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Rather Than Bash the VA, Let’s Learn From Its Successes
A new report by the Veterans Healthcare Policy Institute (VHPI) documents how elements included in many bills passed on Capitol Hill have failed to improve the efficacy of mental health services for our nation’s former service members.1 The authors argue that while these efforts may be well intended, they often compound problems by squandering precious financial resources and stretching an already overtaxed workforce. Clearly, there are shortcomings in the US Department of Veterans Affairs (VA), our nation’s largest integrated health care system, but rather than bash the VA, as the media and Congress tend to favor, let’s learn from its successes as we improve its services.
To do this we must avoid several policy pitfalls. Consider, for example, the VA MISSION Act (38 USC § 1703), which aimed to increase veteran access to quality health care outside the VA system. Studies confirmed that private sector mental health providers are not ready to deliver veteran-specific mental health care.2,3 Indeed, a RAND report found that psychotherapists in the private sector were unlikely to have the requisite skills necessary to deliver high-quality mental health care to service members or veterans.4
The MISSION Act meant to fix this clinical deficit by directing that competency standards be set for non-VA mental health providers who treat veterans for posttraumatic stress disorder (PTSD), traumatic brain injury, and military sexual trauma. But to date, no minimum competency standards have been set for non-VA mental health providers who treat veterans’ common psychological conditions. A license is all they need.
Legislation like the MISSION Act and the newly passed Commander John Scott Hannon Act (38 USC § 101) also assume that veterans who are suicidal or have mental health problems and don’t go to the VA will seek care from private sector providers. Nothing is further from the truth. Many veterans are deeply resistant to seeking mental health care no matter where that care is delivered.4,5 Sometimes veterans believe that mental health problems are a sign of weakness and are loathe to seek help.
To address this issue, the VA pioneered models of integrated mental health and primary care services.6 This means that if a veteran goes to an outpatient primary care clinic at a VA medical facility or community-based outpatient clinic and discusses a mental health or substance abuse problem, the veteran can get immediate care with a mental health provider without making a separate mental health appointment. In addition, the VA already provides routine, annual screening for PTSD and sexual assault as well as depression and substance abuse at all its primary care clinics nationwide. Thanks to comprehensive screening (at a level unknown in most other health care systems) even if a veteran doesn’t spontaneously report a trauma history or mental health distress, VA is able to identify the problem and offer help right in the primary care clinic. This one-stop shopping reduces the shame and stigma of having to make an appointment with a mental health provider, allows treatment to begin immediately, and reduces no shows at follow-up appointments.
Other health care systems are trying to copy the VA model of integrated primary and mental health care, but given our fragmented insurance system, it’s not easy to replicate.7 According to Suzanne Gordon coauthor of the VHPI study, “This VA innovation encourages veterans, socialized by the military to conceal serious mental health problems, to get immediate help. So do many other VA programs, like peer support groups and networks. Legislation needs to strengthen, not weaken, such programs that are almost impossible to reproduce in the private sector.” Outside of VA, mental health challenges faced by veterans likely go undetected, and many veterans will not receive the care that might change, or even save, their lives.
VA best practices include an unprecedented national training initiative on 16 evidence-based psychotherapies that has been in operation for more than a decade.8 These high-quality treatments target debilitating conditions such as depression, PTSD, substance use disorders, insomnia, and chronic pain.9-13 More than 12,700 VA mental health providers have received training in these evidence-based psychotherapies.
“There is no way that non-VA health care systems can ever duplicate the quality of training and supervision that has now been provided, nationally, to VA mental health professionals,” Josef Ruzek, PhD, former Director of the VA National Center for PTSD Dissemination and Training Division told me in a phone conversation (January 14, 2021). “Their program of training and implementation in the very best treatments for veteran mental health conditions stands as an international model of a complex, well-executed, large-scale program to improve mental health service delivery and improve the outcomes of treatment.”
The VA not only paid for the training of these mental health providers, but also contributed substantial efforts to assist in the implementation and sustainability of such practices. These include policy changes mandating their availability at all VA facilities, designation of local evidence-based coordinators at each medical center, and even a nationwide PTSD mentoring program to help PTSD clinic managers make organizational changes and to guide the efforts of any VA clinician seeking advice on how to engage and work with a veteran living with PTSD.14 All these incredible dissemination and implementation endeavors have resulted in a substantial overall decrease in mental health symptoms and substance misuse behaviors and increase in functional outcomes, like improvement in relationship functioning and increase in quality of life for many veterans.
As a trauma psychologist and former VA employee, I urge lawmakers to assure that veterans are not sent to private sector providers who don’t understand their unique needs and aren’t trained to serve them well, and to similarly assure that systems of care are carefully designed to meet the specific needs of veterans.
1. Gordon S, Lemle RB, Ruzek JI, Kudler H. Creating effective solutions, programs, and policies to improve veterans’ mental health care. Published January 2021. Accessed February 22, 2021. https://static1.squarespace.com/static/5b19e25e89c1722037f0fdab/t/6018731daf20e7024b5d6aa8/1612215071469/VHPI_MHReport.pdf
2. Tanielian T, Farris C, Batka C, et al. Ready to serve: community-based provider capacity to deliver culturally competent, quality mental health care to veterans and their families. Published 2014. Accessed February 22, 2021. https://www.rand.org/pubs/research_reports/RR806.html
3. Tanielian T, Farmer CM, Burns RM, et al, Ready or not? Assessing the capacity of New York State health care providers to meet the needs of veterans. Published 2018. Accessed February 22, 2021. https://www.rand.org/pubs/research_reports/RR2298.html.
4. Crawford EF, Elbogen EB, Wagner HR, Kudler H, Calhoun PS, Brancu M, Straits-Troster KA. Surveying treatment preferences in U.S. Iraq-Afghanistan Veterans with PTSD symptoms: a step toward veteran-centered care. J Trauma Stress. 2015 Apr;28(2):118-26. doi: 10.1002/jts.21993.
5. Hoge CW, Castro CA, Messer SC, et al. Combat duty in Iraq and Afghanistan, mental health problems, and barriers to care. New England Journal of Medicine 351:13–22, 2004
6. Zeiss AM, Karlin BE. Integrating mental health and primary care services in the Department of Veterans Affairs Health Care System. J Clin Psychol Med Settings. 2008;15(1):73-78. doi:10.1007/s10880-008-9100-4
7. Gordon S. Wounds of War: How the VA Delivers Health, Healing and Hope to the Nation’s Veterans. Cornell University Press; 2018.
8. Karlin BE, Cross G. From the laboratory to the therapy room: national dissemination and implementation of evidence-based psychotherapies in the U.S. Department of Veterans Affairs Health Care System. Am Psychol. 2014;69(1):19-33. doi:10.1037/a0033888
9. Stewart MO, Raffa SD, Steele JL, et al. National dissemination of interpersonal psychotherapy for depression in veterans: therapist and patient-level outcomes. J Consult Clin Psychol. 2014;82(6):1201-1206. doi:10.1037/a0037410
10. Karlin BE, Ruzek JI, Chard KM, et al. Dissemination of evidence-based psychological treatments for posttraumatic stress disorder in the Veterans Health Administration. J Trauma Stress. 2010;23(6):663-673. doi:10.1002/jts.20588
11. DeMarce JM, Gnys M, Raffa SD, Kumpula M, Karlin BE. Dissemination of cognitive behavioral therapy for substance use disorders in the Department of Veterans Affairs Health Care System: description and evaluation of veteran outcomes [published online ahead of print, 2019 Oct 23]. Subst Abus. 2019;1-7. doi:10.1080/08897077.2019.1674238
12. Karlin BE, Trockel M, Spira AP, Taylor CB, Manber R. National evaluation of the effectiveness of cognitive behavioral therapy for insomnia among older versus younger veterans. Int J Geriatr Psychiatry. 2015;30(3):308-315. doi:10.1002/gps.4143
13. Stewart MO, Karlin BE, Murphy JL, et al. National dissemination of cognitive-behavioral therapy for chronic pain in veterans: therapist and patient-level outcomes. Clin J Pain. 2015;31(8):722-729. doi:10.1097/AJP.0000000000000151
14. Bernardy NC, Hamblen JL, Friedman MJ, Ruzek JI, McFall ME. Implementation of a posttraumatic stress disorder mentoring program to improve treatment services. Psycholog Trauma. 2011;3(3):292-299. doi:10.1037/a0024847
A new report by the Veterans Healthcare Policy Institute (VHPI) documents how elements included in many bills passed on Capitol Hill have failed to improve the efficacy of mental health services for our nation’s former service members.1 The authors argue that while these efforts may be well intended, they often compound problems by squandering precious financial resources and stretching an already overtaxed workforce. Clearly, there are shortcomings in the US Department of Veterans Affairs (VA), our nation’s largest integrated health care system, but rather than bash the VA, as the media and Congress tend to favor, let’s learn from its successes as we improve its services.
To do this we must avoid several policy pitfalls. Consider, for example, the VA MISSION Act (38 USC § 1703), which aimed to increase veteran access to quality health care outside the VA system. Studies confirmed that private sector mental health providers are not ready to deliver veteran-specific mental health care.2,3 Indeed, a RAND report found that psychotherapists in the private sector were unlikely to have the requisite skills necessary to deliver high-quality mental health care to service members or veterans.4
The MISSION Act meant to fix this clinical deficit by directing that competency standards be set for non-VA mental health providers who treat veterans for posttraumatic stress disorder (PTSD), traumatic brain injury, and military sexual trauma. But to date, no minimum competency standards have been set for non-VA mental health providers who treat veterans’ common psychological conditions. A license is all they need.
Legislation like the MISSION Act and the newly passed Commander John Scott Hannon Act (38 USC § 101) also assume that veterans who are suicidal or have mental health problems and don’t go to the VA will seek care from private sector providers. Nothing is further from the truth. Many veterans are deeply resistant to seeking mental health care no matter where that care is delivered.4,5 Sometimes veterans believe that mental health problems are a sign of weakness and are loathe to seek help.
To address this issue, the VA pioneered models of integrated mental health and primary care services.6 This means that if a veteran goes to an outpatient primary care clinic at a VA medical facility or community-based outpatient clinic and discusses a mental health or substance abuse problem, the veteran can get immediate care with a mental health provider without making a separate mental health appointment. In addition, the VA already provides routine, annual screening for PTSD and sexual assault as well as depression and substance abuse at all its primary care clinics nationwide. Thanks to comprehensive screening (at a level unknown in most other health care systems) even if a veteran doesn’t spontaneously report a trauma history or mental health distress, VA is able to identify the problem and offer help right in the primary care clinic. This one-stop shopping reduces the shame and stigma of having to make an appointment with a mental health provider, allows treatment to begin immediately, and reduces no shows at follow-up appointments.
Other health care systems are trying to copy the VA model of integrated primary and mental health care, but given our fragmented insurance system, it’s not easy to replicate.7 According to Suzanne Gordon coauthor of the VHPI study, “This VA innovation encourages veterans, socialized by the military to conceal serious mental health problems, to get immediate help. So do many other VA programs, like peer support groups and networks. Legislation needs to strengthen, not weaken, such programs that are almost impossible to reproduce in the private sector.” Outside of VA, mental health challenges faced by veterans likely go undetected, and many veterans will not receive the care that might change, or even save, their lives.
VA best practices include an unprecedented national training initiative on 16 evidence-based psychotherapies that has been in operation for more than a decade.8 These high-quality treatments target debilitating conditions such as depression, PTSD, substance use disorders, insomnia, and chronic pain.9-13 More than 12,700 VA mental health providers have received training in these evidence-based psychotherapies.
“There is no way that non-VA health care systems can ever duplicate the quality of training and supervision that has now been provided, nationally, to VA mental health professionals,” Josef Ruzek, PhD, former Director of the VA National Center for PTSD Dissemination and Training Division told me in a phone conversation (January 14, 2021). “Their program of training and implementation in the very best treatments for veteran mental health conditions stands as an international model of a complex, well-executed, large-scale program to improve mental health service delivery and improve the outcomes of treatment.”
The VA not only paid for the training of these mental health providers, but also contributed substantial efforts to assist in the implementation and sustainability of such practices. These include policy changes mandating their availability at all VA facilities, designation of local evidence-based coordinators at each medical center, and even a nationwide PTSD mentoring program to help PTSD clinic managers make organizational changes and to guide the efforts of any VA clinician seeking advice on how to engage and work with a veteran living with PTSD.14 All these incredible dissemination and implementation endeavors have resulted in a substantial overall decrease in mental health symptoms and substance misuse behaviors and increase in functional outcomes, like improvement in relationship functioning and increase in quality of life for many veterans.
As a trauma psychologist and former VA employee, I urge lawmakers to assure that veterans are not sent to private sector providers who don’t understand their unique needs and aren’t trained to serve them well, and to similarly assure that systems of care are carefully designed to meet the specific needs of veterans.
A new report by the Veterans Healthcare Policy Institute (VHPI) documents how elements included in many bills passed on Capitol Hill have failed to improve the efficacy of mental health services for our nation’s former service members.1 The authors argue that while these efforts may be well intended, they often compound problems by squandering precious financial resources and stretching an already overtaxed workforce. Clearly, there are shortcomings in the US Department of Veterans Affairs (VA), our nation’s largest integrated health care system, but rather than bash the VA, as the media and Congress tend to favor, let’s learn from its successes as we improve its services.
To do this we must avoid several policy pitfalls. Consider, for example, the VA MISSION Act (38 USC § 1703), which aimed to increase veteran access to quality health care outside the VA system. Studies confirmed that private sector mental health providers are not ready to deliver veteran-specific mental health care.2,3 Indeed, a RAND report found that psychotherapists in the private sector were unlikely to have the requisite skills necessary to deliver high-quality mental health care to service members or veterans.4
The MISSION Act meant to fix this clinical deficit by directing that competency standards be set for non-VA mental health providers who treat veterans for posttraumatic stress disorder (PTSD), traumatic brain injury, and military sexual trauma. But to date, no minimum competency standards have been set for non-VA mental health providers who treat veterans’ common psychological conditions. A license is all they need.
Legislation like the MISSION Act and the newly passed Commander John Scott Hannon Act (38 USC § 101) also assume that veterans who are suicidal or have mental health problems and don’t go to the VA will seek care from private sector providers. Nothing is further from the truth. Many veterans are deeply resistant to seeking mental health care no matter where that care is delivered.4,5 Sometimes veterans believe that mental health problems are a sign of weakness and are loathe to seek help.
To address this issue, the VA pioneered models of integrated mental health and primary care services.6 This means that if a veteran goes to an outpatient primary care clinic at a VA medical facility or community-based outpatient clinic and discusses a mental health or substance abuse problem, the veteran can get immediate care with a mental health provider without making a separate mental health appointment. In addition, the VA already provides routine, annual screening for PTSD and sexual assault as well as depression and substance abuse at all its primary care clinics nationwide. Thanks to comprehensive screening (at a level unknown in most other health care systems) even if a veteran doesn’t spontaneously report a trauma history or mental health distress, VA is able to identify the problem and offer help right in the primary care clinic. This one-stop shopping reduces the shame and stigma of having to make an appointment with a mental health provider, allows treatment to begin immediately, and reduces no shows at follow-up appointments.
Other health care systems are trying to copy the VA model of integrated primary and mental health care, but given our fragmented insurance system, it’s not easy to replicate.7 According to Suzanne Gordon coauthor of the VHPI study, “This VA innovation encourages veterans, socialized by the military to conceal serious mental health problems, to get immediate help. So do many other VA programs, like peer support groups and networks. Legislation needs to strengthen, not weaken, such programs that are almost impossible to reproduce in the private sector.” Outside of VA, mental health challenges faced by veterans likely go undetected, and many veterans will not receive the care that might change, or even save, their lives.
VA best practices include an unprecedented national training initiative on 16 evidence-based psychotherapies that has been in operation for more than a decade.8 These high-quality treatments target debilitating conditions such as depression, PTSD, substance use disorders, insomnia, and chronic pain.9-13 More than 12,700 VA mental health providers have received training in these evidence-based psychotherapies.
“There is no way that non-VA health care systems can ever duplicate the quality of training and supervision that has now been provided, nationally, to VA mental health professionals,” Josef Ruzek, PhD, former Director of the VA National Center for PTSD Dissemination and Training Division told me in a phone conversation (January 14, 2021). “Their program of training and implementation in the very best treatments for veteran mental health conditions stands as an international model of a complex, well-executed, large-scale program to improve mental health service delivery and improve the outcomes of treatment.”
The VA not only paid for the training of these mental health providers, but also contributed substantial efforts to assist in the implementation and sustainability of such practices. These include policy changes mandating their availability at all VA facilities, designation of local evidence-based coordinators at each medical center, and even a nationwide PTSD mentoring program to help PTSD clinic managers make organizational changes and to guide the efforts of any VA clinician seeking advice on how to engage and work with a veteran living with PTSD.14 All these incredible dissemination and implementation endeavors have resulted in a substantial overall decrease in mental health symptoms and substance misuse behaviors and increase in functional outcomes, like improvement in relationship functioning and increase in quality of life for many veterans.
As a trauma psychologist and former VA employee, I urge lawmakers to assure that veterans are not sent to private sector providers who don’t understand their unique needs and aren’t trained to serve them well, and to similarly assure that systems of care are carefully designed to meet the specific needs of veterans.
1. Gordon S, Lemle RB, Ruzek JI, Kudler H. Creating effective solutions, programs, and policies to improve veterans’ mental health care. Published January 2021. Accessed February 22, 2021. https://static1.squarespace.com/static/5b19e25e89c1722037f0fdab/t/6018731daf20e7024b5d6aa8/1612215071469/VHPI_MHReport.pdf
2. Tanielian T, Farris C, Batka C, et al. Ready to serve: community-based provider capacity to deliver culturally competent, quality mental health care to veterans and their families. Published 2014. Accessed February 22, 2021. https://www.rand.org/pubs/research_reports/RR806.html
3. Tanielian T, Farmer CM, Burns RM, et al, Ready or not? Assessing the capacity of New York State health care providers to meet the needs of veterans. Published 2018. Accessed February 22, 2021. https://www.rand.org/pubs/research_reports/RR2298.html.
4. Crawford EF, Elbogen EB, Wagner HR, Kudler H, Calhoun PS, Brancu M, Straits-Troster KA. Surveying treatment preferences in U.S. Iraq-Afghanistan Veterans with PTSD symptoms: a step toward veteran-centered care. J Trauma Stress. 2015 Apr;28(2):118-26. doi: 10.1002/jts.21993.
5. Hoge CW, Castro CA, Messer SC, et al. Combat duty in Iraq and Afghanistan, mental health problems, and barriers to care. New England Journal of Medicine 351:13–22, 2004
6. Zeiss AM, Karlin BE. Integrating mental health and primary care services in the Department of Veterans Affairs Health Care System. J Clin Psychol Med Settings. 2008;15(1):73-78. doi:10.1007/s10880-008-9100-4
7. Gordon S. Wounds of War: How the VA Delivers Health, Healing and Hope to the Nation’s Veterans. Cornell University Press; 2018.
8. Karlin BE, Cross G. From the laboratory to the therapy room: national dissemination and implementation of evidence-based psychotherapies in the U.S. Department of Veterans Affairs Health Care System. Am Psychol. 2014;69(1):19-33. doi:10.1037/a0033888
9. Stewart MO, Raffa SD, Steele JL, et al. National dissemination of interpersonal psychotherapy for depression in veterans: therapist and patient-level outcomes. J Consult Clin Psychol. 2014;82(6):1201-1206. doi:10.1037/a0037410
10. Karlin BE, Ruzek JI, Chard KM, et al. Dissemination of evidence-based psychological treatments for posttraumatic stress disorder in the Veterans Health Administration. J Trauma Stress. 2010;23(6):663-673. doi:10.1002/jts.20588
11. DeMarce JM, Gnys M, Raffa SD, Kumpula M, Karlin BE. Dissemination of cognitive behavioral therapy for substance use disorders in the Department of Veterans Affairs Health Care System: description and evaluation of veteran outcomes [published online ahead of print, 2019 Oct 23]. Subst Abus. 2019;1-7. doi:10.1080/08897077.2019.1674238
12. Karlin BE, Trockel M, Spira AP, Taylor CB, Manber R. National evaluation of the effectiveness of cognitive behavioral therapy for insomnia among older versus younger veterans. Int J Geriatr Psychiatry. 2015;30(3):308-315. doi:10.1002/gps.4143
13. Stewart MO, Karlin BE, Murphy JL, et al. National dissemination of cognitive-behavioral therapy for chronic pain in veterans: therapist and patient-level outcomes. Clin J Pain. 2015;31(8):722-729. doi:10.1097/AJP.0000000000000151
14. Bernardy NC, Hamblen JL, Friedman MJ, Ruzek JI, McFall ME. Implementation of a posttraumatic stress disorder mentoring program to improve treatment services. Psycholog Trauma. 2011;3(3):292-299. doi:10.1037/a0024847
1. Gordon S, Lemle RB, Ruzek JI, Kudler H. Creating effective solutions, programs, and policies to improve veterans’ mental health care. Published January 2021. Accessed February 22, 2021. https://static1.squarespace.com/static/5b19e25e89c1722037f0fdab/t/6018731daf20e7024b5d6aa8/1612215071469/VHPI_MHReport.pdf
2. Tanielian T, Farris C, Batka C, et al. Ready to serve: community-based provider capacity to deliver culturally competent, quality mental health care to veterans and their families. Published 2014. Accessed February 22, 2021. https://www.rand.org/pubs/research_reports/RR806.html
3. Tanielian T, Farmer CM, Burns RM, et al, Ready or not? Assessing the capacity of New York State health care providers to meet the needs of veterans. Published 2018. Accessed February 22, 2021. https://www.rand.org/pubs/research_reports/RR2298.html.
4. Crawford EF, Elbogen EB, Wagner HR, Kudler H, Calhoun PS, Brancu M, Straits-Troster KA. Surveying treatment preferences in U.S. Iraq-Afghanistan Veterans with PTSD symptoms: a step toward veteran-centered care. J Trauma Stress. 2015 Apr;28(2):118-26. doi: 10.1002/jts.21993.
5. Hoge CW, Castro CA, Messer SC, et al. Combat duty in Iraq and Afghanistan, mental health problems, and barriers to care. New England Journal of Medicine 351:13–22, 2004
6. Zeiss AM, Karlin BE. Integrating mental health and primary care services in the Department of Veterans Affairs Health Care System. J Clin Psychol Med Settings. 2008;15(1):73-78. doi:10.1007/s10880-008-9100-4
7. Gordon S. Wounds of War: How the VA Delivers Health, Healing and Hope to the Nation’s Veterans. Cornell University Press; 2018.
8. Karlin BE, Cross G. From the laboratory to the therapy room: national dissemination and implementation of evidence-based psychotherapies in the U.S. Department of Veterans Affairs Health Care System. Am Psychol. 2014;69(1):19-33. doi:10.1037/a0033888
9. Stewart MO, Raffa SD, Steele JL, et al. National dissemination of interpersonal psychotherapy for depression in veterans: therapist and patient-level outcomes. J Consult Clin Psychol. 2014;82(6):1201-1206. doi:10.1037/a0037410
10. Karlin BE, Ruzek JI, Chard KM, et al. Dissemination of evidence-based psychological treatments for posttraumatic stress disorder in the Veterans Health Administration. J Trauma Stress. 2010;23(6):663-673. doi:10.1002/jts.20588
11. DeMarce JM, Gnys M, Raffa SD, Kumpula M, Karlin BE. Dissemination of cognitive behavioral therapy for substance use disorders in the Department of Veterans Affairs Health Care System: description and evaluation of veteran outcomes [published online ahead of print, 2019 Oct 23]. Subst Abus. 2019;1-7. doi:10.1080/08897077.2019.1674238
12. Karlin BE, Trockel M, Spira AP, Taylor CB, Manber R. National evaluation of the effectiveness of cognitive behavioral therapy for insomnia among older versus younger veterans. Int J Geriatr Psychiatry. 2015;30(3):308-315. doi:10.1002/gps.4143
13. Stewart MO, Karlin BE, Murphy JL, et al. National dissemination of cognitive-behavioral therapy for chronic pain in veterans: therapist and patient-level outcomes. Clin J Pain. 2015;31(8):722-729. doi:10.1097/AJP.0000000000000151
14. Bernardy NC, Hamblen JL, Friedman MJ, Ruzek JI, McFall ME. Implementation of a posttraumatic stress disorder mentoring program to improve treatment services. Psycholog Trauma. 2011;3(3):292-299. doi:10.1037/a0024847
Anticipating the care adolescents will need
Adolescents are an increasingly diverse population reflecting changes in the racial, ethnic, and geopolitical milieus of the United States. The World Health Organization classifies adolescence as ages 10 to 19 years.1 However, given the complexity of adolescent development physically, behaviorally, emotionally, and socially, others propose that adolescence may extend to age 24.2
Recognizing the specific challenges adolescents face is key to providing comprehensive longitudinal health care. Moreover, creating an environment of trust helps to ensure open 2-way communication that can facilitate anticipatory guidance.
Our review focuses on common adolescent issues, including injury from vehicles and firearms, tobacco and substance misuse, obesity, behavioral health, sexual health, and social media use. We discuss current trends and recommend strategies to maximize health and wellness.
Start by framing the visit
Confidentiality
Laws governing confidentiality in adolescent health care vary by state. Be aware of the laws pertaining to your practice setting. In addition, health care facilities may have their own policies regarding consent and confidentiality in adolescent care. Discuss confidentiality with both an adolescent and the parent/guardian at the initial visit. And, to help avoid potential misunderstandings, let them know in advance what will (and will not) be divulged.
The American Academy of Pediatrics has developed a useful tip sheet regarding confidentiality laws (www.aap.org/en-us/advocacy-and-policy/aap-health-initiatives/healthy-foster-care-america/Documents/Confidentiality_Laws.pdf). Examples of required (conditional) disclosure include abuse and suicidal or homicidal ideations. Patients should understand that sexually transmitted infections (STIs) are reportable to public health authorities and that potentially injurious behaviors to self or others (eg, excessive drinking prior to driving) may also warrant disclosure(TABLE 13).
Privacy and general visit structure
Create a safe atmosphere where adolescents can discuss personal issues without fear of repercussion or judgment. While parents may prefer to be present during the visit, allowing for time to visit independently with an adolescent offers the opportunity to reinforce issues of privacy and confidentiality. Also discuss your office policies regarding electronic communication, phone communication, and relaying test results.
A useful paradigm for organizing a visit for routine adolescent care is to use an expanded version of the HEADSS mnemonic (TABLE 24,5), which includes questions about an adolescent’s Home, Education, Activities, Drug and alcohol use, Sexual behavior, Suicidality and depression, and other topics. Other validated screening tools include RAAPS (Rapid Adolescent Prevention Screening)6 (www.possibilitiesforchange.com/raaps/); the Guidelines for Adolescent Preventive Services7; and the Bright Futures recommendations for preventive care from the American Academy of Pediatrics.8 Below, we consider important topics addressed with the HEADSS approach.
Continue to: Injury from vehicles and firearms
Injury from vehicles and firearms
Motor vehicle accidents and firearm wounds are the 2 leading causes of adolescent injury. In 2016, of the more than 20,000 deaths in children and adolescents (ages 1-19 years), 20% were due to motor vehicle accidents (4074) and 15% were a result of firearm-related injuries (3143). Among firearm-related deaths, 60% were homicides, 35% were suicides, and 4% were due to accidental discharge.9 The rate of firearm-related deaths among American teens is 36 times greater than that of any other developed nation.9 Currently, 1 of every 3 US households with children younger than 18 has a firearm. Data suggest that in 43% of these households, the firearm is loaded and kept in an unlocked location.10
To aid anticipatory guidance, ask adolescents about firearm and seat belt use, drinking and driving, and suicidal thoughts (TABLE 24,5). Advise them to always wear seat belts whether driving or riding as a passenger. They should never drink and drive (or get in a car with someone who has been drinking). Advise parents that if firearms are present in the household, they should be kept in a secure, locked location. Weapons should be separated from ammunition and safety mechanisms should be engaged on all devices.
Tobacco and substance misuse
Tobacco use, the leading preventable cause of death in the United States,11 is responsible for more deaths than alcohol, motor vehicle accidents, suicides, homicides, and HIV disease combined.12 Most tobacco-associated mortality occurs in individuals who began smoking before the age of 18.12 Individuals who start smoking early are also more likely to continue smoking through adulthood.
Encouragingly, tobacco use has declined significantly among adolescents over the past several decades. Roughly 1 in 25 high school seniors reports daily tobacco use.13 Adolescent smoking behaviors are also changing dramatically with the increasing popularity of electronic cigarettes (“vaping”). Currently, more adolescents vape than smoke cigarettes.13 Vaping has additional health risks including toxic lung injury.
Multiple resources can help combat tobacco and nicotine use in adolescents. The US Preventive Services Task Force recommends that primary care clinicians intervene through education or brief counselling to prevent initiation of tobacco use in school-aged children and adolescents.14 Ask teens about tobacco and electronic cigarette use and encourage them to quit when use is acknowledged. Other helpful office-based tools are the “Quit Line” 800-QUIT-NOW and texting “Quit” to 47848. Smokefree teen (https://teen.smokefree.gov/) is a website that reviews the risks of tobacco and nicotine use and provides age-appropriate cessation tools and tips (including a smartphone app and a live-chat feature). Other useful information is available in a report from the Surgeon General on preventing tobacco use among young adults.15
Continue to: Alcohol use
Alcohol use. Three in 5 high school students report ever having used alcohol.13 As with tobacco, adolescent alcohol use has declined over the past decade. However, binge drinking (≥ 5 drinks on 1 occasion for males; ≥ 4 drinks on 1 occasion for females) remains a common high-risk behavior among adolescents (particularly college students). Based on the Monitoring the Future Survey, 1 in 6 high school seniors reported binge drinking in the past 2 weeks.13 While historically more common among males, rates of binge drinking are now basically similar between male and female adolescents.13
The National Institute on Alcohol Abuse and Alcoholism has a screening and intervention guide specifically for adolescents.16
Illicit drug use. Half of adolescents report using an illicit drug by their senior year in high school.13 Marijuana is the most commonly used substance, and laws governing its use are rapidly changing across the United States. Marijuana is illegal in 10 states and legal in 10 states (and the District of Columbia). The remaining states have varying policies on the medical use of marijuana and the decriminalization of marijuana. In addition, cannabinoid (CBD) products are increasingly available. Frequent cannabis use in adolescence has an adverse impact on general executive function (compared with adult users) and learning.17 Marijuana may serve as a gateway drug in the abuse of other substances,18 and its use should be strongly discouraged in adolescents.
Of note, there has been a sharp rise in the illicit use of prescription drugs, particularly opioids, creating a public health emergency across the United States.19 In 2015, more than 4000 young people, ages 15 to 24, died from a drug-related overdose (> 50% of these attributable to opioids).20 Adolescents with a history of substance abuse and behavioral illness are at particular risk. Many adolescents who misuse opioids and other prescription drugs obtain them from friends and relatives.21
The Substance Abuse and Mental Health Services Administration (SAMHSA) recommends universal screening of adolescents for substance abuse. This screening should be accompanied by a brief intervention to prevent, mitigate, or eliminate substance use, or a referral to appropriate treatment sources. This process of screening, brief intervention, and referral to treatment (SBIRT) is recommended as part of routine health care.22
Continue to: Obesity and physical activity
Obesity and physical activity
The percentage of overweight and obese adolescents in the United States has more than tripled over the past 40 years,23 and 1 in 5 US adolescents is obese.23 Obese teens are at higher risk for multiple chronic diseases, including type 2 diabetes, sleep apnea, and heart disease.24 They are also more likely to be bullied and to have poor self-esteem.25 Only 1 in 5 American high school students engages in 60 or more minutes of moderate-to-vigorous physical activity on 5 or more days per week.26
Regular physical activity is, of course, beneficial for cardiorespiratory fitness, bone health, weight control, and improved indices of behavioral health.26 Adolescents who are physically active consistently demonstrate better school attendance and grades.17 Higher levels of physical fitness are also associated with improved overall cognitive performance.24
General recommendations. The Department of Health and Human Services recommends that adolescents get at least 60 minutes of mostly moderate physical activity every day.26 Encourage adolescents to engage in vigorous physical activity (heavy breathing, sweating) at least 3 days a week. As part of their physical activity patterns, adolescents should also engage in muscle-strengthening and bone-strengthening activities on at least 3 days per week.
Behavioral health
As young people develop their sense of personal identity, they also strive for independence. It can be difficult, at times, to differentiate normal adolescent rebellion from true mental illness. An estimated 17% to 19% of adolescents meet criteria for mental illness, and about 7% have a severe psychiatric disorder.27 Only one-third of adolescents with mental illness receive any mental health services.28
Depression. The 1-year incidence of major depression in adolescents is 3% to 4%, and the lifetime prevalence of depressive symptoms is 25% in all high school students.27 Risk factors include ethnic minority status, poor self-esteem, poor health, recent personal crisis, insomnia, and alcohol/substance abuse. Depression in adolescent girls is correlated with becoming sexually active at a younger age, failure to use contraception, having an STI, and suicide attempts. Depressed boys are more likely to have unprotected intercourse and participate in physical fights.29 Depressed teens have a 2- to 3-fold greater risk for behavioral disorders, anxiety, and attention-deficit/hyperactivity disorder (ADHD).30
Continue to: Suicide
Suicide. Among individuals 15 to 29 years of age, suicide is the second leading cause of death globally, with an annual incidence of 11 to 15 per 100,000.31 Suicide attempts are 10 to 20 times more common than completed suicide.31 Males are more likely than females to die by suicide,32 and boys with a history of attempted suicide have a 30-fold increased risk of subsequent successful suicide.31 Hanging, drug poisoning, and firearms (particularly for males) are the most common means of suicide in adolescents. More than half of adolescents dying by suicide have coexisting depression.31
Characteristics associated with suicidal behaviors in adolescents include impulsivity, poor problem-solving skills, and dichotomous thinking.31 There may be a genetic component as well. In 1 of 5 teenage suicides, a precipitating life event such as the break-up of a relationship, cyber-bullying, or peer rejection is felt to contribute.31
ADHD. The prevalence of ADHD is 7% to 9% in US school-aged children.33 Boys more commonly exhibit hyperactive behaviors, while girls have more inattention. Hyperactivity often diminishes in teens, but inattention and impulsivity persist. Sequelae of ADHD include high-risk sexual behaviors, motor vehicle accidents, incarceration, and substance abuse.34 Poor self-esteem, suicidal ideation, smoking, and obesity are also increased.34 ADHD often persists into adulthood, with implications for social relationships and job performance.34
Eating disorders. The distribution of eating disorders is now known to increasingly include more minorities and males, the latter representing 5% to 10% of cases.35 Eating disorders show a strong genetic tendency and appear to be accelerated by puberty. The most common eating disorder (diagnosed in 0.8%-14% of teens) is eating disorder not otherwise specified (NOS).35 Anorexia nervosa is diagnosed in 0.5% of adolescent girls, and bulimia nervosa in 1% to 2%—particularly among athletes and performers.35 Unanticipated loss of weight, amenorrhea, excessive concern about weight, and deceleration in height/weight curves are potential indicators of an eating disorder. When identified, eating disorders are best managed by a trusted family physician, acting as a coordinator of a multidisciplinary team.
Sexual health
Girls begin to menstruate at an average age of 12, and it takes about 4 years for them to reach reproductive maturity.36 Puberty has been documented to start at younger ages over the past 30 years, likely due to an increase in average body mass index and a decrease in levels of physical activity.37 Girls with early maturation are often insecure and self-conscious, with higher levels of psychological distress.38 In boys, the average age for spermarche (first ejaculation) is 13.39 Boys who mature early tend to be taller, be more confident, and express a good body image.40 Those who have early puberty are more likely to be sexually active or participate in high-risk behaviors.41
Continue to: Pregnancy and contraception
Pregnancy and contraception
Over the past several decades, more US teens have been abstaining from sexual intercourse or have been using effective forms of birth control, particularly condoms and long-acting reversible contraceptives (LARCs).42 Teenage birth rates in girls ages 15 to 19 have declined significantly since the 1980s.42 Despite this, the teenage birth rate in the United States remains higher than in other industrialized nations, and most teen pregnancies are unintended.
There are numerous interventions to reduce teen pregnancy, including sex education, contraceptive counseling, the use of mobile apps that track a user’s monthly fertility cycle or issue reminders to take oral contraceptives,45 and the liberal distribution of contraceptives and condoms. The Contraceptive CHOICE Project shows that providing free (or low-cost) LARCs influences young women to choose these as their preferred contraceptive method.46 Other programs specifically empower girls to convince partners to use condoms and to resist unwanted sexual advances or intimate partner violence.
Adolescents prefer to have their health care providers address the topic of sexual health. Teens are more likely to share information with providers if asked directly about sexual behaviors.47TABLE 24,5 offers tips for anticipatory guidance and potential ways to frame questions with adolescents in this context. State laws vary with regard to the ability of minors to seek contraception, pregnancy testing, or care/screening for STIs without parental consent. Contraceptive counseling combined with effective screening decrease the incidence of STIs and pelvic inflammatory disease for sexually active teens.48
Sexually transmitted infections
Young adolescents often have a limited ability to imagine consequences related to specific actions. In general, there is also an increased desire to engage in experimental behaviors as an expression of developing autonomy, which may expose them to STIs. About half of all STIs contracted in the United States occur in individuals 15 to 24 years of age.49 Girls are at particular risk for the sequelae of these infections, including cervical dysplasia and infertility. Many teens erroneously believe that sexual activities other than intercourse decrease their risk of contracting an STI.50
Human papillomavirus (HPV) infection is the most common STI in adolescence.51 In most cases, HPV is transient and asymptomatic. Oncogenic strains may cause cervical cancer or cancers of the anogenital or oropharyngeal systems. Due to viral latency, it is not recommended to perform HPV typing in men or in women younger than 30 years of age; however, Pap tests are recommended every 3 years for women ages 21 to 29. Primary care providers are pivotal in the public health struggle to prevent HPV infection.
Continue to: Universal immunization of all children...
Universal immunization of all children older than 11 years of age against HPV is strongly advised as part of routine well-child care. Emphasize the proven role of HPV vaccination in preventing cervical52 and oropharyngeal53 cancers. And be prepared to address concerns raised by parents in the context of vaccine safety and the initiation of sexual behaviors (www.cdc.gov/hpv/hcp/answering-questions.html).
Chlamydia is the second most common STI in the United States, usually occurring in individuals younger than 24.54 The CDC estimates that more than 3 million new chlamydial infections occur yearly. These infections are often asymptomatic, particularly in females, but may cause urethritis, cervicitis, epididymitis, proctitis, or pelvic inflammatory disease. Indolent chlamydial infection is the leading cause of tubal infertility in women.54 Routine annual screening for chlamydia is recommended for all sexually active females ≤ 25 years (and for older women with specific risks).55 Annual screening is also recommended for men who have sex with men (MSM).55
Chlamydial infection may be diagnosed with first-catch urine sampling (men or women), urethral swab (men), endocervical swab (women), or self-collected vaginal swab. Nucleic acid amplification testing is the most sensitive test that is widely available.56 First-line treatment includes either azithromycin (1 g orally, single dose) or doxycycline (100 mg orally, twice daily for 7 days).56
Gonorrhea. In 2018, there were more than 500,000 annual cases of gonorrhea, with the majority occurring in those between 15 and 24 years of age.57 Gonorrhea may increase rates of HIV infection transmission up to 5-fold.57 As more adolescents practice oral sex, cases of pharyngeal gonorrhea (and oropharyngeal HPV) have increased. Symptoms of urethritis occur more frequently in men. Screening is recommended for all sexually active women younger than 25.56 Importantly, the organism Neisseria gonorrhoeae has developed significant antibiotic resistance over the past decade. The CDC currently recommends dual therapy for the treatment of gonorrhea using 250 mg of intramuscular ceftriaxone and 1 g of oral azithromycin.56
Syphilis. Rates of syphilis are increasing among individuals ages 15 to 24.51 Screening is particularly recommended for MSM and individuals infected with HIV. Benzathine penicillin G, 50,000 U/kg IM, remains the treatment of choice.56
Continue to: HIV
HIV. Globally, HIV impacts young people disproportionately. HIV infection also facilitates infection with other STIs. In the United States, the highest burden of HIV infection is borne by young MSM, with prevalence among those 18 to 24 years old varying between 26% to 30% (black) and 3% to 5.5% (non-Hispanic white).51 The use of emtricitabine/tenofovir disoproxil fumarate for pre-exposure prophylaxis (PrEP) has recently been approved for the prevention of HIV. PrEP reduces risk by up to 92% for MSM and transgender women.58
Sexual identity
One in 10 high school students self-identifies as “nonheterosexual,” and 1 in 15 reports same-sex sexual contact.59 The term LGBTQ+ includes the communities of lesbian, gay, bisexual, transgender, transsexual, queer, questioning, intersex, and asexual individuals. Developing a safe sense of sexual identity is fundamental to adolescent psychological development, and many adolescents struggle to develop a positive sexual identity. Suicide rates and self-harm behaviors among LGBTQ+ adolescents can be 4 times higher than among their heterosexual peers.60 Rates of mood disorders, substance abuse, and high-risk sexual behaviors are also increased in the LGBTQ+ population.61
The LGBTQ+ community often seeks health care advice and affirmation from primary care providers. Resources to enhance this care are available at www.lgbthealtheducation.org.
Social media
Adolescents today have more media exposure than any prior generation, with smartphone and computer use increasing exponentially. Most (95%) teens have access to a smartphone,62 45% describe themselves as constantly connected to the Internet, and 14% feel that social media is “addictive.”62 Most manage their social media portfolio on multiple sites. Patterns of adolescents' online activities show that boys prefer online gaming, while girls tend to spend more time on social networking.62
Whether extensive media use is psychologically beneficial or deleterious has been widely debated. Increased time online correlates with decreased levels of physical activity.63 And sleep disturbances have been associated with excessive screen time and the presence of mobile devices in the bedroom.64 The use of social media prior to bedtime also has an adverse impact on academic performance—particularly for girls. This adverse impact on academics persists after correcting for daytime sleepiness, body mass index, and number of hours spent on homework.64
Continue to: Due to growing concerns...
Due to growing concerns about the risks of social media in children and adolescents, the American Academy of Pediatrics has developed the Family Media Plan (www.healthychildren.org/English/media/Pages/default.aspx). Some specific questions that providers may ask are outlined in TABLE 3.64 The Family Media Plan can provide age-specific guidelines to assist parents or caregivers in answering these questions.
Cyber-bullying. One in 3 adolescents (primarily female) has been a victim of cyber-bullying.65 Sadly, 1 in 5 teens has received some form of electronic sexual solicitation.66 The likelihood of unsolicited stranger contact correlates with teens’ online habits and the amount of information disclosed. Predictors include female sex, visiting chat rooms, posting photos, and disclosing personal information. Restricting computer use to an area with parental supervision or installing monitoring programs does not seem to exert any protective influence on cyber-bullying or unsolicited stranger contact.65 While 63% of cyber-bullying victims feel upset, embarrassed, or stressed by these contacts,66 few events are actually reported. To address this, some states have adopted laws adding cyber-bullying to school disciplinary codes.
Negative health impacts associated with cyber-bullying include anxiety, sadness, and greater difficulty in concentrating on school work.65 Victims of bullying are more likely to have school disciplinary actions and depression and to be truant or to carry weapons to school.66 Cyber-bullying is uniquely destructive due to its ubiquitous presence. A sense of relative anonymity online may encourage perpetrators to act more cruelly, with less concern for punishment.
Young people are also more likely to share passwords as a sign of friendship. This may result in others assuming their identity online. Adolescents rarely disclose bullying to parents or other adults, fearing restriction of Internet access, and many of them think that adults may downplay the seriousness of the events.66
CORRESPONDENCE
Mark B. Stephens, MD, Penn State Health Medical Group, 1850 East Park Avenue, State College, PA 16803; mstephens3@pennstatehealth.psu.edu.
1. World Health Organization. Adolescent health. Accessed February 23, 2021. www.who.int/maternal_child_adolescent/adolescence/en/
2. Sawyer SM, Azzopardi PS, Wickremarathne D, et al. The age of adolescence. Lancet Child Adolesc Health. 2018;2:223-228.
3. Pathak PR, Chou A. Confidential care for adoloscents in the U.S. healthcare system. J Patient Cent Res Rev. 2019;6:46-50.
4. AMA Journal of Ethics. HEADSS: the “review of systems” for adolescents. Accessed February 23, 2021. https://journalofethics.ama-assn.org/article/headss-review-systems-adolescents/2005-03
5. Cohen E, MacKenzie RG, Yates GL. HEADSS, a psychosocial risk assessment instrument: implications for designing effective intervention programs for runaway youth. J Adolesc Health. 1991;12:539-544.
6. Possibilities for Change. Rapid Adolescent Prevention Screening (RAAPS). Accessed February 23, 2021. www.possibilitiesforchange.com/raaps/
7. Elster AB, Kuznets NJ. AMA Guidelines for Adolescent Preventive Services (GAPS): Recommendations and Rationale. Williams & Wilkins; 1994.
8. AAP. Engaging patients and families - periodicity schedule. Accessed February 23, 2021. www.aap.org/en-us/professional-resources/practice-support/Pages/PeriodicitySchedule.aspx
9. Cunningham RM, Walton MA, Carter PM. The major causes of death in children and adolescents in the United States. N Eng J Med. 2018;379:2468-2475.
10. Schuster MA, Franke TM, Bastian AM, et al. Firearm storage patterns in US homes with children. Am J Public Health. 2000;90:588-594.
11. Mokdad AH, Marks JS, Stroup DF, et al. Actual causes of death in the United States. JAMA. 2004;291:1238-1245.
12. HHS. Health consequences of smoking, surgeon general fact sheet. Accessed February 23, 2021. www.hhs.gov/surgeongeneral/reports-and-publications/tobacco/consequences-smoking-factsheet/index.html
13. Johnston LD, Miech RA, O’Malley PM, et al. Monitoring the future: national survey results on drug use, 1975-2017. The University of Michigan. 2018. Accessed February 23, 2021. https://eric.ed.gov/?id=ED589762
14. US Preventive Services Task Force. Prevention and cessation of tobacco use in children and adolescents: primary care interventions. Accessed February 23, 2021. www.uspreventiveservicestaskforce.org/uspstf/recommendation/tobacco-and-nicotine-use-prevention-in-children-and-adolescents-primary-care-interventions
15. HHS. Preventing Tobacco Use Among Youth and Young Adults: A Report of the Surgeon General. Atlanta, GA: HHS, CDC, NCCDPHP, OSH; 2012. Accessed February 23, 2021. www.ncbi.nlm.nih.gov/books/NBK99237/
16. NIH. Alcohol screening and brief intervention for youth: a pocket guide. Accessed February 23, 2021. https://pubs.niaaa.nih.gov/publications/Practitioner/YouthGuide/YouthGuidePocket.pdf
17. Gorey C, Kuhns L, Smaragdi E, et al. Age-related differences in the impact of cannabis use on the brain and cognition: a systematic review. Eur Arch Psychiatry Clin Neurosci. 2019;269:37-58.
18. Secades-Villa R, Garcia-Rodriguez O, Jin CJ, et al. Probability and predictors of the cannabis gateway effect: a national study. Int J Drug Policy. 2015;26:135-142.
19. Kann L, McManus T, Harris WA, et al. Youth risk behavior surveillance—United States, 2017. MMWR Surveill Summ. 2018;67:1-114.
20. NIH. Drug overdoses in youth. How do drug overdoses happen?. Accessed February 23, 2021. https://teens.drugabuse.gov/drug-facts/drug-overdoses-youth
21. Branstetter SA, Low S, Furman W. The influence of parents and friends on adolescent substance use: a multidimensional approach. J Subst Use. 2011;162:150-160.
22. AAP. Committee on Substance Use and Prevention. Substance use screening, brief intervention, and referral to treatment. Pediatrics. 2016;138:e20161210.
23. Hales CM, Carroll MD, Fryar CD, et al. Prevalence of obesity among adults and youth: United States, 2015–2016. NCHS Data Brief. 2017;288:1-8.
24. Halfon N, Larson K, Slusser W. Associations between obesity and comorbid mental health, developmental and physical health conditions in a nationally representative sample of US children aged 10 to 17. Acad Pediatr. 2013;13:6-13.
25. Griffiths LJ, Parsons TJ, Hill AJ. Self-esteem and quality of life in obese children and adolescents: a systematic review. Int J Pediatr Obes. 2010;5:282-304.
26. National Physical Activity Plan Alliance. The 2018 United States report card on physical activity for children and youth. Accessed February 23, 2021. http://physicalactivityplan.org/projects/PA/2018/2018%20US%20Report%20Card%20Full%20Version_WEB.PDF?pdf=page-link
27. HHS. NIMH. Child and adolescent mental health. Accessed February 23, 2021. www.nimh.nih.gov/health/topics/child-and-adolescent-mental-health/index.shtml
28. Yonek JC, Jordan N, Dunlop D, et al. Patient-centered medical home care for adolescents in need of mental health treatment. J Adolesc Health. 2018;63:172-180.
29. Brooks TL, Harris SK, Thrall JS, et al. Association of adolescent risk behaviors with mental health symptoms in high school students. |J Adolesc Health. 2002;31:240-246.
30. Weller BE, Blanford KL, Butler AM. Estimated prevalence of psychiatric comorbidities in US adolescents with depression by race/ethnicity, 2011-2012. J Adolesc Health. 2018;62:716-721.
31. Bilsen J. Suicide and youth: risk factors. Front Psychiatry. 2018;9:540.
32. Shain B, AAP Committee on Adolescence. Suicide and suicide attempts in adolescents. Pediatrics. 2016;138:e20161420.
33. Brahmbhatt K, Hilty DM, Hah M, et al. Diagnosis and treatment of attention deficit hyperactivity disorder during adolescence in the primary care setting: review and future directions. J Adolesc Health. 2016;59:135-143.
34. Bravender T. Attention-deficit/hyperactivity disorder and disordered eating. [editorial] J Adolesc Health. 2017;61:125-126.
35. Rosen DS, AAP Committee on Adolescence. Identification and management of eating disorders in children and adolescents. Pediatrics. 2010;126:1240-1253.
36. Susman EJ, Houts RM, Steinberg L, et al. Longitudinal development of secondary sexual characteristics in girls and boys between ages 9 ½ and 15 ½ years. Arch Pediatr Adolesc Med. 2010;164:166-173.
37. Kaplowitz PB. Link between body fat and the timing of puberty. Pediatrics. 2008;121(suppl 3):S208-S217.
38. Ge X, Conger RD, Elder GH. Coming of age too early: pubertal influences on girl’s vulnerability to psychologic distress. Child Dev. 1996;67:3386-3400.
39. Jørgensen M, Keiding N, Skakkebaek NE. Estimation of spermarche from longitudinal spermaturia data. Biometrics. 1991;47:177-193.
40. Kar SK, Choudhury A, Singh AP. Understanding normal development of adolescent sexuality: a bumpy ride. J Hum Reprod Sci. 2015;8:70-74.
41. Susman EJ, Dorn LD, Schiefelbein VL. Puberty, sexuality and health. In: Lerner MA, Easterbrooks MA, Mistry J (eds). Comprehensive Handbook of Psychology. Wiley; 2003.
42. Lindberg LD, Santelli JS, Desai S. Changing patterns of contraceptive use and the decline in rates of pregnancy and birth among U.S. adolescents, 2007-2014. J Adolesc Health. 2018;63:253-256.
43. Guttmacher Institute. Teen pregnancy. www.guttmacher.org/united-states/teens/teen-pregnancy. Accessed February 23, 2021.
44. CDC. Social determinants and eliminating disparities in teen pregnancy. Accessed February 23, 2021. www.cdc.gov/teenpregnancy/about/social-determinants-disparities-teen-pregnancy.htm
45. Widman L, Nesi J, Kamke K, et al. Technology-based interventions to reduce sexually transmitted infection and unintended pregnancy among youth. J Adolesc Health. 2018;62:651-660.
46. Secura GM, Allsworth JE, Madden T, et al. The Contraceptive CHOICE Project: reducing barriers to long-acting reversible contraception. Am J Obstet Gynecol. 2010;203:115.e1-115.e7.
47. Ham P, Allen C. Adolescent health screening and counseling. Am Fam Physician. 2012;86:1109-1116.
48. ACOG. Committee on Adolescent Health Care. Adolescent pregnancy, contraception and sexual activity. 2017. Accessed February 23, 2021. www.acog.org/clinical/clinical-guidance/committee-opinion/articles/2017/05/adolescent-pregnancy-contraception-and-sexual-activity
49. Wangu Z, Burstein GR. Adolescent sexuality: updates to the sexually transmitted infection guidelines. Pediatr Clin N Am. 2017;64:389-411.
50. Holway GV, Hernandez SM. Oral sex and condom use in a U.S. national sample of adolescents and young adults. J Adolesc Health. 2018;62:402-410.
51. CDC. STDs in adults and adolescents. Accessed February 23, 2021. www.cdc.gov/std/stats17/adolescents.htm
52. McClung N, Gargano J, Bennett N, et al. Trends in human papillomavirus vaccine types 16 and 18 in cervical precancers, 2008-2014. Accessed February 23, 2021. https://cebp.aacrjournals.org/content/28/3/602
53. Timbang MR, Sim MW, Bewley AF, et al. HPV-related oropharyngeal cancer: a review on burden of the disease and opportunities for prevention and early detection. Hum Vaccin Immunother. 2019;15:1920-1928.
54. Carey AJ, Beagley KW. Chlamydia trachomatis, a hidden epidemic: effects on female reproduction and options for treatment. Am J Reprod Immunol. 2010;63:576-586.
55. USPSTF. Chlamydia and gonorrhea screening. Accessed February 23, 2021. www.uspreventiveservicestaskforce.org/Page/Document/RecommendationStatementFinal/chlamydia-and-gonorrhea-screening
56. Workowski KA, Bolan GA. Sexually transmitted diseases treatment guidelines, 2015. MMWR Morb Mortal Wkly Rep. 2015;64:1-135.
57. CDC. Sexually transmitted disease surveillance 2018. Accessed February 23, 2021. www.cdc.gov/std/stats18/gonorrhea.htm
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59. Kann L, McManus T, Harris WA, et al. Youth risk behavior surveillance–United States, 2015. MMWR Surveill Summ. 2016;65:1-174.
60. CDC. LGBT youth. Accessed February 23, 2021. www.cdc.gov/lgbthealth/youth.htm
61. Johns MM, Lowry R, Rasberry CN, et al. Violence victimization, substance use, and suicide risk among sexual minority high school students – United States, 2015-2017. MMWR Morb Mortal Wkly Rep. 2018;67:1211-1215.
62. Pew Research Center. Teens, social media & technology 2018. . Accessed February 23, 2021. www.pewinternet.org/2018/05/31/teens-social-media-technology-2018/
63. Chassiakos YLR, Radesky J, Christakis D, et al. Children and adolescents and digital media. Pediatrics. 2016;138:e20162593.
64. Arora T, Albahri A, Omar OM, et al. The prospective association between electronic device use before bedtime and academic attainment in adolescents. J Adolesc Health. 2018;63:451-458.
65. Mishna F, Saini M, Solomon S. Ongoing and online: children and youth’s perceptions of cyber bullying. Child Youth Serv Rev. 2009;31:1222-1228.
66. Sengupta A, Chaudhuri A. Are social networking sites a source of online harassment for teens? Evidence from survey data. Child Youth Serv Rev. 2011;33:284-290.
Adolescents are an increasingly diverse population reflecting changes in the racial, ethnic, and geopolitical milieus of the United States. The World Health Organization classifies adolescence as ages 10 to 19 years.1 However, given the complexity of adolescent development physically, behaviorally, emotionally, and socially, others propose that adolescence may extend to age 24.2
Recognizing the specific challenges adolescents face is key to providing comprehensive longitudinal health care. Moreover, creating an environment of trust helps to ensure open 2-way communication that can facilitate anticipatory guidance.
Our review focuses on common adolescent issues, including injury from vehicles and firearms, tobacco and substance misuse, obesity, behavioral health, sexual health, and social media use. We discuss current trends and recommend strategies to maximize health and wellness.
Start by framing the visit
Confidentiality
Laws governing confidentiality in adolescent health care vary by state. Be aware of the laws pertaining to your practice setting. In addition, health care facilities may have their own policies regarding consent and confidentiality in adolescent care. Discuss confidentiality with both an adolescent and the parent/guardian at the initial visit. And, to help avoid potential misunderstandings, let them know in advance what will (and will not) be divulged.
The American Academy of Pediatrics has developed a useful tip sheet regarding confidentiality laws (www.aap.org/en-us/advocacy-and-policy/aap-health-initiatives/healthy-foster-care-america/Documents/Confidentiality_Laws.pdf). Examples of required (conditional) disclosure include abuse and suicidal or homicidal ideations. Patients should understand that sexually transmitted infections (STIs) are reportable to public health authorities and that potentially injurious behaviors to self or others (eg, excessive drinking prior to driving) may also warrant disclosure(TABLE 13).
Privacy and general visit structure
Create a safe atmosphere where adolescents can discuss personal issues without fear of repercussion or judgment. While parents may prefer to be present during the visit, allowing for time to visit independently with an adolescent offers the opportunity to reinforce issues of privacy and confidentiality. Also discuss your office policies regarding electronic communication, phone communication, and relaying test results.
A useful paradigm for organizing a visit for routine adolescent care is to use an expanded version of the HEADSS mnemonic (TABLE 24,5), which includes questions about an adolescent’s Home, Education, Activities, Drug and alcohol use, Sexual behavior, Suicidality and depression, and other topics. Other validated screening tools include RAAPS (Rapid Adolescent Prevention Screening)6 (www.possibilitiesforchange.com/raaps/); the Guidelines for Adolescent Preventive Services7; and the Bright Futures recommendations for preventive care from the American Academy of Pediatrics.8 Below, we consider important topics addressed with the HEADSS approach.
Continue to: Injury from vehicles and firearms
Injury from vehicles and firearms
Motor vehicle accidents and firearm wounds are the 2 leading causes of adolescent injury. In 2016, of the more than 20,000 deaths in children and adolescents (ages 1-19 years), 20% were due to motor vehicle accidents (4074) and 15% were a result of firearm-related injuries (3143). Among firearm-related deaths, 60% were homicides, 35% were suicides, and 4% were due to accidental discharge.9 The rate of firearm-related deaths among American teens is 36 times greater than that of any other developed nation.9 Currently, 1 of every 3 US households with children younger than 18 has a firearm. Data suggest that in 43% of these households, the firearm is loaded and kept in an unlocked location.10
To aid anticipatory guidance, ask adolescents about firearm and seat belt use, drinking and driving, and suicidal thoughts (TABLE 24,5). Advise them to always wear seat belts whether driving or riding as a passenger. They should never drink and drive (or get in a car with someone who has been drinking). Advise parents that if firearms are present in the household, they should be kept in a secure, locked location. Weapons should be separated from ammunition and safety mechanisms should be engaged on all devices.
Tobacco and substance misuse
Tobacco use, the leading preventable cause of death in the United States,11 is responsible for more deaths than alcohol, motor vehicle accidents, suicides, homicides, and HIV disease combined.12 Most tobacco-associated mortality occurs in individuals who began smoking before the age of 18.12 Individuals who start smoking early are also more likely to continue smoking through adulthood.
Encouragingly, tobacco use has declined significantly among adolescents over the past several decades. Roughly 1 in 25 high school seniors reports daily tobacco use.13 Adolescent smoking behaviors are also changing dramatically with the increasing popularity of electronic cigarettes (“vaping”). Currently, more adolescents vape than smoke cigarettes.13 Vaping has additional health risks including toxic lung injury.
Multiple resources can help combat tobacco and nicotine use in adolescents. The US Preventive Services Task Force recommends that primary care clinicians intervene through education or brief counselling to prevent initiation of tobacco use in school-aged children and adolescents.14 Ask teens about tobacco and electronic cigarette use and encourage them to quit when use is acknowledged. Other helpful office-based tools are the “Quit Line” 800-QUIT-NOW and texting “Quit” to 47848. Smokefree teen (https://teen.smokefree.gov/) is a website that reviews the risks of tobacco and nicotine use and provides age-appropriate cessation tools and tips (including a smartphone app and a live-chat feature). Other useful information is available in a report from the Surgeon General on preventing tobacco use among young adults.15
Continue to: Alcohol use
Alcohol use. Three in 5 high school students report ever having used alcohol.13 As with tobacco, adolescent alcohol use has declined over the past decade. However, binge drinking (≥ 5 drinks on 1 occasion for males; ≥ 4 drinks on 1 occasion for females) remains a common high-risk behavior among adolescents (particularly college students). Based on the Monitoring the Future Survey, 1 in 6 high school seniors reported binge drinking in the past 2 weeks.13 While historically more common among males, rates of binge drinking are now basically similar between male and female adolescents.13
The National Institute on Alcohol Abuse and Alcoholism has a screening and intervention guide specifically for adolescents.16
Illicit drug use. Half of adolescents report using an illicit drug by their senior year in high school.13 Marijuana is the most commonly used substance, and laws governing its use are rapidly changing across the United States. Marijuana is illegal in 10 states and legal in 10 states (and the District of Columbia). The remaining states have varying policies on the medical use of marijuana and the decriminalization of marijuana. In addition, cannabinoid (CBD) products are increasingly available. Frequent cannabis use in adolescence has an adverse impact on general executive function (compared with adult users) and learning.17 Marijuana may serve as a gateway drug in the abuse of other substances,18 and its use should be strongly discouraged in adolescents.
Of note, there has been a sharp rise in the illicit use of prescription drugs, particularly opioids, creating a public health emergency across the United States.19 In 2015, more than 4000 young people, ages 15 to 24, died from a drug-related overdose (> 50% of these attributable to opioids).20 Adolescents with a history of substance abuse and behavioral illness are at particular risk. Many adolescents who misuse opioids and other prescription drugs obtain them from friends and relatives.21
The Substance Abuse and Mental Health Services Administration (SAMHSA) recommends universal screening of adolescents for substance abuse. This screening should be accompanied by a brief intervention to prevent, mitigate, or eliminate substance use, or a referral to appropriate treatment sources. This process of screening, brief intervention, and referral to treatment (SBIRT) is recommended as part of routine health care.22
Continue to: Obesity and physical activity
Obesity and physical activity
The percentage of overweight and obese adolescents in the United States has more than tripled over the past 40 years,23 and 1 in 5 US adolescents is obese.23 Obese teens are at higher risk for multiple chronic diseases, including type 2 diabetes, sleep apnea, and heart disease.24 They are also more likely to be bullied and to have poor self-esteem.25 Only 1 in 5 American high school students engages in 60 or more minutes of moderate-to-vigorous physical activity on 5 or more days per week.26
Regular physical activity is, of course, beneficial for cardiorespiratory fitness, bone health, weight control, and improved indices of behavioral health.26 Adolescents who are physically active consistently demonstrate better school attendance and grades.17 Higher levels of physical fitness are also associated with improved overall cognitive performance.24
General recommendations. The Department of Health and Human Services recommends that adolescents get at least 60 minutes of mostly moderate physical activity every day.26 Encourage adolescents to engage in vigorous physical activity (heavy breathing, sweating) at least 3 days a week. As part of their physical activity patterns, adolescents should also engage in muscle-strengthening and bone-strengthening activities on at least 3 days per week.
Behavioral health
As young people develop their sense of personal identity, they also strive for independence. It can be difficult, at times, to differentiate normal adolescent rebellion from true mental illness. An estimated 17% to 19% of adolescents meet criteria for mental illness, and about 7% have a severe psychiatric disorder.27 Only one-third of adolescents with mental illness receive any mental health services.28
Depression. The 1-year incidence of major depression in adolescents is 3% to 4%, and the lifetime prevalence of depressive symptoms is 25% in all high school students.27 Risk factors include ethnic minority status, poor self-esteem, poor health, recent personal crisis, insomnia, and alcohol/substance abuse. Depression in adolescent girls is correlated with becoming sexually active at a younger age, failure to use contraception, having an STI, and suicide attempts. Depressed boys are more likely to have unprotected intercourse and participate in physical fights.29 Depressed teens have a 2- to 3-fold greater risk for behavioral disorders, anxiety, and attention-deficit/hyperactivity disorder (ADHD).30
Continue to: Suicide
Suicide. Among individuals 15 to 29 years of age, suicide is the second leading cause of death globally, with an annual incidence of 11 to 15 per 100,000.31 Suicide attempts are 10 to 20 times more common than completed suicide.31 Males are more likely than females to die by suicide,32 and boys with a history of attempted suicide have a 30-fold increased risk of subsequent successful suicide.31 Hanging, drug poisoning, and firearms (particularly for males) are the most common means of suicide in adolescents. More than half of adolescents dying by suicide have coexisting depression.31
Characteristics associated with suicidal behaviors in adolescents include impulsivity, poor problem-solving skills, and dichotomous thinking.31 There may be a genetic component as well. In 1 of 5 teenage suicides, a precipitating life event such as the break-up of a relationship, cyber-bullying, or peer rejection is felt to contribute.31
ADHD. The prevalence of ADHD is 7% to 9% in US school-aged children.33 Boys more commonly exhibit hyperactive behaviors, while girls have more inattention. Hyperactivity often diminishes in teens, but inattention and impulsivity persist. Sequelae of ADHD include high-risk sexual behaviors, motor vehicle accidents, incarceration, and substance abuse.34 Poor self-esteem, suicidal ideation, smoking, and obesity are also increased.34 ADHD often persists into adulthood, with implications for social relationships and job performance.34
Eating disorders. The distribution of eating disorders is now known to increasingly include more minorities and males, the latter representing 5% to 10% of cases.35 Eating disorders show a strong genetic tendency and appear to be accelerated by puberty. The most common eating disorder (diagnosed in 0.8%-14% of teens) is eating disorder not otherwise specified (NOS).35 Anorexia nervosa is diagnosed in 0.5% of adolescent girls, and bulimia nervosa in 1% to 2%—particularly among athletes and performers.35 Unanticipated loss of weight, amenorrhea, excessive concern about weight, and deceleration in height/weight curves are potential indicators of an eating disorder. When identified, eating disorders are best managed by a trusted family physician, acting as a coordinator of a multidisciplinary team.
Sexual health
Girls begin to menstruate at an average age of 12, and it takes about 4 years for them to reach reproductive maturity.36 Puberty has been documented to start at younger ages over the past 30 years, likely due to an increase in average body mass index and a decrease in levels of physical activity.37 Girls with early maturation are often insecure and self-conscious, with higher levels of psychological distress.38 In boys, the average age for spermarche (first ejaculation) is 13.39 Boys who mature early tend to be taller, be more confident, and express a good body image.40 Those who have early puberty are more likely to be sexually active or participate in high-risk behaviors.41
Continue to: Pregnancy and contraception
Pregnancy and contraception
Over the past several decades, more US teens have been abstaining from sexual intercourse or have been using effective forms of birth control, particularly condoms and long-acting reversible contraceptives (LARCs).42 Teenage birth rates in girls ages 15 to 19 have declined significantly since the 1980s.42 Despite this, the teenage birth rate in the United States remains higher than in other industrialized nations, and most teen pregnancies are unintended.
There are numerous interventions to reduce teen pregnancy, including sex education, contraceptive counseling, the use of mobile apps that track a user’s monthly fertility cycle or issue reminders to take oral contraceptives,45 and the liberal distribution of contraceptives and condoms. The Contraceptive CHOICE Project shows that providing free (or low-cost) LARCs influences young women to choose these as their preferred contraceptive method.46 Other programs specifically empower girls to convince partners to use condoms and to resist unwanted sexual advances or intimate partner violence.
Adolescents prefer to have their health care providers address the topic of sexual health. Teens are more likely to share information with providers if asked directly about sexual behaviors.47TABLE 24,5 offers tips for anticipatory guidance and potential ways to frame questions with adolescents in this context. State laws vary with regard to the ability of minors to seek contraception, pregnancy testing, or care/screening for STIs without parental consent. Contraceptive counseling combined with effective screening decrease the incidence of STIs and pelvic inflammatory disease for sexually active teens.48
Sexually transmitted infections
Young adolescents often have a limited ability to imagine consequences related to specific actions. In general, there is also an increased desire to engage in experimental behaviors as an expression of developing autonomy, which may expose them to STIs. About half of all STIs contracted in the United States occur in individuals 15 to 24 years of age.49 Girls are at particular risk for the sequelae of these infections, including cervical dysplasia and infertility. Many teens erroneously believe that sexual activities other than intercourse decrease their risk of contracting an STI.50
Human papillomavirus (HPV) infection is the most common STI in adolescence.51 In most cases, HPV is transient and asymptomatic. Oncogenic strains may cause cervical cancer or cancers of the anogenital or oropharyngeal systems. Due to viral latency, it is not recommended to perform HPV typing in men or in women younger than 30 years of age; however, Pap tests are recommended every 3 years for women ages 21 to 29. Primary care providers are pivotal in the public health struggle to prevent HPV infection.
Continue to: Universal immunization of all children...
Universal immunization of all children older than 11 years of age against HPV is strongly advised as part of routine well-child care. Emphasize the proven role of HPV vaccination in preventing cervical52 and oropharyngeal53 cancers. And be prepared to address concerns raised by parents in the context of vaccine safety and the initiation of sexual behaviors (www.cdc.gov/hpv/hcp/answering-questions.html).
Chlamydia is the second most common STI in the United States, usually occurring in individuals younger than 24.54 The CDC estimates that more than 3 million new chlamydial infections occur yearly. These infections are often asymptomatic, particularly in females, but may cause urethritis, cervicitis, epididymitis, proctitis, or pelvic inflammatory disease. Indolent chlamydial infection is the leading cause of tubal infertility in women.54 Routine annual screening for chlamydia is recommended for all sexually active females ≤ 25 years (and for older women with specific risks).55 Annual screening is also recommended for men who have sex with men (MSM).55
Chlamydial infection may be diagnosed with first-catch urine sampling (men or women), urethral swab (men), endocervical swab (women), or self-collected vaginal swab. Nucleic acid amplification testing is the most sensitive test that is widely available.56 First-line treatment includes either azithromycin (1 g orally, single dose) or doxycycline (100 mg orally, twice daily for 7 days).56
Gonorrhea. In 2018, there were more than 500,000 annual cases of gonorrhea, with the majority occurring in those between 15 and 24 years of age.57 Gonorrhea may increase rates of HIV infection transmission up to 5-fold.57 As more adolescents practice oral sex, cases of pharyngeal gonorrhea (and oropharyngeal HPV) have increased. Symptoms of urethritis occur more frequently in men. Screening is recommended for all sexually active women younger than 25.56 Importantly, the organism Neisseria gonorrhoeae has developed significant antibiotic resistance over the past decade. The CDC currently recommends dual therapy for the treatment of gonorrhea using 250 mg of intramuscular ceftriaxone and 1 g of oral azithromycin.56
Syphilis. Rates of syphilis are increasing among individuals ages 15 to 24.51 Screening is particularly recommended for MSM and individuals infected with HIV. Benzathine penicillin G, 50,000 U/kg IM, remains the treatment of choice.56
Continue to: HIV
HIV. Globally, HIV impacts young people disproportionately. HIV infection also facilitates infection with other STIs. In the United States, the highest burden of HIV infection is borne by young MSM, with prevalence among those 18 to 24 years old varying between 26% to 30% (black) and 3% to 5.5% (non-Hispanic white).51 The use of emtricitabine/tenofovir disoproxil fumarate for pre-exposure prophylaxis (PrEP) has recently been approved for the prevention of HIV. PrEP reduces risk by up to 92% for MSM and transgender women.58
Sexual identity
One in 10 high school students self-identifies as “nonheterosexual,” and 1 in 15 reports same-sex sexual contact.59 The term LGBTQ+ includes the communities of lesbian, gay, bisexual, transgender, transsexual, queer, questioning, intersex, and asexual individuals. Developing a safe sense of sexual identity is fundamental to adolescent psychological development, and many adolescents struggle to develop a positive sexual identity. Suicide rates and self-harm behaviors among LGBTQ+ adolescents can be 4 times higher than among their heterosexual peers.60 Rates of mood disorders, substance abuse, and high-risk sexual behaviors are also increased in the LGBTQ+ population.61
The LGBTQ+ community often seeks health care advice and affirmation from primary care providers. Resources to enhance this care are available at www.lgbthealtheducation.org.
Social media
Adolescents today have more media exposure than any prior generation, with smartphone and computer use increasing exponentially. Most (95%) teens have access to a smartphone,62 45% describe themselves as constantly connected to the Internet, and 14% feel that social media is “addictive.”62 Most manage their social media portfolio on multiple sites. Patterns of adolescents' online activities show that boys prefer online gaming, while girls tend to spend more time on social networking.62
Whether extensive media use is psychologically beneficial or deleterious has been widely debated. Increased time online correlates with decreased levels of physical activity.63 And sleep disturbances have been associated with excessive screen time and the presence of mobile devices in the bedroom.64 The use of social media prior to bedtime also has an adverse impact on academic performance—particularly for girls. This adverse impact on academics persists after correcting for daytime sleepiness, body mass index, and number of hours spent on homework.64
Continue to: Due to growing concerns...
Due to growing concerns about the risks of social media in children and adolescents, the American Academy of Pediatrics has developed the Family Media Plan (www.healthychildren.org/English/media/Pages/default.aspx). Some specific questions that providers may ask are outlined in TABLE 3.64 The Family Media Plan can provide age-specific guidelines to assist parents or caregivers in answering these questions.
Cyber-bullying. One in 3 adolescents (primarily female) has been a victim of cyber-bullying.65 Sadly, 1 in 5 teens has received some form of electronic sexual solicitation.66 The likelihood of unsolicited stranger contact correlates with teens’ online habits and the amount of information disclosed. Predictors include female sex, visiting chat rooms, posting photos, and disclosing personal information. Restricting computer use to an area with parental supervision or installing monitoring programs does not seem to exert any protective influence on cyber-bullying or unsolicited stranger contact.65 While 63% of cyber-bullying victims feel upset, embarrassed, or stressed by these contacts,66 few events are actually reported. To address this, some states have adopted laws adding cyber-bullying to school disciplinary codes.
Negative health impacts associated with cyber-bullying include anxiety, sadness, and greater difficulty in concentrating on school work.65 Victims of bullying are more likely to have school disciplinary actions and depression and to be truant or to carry weapons to school.66 Cyber-bullying is uniquely destructive due to its ubiquitous presence. A sense of relative anonymity online may encourage perpetrators to act more cruelly, with less concern for punishment.
Young people are also more likely to share passwords as a sign of friendship. This may result in others assuming their identity online. Adolescents rarely disclose bullying to parents or other adults, fearing restriction of Internet access, and many of them think that adults may downplay the seriousness of the events.66
CORRESPONDENCE
Mark B. Stephens, MD, Penn State Health Medical Group, 1850 East Park Avenue, State College, PA 16803; mstephens3@pennstatehealth.psu.edu.
Adolescents are an increasingly diverse population reflecting changes in the racial, ethnic, and geopolitical milieus of the United States. The World Health Organization classifies adolescence as ages 10 to 19 years.1 However, given the complexity of adolescent development physically, behaviorally, emotionally, and socially, others propose that adolescence may extend to age 24.2
Recognizing the specific challenges adolescents face is key to providing comprehensive longitudinal health care. Moreover, creating an environment of trust helps to ensure open 2-way communication that can facilitate anticipatory guidance.
Our review focuses on common adolescent issues, including injury from vehicles and firearms, tobacco and substance misuse, obesity, behavioral health, sexual health, and social media use. We discuss current trends and recommend strategies to maximize health and wellness.
Start by framing the visit
Confidentiality
Laws governing confidentiality in adolescent health care vary by state. Be aware of the laws pertaining to your practice setting. In addition, health care facilities may have their own policies regarding consent and confidentiality in adolescent care. Discuss confidentiality with both an adolescent and the parent/guardian at the initial visit. And, to help avoid potential misunderstandings, let them know in advance what will (and will not) be divulged.
The American Academy of Pediatrics has developed a useful tip sheet regarding confidentiality laws (www.aap.org/en-us/advocacy-and-policy/aap-health-initiatives/healthy-foster-care-america/Documents/Confidentiality_Laws.pdf). Examples of required (conditional) disclosure include abuse and suicidal or homicidal ideations. Patients should understand that sexually transmitted infections (STIs) are reportable to public health authorities and that potentially injurious behaviors to self or others (eg, excessive drinking prior to driving) may also warrant disclosure(TABLE 13).
Privacy and general visit structure
Create a safe atmosphere where adolescents can discuss personal issues without fear of repercussion or judgment. While parents may prefer to be present during the visit, allowing for time to visit independently with an adolescent offers the opportunity to reinforce issues of privacy and confidentiality. Also discuss your office policies regarding electronic communication, phone communication, and relaying test results.
A useful paradigm for organizing a visit for routine adolescent care is to use an expanded version of the HEADSS mnemonic (TABLE 24,5), which includes questions about an adolescent’s Home, Education, Activities, Drug and alcohol use, Sexual behavior, Suicidality and depression, and other topics. Other validated screening tools include RAAPS (Rapid Adolescent Prevention Screening)6 (www.possibilitiesforchange.com/raaps/); the Guidelines for Adolescent Preventive Services7; and the Bright Futures recommendations for preventive care from the American Academy of Pediatrics.8 Below, we consider important topics addressed with the HEADSS approach.
Continue to: Injury from vehicles and firearms
Injury from vehicles and firearms
Motor vehicle accidents and firearm wounds are the 2 leading causes of adolescent injury. In 2016, of the more than 20,000 deaths in children and adolescents (ages 1-19 years), 20% were due to motor vehicle accidents (4074) and 15% were a result of firearm-related injuries (3143). Among firearm-related deaths, 60% were homicides, 35% were suicides, and 4% were due to accidental discharge.9 The rate of firearm-related deaths among American teens is 36 times greater than that of any other developed nation.9 Currently, 1 of every 3 US households with children younger than 18 has a firearm. Data suggest that in 43% of these households, the firearm is loaded and kept in an unlocked location.10
To aid anticipatory guidance, ask adolescents about firearm and seat belt use, drinking and driving, and suicidal thoughts (TABLE 24,5). Advise them to always wear seat belts whether driving or riding as a passenger. They should never drink and drive (or get in a car with someone who has been drinking). Advise parents that if firearms are present in the household, they should be kept in a secure, locked location. Weapons should be separated from ammunition and safety mechanisms should be engaged on all devices.
Tobacco and substance misuse
Tobacco use, the leading preventable cause of death in the United States,11 is responsible for more deaths than alcohol, motor vehicle accidents, suicides, homicides, and HIV disease combined.12 Most tobacco-associated mortality occurs in individuals who began smoking before the age of 18.12 Individuals who start smoking early are also more likely to continue smoking through adulthood.
Encouragingly, tobacco use has declined significantly among adolescents over the past several decades. Roughly 1 in 25 high school seniors reports daily tobacco use.13 Adolescent smoking behaviors are also changing dramatically with the increasing popularity of electronic cigarettes (“vaping”). Currently, more adolescents vape than smoke cigarettes.13 Vaping has additional health risks including toxic lung injury.
Multiple resources can help combat tobacco and nicotine use in adolescents. The US Preventive Services Task Force recommends that primary care clinicians intervene through education or brief counselling to prevent initiation of tobacco use in school-aged children and adolescents.14 Ask teens about tobacco and electronic cigarette use and encourage them to quit when use is acknowledged. Other helpful office-based tools are the “Quit Line” 800-QUIT-NOW and texting “Quit” to 47848. Smokefree teen (https://teen.smokefree.gov/) is a website that reviews the risks of tobacco and nicotine use and provides age-appropriate cessation tools and tips (including a smartphone app and a live-chat feature). Other useful information is available in a report from the Surgeon General on preventing tobacco use among young adults.15
Continue to: Alcohol use
Alcohol use. Three in 5 high school students report ever having used alcohol.13 As with tobacco, adolescent alcohol use has declined over the past decade. However, binge drinking (≥ 5 drinks on 1 occasion for males; ≥ 4 drinks on 1 occasion for females) remains a common high-risk behavior among adolescents (particularly college students). Based on the Monitoring the Future Survey, 1 in 6 high school seniors reported binge drinking in the past 2 weeks.13 While historically more common among males, rates of binge drinking are now basically similar between male and female adolescents.13
The National Institute on Alcohol Abuse and Alcoholism has a screening and intervention guide specifically for adolescents.16
Illicit drug use. Half of adolescents report using an illicit drug by their senior year in high school.13 Marijuana is the most commonly used substance, and laws governing its use are rapidly changing across the United States. Marijuana is illegal in 10 states and legal in 10 states (and the District of Columbia). The remaining states have varying policies on the medical use of marijuana and the decriminalization of marijuana. In addition, cannabinoid (CBD) products are increasingly available. Frequent cannabis use in adolescence has an adverse impact on general executive function (compared with adult users) and learning.17 Marijuana may serve as a gateway drug in the abuse of other substances,18 and its use should be strongly discouraged in adolescents.
Of note, there has been a sharp rise in the illicit use of prescription drugs, particularly opioids, creating a public health emergency across the United States.19 In 2015, more than 4000 young people, ages 15 to 24, died from a drug-related overdose (> 50% of these attributable to opioids).20 Adolescents with a history of substance abuse and behavioral illness are at particular risk. Many adolescents who misuse opioids and other prescription drugs obtain them from friends and relatives.21
The Substance Abuse and Mental Health Services Administration (SAMHSA) recommends universal screening of adolescents for substance abuse. This screening should be accompanied by a brief intervention to prevent, mitigate, or eliminate substance use, or a referral to appropriate treatment sources. This process of screening, brief intervention, and referral to treatment (SBIRT) is recommended as part of routine health care.22
Continue to: Obesity and physical activity
Obesity and physical activity
The percentage of overweight and obese adolescents in the United States has more than tripled over the past 40 years,23 and 1 in 5 US adolescents is obese.23 Obese teens are at higher risk for multiple chronic diseases, including type 2 diabetes, sleep apnea, and heart disease.24 They are also more likely to be bullied and to have poor self-esteem.25 Only 1 in 5 American high school students engages in 60 or more minutes of moderate-to-vigorous physical activity on 5 or more days per week.26
Regular physical activity is, of course, beneficial for cardiorespiratory fitness, bone health, weight control, and improved indices of behavioral health.26 Adolescents who are physically active consistently demonstrate better school attendance and grades.17 Higher levels of physical fitness are also associated with improved overall cognitive performance.24
General recommendations. The Department of Health and Human Services recommends that adolescents get at least 60 minutes of mostly moderate physical activity every day.26 Encourage adolescents to engage in vigorous physical activity (heavy breathing, sweating) at least 3 days a week. As part of their physical activity patterns, adolescents should also engage in muscle-strengthening and bone-strengthening activities on at least 3 days per week.
Behavioral health
As young people develop their sense of personal identity, they also strive for independence. It can be difficult, at times, to differentiate normal adolescent rebellion from true mental illness. An estimated 17% to 19% of adolescents meet criteria for mental illness, and about 7% have a severe psychiatric disorder.27 Only one-third of adolescents with mental illness receive any mental health services.28
Depression. The 1-year incidence of major depression in adolescents is 3% to 4%, and the lifetime prevalence of depressive symptoms is 25% in all high school students.27 Risk factors include ethnic minority status, poor self-esteem, poor health, recent personal crisis, insomnia, and alcohol/substance abuse. Depression in adolescent girls is correlated with becoming sexually active at a younger age, failure to use contraception, having an STI, and suicide attempts. Depressed boys are more likely to have unprotected intercourse and participate in physical fights.29 Depressed teens have a 2- to 3-fold greater risk for behavioral disorders, anxiety, and attention-deficit/hyperactivity disorder (ADHD).30
Continue to: Suicide
Suicide. Among individuals 15 to 29 years of age, suicide is the second leading cause of death globally, with an annual incidence of 11 to 15 per 100,000.31 Suicide attempts are 10 to 20 times more common than completed suicide.31 Males are more likely than females to die by suicide,32 and boys with a history of attempted suicide have a 30-fold increased risk of subsequent successful suicide.31 Hanging, drug poisoning, and firearms (particularly for males) are the most common means of suicide in adolescents. More than half of adolescents dying by suicide have coexisting depression.31
Characteristics associated with suicidal behaviors in adolescents include impulsivity, poor problem-solving skills, and dichotomous thinking.31 There may be a genetic component as well. In 1 of 5 teenage suicides, a precipitating life event such as the break-up of a relationship, cyber-bullying, or peer rejection is felt to contribute.31
ADHD. The prevalence of ADHD is 7% to 9% in US school-aged children.33 Boys more commonly exhibit hyperactive behaviors, while girls have more inattention. Hyperactivity often diminishes in teens, but inattention and impulsivity persist. Sequelae of ADHD include high-risk sexual behaviors, motor vehicle accidents, incarceration, and substance abuse.34 Poor self-esteem, suicidal ideation, smoking, and obesity are also increased.34 ADHD often persists into adulthood, with implications for social relationships and job performance.34
Eating disorders. The distribution of eating disorders is now known to increasingly include more minorities and males, the latter representing 5% to 10% of cases.35 Eating disorders show a strong genetic tendency and appear to be accelerated by puberty. The most common eating disorder (diagnosed in 0.8%-14% of teens) is eating disorder not otherwise specified (NOS).35 Anorexia nervosa is diagnosed in 0.5% of adolescent girls, and bulimia nervosa in 1% to 2%—particularly among athletes and performers.35 Unanticipated loss of weight, amenorrhea, excessive concern about weight, and deceleration in height/weight curves are potential indicators of an eating disorder. When identified, eating disorders are best managed by a trusted family physician, acting as a coordinator of a multidisciplinary team.
Sexual health
Girls begin to menstruate at an average age of 12, and it takes about 4 years for them to reach reproductive maturity.36 Puberty has been documented to start at younger ages over the past 30 years, likely due to an increase in average body mass index and a decrease in levels of physical activity.37 Girls with early maturation are often insecure and self-conscious, with higher levels of psychological distress.38 In boys, the average age for spermarche (first ejaculation) is 13.39 Boys who mature early tend to be taller, be more confident, and express a good body image.40 Those who have early puberty are more likely to be sexually active or participate in high-risk behaviors.41
Continue to: Pregnancy and contraception
Pregnancy and contraception
Over the past several decades, more US teens have been abstaining from sexual intercourse or have been using effective forms of birth control, particularly condoms and long-acting reversible contraceptives (LARCs).42 Teenage birth rates in girls ages 15 to 19 have declined significantly since the 1980s.42 Despite this, the teenage birth rate in the United States remains higher than in other industrialized nations, and most teen pregnancies are unintended.
There are numerous interventions to reduce teen pregnancy, including sex education, contraceptive counseling, the use of mobile apps that track a user’s monthly fertility cycle or issue reminders to take oral contraceptives,45 and the liberal distribution of contraceptives and condoms. The Contraceptive CHOICE Project shows that providing free (or low-cost) LARCs influences young women to choose these as their preferred contraceptive method.46 Other programs specifically empower girls to convince partners to use condoms and to resist unwanted sexual advances or intimate partner violence.
Adolescents prefer to have their health care providers address the topic of sexual health. Teens are more likely to share information with providers if asked directly about sexual behaviors.47TABLE 24,5 offers tips for anticipatory guidance and potential ways to frame questions with adolescents in this context. State laws vary with regard to the ability of minors to seek contraception, pregnancy testing, or care/screening for STIs without parental consent. Contraceptive counseling combined with effective screening decrease the incidence of STIs and pelvic inflammatory disease for sexually active teens.48
Sexually transmitted infections
Young adolescents often have a limited ability to imagine consequences related to specific actions. In general, there is also an increased desire to engage in experimental behaviors as an expression of developing autonomy, which may expose them to STIs. About half of all STIs contracted in the United States occur in individuals 15 to 24 years of age.49 Girls are at particular risk for the sequelae of these infections, including cervical dysplasia and infertility. Many teens erroneously believe that sexual activities other than intercourse decrease their risk of contracting an STI.50
Human papillomavirus (HPV) infection is the most common STI in adolescence.51 In most cases, HPV is transient and asymptomatic. Oncogenic strains may cause cervical cancer or cancers of the anogenital or oropharyngeal systems. Due to viral latency, it is not recommended to perform HPV typing in men or in women younger than 30 years of age; however, Pap tests are recommended every 3 years for women ages 21 to 29. Primary care providers are pivotal in the public health struggle to prevent HPV infection.
Continue to: Universal immunization of all children...
Universal immunization of all children older than 11 years of age against HPV is strongly advised as part of routine well-child care. Emphasize the proven role of HPV vaccination in preventing cervical52 and oropharyngeal53 cancers. And be prepared to address concerns raised by parents in the context of vaccine safety and the initiation of sexual behaviors (www.cdc.gov/hpv/hcp/answering-questions.html).
Chlamydia is the second most common STI in the United States, usually occurring in individuals younger than 24.54 The CDC estimates that more than 3 million new chlamydial infections occur yearly. These infections are often asymptomatic, particularly in females, but may cause urethritis, cervicitis, epididymitis, proctitis, or pelvic inflammatory disease. Indolent chlamydial infection is the leading cause of tubal infertility in women.54 Routine annual screening for chlamydia is recommended for all sexually active females ≤ 25 years (and for older women with specific risks).55 Annual screening is also recommended for men who have sex with men (MSM).55
Chlamydial infection may be diagnosed with first-catch urine sampling (men or women), urethral swab (men), endocervical swab (women), or self-collected vaginal swab. Nucleic acid amplification testing is the most sensitive test that is widely available.56 First-line treatment includes either azithromycin (1 g orally, single dose) or doxycycline (100 mg orally, twice daily for 7 days).56
Gonorrhea. In 2018, there were more than 500,000 annual cases of gonorrhea, with the majority occurring in those between 15 and 24 years of age.57 Gonorrhea may increase rates of HIV infection transmission up to 5-fold.57 As more adolescents practice oral sex, cases of pharyngeal gonorrhea (and oropharyngeal HPV) have increased. Symptoms of urethritis occur more frequently in men. Screening is recommended for all sexually active women younger than 25.56 Importantly, the organism Neisseria gonorrhoeae has developed significant antibiotic resistance over the past decade. The CDC currently recommends dual therapy for the treatment of gonorrhea using 250 mg of intramuscular ceftriaxone and 1 g of oral azithromycin.56
Syphilis. Rates of syphilis are increasing among individuals ages 15 to 24.51 Screening is particularly recommended for MSM and individuals infected with HIV. Benzathine penicillin G, 50,000 U/kg IM, remains the treatment of choice.56
Continue to: HIV
HIV. Globally, HIV impacts young people disproportionately. HIV infection also facilitates infection with other STIs. In the United States, the highest burden of HIV infection is borne by young MSM, with prevalence among those 18 to 24 years old varying between 26% to 30% (black) and 3% to 5.5% (non-Hispanic white).51 The use of emtricitabine/tenofovir disoproxil fumarate for pre-exposure prophylaxis (PrEP) has recently been approved for the prevention of HIV. PrEP reduces risk by up to 92% for MSM and transgender women.58
Sexual identity
One in 10 high school students self-identifies as “nonheterosexual,” and 1 in 15 reports same-sex sexual contact.59 The term LGBTQ+ includes the communities of lesbian, gay, bisexual, transgender, transsexual, queer, questioning, intersex, and asexual individuals. Developing a safe sense of sexual identity is fundamental to adolescent psychological development, and many adolescents struggle to develop a positive sexual identity. Suicide rates and self-harm behaviors among LGBTQ+ adolescents can be 4 times higher than among their heterosexual peers.60 Rates of mood disorders, substance abuse, and high-risk sexual behaviors are also increased in the LGBTQ+ population.61
The LGBTQ+ community often seeks health care advice and affirmation from primary care providers. Resources to enhance this care are available at www.lgbthealtheducation.org.
Social media
Adolescents today have more media exposure than any prior generation, with smartphone and computer use increasing exponentially. Most (95%) teens have access to a smartphone,62 45% describe themselves as constantly connected to the Internet, and 14% feel that social media is “addictive.”62 Most manage their social media portfolio on multiple sites. Patterns of adolescents' online activities show that boys prefer online gaming, while girls tend to spend more time on social networking.62
Whether extensive media use is psychologically beneficial or deleterious has been widely debated. Increased time online correlates with decreased levels of physical activity.63 And sleep disturbances have been associated with excessive screen time and the presence of mobile devices in the bedroom.64 The use of social media prior to bedtime also has an adverse impact on academic performance—particularly for girls. This adverse impact on academics persists after correcting for daytime sleepiness, body mass index, and number of hours spent on homework.64
Continue to: Due to growing concerns...
Due to growing concerns about the risks of social media in children and adolescents, the American Academy of Pediatrics has developed the Family Media Plan (www.healthychildren.org/English/media/Pages/default.aspx). Some specific questions that providers may ask are outlined in TABLE 3.64 The Family Media Plan can provide age-specific guidelines to assist parents or caregivers in answering these questions.
Cyber-bullying. One in 3 adolescents (primarily female) has been a victim of cyber-bullying.65 Sadly, 1 in 5 teens has received some form of electronic sexual solicitation.66 The likelihood of unsolicited stranger contact correlates with teens’ online habits and the amount of information disclosed. Predictors include female sex, visiting chat rooms, posting photos, and disclosing personal information. Restricting computer use to an area with parental supervision or installing monitoring programs does not seem to exert any protective influence on cyber-bullying or unsolicited stranger contact.65 While 63% of cyber-bullying victims feel upset, embarrassed, or stressed by these contacts,66 few events are actually reported. To address this, some states have adopted laws adding cyber-bullying to school disciplinary codes.
Negative health impacts associated with cyber-bullying include anxiety, sadness, and greater difficulty in concentrating on school work.65 Victims of bullying are more likely to have school disciplinary actions and depression and to be truant or to carry weapons to school.66 Cyber-bullying is uniquely destructive due to its ubiquitous presence. A sense of relative anonymity online may encourage perpetrators to act more cruelly, with less concern for punishment.
Young people are also more likely to share passwords as a sign of friendship. This may result in others assuming their identity online. Adolescents rarely disclose bullying to parents or other adults, fearing restriction of Internet access, and many of them think that adults may downplay the seriousness of the events.66
CORRESPONDENCE
Mark B. Stephens, MD, Penn State Health Medical Group, 1850 East Park Avenue, State College, PA 16803; mstephens3@pennstatehealth.psu.edu.
1. World Health Organization. Adolescent health. Accessed February 23, 2021. www.who.int/maternal_child_adolescent/adolescence/en/
2. Sawyer SM, Azzopardi PS, Wickremarathne D, et al. The age of adolescence. Lancet Child Adolesc Health. 2018;2:223-228.
3. Pathak PR, Chou A. Confidential care for adoloscents in the U.S. healthcare system. J Patient Cent Res Rev. 2019;6:46-50.
4. AMA Journal of Ethics. HEADSS: the “review of systems” for adolescents. Accessed February 23, 2021. https://journalofethics.ama-assn.org/article/headss-review-systems-adolescents/2005-03
5. Cohen E, MacKenzie RG, Yates GL. HEADSS, a psychosocial risk assessment instrument: implications for designing effective intervention programs for runaway youth. J Adolesc Health. 1991;12:539-544.
6. Possibilities for Change. Rapid Adolescent Prevention Screening (RAAPS). Accessed February 23, 2021. www.possibilitiesforchange.com/raaps/
7. Elster AB, Kuznets NJ. AMA Guidelines for Adolescent Preventive Services (GAPS): Recommendations and Rationale. Williams & Wilkins; 1994.
8. AAP. Engaging patients and families - periodicity schedule. Accessed February 23, 2021. www.aap.org/en-us/professional-resources/practice-support/Pages/PeriodicitySchedule.aspx
9. Cunningham RM, Walton MA, Carter PM. The major causes of death in children and adolescents in the United States. N Eng J Med. 2018;379:2468-2475.
10. Schuster MA, Franke TM, Bastian AM, et al. Firearm storage patterns in US homes with children. Am J Public Health. 2000;90:588-594.
11. Mokdad AH, Marks JS, Stroup DF, et al. Actual causes of death in the United States. JAMA. 2004;291:1238-1245.
12. HHS. Health consequences of smoking, surgeon general fact sheet. Accessed February 23, 2021. www.hhs.gov/surgeongeneral/reports-and-publications/tobacco/consequences-smoking-factsheet/index.html
13. Johnston LD, Miech RA, O’Malley PM, et al. Monitoring the future: national survey results on drug use, 1975-2017. The University of Michigan. 2018. Accessed February 23, 2021. https://eric.ed.gov/?id=ED589762
14. US Preventive Services Task Force. Prevention and cessation of tobacco use in children and adolescents: primary care interventions. Accessed February 23, 2021. www.uspreventiveservicestaskforce.org/uspstf/recommendation/tobacco-and-nicotine-use-prevention-in-children-and-adolescents-primary-care-interventions
15. HHS. Preventing Tobacco Use Among Youth and Young Adults: A Report of the Surgeon General. Atlanta, GA: HHS, CDC, NCCDPHP, OSH; 2012. Accessed February 23, 2021. www.ncbi.nlm.nih.gov/books/NBK99237/
16. NIH. Alcohol screening and brief intervention for youth: a pocket guide. Accessed February 23, 2021. https://pubs.niaaa.nih.gov/publications/Practitioner/YouthGuide/YouthGuidePocket.pdf
17. Gorey C, Kuhns L, Smaragdi E, et al. Age-related differences in the impact of cannabis use on the brain and cognition: a systematic review. Eur Arch Psychiatry Clin Neurosci. 2019;269:37-58.
18. Secades-Villa R, Garcia-Rodriguez O, Jin CJ, et al. Probability and predictors of the cannabis gateway effect: a national study. Int J Drug Policy. 2015;26:135-142.
19. Kann L, McManus T, Harris WA, et al. Youth risk behavior surveillance—United States, 2017. MMWR Surveill Summ. 2018;67:1-114.
20. NIH. Drug overdoses in youth. How do drug overdoses happen?. Accessed February 23, 2021. https://teens.drugabuse.gov/drug-facts/drug-overdoses-youth
21. Branstetter SA, Low S, Furman W. The influence of parents and friends on adolescent substance use: a multidimensional approach. J Subst Use. 2011;162:150-160.
22. AAP. Committee on Substance Use and Prevention. Substance use screening, brief intervention, and referral to treatment. Pediatrics. 2016;138:e20161210.
23. Hales CM, Carroll MD, Fryar CD, et al. Prevalence of obesity among adults and youth: United States, 2015–2016. NCHS Data Brief. 2017;288:1-8.
24. Halfon N, Larson K, Slusser W. Associations between obesity and comorbid mental health, developmental and physical health conditions in a nationally representative sample of US children aged 10 to 17. Acad Pediatr. 2013;13:6-13.
25. Griffiths LJ, Parsons TJ, Hill AJ. Self-esteem and quality of life in obese children and adolescents: a systematic review. Int J Pediatr Obes. 2010;5:282-304.
26. National Physical Activity Plan Alliance. The 2018 United States report card on physical activity for children and youth. Accessed February 23, 2021. http://physicalactivityplan.org/projects/PA/2018/2018%20US%20Report%20Card%20Full%20Version_WEB.PDF?pdf=page-link
27. HHS. NIMH. Child and adolescent mental health. Accessed February 23, 2021. www.nimh.nih.gov/health/topics/child-and-adolescent-mental-health/index.shtml
28. Yonek JC, Jordan N, Dunlop D, et al. Patient-centered medical home care for adolescents in need of mental health treatment. J Adolesc Health. 2018;63:172-180.
29. Brooks TL, Harris SK, Thrall JS, et al. Association of adolescent risk behaviors with mental health symptoms in high school students. |J Adolesc Health. 2002;31:240-246.
30. Weller BE, Blanford KL, Butler AM. Estimated prevalence of psychiatric comorbidities in US adolescents with depression by race/ethnicity, 2011-2012. J Adolesc Health. 2018;62:716-721.
31. Bilsen J. Suicide and youth: risk factors. Front Psychiatry. 2018;9:540.
32. Shain B, AAP Committee on Adolescence. Suicide and suicide attempts in adolescents. Pediatrics. 2016;138:e20161420.
33. Brahmbhatt K, Hilty DM, Hah M, et al. Diagnosis and treatment of attention deficit hyperactivity disorder during adolescence in the primary care setting: review and future directions. J Adolesc Health. 2016;59:135-143.
34. Bravender T. Attention-deficit/hyperactivity disorder and disordered eating. [editorial] J Adolesc Health. 2017;61:125-126.
35. Rosen DS, AAP Committee on Adolescence. Identification and management of eating disorders in children and adolescents. Pediatrics. 2010;126:1240-1253.
36. Susman EJ, Houts RM, Steinberg L, et al. Longitudinal development of secondary sexual characteristics in girls and boys between ages 9 ½ and 15 ½ years. Arch Pediatr Adolesc Med. 2010;164:166-173.
37. Kaplowitz PB. Link between body fat and the timing of puberty. Pediatrics. 2008;121(suppl 3):S208-S217.
38. Ge X, Conger RD, Elder GH. Coming of age too early: pubertal influences on girl’s vulnerability to psychologic distress. Child Dev. 1996;67:3386-3400.
39. Jørgensen M, Keiding N, Skakkebaek NE. Estimation of spermarche from longitudinal spermaturia data. Biometrics. 1991;47:177-193.
40. Kar SK, Choudhury A, Singh AP. Understanding normal development of adolescent sexuality: a bumpy ride. J Hum Reprod Sci. 2015;8:70-74.
41. Susman EJ, Dorn LD, Schiefelbein VL. Puberty, sexuality and health. In: Lerner MA, Easterbrooks MA, Mistry J (eds). Comprehensive Handbook of Psychology. Wiley; 2003.
42. Lindberg LD, Santelli JS, Desai S. Changing patterns of contraceptive use and the decline in rates of pregnancy and birth among U.S. adolescents, 2007-2014. J Adolesc Health. 2018;63:253-256.
43. Guttmacher Institute. Teen pregnancy. www.guttmacher.org/united-states/teens/teen-pregnancy. Accessed February 23, 2021.
44. CDC. Social determinants and eliminating disparities in teen pregnancy. Accessed February 23, 2021. www.cdc.gov/teenpregnancy/about/social-determinants-disparities-teen-pregnancy.htm
45. Widman L, Nesi J, Kamke K, et al. Technology-based interventions to reduce sexually transmitted infection and unintended pregnancy among youth. J Adolesc Health. 2018;62:651-660.
46. Secura GM, Allsworth JE, Madden T, et al. The Contraceptive CHOICE Project: reducing barriers to long-acting reversible contraception. Am J Obstet Gynecol. 2010;203:115.e1-115.e7.
47. Ham P, Allen C. Adolescent health screening and counseling. Am Fam Physician. 2012;86:1109-1116.
48. ACOG. Committee on Adolescent Health Care. Adolescent pregnancy, contraception and sexual activity. 2017. Accessed February 23, 2021. www.acog.org/clinical/clinical-guidance/committee-opinion/articles/2017/05/adolescent-pregnancy-contraception-and-sexual-activity
49. Wangu Z, Burstein GR. Adolescent sexuality: updates to the sexually transmitted infection guidelines. Pediatr Clin N Am. 2017;64:389-411.
50. Holway GV, Hernandez SM. Oral sex and condom use in a U.S. national sample of adolescents and young adults. J Adolesc Health. 2018;62:402-410.
51. CDC. STDs in adults and adolescents. Accessed February 23, 2021. www.cdc.gov/std/stats17/adolescents.htm
52. McClung N, Gargano J, Bennett N, et al. Trends in human papillomavirus vaccine types 16 and 18 in cervical precancers, 2008-2014. Accessed February 23, 2021. https://cebp.aacrjournals.org/content/28/3/602
53. Timbang MR, Sim MW, Bewley AF, et al. HPV-related oropharyngeal cancer: a review on burden of the disease and opportunities for prevention and early detection. Hum Vaccin Immunother. 2019;15:1920-1928.
54. Carey AJ, Beagley KW. Chlamydia trachomatis, a hidden epidemic: effects on female reproduction and options for treatment. Am J Reprod Immunol. 2010;63:576-586.
55. USPSTF. Chlamydia and gonorrhea screening. Accessed February 23, 2021. www.uspreventiveservicestaskforce.org/Page/Document/RecommendationStatementFinal/chlamydia-and-gonorrhea-screening
56. Workowski KA, Bolan GA. Sexually transmitted diseases treatment guidelines, 2015. MMWR Morb Mortal Wkly Rep. 2015;64:1-135.
57. CDC. Sexually transmitted disease surveillance 2018. Accessed February 23, 2021. www.cdc.gov/std/stats18/gonorrhea.htm
5
59. Kann L, McManus T, Harris WA, et al. Youth risk behavior surveillance–United States, 2015. MMWR Surveill Summ. 2016;65:1-174.
60. CDC. LGBT youth. Accessed February 23, 2021. www.cdc.gov/lgbthealth/youth.htm
61. Johns MM, Lowry R, Rasberry CN, et al. Violence victimization, substance use, and suicide risk among sexual minority high school students – United States, 2015-2017. MMWR Morb Mortal Wkly Rep. 2018;67:1211-1215.
62. Pew Research Center. Teens, social media & technology 2018. . Accessed February 23, 2021. www.pewinternet.org/2018/05/31/teens-social-media-technology-2018/
63. Chassiakos YLR, Radesky J, Christakis D, et al. Children and adolescents and digital media. Pediatrics. 2016;138:e20162593.
64. Arora T, Albahri A, Omar OM, et al. The prospective association between electronic device use before bedtime and academic attainment in adolescents. J Adolesc Health. 2018;63:451-458.
65. Mishna F, Saini M, Solomon S. Ongoing and online: children and youth’s perceptions of cyber bullying. Child Youth Serv Rev. 2009;31:1222-1228.
66. Sengupta A, Chaudhuri A. Are social networking sites a source of online harassment for teens? Evidence from survey data. Child Youth Serv Rev. 2011;33:284-290.
1. World Health Organization. Adolescent health. Accessed February 23, 2021. www.who.int/maternal_child_adolescent/adolescence/en/
2. Sawyer SM, Azzopardi PS, Wickremarathne D, et al. The age of adolescence. Lancet Child Adolesc Health. 2018;2:223-228.
3. Pathak PR, Chou A. Confidential care for adoloscents in the U.S. healthcare system. J Patient Cent Res Rev. 2019;6:46-50.
4. AMA Journal of Ethics. HEADSS: the “review of systems” for adolescents. Accessed February 23, 2021. https://journalofethics.ama-assn.org/article/headss-review-systems-adolescents/2005-03
5. Cohen E, MacKenzie RG, Yates GL. HEADSS, a psychosocial risk assessment instrument: implications for designing effective intervention programs for runaway youth. J Adolesc Health. 1991;12:539-544.
6. Possibilities for Change. Rapid Adolescent Prevention Screening (RAAPS). Accessed February 23, 2021. www.possibilitiesforchange.com/raaps/
7. Elster AB, Kuznets NJ. AMA Guidelines for Adolescent Preventive Services (GAPS): Recommendations and Rationale. Williams & Wilkins; 1994.
8. AAP. Engaging patients and families - periodicity schedule. Accessed February 23, 2021. www.aap.org/en-us/professional-resources/practice-support/Pages/PeriodicitySchedule.aspx
9. Cunningham RM, Walton MA, Carter PM. The major causes of death in children and adolescents in the United States. N Eng J Med. 2018;379:2468-2475.
10. Schuster MA, Franke TM, Bastian AM, et al. Firearm storage patterns in US homes with children. Am J Public Health. 2000;90:588-594.
11. Mokdad AH, Marks JS, Stroup DF, et al. Actual causes of death in the United States. JAMA. 2004;291:1238-1245.
12. HHS. Health consequences of smoking, surgeon general fact sheet. Accessed February 23, 2021. www.hhs.gov/surgeongeneral/reports-and-publications/tobacco/consequences-smoking-factsheet/index.html
13. Johnston LD, Miech RA, O’Malley PM, et al. Monitoring the future: national survey results on drug use, 1975-2017. The University of Michigan. 2018. Accessed February 23, 2021. https://eric.ed.gov/?id=ED589762
14. US Preventive Services Task Force. Prevention and cessation of tobacco use in children and adolescents: primary care interventions. Accessed February 23, 2021. www.uspreventiveservicestaskforce.org/uspstf/recommendation/tobacco-and-nicotine-use-prevention-in-children-and-adolescents-primary-care-interventions
15. HHS. Preventing Tobacco Use Among Youth and Young Adults: A Report of the Surgeon General. Atlanta, GA: HHS, CDC, NCCDPHP, OSH; 2012. Accessed February 23, 2021. www.ncbi.nlm.nih.gov/books/NBK99237/
16. NIH. Alcohol screening and brief intervention for youth: a pocket guide. Accessed February 23, 2021. https://pubs.niaaa.nih.gov/publications/Practitioner/YouthGuide/YouthGuidePocket.pdf
17. Gorey C, Kuhns L, Smaragdi E, et al. Age-related differences in the impact of cannabis use on the brain and cognition: a systematic review. Eur Arch Psychiatry Clin Neurosci. 2019;269:37-58.
18. Secades-Villa R, Garcia-Rodriguez O, Jin CJ, et al. Probability and predictors of the cannabis gateway effect: a national study. Int J Drug Policy. 2015;26:135-142.
19. Kann L, McManus T, Harris WA, et al. Youth risk behavior surveillance—United States, 2017. MMWR Surveill Summ. 2018;67:1-114.
20. NIH. Drug overdoses in youth. How do drug overdoses happen?. Accessed February 23, 2021. https://teens.drugabuse.gov/drug-facts/drug-overdoses-youth
21. Branstetter SA, Low S, Furman W. The influence of parents and friends on adolescent substance use: a multidimensional approach. J Subst Use. 2011;162:150-160.
22. AAP. Committee on Substance Use and Prevention. Substance use screening, brief intervention, and referral to treatment. Pediatrics. 2016;138:e20161210.
23. Hales CM, Carroll MD, Fryar CD, et al. Prevalence of obesity among adults and youth: United States, 2015–2016. NCHS Data Brief. 2017;288:1-8.
24. Halfon N, Larson K, Slusser W. Associations between obesity and comorbid mental health, developmental and physical health conditions in a nationally representative sample of US children aged 10 to 17. Acad Pediatr. 2013;13:6-13.
25. Griffiths LJ, Parsons TJ, Hill AJ. Self-esteem and quality of life in obese children and adolescents: a systematic review. Int J Pediatr Obes. 2010;5:282-304.
26. National Physical Activity Plan Alliance. The 2018 United States report card on physical activity for children and youth. Accessed February 23, 2021. http://physicalactivityplan.org/projects/PA/2018/2018%20US%20Report%20Card%20Full%20Version_WEB.PDF?pdf=page-link
27. HHS. NIMH. Child and adolescent mental health. Accessed February 23, 2021. www.nimh.nih.gov/health/topics/child-and-adolescent-mental-health/index.shtml
28. Yonek JC, Jordan N, Dunlop D, et al. Patient-centered medical home care for adolescents in need of mental health treatment. J Adolesc Health. 2018;63:172-180.
29. Brooks TL, Harris SK, Thrall JS, et al. Association of adolescent risk behaviors with mental health symptoms in high school students. |J Adolesc Health. 2002;31:240-246.
30. Weller BE, Blanford KL, Butler AM. Estimated prevalence of psychiatric comorbidities in US adolescents with depression by race/ethnicity, 2011-2012. J Adolesc Health. 2018;62:716-721.
31. Bilsen J. Suicide and youth: risk factors. Front Psychiatry. 2018;9:540.
32. Shain B, AAP Committee on Adolescence. Suicide and suicide attempts in adolescents. Pediatrics. 2016;138:e20161420.
33. Brahmbhatt K, Hilty DM, Hah M, et al. Diagnosis and treatment of attention deficit hyperactivity disorder during adolescence in the primary care setting: review and future directions. J Adolesc Health. 2016;59:135-143.
34. Bravender T. Attention-deficit/hyperactivity disorder and disordered eating. [editorial] J Adolesc Health. 2017;61:125-126.
35. Rosen DS, AAP Committee on Adolescence. Identification and management of eating disorders in children and adolescents. Pediatrics. 2010;126:1240-1253.
36. Susman EJ, Houts RM, Steinberg L, et al. Longitudinal development of secondary sexual characteristics in girls and boys between ages 9 ½ and 15 ½ years. Arch Pediatr Adolesc Med. 2010;164:166-173.
37. Kaplowitz PB. Link between body fat and the timing of puberty. Pediatrics. 2008;121(suppl 3):S208-S217.
38. Ge X, Conger RD, Elder GH. Coming of age too early: pubertal influences on girl’s vulnerability to psychologic distress. Child Dev. 1996;67:3386-3400.
39. Jørgensen M, Keiding N, Skakkebaek NE. Estimation of spermarche from longitudinal spermaturia data. Biometrics. 1991;47:177-193.
40. Kar SK, Choudhury A, Singh AP. Understanding normal development of adolescent sexuality: a bumpy ride. J Hum Reprod Sci. 2015;8:70-74.
41. Susman EJ, Dorn LD, Schiefelbein VL. Puberty, sexuality and health. In: Lerner MA, Easterbrooks MA, Mistry J (eds). Comprehensive Handbook of Psychology. Wiley; 2003.
42. Lindberg LD, Santelli JS, Desai S. Changing patterns of contraceptive use and the decline in rates of pregnancy and birth among U.S. adolescents, 2007-2014. J Adolesc Health. 2018;63:253-256.
43. Guttmacher Institute. Teen pregnancy. www.guttmacher.org/united-states/teens/teen-pregnancy. Accessed February 23, 2021.
44. CDC. Social determinants and eliminating disparities in teen pregnancy. Accessed February 23, 2021. www.cdc.gov/teenpregnancy/about/social-determinants-disparities-teen-pregnancy.htm
45. Widman L, Nesi J, Kamke K, et al. Technology-based interventions to reduce sexually transmitted infection and unintended pregnancy among youth. J Adolesc Health. 2018;62:651-660.
46. Secura GM, Allsworth JE, Madden T, et al. The Contraceptive CHOICE Project: reducing barriers to long-acting reversible contraception. Am J Obstet Gynecol. 2010;203:115.e1-115.e7.
47. Ham P, Allen C. Adolescent health screening and counseling. Am Fam Physician. 2012;86:1109-1116.
48. ACOG. Committee on Adolescent Health Care. Adolescent pregnancy, contraception and sexual activity. 2017. Accessed February 23, 2021. www.acog.org/clinical/clinical-guidance/committee-opinion/articles/2017/05/adolescent-pregnancy-contraception-and-sexual-activity
49. Wangu Z, Burstein GR. Adolescent sexuality: updates to the sexually transmitted infection guidelines. Pediatr Clin N Am. 2017;64:389-411.
50. Holway GV, Hernandez SM. Oral sex and condom use in a U.S. national sample of adolescents and young adults. J Adolesc Health. 2018;62:402-410.
51. CDC. STDs in adults and adolescents. Accessed February 23, 2021. www.cdc.gov/std/stats17/adolescents.htm
52. McClung N, Gargano J, Bennett N, et al. Trends in human papillomavirus vaccine types 16 and 18 in cervical precancers, 2008-2014. Accessed February 23, 2021. https://cebp.aacrjournals.org/content/28/3/602
53. Timbang MR, Sim MW, Bewley AF, et al. HPV-related oropharyngeal cancer: a review on burden of the disease and opportunities for prevention and early detection. Hum Vaccin Immunother. 2019;15:1920-1928.
54. Carey AJ, Beagley KW. Chlamydia trachomatis, a hidden epidemic: effects on female reproduction and options for treatment. Am J Reprod Immunol. 2010;63:576-586.
55. USPSTF. Chlamydia and gonorrhea screening. Accessed February 23, 2021. www.uspreventiveservicestaskforce.org/Page/Document/RecommendationStatementFinal/chlamydia-and-gonorrhea-screening
56. Workowski KA, Bolan GA. Sexually transmitted diseases treatment guidelines, 2015. MMWR Morb Mortal Wkly Rep. 2015;64:1-135.
57. CDC. Sexually transmitted disease surveillance 2018. Accessed February 23, 2021. www.cdc.gov/std/stats18/gonorrhea.htm
5
59. Kann L, McManus T, Harris WA, et al. Youth risk behavior surveillance–United States, 2015. MMWR Surveill Summ. 2016;65:1-174.
60. CDC. LGBT youth. Accessed February 23, 2021. www.cdc.gov/lgbthealth/youth.htm
61. Johns MM, Lowry R, Rasberry CN, et al. Violence victimization, substance use, and suicide risk among sexual minority high school students – United States, 2015-2017. MMWR Morb Mortal Wkly Rep. 2018;67:1211-1215.
62. Pew Research Center. Teens, social media & technology 2018. . Accessed February 23, 2021. www.pewinternet.org/2018/05/31/teens-social-media-technology-2018/
63. Chassiakos YLR, Radesky J, Christakis D, et al. Children and adolescents and digital media. Pediatrics. 2016;138:e20162593.
64. Arora T, Albahri A, Omar OM, et al. The prospective association between electronic device use before bedtime and academic attainment in adolescents. J Adolesc Health. 2018;63:451-458.
65. Mishna F, Saini M, Solomon S. Ongoing and online: children and youth’s perceptions of cyber bullying. Child Youth Serv Rev. 2009;31:1222-1228.
66. Sengupta A, Chaudhuri A. Are social networking sites a source of online harassment for teens? Evidence from survey data. Child Youth Serv Rev. 2011;33:284-290.
PRACTICE RECOMMENDATIONS
› Consider using a 2-question screening tool for adolescents that asks about personal use of alcohol and use of alcohol by friends; this resource offers a risk assessment with recommendations. C
› Consider using the American Academy of Pediatrics Family Media Plan to provide age-specific guidelines to help parents or caregivers establish rules for online activities. C
Strength of recommendation (SOR)
A Good-quality patient-oriented evidence
B Inconsistent or limited-quality patient-oriented evidence
C Consensus, usual practice, opinion, disease-oriented evidence, case series
U.S. suicide rate in 2019 took first downturn in 14 years
In 2019, the U.S. suicide rate dropped for the first time in 14 years, driven largely by a significant decline in firearm-related deaths, according to a new analysis of National Vital Statistics System data.
Since firearms are the “most common and most lethal” mechanism of suicide, the drop in deaths is “particularly encouraging,” Deborah M. Stone, ScD, MSW, MPH, and associates wrote in the Morbidity and Mortality Weekly Report.
The national suicide rate decreased from 14.2 per 100,000 population in 2018 to 13.9 per 100,000 in 2019, a statistically significant drop of 2.1% that reversed a 20-year trend that saw the rate increase by 33% since 1999, they said.
The rate for firearm use, which is involved in half of all suicides, declined from 7.0 per 100,000 to 6.8, for a significant change of 2.9%, said Dr. Stone and associates at the Centers for Disease Control and Prevention’s National Center for Injury Prevention and Control.
The only other method with a drop in suicide rate from 2018 to 2019 was suffocation – the second most common mechanism of injury – but the relative change of 2.3% was not significant, they noted.
Significant declines also occurred in several subgroups: Whites; those aged 15-24, 55-64, and 65-74 years; and those living in counties classified as large fringe metropolitan or micropolitan (urban cluster of ≥ 10,000 but less than 50,000 population), they said, based on data from the National Vital Statistics System.
the investigators wrote.
The states with significant increases were Hawaii (30.3%) and Nebraska (20.1%), while declines in the suicide rate were significant in five states – Idaho, Indiana, Massachusetts, North Carolina, and Virginia, Dr. Stone and associates reported. Altogether, the rate fell in 31 states, increased in 18, and did not change in 2.
The significance of those changes varied between males and females. Declines were significant for females in Indiana, Massachusetts, and Washington, and for males in Florida, Kentucky, Massachusetts, North Carolina, and West Virginia. Minnesota was the only state with a significant increase among females, with Hawaii and Wyoming posting increases for males, they said.
As the response to the COVID-19 pandemic continues, the investigators pointed out, “prevention is more important than ever. Past research indicates that suicide rates remain stable or decline during infrastructure disruption (e.g., natural disasters), only to rise afterwards as the longer-term sequelae unfold in persons, families, and communities.”
In 2019, the U.S. suicide rate dropped for the first time in 14 years, driven largely by a significant decline in firearm-related deaths, according to a new analysis of National Vital Statistics System data.
Since firearms are the “most common and most lethal” mechanism of suicide, the drop in deaths is “particularly encouraging,” Deborah M. Stone, ScD, MSW, MPH, and associates wrote in the Morbidity and Mortality Weekly Report.
The national suicide rate decreased from 14.2 per 100,000 population in 2018 to 13.9 per 100,000 in 2019, a statistically significant drop of 2.1% that reversed a 20-year trend that saw the rate increase by 33% since 1999, they said.
The rate for firearm use, which is involved in half of all suicides, declined from 7.0 per 100,000 to 6.8, for a significant change of 2.9%, said Dr. Stone and associates at the Centers for Disease Control and Prevention’s National Center for Injury Prevention and Control.
The only other method with a drop in suicide rate from 2018 to 2019 was suffocation – the second most common mechanism of injury – but the relative change of 2.3% was not significant, they noted.
Significant declines also occurred in several subgroups: Whites; those aged 15-24, 55-64, and 65-74 years; and those living in counties classified as large fringe metropolitan or micropolitan (urban cluster of ≥ 10,000 but less than 50,000 population), they said, based on data from the National Vital Statistics System.
the investigators wrote.
The states with significant increases were Hawaii (30.3%) and Nebraska (20.1%), while declines in the suicide rate were significant in five states – Idaho, Indiana, Massachusetts, North Carolina, and Virginia, Dr. Stone and associates reported. Altogether, the rate fell in 31 states, increased in 18, and did not change in 2.
The significance of those changes varied between males and females. Declines were significant for females in Indiana, Massachusetts, and Washington, and for males in Florida, Kentucky, Massachusetts, North Carolina, and West Virginia. Minnesota was the only state with a significant increase among females, with Hawaii and Wyoming posting increases for males, they said.
As the response to the COVID-19 pandemic continues, the investigators pointed out, “prevention is more important than ever. Past research indicates that suicide rates remain stable or decline during infrastructure disruption (e.g., natural disasters), only to rise afterwards as the longer-term sequelae unfold in persons, families, and communities.”
In 2019, the U.S. suicide rate dropped for the first time in 14 years, driven largely by a significant decline in firearm-related deaths, according to a new analysis of National Vital Statistics System data.
Since firearms are the “most common and most lethal” mechanism of suicide, the drop in deaths is “particularly encouraging,” Deborah M. Stone, ScD, MSW, MPH, and associates wrote in the Morbidity and Mortality Weekly Report.
The national suicide rate decreased from 14.2 per 100,000 population in 2018 to 13.9 per 100,000 in 2019, a statistically significant drop of 2.1% that reversed a 20-year trend that saw the rate increase by 33% since 1999, they said.
The rate for firearm use, which is involved in half of all suicides, declined from 7.0 per 100,000 to 6.8, for a significant change of 2.9%, said Dr. Stone and associates at the Centers for Disease Control and Prevention’s National Center for Injury Prevention and Control.
The only other method with a drop in suicide rate from 2018 to 2019 was suffocation – the second most common mechanism of injury – but the relative change of 2.3% was not significant, they noted.
Significant declines also occurred in several subgroups: Whites; those aged 15-24, 55-64, and 65-74 years; and those living in counties classified as large fringe metropolitan or micropolitan (urban cluster of ≥ 10,000 but less than 50,000 population), they said, based on data from the National Vital Statistics System.
the investigators wrote.
The states with significant increases were Hawaii (30.3%) and Nebraska (20.1%), while declines in the suicide rate were significant in five states – Idaho, Indiana, Massachusetts, North Carolina, and Virginia, Dr. Stone and associates reported. Altogether, the rate fell in 31 states, increased in 18, and did not change in 2.
The significance of those changes varied between males and females. Declines were significant for females in Indiana, Massachusetts, and Washington, and for males in Florida, Kentucky, Massachusetts, North Carolina, and West Virginia. Minnesota was the only state with a significant increase among females, with Hawaii and Wyoming posting increases for males, they said.
As the response to the COVID-19 pandemic continues, the investigators pointed out, “prevention is more important than ever. Past research indicates that suicide rates remain stable or decline during infrastructure disruption (e.g., natural disasters), only to rise afterwards as the longer-term sequelae unfold in persons, families, and communities.”
FROM MMWR
Which detoxification regimens are effective for alcohol withdrawal syndrome?
EVIDENCE SUMMARY
Benzodiazepines work—but how do they compare?
A 2010 Cochrane meta-analysis of 64 RCTs and controlled clinical trials (CCTs; N = 4309) evaluated the use of benzodiazepines for treatment of AWS in adults.1 This systematic review compared benzodiazepines
- vs placebo (10 studies)
- vs other drugs, including phenobarbital, carbamazepine, topiramate, lamotrigine, gabapentin, haloperidol, clonidine, hydroxyzine, propranolol, and baclofen (42 studies)
- to other benzodiazepines, including chlordiazepoxide, alprazolam, diazepam, and lorazepam (18 studies)
- in combination with other drugs vs other drugs alone (3 studies)
- administered on a fixed schedule vs symptom-triggered administration (3 studies).
Primary outcomes included efficacy (alcohol withdrawal seizures, alcohol withdrawal delirium, alcohol withdrawal symptoms, global improvement), safety (adverse events and severe, life-threatening adverse events), and acceptability (dropouts and dropouts due to adverse events).
Benzodiazepines performed better than placebo for seizures in 3 studies (N = 324), with a relative risk (RR) of 0.16 (95% confidence interval [CI], 0.04-0.69). Studies assessing the described outcomes between benzodiazepines and other drugs were often of small sample size and heterogeneous in interventions and outcomes, limiting the ability to draw clear conclusions regarding benzodiazepine superiority. Comparisons of different benzodiazepines with each other and comparisons of benzodiazepines combined with other drugs vs other drugs alone did not reach statistical significance. Data on harms of benzodiazepines were lacking.
Anticonvulsants are not better than placebo for AWS
Another 2010 Cochrane meta-analysis of 56 RCTs and CCTs (N = 4076) evaluated the use of anticonvulsants for AWS.2 This systematic review compared anticonvulsants
- vs placebo (17 studies)
- vs other drugs, such as bromocriptine, piracetam, gamma-hydroxybutyric acid, trifluoperazine, clonidine, and various benzodiazepines (32 studies)
- to other anticonvulsants (10 studies)
- in combination with other drugs vs other drugs alone (6 studies)
- in combination with other drugs vs different anticonvulsants (1 study).
Primary outcomes included reductions in alcohol withdrawal seizures, adverse events, and acceptability of medication as indicated by participant dropouts.
Anticonvulsants were not superior to placebo for any outcome. Three studies (N = 260) favored carbamazepine over benzodiazepine (oxazepam or lorazepam) for 1 secondary outcome: a reduction of Clinical Institute Withdrawal Assessment of Alcohol Scale (CIWA-Ar) score (maximum score of 7; mean difference [MD] = –1 [95% CI, –1.9 to –0.2]).
Continue to: Gabapentin is effective; less sedating than chlordiazepoxide
Gabapentin is effective; less sedating than chlordiazepoxide
A 2013 RCT of US veterans with AWS (N = 26; 25 men; average age, 53.5 years) compared gabapentin and chlordiazepoxide.3 Endpoints were ratings on the Epworth Sleepiness Scale (ESS; maximum score = 24), Penn Alcohol Craving Scale (PACS; maximum score, 30), and CIWA-Ar.
In the early treatment period (Days 1-4), ESS and PACS scores did not differ significantly between groups. At end of treatment (Days 5-7), ESS and PACS scores were lower in gabapentin-treated patients (ESS: MD = –3.7; 95% CI, –7.2 to –0.19; P = .04; PACS: MD = –6.05; 95% CI –12.82 to 0.72; P = .08). CIWA-Ar did not differ between treatment groups.
Recommendations from others
In January 2020, the American Society of Addiction Medicine (ASAM) published a clinical practice guideline for alcohol withdrawal management. Protocols for diagnosis, assessment, level of care determination, and management are delineated.4
Benzodiazepines are the first-line treatment for moderate-to-severe AWS, or when there is risk for severe AWS. In the ambulatory setting, when AWS is mild and there is no risk for worsening, AWS can be managed with supportive care or with either benzodiazepines, gabapentin, or carbamazepine as monotherapy. ASAM recommends long-acting benzodiazepines (eg, chlordiazepoxide or diazepam) over short-acting benzodiazepines (eg, alprazolam or lorazepam), except in the elderly and those with liver or lung disease.5
Editor’s takeaway
Dozens of small trials and meta-analyses confirm the benefits (sometimes marginal) of sedation to treat alcohol withdrawal. Given that the evidence fails to point to the superiority of 1 agent over another, it seems reasonable to make treatment decisions based on physician and perhaps patient preference. This review does not support a change in clinical practice.
1. Amato L, Minozzi S, Vecchi S, et al. Benzodiazepines for alcohol withdrawal. Cochrane Database Syst Rev. 2010;(3):CD005063.
2. Minozzi S, Amato L, Vecchi S, et al. Anticonvulsants for alcohol withdrawal. Cochrane Database Syst Rev. 2010;(3):CD005064.
3. Stock CJ, Carpenter L, Ying J, et al. Gabapentin versus chlordiazepoxide for outpatient alcohol detoxification treatment. Ann Pharmacother. 2013;47:961-969.
4. American Society of Addiction Medicine. The ASAM Clinical Practice Guideline on Alcohol Withdrawal Management 2020. Accessed March 2, 2021. www.asam.org/docs/default-source/quality-science/the_asam_clinical_practice_guideline_on_alcohol-1.pdf
5. Ries RK, Fiellin DA, Miller SC, et al. The ASAM Principles of Addiction Medicine. 4th ed. Lippincott Williams & Wilkins; 2014.
EVIDENCE SUMMARY
Benzodiazepines work—but how do they compare?
A 2010 Cochrane meta-analysis of 64 RCTs and controlled clinical trials (CCTs; N = 4309) evaluated the use of benzodiazepines for treatment of AWS in adults.1 This systematic review compared benzodiazepines
- vs placebo (10 studies)
- vs other drugs, including phenobarbital, carbamazepine, topiramate, lamotrigine, gabapentin, haloperidol, clonidine, hydroxyzine, propranolol, and baclofen (42 studies)
- to other benzodiazepines, including chlordiazepoxide, alprazolam, diazepam, and lorazepam (18 studies)
- in combination with other drugs vs other drugs alone (3 studies)
- administered on a fixed schedule vs symptom-triggered administration (3 studies).
Primary outcomes included efficacy (alcohol withdrawal seizures, alcohol withdrawal delirium, alcohol withdrawal symptoms, global improvement), safety (adverse events and severe, life-threatening adverse events), and acceptability (dropouts and dropouts due to adverse events).
Benzodiazepines performed better than placebo for seizures in 3 studies (N = 324), with a relative risk (RR) of 0.16 (95% confidence interval [CI], 0.04-0.69). Studies assessing the described outcomes between benzodiazepines and other drugs were often of small sample size and heterogeneous in interventions and outcomes, limiting the ability to draw clear conclusions regarding benzodiazepine superiority. Comparisons of different benzodiazepines with each other and comparisons of benzodiazepines combined with other drugs vs other drugs alone did not reach statistical significance. Data on harms of benzodiazepines were lacking.
Anticonvulsants are not better than placebo for AWS
Another 2010 Cochrane meta-analysis of 56 RCTs and CCTs (N = 4076) evaluated the use of anticonvulsants for AWS.2 This systematic review compared anticonvulsants
- vs placebo (17 studies)
- vs other drugs, such as bromocriptine, piracetam, gamma-hydroxybutyric acid, trifluoperazine, clonidine, and various benzodiazepines (32 studies)
- to other anticonvulsants (10 studies)
- in combination with other drugs vs other drugs alone (6 studies)
- in combination with other drugs vs different anticonvulsants (1 study).
Primary outcomes included reductions in alcohol withdrawal seizures, adverse events, and acceptability of medication as indicated by participant dropouts.
Anticonvulsants were not superior to placebo for any outcome. Three studies (N = 260) favored carbamazepine over benzodiazepine (oxazepam or lorazepam) for 1 secondary outcome: a reduction of Clinical Institute Withdrawal Assessment of Alcohol Scale (CIWA-Ar) score (maximum score of 7; mean difference [MD] = –1 [95% CI, –1.9 to –0.2]).
Continue to: Gabapentin is effective; less sedating than chlordiazepoxide
Gabapentin is effective; less sedating than chlordiazepoxide
A 2013 RCT of US veterans with AWS (N = 26; 25 men; average age, 53.5 years) compared gabapentin and chlordiazepoxide.3 Endpoints were ratings on the Epworth Sleepiness Scale (ESS; maximum score = 24), Penn Alcohol Craving Scale (PACS; maximum score, 30), and CIWA-Ar.
In the early treatment period (Days 1-4), ESS and PACS scores did not differ significantly between groups. At end of treatment (Days 5-7), ESS and PACS scores were lower in gabapentin-treated patients (ESS: MD = –3.7; 95% CI, –7.2 to –0.19; P = .04; PACS: MD = –6.05; 95% CI –12.82 to 0.72; P = .08). CIWA-Ar did not differ between treatment groups.
Recommendations from others
In January 2020, the American Society of Addiction Medicine (ASAM) published a clinical practice guideline for alcohol withdrawal management. Protocols for diagnosis, assessment, level of care determination, and management are delineated.4
Benzodiazepines are the first-line treatment for moderate-to-severe AWS, or when there is risk for severe AWS. In the ambulatory setting, when AWS is mild and there is no risk for worsening, AWS can be managed with supportive care or with either benzodiazepines, gabapentin, or carbamazepine as monotherapy. ASAM recommends long-acting benzodiazepines (eg, chlordiazepoxide or diazepam) over short-acting benzodiazepines (eg, alprazolam or lorazepam), except in the elderly and those with liver or lung disease.5
Editor’s takeaway
Dozens of small trials and meta-analyses confirm the benefits (sometimes marginal) of sedation to treat alcohol withdrawal. Given that the evidence fails to point to the superiority of 1 agent over another, it seems reasonable to make treatment decisions based on physician and perhaps patient preference. This review does not support a change in clinical practice.
EVIDENCE SUMMARY
Benzodiazepines work—but how do they compare?
A 2010 Cochrane meta-analysis of 64 RCTs and controlled clinical trials (CCTs; N = 4309) evaluated the use of benzodiazepines for treatment of AWS in adults.1 This systematic review compared benzodiazepines
- vs placebo (10 studies)
- vs other drugs, including phenobarbital, carbamazepine, topiramate, lamotrigine, gabapentin, haloperidol, clonidine, hydroxyzine, propranolol, and baclofen (42 studies)
- to other benzodiazepines, including chlordiazepoxide, alprazolam, diazepam, and lorazepam (18 studies)
- in combination with other drugs vs other drugs alone (3 studies)
- administered on a fixed schedule vs symptom-triggered administration (3 studies).
Primary outcomes included efficacy (alcohol withdrawal seizures, alcohol withdrawal delirium, alcohol withdrawal symptoms, global improvement), safety (adverse events and severe, life-threatening adverse events), and acceptability (dropouts and dropouts due to adverse events).
Benzodiazepines performed better than placebo for seizures in 3 studies (N = 324), with a relative risk (RR) of 0.16 (95% confidence interval [CI], 0.04-0.69). Studies assessing the described outcomes between benzodiazepines and other drugs were often of small sample size and heterogeneous in interventions and outcomes, limiting the ability to draw clear conclusions regarding benzodiazepine superiority. Comparisons of different benzodiazepines with each other and comparisons of benzodiazepines combined with other drugs vs other drugs alone did not reach statistical significance. Data on harms of benzodiazepines were lacking.
Anticonvulsants are not better than placebo for AWS
Another 2010 Cochrane meta-analysis of 56 RCTs and CCTs (N = 4076) evaluated the use of anticonvulsants for AWS.2 This systematic review compared anticonvulsants
- vs placebo (17 studies)
- vs other drugs, such as bromocriptine, piracetam, gamma-hydroxybutyric acid, trifluoperazine, clonidine, and various benzodiazepines (32 studies)
- to other anticonvulsants (10 studies)
- in combination with other drugs vs other drugs alone (6 studies)
- in combination with other drugs vs different anticonvulsants (1 study).
Primary outcomes included reductions in alcohol withdrawal seizures, adverse events, and acceptability of medication as indicated by participant dropouts.
Anticonvulsants were not superior to placebo for any outcome. Three studies (N = 260) favored carbamazepine over benzodiazepine (oxazepam or lorazepam) for 1 secondary outcome: a reduction of Clinical Institute Withdrawal Assessment of Alcohol Scale (CIWA-Ar) score (maximum score of 7; mean difference [MD] = –1 [95% CI, –1.9 to –0.2]).
Continue to: Gabapentin is effective; less sedating than chlordiazepoxide
Gabapentin is effective; less sedating than chlordiazepoxide
A 2013 RCT of US veterans with AWS (N = 26; 25 men; average age, 53.5 years) compared gabapentin and chlordiazepoxide.3 Endpoints were ratings on the Epworth Sleepiness Scale (ESS; maximum score = 24), Penn Alcohol Craving Scale (PACS; maximum score, 30), and CIWA-Ar.
In the early treatment period (Days 1-4), ESS and PACS scores did not differ significantly between groups. At end of treatment (Days 5-7), ESS and PACS scores were lower in gabapentin-treated patients (ESS: MD = –3.7; 95% CI, –7.2 to –0.19; P = .04; PACS: MD = –6.05; 95% CI –12.82 to 0.72; P = .08). CIWA-Ar did not differ between treatment groups.
Recommendations from others
In January 2020, the American Society of Addiction Medicine (ASAM) published a clinical practice guideline for alcohol withdrawal management. Protocols for diagnosis, assessment, level of care determination, and management are delineated.4
Benzodiazepines are the first-line treatment for moderate-to-severe AWS, or when there is risk for severe AWS. In the ambulatory setting, when AWS is mild and there is no risk for worsening, AWS can be managed with supportive care or with either benzodiazepines, gabapentin, or carbamazepine as monotherapy. ASAM recommends long-acting benzodiazepines (eg, chlordiazepoxide or diazepam) over short-acting benzodiazepines (eg, alprazolam or lorazepam), except in the elderly and those with liver or lung disease.5
Editor’s takeaway
Dozens of small trials and meta-analyses confirm the benefits (sometimes marginal) of sedation to treat alcohol withdrawal. Given that the evidence fails to point to the superiority of 1 agent over another, it seems reasonable to make treatment decisions based on physician and perhaps patient preference. This review does not support a change in clinical practice.
1. Amato L, Minozzi S, Vecchi S, et al. Benzodiazepines for alcohol withdrawal. Cochrane Database Syst Rev. 2010;(3):CD005063.
2. Minozzi S, Amato L, Vecchi S, et al. Anticonvulsants for alcohol withdrawal. Cochrane Database Syst Rev. 2010;(3):CD005064.
3. Stock CJ, Carpenter L, Ying J, et al. Gabapentin versus chlordiazepoxide for outpatient alcohol detoxification treatment. Ann Pharmacother. 2013;47:961-969.
4. American Society of Addiction Medicine. The ASAM Clinical Practice Guideline on Alcohol Withdrawal Management 2020. Accessed March 2, 2021. www.asam.org/docs/default-source/quality-science/the_asam_clinical_practice_guideline_on_alcohol-1.pdf
5. Ries RK, Fiellin DA, Miller SC, et al. The ASAM Principles of Addiction Medicine. 4th ed. Lippincott Williams & Wilkins; 2014.
1. Amato L, Minozzi S, Vecchi S, et al. Benzodiazepines for alcohol withdrawal. Cochrane Database Syst Rev. 2010;(3):CD005063.
2. Minozzi S, Amato L, Vecchi S, et al. Anticonvulsants for alcohol withdrawal. Cochrane Database Syst Rev. 2010;(3):CD005064.
3. Stock CJ, Carpenter L, Ying J, et al. Gabapentin versus chlordiazepoxide for outpatient alcohol detoxification treatment. Ann Pharmacother. 2013;47:961-969.
4. American Society of Addiction Medicine. The ASAM Clinical Practice Guideline on Alcohol Withdrawal Management 2020. Accessed March 2, 2021. www.asam.org/docs/default-source/quality-science/the_asam_clinical_practice_guideline_on_alcohol-1.pdf
5. Ries RK, Fiellin DA, Miller SC, et al. The ASAM Principles of Addiction Medicine. 4th ed. Lippincott Williams & Wilkins; 2014.
EVIDENCE-BASED ANSWER:
Benzodiazepines remain the first-line regimen for alcohol withdrawal syndrome (AWS) and are the only class more effective than placebo for reducing seizure (strength of recommendation [SOR]: B, based on 3 medium-quality randomized controlled trials [RCTs]). Anticonvulsants are no more effective than placebo at reducing seizures (SOR: B, based on 10 moderate-quality RCTs). Gabapentin reduces withdrawal symptoms and is less sedating than benzodiazepines (SOR: B, based on 1 medium-quality RCT). Carbamazepine also reduces withdrawal symptoms (SOR: B, based on 3 RCTs). Evidence of benzodiazepine superiority to other drugs with respect to safety is lacking (SOR: A, based on a meta-analysis).
14-year-old girl • history of bullying • lack of social support • multiple linear scars on breasts • Dx?
THE CASE
A 14-year-old girl with no significant medical history presented to the office accompanied by her mother for a routine well-adolescent visit. She attended school online due to a history of severe bullying and, when interviewed alone, admitted to a lack of a social life as a result. On questioning, she denied tobacco, alcohol, or illicit drug use. Her gender identity was female. Her sexual orientation was toward both males and females, but she was not sexually active. She denied exposure to physical or emotional violence at home and said she did not feel depressed or think about suicide.
Physical examination revealed multiple erythematous linear scars surrounding the areola of both breasts. When questioned about these lesions, she admitted to cutting herself on the breasts during the past several months but again denied suicidal intent. She believed that her behavior was a normal coping mechanism.
The physical exam was otherwise normal. Lab results, including thyroid-stimulating hormone and complete blood count, were within normal limits.
THE DIAGNOSIS
The physical exam findings and the patient’s self report pointed to a diagnosis of nonsuicidal self-injurious (NSSI) behavior involving cutting.
DISCUSSION
The NSSI behavior displayed by this patient is a common biopsychosocial disorder observed in adolescents. Self-injury is defined as the deliberate injuring of body tissues without suicidal intent.1 Self-injurious behavior typically begins when patients are 13 to 16 years of age, and cutting is the most common form. Most acts occur on the arms, legs, wrists, and stomach.2 Studies have shown that the prevalence of this behavior is on the rise among adolescents, from about 7% in 2014 to between 14% and 24% in 2015.3
Risk for suicide. Although a feature of NSSI is the lack of suicidal intent, this type of high-risk behavior is associated with past, present, and future suicide attempts. It is important for physicians to identify NSSI in an adolescent, as it is linked to a 7-fold increased risk for a suicide attempt.3
Screening for NSSI. Less than one-fifth of adolescents who injure themselves come to the attention of health care providers.4 We propose that primary care physicians add NSSI to the list of risky behaviors—including drug abuse, sexual activity, and depression—for which they screen during well-child visits.
Continue to: Identifying risk factors
Identifying risk factors. The case patient experienced bullying and reported a nonheterosexual orientation, both of which have been demonstrated as strong risk factors for NSSI.5 Female gender has also been identified as a risk factor for NSSI.3
In adolescent psychiatric samples, prevalence rates of NSSI were found to be as high as 60% for 1 incident of NSSI and around 50% for repetitive NSSI.6 NSSI coincides with other psychiatric comorbidities, including eating disorders, mood disorders (depression), anxiety disorders, posttraumatic stress disorder, and borderline personality disorder.3 In a study of 93 subjects, each of whom was a self-reported abuse survivor with a history of self-injury, 96% were in therapy for diagnoses that included posttraumatic stress disorder (73%), dissociative disorder (40%), borderline personality disorder (37%), and multiple personality disorder (29%).7
The experience of adverse childhood events also increases risk for NSSI. This includes parental neglect, abuse, or deprivation.6 Insecure paternal attachment and parental neglect are significant predictors for women, while childhood separation is a primary predictor for men.8 Indirect childhood maltreatment, such as witnessing domestic violence or increased parental critique, is also associated with NSSI.8 NSSI is also more prevalent among young people who identify with a subculture such as gothic or emo.6
Why they do it and how to help
In multiple studies aimed at identifying reasons for self-injury, converging evidence suggests that nearly all patients act with the intent of alleviating negative affect.9 Patients self-harm to regulate distress, anxiety, and frustration that they perceive to be intolerable.9 They may self-harm to generate feeling when emotionally empty or to avert suicidal intent.9 For others, self-harm is a way to communicate their distress.
How to proceed. After a physician identifies NSSI, the patient should be assessed for suicidality and medical severity of the injury.3 Factors associated with higher likelihood of suicidality in patients with NSSI include multiple self-injurious methods and locations, early age of onset, longer history of NSSI, recent worsening of the injuries, simultaneous substance use, and the perception that the patient is addicted to self-injury.10
Continue to: It is also important...
It is also important to ask the patient whether she or he has told anyone about the behavior. Participation in NSSI communities may reinforce it.3
Treatment found to be effective for NSSI involves dialectical behavioral therapy, cognitive behavioral therapy, and mentalization-based therapy.11
Our patient was admitted to the hospital several weeks after her well visit because she expressed suicidal ideation. After being discharged, she was referred to outpatient Psychiatry with a treatment plan that included cognitive behavioral therapy.
THE TAKEAWAY
While our patient may have concealed her self-injurious experience because of stigma and concern about others’ reactions, there were several risk factors for NSSI in her history that prompted further investigation with a skin exam.
If a patient presents with 1 or more risk factors, an initial assessment for possible NSSI should be performed with detailed history-taking and a skin exam. Once NSSI is identified, the initial response and tone of questioning toward the patient need to convey a sense of genuine curiosity about the patient’s experience. From there, the physician can avail the patient to the proper treatment modalities.
NSSI patients can be resistant to sharing and participating in support groups. However, a referred counselor can follow up with a stepwise approach to slowly gain the trust of the individual, find the root cause, and get the patient to a point where she or he is ready to start the necessary treatment.
1. Klonsky ED, Glenn CR. Resisting urges to self-injure. Behav Cogn Psychother. 2008;36:211-220. doi: 10.1017/S1352465808004128
2. Whitlock J, Eckenrode J, Silverman D. Self-injurious behaviors in a college population. Pediatrics. 2006;117:1939-1948. doi: 10.1542/peds.2005-2543
3. Lewis SP, Heath NL. Non-suicidal self-injury among youth. J Pediatr. 2015;166:526-630. doi: 10.1016/j.jpeds.2014.11.062
4. Ystgaard M, Arensman E, Hawton K, et al. Deliberate self-harm in adolescents: comparison between those who receive help following self-harm and those who do not. J Adolesc. 2009;32: 875-891.
5. Lereya ST, Copeland WE, Costello EJ, et al. Adult mental health consequences of peer bullying and maltreatment in childhood: two cohorts in two countries. Lancet Psychiatry. 2015;2:524-531. doi: 10.1016/S2215-0366(15)00165-0
6. Brown RC, Plener PL. Non-suicidal self-injury in adolescence. Curr Psychiatry Rep. 2017;19:20. doi: 10.1007/s11920-017-0767-9
7. Briere J, Gil E. Self-mutilation in clinical and general population samples: prevalence, correlates, and functions. Am J Orthopsychiatry. 1998;68:609-620. doi:10.1037/h0080369
8. Gratz KL, Conrad SD, Roemer L. Risk factors for deliberate self-harm among college students. Am J Orthopsychiatry. 2002;1:128-140. doi: 10.1037//0002-9432.72.1.128
9. Klonsky ED. The functions of deliberate self-injury: a review of the evidence. Clin Psychol Rev. 2007;27:226-239.
10. Nock MK, Joiner Jr. TE, Gordon KH, et al. Non-suicidal self-injury among adolescents: diagnostic correlates and relation to suicide attempts. Psychiatry Res. 2006;144:65-72. doi: 10.1016/j.psychres.2006.05.010
11. Lewis SP, Baker TG. The possible risks of self-injury websites: a content analysis. Arch Suicide Res. 2011;15:390-396. doi: 10.1080/13811118.2011.616154
THE CASE
A 14-year-old girl with no significant medical history presented to the office accompanied by her mother for a routine well-adolescent visit. She attended school online due to a history of severe bullying and, when interviewed alone, admitted to a lack of a social life as a result. On questioning, she denied tobacco, alcohol, or illicit drug use. Her gender identity was female. Her sexual orientation was toward both males and females, but she was not sexually active. She denied exposure to physical or emotional violence at home and said she did not feel depressed or think about suicide.
Physical examination revealed multiple erythematous linear scars surrounding the areola of both breasts. When questioned about these lesions, she admitted to cutting herself on the breasts during the past several months but again denied suicidal intent. She believed that her behavior was a normal coping mechanism.
The physical exam was otherwise normal. Lab results, including thyroid-stimulating hormone and complete blood count, were within normal limits.
THE DIAGNOSIS
The physical exam findings and the patient’s self report pointed to a diagnosis of nonsuicidal self-injurious (NSSI) behavior involving cutting.
DISCUSSION
The NSSI behavior displayed by this patient is a common biopsychosocial disorder observed in adolescents. Self-injury is defined as the deliberate injuring of body tissues without suicidal intent.1 Self-injurious behavior typically begins when patients are 13 to 16 years of age, and cutting is the most common form. Most acts occur on the arms, legs, wrists, and stomach.2 Studies have shown that the prevalence of this behavior is on the rise among adolescents, from about 7% in 2014 to between 14% and 24% in 2015.3
Risk for suicide. Although a feature of NSSI is the lack of suicidal intent, this type of high-risk behavior is associated with past, present, and future suicide attempts. It is important for physicians to identify NSSI in an adolescent, as it is linked to a 7-fold increased risk for a suicide attempt.3
Screening for NSSI. Less than one-fifth of adolescents who injure themselves come to the attention of health care providers.4 We propose that primary care physicians add NSSI to the list of risky behaviors—including drug abuse, sexual activity, and depression—for which they screen during well-child visits.
Continue to: Identifying risk factors
Identifying risk factors. The case patient experienced bullying and reported a nonheterosexual orientation, both of which have been demonstrated as strong risk factors for NSSI.5 Female gender has also been identified as a risk factor for NSSI.3
In adolescent psychiatric samples, prevalence rates of NSSI were found to be as high as 60% for 1 incident of NSSI and around 50% for repetitive NSSI.6 NSSI coincides with other psychiatric comorbidities, including eating disorders, mood disorders (depression), anxiety disorders, posttraumatic stress disorder, and borderline personality disorder.3 In a study of 93 subjects, each of whom was a self-reported abuse survivor with a history of self-injury, 96% were in therapy for diagnoses that included posttraumatic stress disorder (73%), dissociative disorder (40%), borderline personality disorder (37%), and multiple personality disorder (29%).7
The experience of adverse childhood events also increases risk for NSSI. This includes parental neglect, abuse, or deprivation.6 Insecure paternal attachment and parental neglect are significant predictors for women, while childhood separation is a primary predictor for men.8 Indirect childhood maltreatment, such as witnessing domestic violence or increased parental critique, is also associated with NSSI.8 NSSI is also more prevalent among young people who identify with a subculture such as gothic or emo.6
Why they do it and how to help
In multiple studies aimed at identifying reasons for self-injury, converging evidence suggests that nearly all patients act with the intent of alleviating negative affect.9 Patients self-harm to regulate distress, anxiety, and frustration that they perceive to be intolerable.9 They may self-harm to generate feeling when emotionally empty or to avert suicidal intent.9 For others, self-harm is a way to communicate their distress.
How to proceed. After a physician identifies NSSI, the patient should be assessed for suicidality and medical severity of the injury.3 Factors associated with higher likelihood of suicidality in patients with NSSI include multiple self-injurious methods and locations, early age of onset, longer history of NSSI, recent worsening of the injuries, simultaneous substance use, and the perception that the patient is addicted to self-injury.10
Continue to: It is also important...
It is also important to ask the patient whether she or he has told anyone about the behavior. Participation in NSSI communities may reinforce it.3
Treatment found to be effective for NSSI involves dialectical behavioral therapy, cognitive behavioral therapy, and mentalization-based therapy.11
Our patient was admitted to the hospital several weeks after her well visit because she expressed suicidal ideation. After being discharged, she was referred to outpatient Psychiatry with a treatment plan that included cognitive behavioral therapy.
THE TAKEAWAY
While our patient may have concealed her self-injurious experience because of stigma and concern about others’ reactions, there were several risk factors for NSSI in her history that prompted further investigation with a skin exam.
If a patient presents with 1 or more risk factors, an initial assessment for possible NSSI should be performed with detailed history-taking and a skin exam. Once NSSI is identified, the initial response and tone of questioning toward the patient need to convey a sense of genuine curiosity about the patient’s experience. From there, the physician can avail the patient to the proper treatment modalities.
NSSI patients can be resistant to sharing and participating in support groups. However, a referred counselor can follow up with a stepwise approach to slowly gain the trust of the individual, find the root cause, and get the patient to a point where she or he is ready to start the necessary treatment.
THE CASE
A 14-year-old girl with no significant medical history presented to the office accompanied by her mother for a routine well-adolescent visit. She attended school online due to a history of severe bullying and, when interviewed alone, admitted to a lack of a social life as a result. On questioning, she denied tobacco, alcohol, or illicit drug use. Her gender identity was female. Her sexual orientation was toward both males and females, but she was not sexually active. She denied exposure to physical or emotional violence at home and said she did not feel depressed or think about suicide.
Physical examination revealed multiple erythematous linear scars surrounding the areola of both breasts. When questioned about these lesions, she admitted to cutting herself on the breasts during the past several months but again denied suicidal intent. She believed that her behavior was a normal coping mechanism.
The physical exam was otherwise normal. Lab results, including thyroid-stimulating hormone and complete blood count, were within normal limits.
THE DIAGNOSIS
The physical exam findings and the patient’s self report pointed to a diagnosis of nonsuicidal self-injurious (NSSI) behavior involving cutting.
DISCUSSION
The NSSI behavior displayed by this patient is a common biopsychosocial disorder observed in adolescents. Self-injury is defined as the deliberate injuring of body tissues without suicidal intent.1 Self-injurious behavior typically begins when patients are 13 to 16 years of age, and cutting is the most common form. Most acts occur on the arms, legs, wrists, and stomach.2 Studies have shown that the prevalence of this behavior is on the rise among adolescents, from about 7% in 2014 to between 14% and 24% in 2015.3
Risk for suicide. Although a feature of NSSI is the lack of suicidal intent, this type of high-risk behavior is associated with past, present, and future suicide attempts. It is important for physicians to identify NSSI in an adolescent, as it is linked to a 7-fold increased risk for a suicide attempt.3
Screening for NSSI. Less than one-fifth of adolescents who injure themselves come to the attention of health care providers.4 We propose that primary care physicians add NSSI to the list of risky behaviors—including drug abuse, sexual activity, and depression—for which they screen during well-child visits.
Continue to: Identifying risk factors
Identifying risk factors. The case patient experienced bullying and reported a nonheterosexual orientation, both of which have been demonstrated as strong risk factors for NSSI.5 Female gender has also been identified as a risk factor for NSSI.3
In adolescent psychiatric samples, prevalence rates of NSSI were found to be as high as 60% for 1 incident of NSSI and around 50% for repetitive NSSI.6 NSSI coincides with other psychiatric comorbidities, including eating disorders, mood disorders (depression), anxiety disorders, posttraumatic stress disorder, and borderline personality disorder.3 In a study of 93 subjects, each of whom was a self-reported abuse survivor with a history of self-injury, 96% were in therapy for diagnoses that included posttraumatic stress disorder (73%), dissociative disorder (40%), borderline personality disorder (37%), and multiple personality disorder (29%).7
The experience of adverse childhood events also increases risk for NSSI. This includes parental neglect, abuse, or deprivation.6 Insecure paternal attachment and parental neglect are significant predictors for women, while childhood separation is a primary predictor for men.8 Indirect childhood maltreatment, such as witnessing domestic violence or increased parental critique, is also associated with NSSI.8 NSSI is also more prevalent among young people who identify with a subculture such as gothic or emo.6
Why they do it and how to help
In multiple studies aimed at identifying reasons for self-injury, converging evidence suggests that nearly all patients act with the intent of alleviating negative affect.9 Patients self-harm to regulate distress, anxiety, and frustration that they perceive to be intolerable.9 They may self-harm to generate feeling when emotionally empty or to avert suicidal intent.9 For others, self-harm is a way to communicate their distress.
How to proceed. After a physician identifies NSSI, the patient should be assessed for suicidality and medical severity of the injury.3 Factors associated with higher likelihood of suicidality in patients with NSSI include multiple self-injurious methods and locations, early age of onset, longer history of NSSI, recent worsening of the injuries, simultaneous substance use, and the perception that the patient is addicted to self-injury.10
Continue to: It is also important...
It is also important to ask the patient whether she or he has told anyone about the behavior. Participation in NSSI communities may reinforce it.3
Treatment found to be effective for NSSI involves dialectical behavioral therapy, cognitive behavioral therapy, and mentalization-based therapy.11
Our patient was admitted to the hospital several weeks after her well visit because she expressed suicidal ideation. After being discharged, she was referred to outpatient Psychiatry with a treatment plan that included cognitive behavioral therapy.
THE TAKEAWAY
While our patient may have concealed her self-injurious experience because of stigma and concern about others’ reactions, there were several risk factors for NSSI in her history that prompted further investigation with a skin exam.
If a patient presents with 1 or more risk factors, an initial assessment for possible NSSI should be performed with detailed history-taking and a skin exam. Once NSSI is identified, the initial response and tone of questioning toward the patient need to convey a sense of genuine curiosity about the patient’s experience. From there, the physician can avail the patient to the proper treatment modalities.
NSSI patients can be resistant to sharing and participating in support groups. However, a referred counselor can follow up with a stepwise approach to slowly gain the trust of the individual, find the root cause, and get the patient to a point where she or he is ready to start the necessary treatment.
1. Klonsky ED, Glenn CR. Resisting urges to self-injure. Behav Cogn Psychother. 2008;36:211-220. doi: 10.1017/S1352465808004128
2. Whitlock J, Eckenrode J, Silverman D. Self-injurious behaviors in a college population. Pediatrics. 2006;117:1939-1948. doi: 10.1542/peds.2005-2543
3. Lewis SP, Heath NL. Non-suicidal self-injury among youth. J Pediatr. 2015;166:526-630. doi: 10.1016/j.jpeds.2014.11.062
4. Ystgaard M, Arensman E, Hawton K, et al. Deliberate self-harm in adolescents: comparison between those who receive help following self-harm and those who do not. J Adolesc. 2009;32: 875-891.
5. Lereya ST, Copeland WE, Costello EJ, et al. Adult mental health consequences of peer bullying and maltreatment in childhood: two cohorts in two countries. Lancet Psychiatry. 2015;2:524-531. doi: 10.1016/S2215-0366(15)00165-0
6. Brown RC, Plener PL. Non-suicidal self-injury in adolescence. Curr Psychiatry Rep. 2017;19:20. doi: 10.1007/s11920-017-0767-9
7. Briere J, Gil E. Self-mutilation in clinical and general population samples: prevalence, correlates, and functions. Am J Orthopsychiatry. 1998;68:609-620. doi:10.1037/h0080369
8. Gratz KL, Conrad SD, Roemer L. Risk factors for deliberate self-harm among college students. Am J Orthopsychiatry. 2002;1:128-140. doi: 10.1037//0002-9432.72.1.128
9. Klonsky ED. The functions of deliberate self-injury: a review of the evidence. Clin Psychol Rev. 2007;27:226-239.
10. Nock MK, Joiner Jr. TE, Gordon KH, et al. Non-suicidal self-injury among adolescents: diagnostic correlates and relation to suicide attempts. Psychiatry Res. 2006;144:65-72. doi: 10.1016/j.psychres.2006.05.010
11. Lewis SP, Baker TG. The possible risks of self-injury websites: a content analysis. Arch Suicide Res. 2011;15:390-396. doi: 10.1080/13811118.2011.616154
1. Klonsky ED, Glenn CR. Resisting urges to self-injure. Behav Cogn Psychother. 2008;36:211-220. doi: 10.1017/S1352465808004128
2. Whitlock J, Eckenrode J, Silverman D. Self-injurious behaviors in a college population. Pediatrics. 2006;117:1939-1948. doi: 10.1542/peds.2005-2543
3. Lewis SP, Heath NL. Non-suicidal self-injury among youth. J Pediatr. 2015;166:526-630. doi: 10.1016/j.jpeds.2014.11.062
4. Ystgaard M, Arensman E, Hawton K, et al. Deliberate self-harm in adolescents: comparison between those who receive help following self-harm and those who do not. J Adolesc. 2009;32: 875-891.
5. Lereya ST, Copeland WE, Costello EJ, et al. Adult mental health consequences of peer bullying and maltreatment in childhood: two cohorts in two countries. Lancet Psychiatry. 2015;2:524-531. doi: 10.1016/S2215-0366(15)00165-0
6. Brown RC, Plener PL. Non-suicidal self-injury in adolescence. Curr Psychiatry Rep. 2017;19:20. doi: 10.1007/s11920-017-0767-9
7. Briere J, Gil E. Self-mutilation in clinical and general population samples: prevalence, correlates, and functions. Am J Orthopsychiatry. 1998;68:609-620. doi:10.1037/h0080369
8. Gratz KL, Conrad SD, Roemer L. Risk factors for deliberate self-harm among college students. Am J Orthopsychiatry. 2002;1:128-140. doi: 10.1037//0002-9432.72.1.128
9. Klonsky ED. The functions of deliberate self-injury: a review of the evidence. Clin Psychol Rev. 2007;27:226-239.
10. Nock MK, Joiner Jr. TE, Gordon KH, et al. Non-suicidal self-injury among adolescents: diagnostic correlates and relation to suicide attempts. Psychiatry Res. 2006;144:65-72. doi: 10.1016/j.psychres.2006.05.010
11. Lewis SP, Baker TG. The possible risks of self-injury websites: a content analysis. Arch Suicide Res. 2011;15:390-396. doi: 10.1080/13811118.2011.616154
Functional neurological disorder: A practical guide to an elusive Dx
CASE
John D,* a 25-year-old patient with an otherwise unremarkable medical history, describes 2 months of daily headache, lower-extremity weakness, and unsteady gait that began fairly suddenly during his first deployment in the US Army. He explains that these symptoms affected his ability to perform his duties and necessitated an early return stateside for evaluation and treatment.
Mr. D denies precipitating trauma or unusual environmental exposures. He reports that, stateside now, symptoms continue to affect his ability to work and attend to personal and family responsibilities.
Asked about stressors, Mr. D notes the birth of his first child approximately 3 months ago, while he was deployed, and marital stressors. He denies suicidal or homicidal ideation.
* The patient’s name has been changed to protect his identity.
The challenge of identifying and managing FND
A functional neurological disorder (FND) is a constellation of psychological, physiological, and neurological symptoms, without an identifiable organic etiology, a conscious decision, or secondary gain for the patient,1 that adversely impacts functioning in 1 or more significant life domains.
Given the high throughput of patients in primary care practices, family physicians can expect to encounter suspected cases of FND in their practices. Regrettably, however, a lack of familiarity with the disorder and its related problems (eg, nonorganic paralysis, sensory loss, nonepileptic seizures, and abnormal movements) can add as much as $20,000 in excess direct and indirect costs of care for every such patient.1 In this article, we synthesize the recent literature on FND so that family physicians can expand their acumen in understanding, identifying, and evaluating patients whose presentation suggests FND.
An underrecognized entity
A precise estimate of the prevalence of FND is difficult to determine because the disorder is underrecognized and misdiagnosed and because it is often accompanied by the confounding of psychological and physiological comorbidities. A 2012 study estimated the annual incidence of FND to be 4 to 12 cases for every 100,000 people2; in primary care and outpatient neurology settings, prevalence is 6% to 22% of all patients.3,4 Stone and colleagues identified functional neurological symptoms as the second most common reason for outpatient neurology consultation,5 with 1 nonepileptic seizure patient seen for every 6 epileptic patients, and functional weakness presenting at the same rate as multiple sclerosis.6
Continue to: Demographics of patients with FND...
Demographics of patients with FND vary, depending on presenting neurological symptoms and disorder subtype. Existing data indicate a correlation between FND and younger age, female sex, physical disability,7 and a history of abuse or trauma.3,8 A challenge in concretely ascertaining the prevalence of FND is that conditions such as fibromyalgia, chronic pelvic pain, globus hystericus, and nonepileptic seizures can also be characterized as medically unexplained functional disorders, even within the network of neurology care.4
Misdiagnosis and bias are not uncommon
Ambiguity in classifying and evaluating FND can affect physicians’ perceptions, assessment, and care of patients with suggestive presenting symptoms. A major early challenge in diagnosing FND is the inconsistency of characterizing terminology (pseudoneurological, somatic, dissociative, conversion, psychogenic, hysterical, factitious, functional, medically unexplained9,10) and definitions in the literature. Neurological symptoms of unidentifiable organic cause can greatly diminish quality of life4; FND is a scientifically and clinically useful diagnosis for many combinations of nonrandomly co-occurring symptoms and clinical signs.
The pitfall of misdiagnosis. Remain cautious about making a diagnosis of FND by exclusion, which might yield an incorrect or false-negative finding because of an atypical presentation. It is important to avoid misdiagnosis by prematurely closing the differential diagnosis; instead, keep in mind that a medically unexplained diagnosis might be better explained by conducting a robust social and medical history and obtaining additional or collateral data, or both, along with appropriate consultation.4,9
Misdiagnosis can lead to a circuitous and costly work-up, with the potential to increase the patient’s distress. You can reduce this burden with early recognition of FND and centralized management of multidisciplinary care, which are more likely to lead to an accurate and timely diagnosis—paramount to empowering patients with access to the correct information and meaningful support needed to enhance treatment and self-care.9
Bias, haste, and dismissal are unproductive. Even with a clear definition of FND, it is not uncommon for a physician to rapidly assess a patient’s clinical signs, make a diagnosis of “unknown etiology,” or openly question the veracity of complaints. Furthermore, be aware of inadvertently characterizing FND using the prefix “pseudo” or the term “hysterical,” which can be psychologically discomforting for many patients, who legitimately experience inexplicable symptoms. Such pejoratives can lead to stigmatizing and misleading assessments and treatment paths4—courses of action that can cause early and, possibly, irreparable harm to the patient–physician relationship and increase the patient’s inclination to go “doctor-shopping,” with associated loss of continuity of care.
Why is it difficult to diagnose FND?
The latest (5th) edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) describes conversion, somatoform disorder, and FND synonymously.DSM-5 diagnostic criteria for conversion disorderare11:
- a specified type of symptom or deficit of altered voluntary motor or sensory function (eg, weakness, difficulty swallowing, slurred speech, seizures)
- clinical evidence of the incompatibility of the symptom or deficit and any recognized neurological or medical disorder
- incapability of better explaining the symptom or deficit as another medical or mental disorder.
- The symptom or deficit causes distress or impairment that (1) is clinically significant in occupational, social, or other important areas of function or (2) warrants medical evaluation.
The overarching feature of these criteria is the inconsistency of symptoms with recognized neurological, physiological, or psychiatric conditions. Although identification of psychological factors can help clarify and provide a treatment direction, such identification is not essential for making a diagnosis of FND. Malingering does not need to be refuted as part of establishing the diagnosis.12
Continue to: In contrast...
In contrast, the World Health Organization’s ICD-10 Classification of Mental and Behavioural Disorders groups diagnostic criteria for FND among the dissociative disorders13:
- Clinical features are specified for the individual dissociative disorder (motor, sensory, convulsions, mixed).
- Evidence is absent of a physical disorder that might explain symptoms.
- Evidence of psychological causation is present in clear temporal association with stressful events and problems or disturbed relationships, even if the patient denies such association.
Note the emphasis on psychological causation and exclusion of purposeful simulation of symptoms, as opposed to a primarily unconscious disconnection from the patient’s body or environment.
ICD-10 guidelines acknowledge the difficulty of finding definitive evidence of a psychological cause and recommend provisional diagnosis of FND if psychological factors are not readily apparent.14 Of note, many patients with FND are affected psychologically by their condition, with an impact on mood, behaviors, and interpersonal interactions, although not necessarily to a clinically diagnostic degree. Therefore, a psychiatric diagnosis alone is not a necessary precursor for the diagnosis of an FND.
CASE
History. Mr. D’s history is positive for light alcohol consumption (“2 or 3 cans of beer on weekends”) and chewing tobacco (he reports stopping 6 months earlier) and negative for substance abuse. The family history is positive for maternal hypertension and paternal suicide when the patient was 10 years old (no other known paternal history).
Physical findings. The review of systems is positive for intermittent palpitations, lower-extremity weakness causing unsteady gait, and generalized headache.
Vital signs are within normal limits, including blood pressure (120/82 mm Hg) and heart rate (110 beats/min). The patient is not in acute distress; he is awake, alert, and oriented × 3. No murmurs are heard; lungs are clear bilaterally to auscultation. There is no tenderness on abdominal palpation, and no hepatomegaly or splenomegaly; bowel sounds are normal. No significant bruising or lacerations are noted.
Neurology exam. Cranial nerves II-XII are intact. Pupils are equal and reactive to light. Reflexes are 2+ bilaterally. Muscle strength and tone are normal; no tremors are noted. Babinski signs are normal. A Romberg test is positive (swaying).
Continue to: Mr. D has an antalgic gait...
Mr. D has an antalgic gait with significant swaying (without falling); bent posture; and unsteadiness that requires a cane. However, he is able to get up and off the exam table without assistance, and to propel himself, by rolling a chair forward and backward, without difficulty.
Conducting a diagnostic examination
Taking the history. Certain clues can aid in the diagnosis of FND (TABLE 1).15 For example, the patient might have been seen in multiple specialty practices for a multitude of vague symptoms indicative of potentially related conditions (eg, chronic fatigue, allergies and sensitivities, fibromyalgia, and other chronic pain). The history might include repeated surgeries to investigate those symptoms (eg, laparoscopy, or hysterectomy at an early age). Taking time and care to explore all clinical clues, patient reports, and collateral data are therefore key to making an accurate diagnosis.
Note any discrepancies between the severity of reported symptoms and functional ability. A technique that can help elucidate a complex or ambiguous medical presentation is to ask the patient to list all their symptoms at the beginning of the interview. This has threefold benefit: You get a broad picture of the problem; the patient is unburdened of their concerns and experiences your validation; and a long list of symptoms can be an early clue to a diagnosis of FND.
Other helpful questions to determine the impact of symptoms on the patient’s well-being include inquiries about16:
- functional impairment
- onset and course of symptoms
- potential causal or correlating events
- dissociative episodes
- previous diagnoses and treatments
- the patient’s perceptions of, and emotional response to, their illness
- a history of abuse.
The physical examination to determine the presence of FND varies, depending on the functional area of impact (eg, motor, neurological, sensory, speech and swallowing). Pay particular attention to presenting signs and clues, and balance them with the patient’s report (or lack of report). Endeavor to demonstrate positive functional signs, such as a positive Hoover test, which relies on the principle of synergistic muscle contraction. You might see evidence of inconsistency, such as weakness or a change in gait, under observation, that seemingly resolves when the patient is getting on and off the exam table.16Table 215-24 describes areas affected by FND, characteristics of the disorder, and related diagnostic examinations.
Table 315,18,19 reviews validated special exams that can aid in making the diagnosis. Additional special tests are discussed in the literature.15-24 These tests can be helpful in narrowing the differential diagnosis but have not been validated and should be used with caution.
Some clinical signs associated with FND might be affected by other factors, including socioeconomic status, limited access to health care, low health literacy, poor communication skills, and physician bias. Keep these factors in mind during the visit, to avoid contributing further to health disparities among groups of patients affected by these problems.
Continue to: CASE
CASE
The work-up over the next month for Mr. D includes numerous studies, all yielding results that are negative or within normal limits: visual acuity; electrocardiography and an event monitor; laboratory testing (including a complete blood count, comprehensive metabolic panel, thyroid-stimulating hormone, creatine kinase, erythrocyte sedimentation rate, C-reactive protein, vitamin B12, folate, and vitamin D); magnetic resonance imaging of the brain and lumbar spine; lumbar puncture; and electromyography.
The score on the 9-item Patient Health Questionnaire for depression is 4 (severity: “none or minimal”); on the 7-item Generalized Anxiety Disorder scale, 0 (“no anxiety disorder”).
Referral. A neurology work-up of headache, lower extremity weakness, and unsteady gait to address several diagnostic possibilities, including migraine and multiple sclerosis, is within normal limits. A cardiology work-up of palpitations is negative for arrhythmias and other concerning findings.
Mr. D declines psychiatric and psychological evaluations.
Building a differential diagnosisis a formidable task
The differential diagnosis of FND is vast. It includes neurological, physiological, and psychiatric symptoms and disorders; somatization; and malingering (Table 4).6 Any disorder or condition in these areas that is in the differential diagnosis can be precipitated or exacerbated by stress; most, however, do not involve loss of physical function.12 In addition, the diagnosis of an FND does not necessarily exclude an organic disorder.
A patient’s presentation becomes complicated—and more difficult to treat—when functional symptoms and an unrelated underlying or early-stage neurological condition coexist. For example, a patient with epilepsy might also have dissociative seizures atop their organic disorder. Neurological disease is considered a risk factor for an overlying FND—just as the risk of depression or anxiety runs concurrently with other chronic diseases.14
Focus on clinical signs to narrow the differential. A thorough social and medical history and physical examination, as discussed earlier, help narrow the differential diagnosis of organic and medically unexplained disorders. Well-defined imaging or laboratory protocols do not exist to guide physicians to a definitive diagnosis, however.
Continue to: Psychiatric conditions
Psychiatric conditions can coexist with the diagnosis of FND, but might be unrelated. A systematic review of the literature showed that 17% to 42% of patients with FND had a concurrent anxiety disorder. Depression disorders were co-diagnosed in 19% to 71% of patients with FND; dissociative and personality disorders were noted, as well.25 However, coexisting psychiatric diagnosis might more likely be associated with distress from the presenting functional neurological symptoms, not linked to the FND diagnosis itself.12 This shift in understanding is reflected in the description of FND in the DSM-5.11
CASE
Mr. D reports debilitating headaches at return office visits. Trials of abortive triptans provide no relief; neither do control medications (beta-blockers, coenzyme Q10, magnesium, onabotulinumtoxinA [Botox], topiramate, and valproate). Lower-extremity weakness and unsteadiness are managed with supportive devices, including a cane, and physical therapy.
Importance of establishing a multidisciplinary approach
The complexity of FND lends itself to a multidisciplinary approach during evaluation and, eventually, for treatment. The assessment and diagnostic intervention that you provide, along with the contributions of consulted specialists (including neurology, physical and occupational therapy, psychiatry, psychology, and other mental health professionals) establishes a team-based approach that can increase the patient’s sense of support and reduce excessive testing and unnecessary medications, surgeries, and other treatments.26
Family physicians are in the ideal position to recognize the patient’s functional capacity and the quality of symptoms and to provide timely referral (eg, to Neurology and Psychiatry) for confirmation of the diagnosis and then treatment.
Evidence-based treatment options include:
- psychotherapy, with an emphasis on cognitive behavioral therapy
- physical therapy
- psychopharmacology
- promising combinations of physical and psychological treatment to improve long-term functionality.27
A promising diagnostic tool
The most significant update in the FND literature is on functional neuroimaging for assessing the disorder. Early findings suggest an intricate relationship between mind and body regarding the pathological distortion in FND. And, there is clear evidence that neuroimaging—specifically, functional magnetic resonance imaging—shows changes in brain activity that correspond to the patient’s symptom report. That said, imaging is not the recommended standard of care in the initial work-up of FND because of its cost and the fact that the diagnosis is principally a clinical undertaking.17,28
Call to action
Offer a generous ear. Begin the diagnostic pursuit by listening carefully and fully to the patient’s complaints, without arriving at a diagnosis with unwarranted bias or haste. This endeavor might require support from other clinical staff (eg, nurses, social workers, case managers) because the diagnostic process can be arduous and lengthy.
Continue to: Convey the diagnosis with sensitivity
Convey the diagnosis with sensitivity. Inquire about the patient’s perceptions and impairments to best personalize your diagnostic explanations. Delivery of the diagnosis might affect the patient’s acceptance and compliance with further testing and treatment of what is generally a persistent and treatment-resistant disorder; poor delivery of diagnostic information can impair the patient–physician relationship and increase the risk of disjointed care. Many patients find that improved patient–physician communication is therapeutic.29
Let the patient know that you’re taking her seriously. Validate patient concerns with a nonstigmatizing diagnostic label; discuss the diagnostic parameters and cause of symptoms in layman’s terms; and emphasize the potential for reversibility.30 Some patients are not satisfied with having a diagnosis of FND until they are reassured with normal results of testing and provided with referral; even then, some seek further reassurance.
Key tenets of managing care for patients who have been given a diagnosis of FND include:
- nonjudgmental, positive regard
- meaningful expression of empathy
- multidisciplinary coordination
- avoidance of unnecessary testing and harmful treatments
- descriptive and contextual explanations of the diagnosis.
Last, keep in mind that the course of treatment for FND is potentially prolonged and multilayered.
CASE
After many visits with his family physician and the neurology and cardiology specialists, as well as an extensive work-up, the physician approaches Mr. D with the possibility of a diagnosis of FND and proposes a multidisciplinary plan that includes:
- a course of physical and occupational therapy
- development of individualized cognitive behavioral tools
- weekly personal and marital counseling
- initiation of a selective serotonin reuptake inhibitor for anxiety
- monthly visits with his family physician.
Months after his return from deployment for evaluation and treatment, Mr. D is able to return to military duty. He reports that his quality of life has improved.
CORRESPONDENCE
Roselyn W. Clemente Fuentes, MD, FAAFP, Eglin Family Medicine Residency, 307 Boatner Road, Eglin AFB, FL 32547; roselynjan.w.fuentes.mil@mail.mil.
1. Konnopka A, Schaefert R, Heinrich S, et al. Economics of medically unexplained symptoms: a systematic review of the literature. Psychother Psychosom. 2012;81:265-275.
2. Carson AJ, Brown R, David AS, et al; on behalf of UK-FNS. Functional (conversion) neurological symptoms: research since the millennium. J Neurol Neurosurg Psychiatry. 2012;83:842-850.
3. Stone J, Carson A, Duncan R, et al. Who is referred to neurology clinics?—the diagnoses made in 3781 new patients. Clin Neurol Neurosurg. 2010;112:747-751.
4. Evens A, Vendetta L, Krebs K, et al. Medically unexplained neurologic symptoms: a primer for physicians who make the initial encounter. Am J Med. 2015;128:1059-1064.
5. Stone J, Reuber M, Carson A. Functional symptoms in neurology: mimics and chameleons. Pract Neurol. 2013;13:104-113.
6. Stone J, Warlow C, Sharpe M. The symptom of functional weakness: a controlled study of 107 patients. Brain. 2010;133:1537-1551.
7. Carson A, Stone J, Hibberd C, et al. Disability, distress and unemployment in neurology outpatients with symptoms ‘unexplained by organic disease’. J Neurol Neurosurg Psychiatry. 2011;82:810-813.
8. Fink P, Hansen MS, Oxhøj M-L. The prevalence of somatoform disorders among internal medical inpatients. J Psychosom Res. 2004;56:413-418.
9. Thomas LE. Are your patient’s medically unexplained symptoms really “all in her head”? Med Hypotheses. 2012;78:542-547.
10. Ding JM, Kanaan RAA. What should we say to patients with unexplained neurological symptoms? How explanation affects offence. J Psychosom Res. 2016;91:55-60.
11. Diagnostic and Statistical Manual of Mental Disorders (DSM-5). 5th ed. American Psychiatric Association; 2013.
12. Stone J, LaFrance WC Jr, Levenson JL, et al. Issues for DSM-5: Conversion disorder. Am J Psychiatry. 2010;167:626-627.
13. The ICD-10 Classification of Mental and Behavioural Disorders: Clinical Descriptions and Diagnostic Guidelines. World Health Organization; 1994. Accessed January 21, 2021. www.who.int/classifications/icd/en/bluebook.pdf
14. Stone J, Carson A, Duncan R, et al. Which neurological diseases are most likely to be associated with “symptoms unexplained by organic disease.” J Neurol. 2012;259:33-38.
15. Shaibani A, Sabbagh M. Pseudoneurologic syndromes: recognition and diagnosis. Am Fam Physician. 1998;57:2485-2494.
16. Stone J, Carson A, Sharpe M. Functional symptoms and signs in neurology: assessment and diagnosis. J Neurol Neurosurg Psychiatry. 2005;76(suppl 1):i2-i12.
17. Vuilleumier P. Brain circuits implicated in psychogenic paralysis in conversion disorders and hypnosis. Neurophysiol Clin. 2014;44:323-337.
18. McKee K, Glass S, Adams C, et al. The inpatient assessment and management of motor functional neurological disorders: an interdisciplinary perspective. Psychosomatics. 2018;59:358-368.
19. Daum C, Hubschmid M, Aybek S. The value of ‘positive’ clinical signs for weakness, sensory and gait disorders in conversion disorder: a systematic and narrative review. J Neurol Neurosurg Psychiatry. 2014;85:180-190.
20. Brown P, Thompson PD. Electrophysiological aids to the diagnosis of psychogenic jerks, spasms, and tremor. Mov Disord. 2001;16:595-599.
21. Ludwig L, McWhirter L, Williams S, et al. Functional coma. In: Hallett M, Stone J, Carson A, eds. Handbook of Clinical Neurology: Volume 139: Functional Neurologic Disorders. 1st ed. Academic Press; 2016:313.
22. Miller NR, Subramanian PS, Patel VR. Walsh and Hoyt’s Clinical Neuro-ophthalmology. 3rd ed. Wolters Kluwer; 2016:512-513.
23. Takazaki K, Stransky AD, Miller G. Psychogenic nonepileptic seizures: diagnosis, management, and bioethics. Pediatr Neurol. 2016;62:3-8.
24. Sahaya K, Dholakia SA, Sahota PK. Psychogenic non-epileptic seizures: a challenging entity. J Clin Neurosci. 2011;18:1602-1607.
25. Gelauff J, Stone J, Edwards M, et al. The prognosis of functional (psychogenic) motor symptoms: a systematic review. J Neurol Neurosurg Psychiatry. 2014;85:220-226.
26. Kranick SM, Gorrindo T, Hallett M. Psychogenic movement disorders and motor conversion: a roadmap for collaboration between neurology and psychiatry. Psychosomatics. 2011;52:109-116.
27. Edwards MJ, Bhatia KP. Functional (psychogenic) movement disorders: merging mind and brain. Lancet Neurol. 2012;11:250-260.
28. Burgmer M, Kugel H, Pfleiderer B, et al. The mirror neuron system under hypnosis—brain substrates of voluntary and involuntary motor activation in hypnotic paralysis. Cortex. 2013;49:437-445.
29. van Bokhoven MA, Koch H, van der Weijden T, et al. Influence of watchful waiting on satisfaction and anxiety among patients seeking care for unexplained complaints, Ann Fam Med. 2009;7:112-120.
30. Stone J, Carson A, Hallet M. Explanation as treatment for functional neurologic disorders. Handb Clin Neurol. 2016;139:543-553.
CASE
John D,* a 25-year-old patient with an otherwise unremarkable medical history, describes 2 months of daily headache, lower-extremity weakness, and unsteady gait that began fairly suddenly during his first deployment in the US Army. He explains that these symptoms affected his ability to perform his duties and necessitated an early return stateside for evaluation and treatment.
Mr. D denies precipitating trauma or unusual environmental exposures. He reports that, stateside now, symptoms continue to affect his ability to work and attend to personal and family responsibilities.
Asked about stressors, Mr. D notes the birth of his first child approximately 3 months ago, while he was deployed, and marital stressors. He denies suicidal or homicidal ideation.
* The patient’s name has been changed to protect his identity.
The challenge of identifying and managing FND
A functional neurological disorder (FND) is a constellation of psychological, physiological, and neurological symptoms, without an identifiable organic etiology, a conscious decision, or secondary gain for the patient,1 that adversely impacts functioning in 1 or more significant life domains.
Given the high throughput of patients in primary care practices, family physicians can expect to encounter suspected cases of FND in their practices. Regrettably, however, a lack of familiarity with the disorder and its related problems (eg, nonorganic paralysis, sensory loss, nonepileptic seizures, and abnormal movements) can add as much as $20,000 in excess direct and indirect costs of care for every such patient.1 In this article, we synthesize the recent literature on FND so that family physicians can expand their acumen in understanding, identifying, and evaluating patients whose presentation suggests FND.
An underrecognized entity
A precise estimate of the prevalence of FND is difficult to determine because the disorder is underrecognized and misdiagnosed and because it is often accompanied by the confounding of psychological and physiological comorbidities. A 2012 study estimated the annual incidence of FND to be 4 to 12 cases for every 100,000 people2; in primary care and outpatient neurology settings, prevalence is 6% to 22% of all patients.3,4 Stone and colleagues identified functional neurological symptoms as the second most common reason for outpatient neurology consultation,5 with 1 nonepileptic seizure patient seen for every 6 epileptic patients, and functional weakness presenting at the same rate as multiple sclerosis.6
Continue to: Demographics of patients with FND...
Demographics of patients with FND vary, depending on presenting neurological symptoms and disorder subtype. Existing data indicate a correlation between FND and younger age, female sex, physical disability,7 and a history of abuse or trauma.3,8 A challenge in concretely ascertaining the prevalence of FND is that conditions such as fibromyalgia, chronic pelvic pain, globus hystericus, and nonepileptic seizures can also be characterized as medically unexplained functional disorders, even within the network of neurology care.4
Misdiagnosis and bias are not uncommon
Ambiguity in classifying and evaluating FND can affect physicians’ perceptions, assessment, and care of patients with suggestive presenting symptoms. A major early challenge in diagnosing FND is the inconsistency of characterizing terminology (pseudoneurological, somatic, dissociative, conversion, psychogenic, hysterical, factitious, functional, medically unexplained9,10) and definitions in the literature. Neurological symptoms of unidentifiable organic cause can greatly diminish quality of life4; FND is a scientifically and clinically useful diagnosis for many combinations of nonrandomly co-occurring symptoms and clinical signs.
The pitfall of misdiagnosis. Remain cautious about making a diagnosis of FND by exclusion, which might yield an incorrect or false-negative finding because of an atypical presentation. It is important to avoid misdiagnosis by prematurely closing the differential diagnosis; instead, keep in mind that a medically unexplained diagnosis might be better explained by conducting a robust social and medical history and obtaining additional or collateral data, or both, along with appropriate consultation.4,9
Misdiagnosis can lead to a circuitous and costly work-up, with the potential to increase the patient’s distress. You can reduce this burden with early recognition of FND and centralized management of multidisciplinary care, which are more likely to lead to an accurate and timely diagnosis—paramount to empowering patients with access to the correct information and meaningful support needed to enhance treatment and self-care.9
Bias, haste, and dismissal are unproductive. Even with a clear definition of FND, it is not uncommon for a physician to rapidly assess a patient’s clinical signs, make a diagnosis of “unknown etiology,” or openly question the veracity of complaints. Furthermore, be aware of inadvertently characterizing FND using the prefix “pseudo” or the term “hysterical,” which can be psychologically discomforting for many patients, who legitimately experience inexplicable symptoms. Such pejoratives can lead to stigmatizing and misleading assessments and treatment paths4—courses of action that can cause early and, possibly, irreparable harm to the patient–physician relationship and increase the patient’s inclination to go “doctor-shopping,” with associated loss of continuity of care.
Why is it difficult to diagnose FND?
The latest (5th) edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) describes conversion, somatoform disorder, and FND synonymously.DSM-5 diagnostic criteria for conversion disorderare11:
- a specified type of symptom or deficit of altered voluntary motor or sensory function (eg, weakness, difficulty swallowing, slurred speech, seizures)
- clinical evidence of the incompatibility of the symptom or deficit and any recognized neurological or medical disorder
- incapability of better explaining the symptom or deficit as another medical or mental disorder.
- The symptom or deficit causes distress or impairment that (1) is clinically significant in occupational, social, or other important areas of function or (2) warrants medical evaluation.
The overarching feature of these criteria is the inconsistency of symptoms with recognized neurological, physiological, or psychiatric conditions. Although identification of psychological factors can help clarify and provide a treatment direction, such identification is not essential for making a diagnosis of FND. Malingering does not need to be refuted as part of establishing the diagnosis.12
Continue to: In contrast...
In contrast, the World Health Organization’s ICD-10 Classification of Mental and Behavioural Disorders groups diagnostic criteria for FND among the dissociative disorders13:
- Clinical features are specified for the individual dissociative disorder (motor, sensory, convulsions, mixed).
- Evidence is absent of a physical disorder that might explain symptoms.
- Evidence of psychological causation is present in clear temporal association with stressful events and problems or disturbed relationships, even if the patient denies such association.
Note the emphasis on psychological causation and exclusion of purposeful simulation of symptoms, as opposed to a primarily unconscious disconnection from the patient’s body or environment.
ICD-10 guidelines acknowledge the difficulty of finding definitive evidence of a psychological cause and recommend provisional diagnosis of FND if psychological factors are not readily apparent.14 Of note, many patients with FND are affected psychologically by their condition, with an impact on mood, behaviors, and interpersonal interactions, although not necessarily to a clinically diagnostic degree. Therefore, a psychiatric diagnosis alone is not a necessary precursor for the diagnosis of an FND.
CASE
History. Mr. D’s history is positive for light alcohol consumption (“2 or 3 cans of beer on weekends”) and chewing tobacco (he reports stopping 6 months earlier) and negative for substance abuse. The family history is positive for maternal hypertension and paternal suicide when the patient was 10 years old (no other known paternal history).
Physical findings. The review of systems is positive for intermittent palpitations, lower-extremity weakness causing unsteady gait, and generalized headache.
Vital signs are within normal limits, including blood pressure (120/82 mm Hg) and heart rate (110 beats/min). The patient is not in acute distress; he is awake, alert, and oriented × 3. No murmurs are heard; lungs are clear bilaterally to auscultation. There is no tenderness on abdominal palpation, and no hepatomegaly or splenomegaly; bowel sounds are normal. No significant bruising or lacerations are noted.
Neurology exam. Cranial nerves II-XII are intact. Pupils are equal and reactive to light. Reflexes are 2+ bilaterally. Muscle strength and tone are normal; no tremors are noted. Babinski signs are normal. A Romberg test is positive (swaying).
Continue to: Mr. D has an antalgic gait...
Mr. D has an antalgic gait with significant swaying (without falling); bent posture; and unsteadiness that requires a cane. However, he is able to get up and off the exam table without assistance, and to propel himself, by rolling a chair forward and backward, without difficulty.
Conducting a diagnostic examination
Taking the history. Certain clues can aid in the diagnosis of FND (TABLE 1).15 For example, the patient might have been seen in multiple specialty practices for a multitude of vague symptoms indicative of potentially related conditions (eg, chronic fatigue, allergies and sensitivities, fibromyalgia, and other chronic pain). The history might include repeated surgeries to investigate those symptoms (eg, laparoscopy, or hysterectomy at an early age). Taking time and care to explore all clinical clues, patient reports, and collateral data are therefore key to making an accurate diagnosis.
Note any discrepancies between the severity of reported symptoms and functional ability. A technique that can help elucidate a complex or ambiguous medical presentation is to ask the patient to list all their symptoms at the beginning of the interview. This has threefold benefit: You get a broad picture of the problem; the patient is unburdened of their concerns and experiences your validation; and a long list of symptoms can be an early clue to a diagnosis of FND.
Other helpful questions to determine the impact of symptoms on the patient’s well-being include inquiries about16:
- functional impairment
- onset and course of symptoms
- potential causal or correlating events
- dissociative episodes
- previous diagnoses and treatments
- the patient’s perceptions of, and emotional response to, their illness
- a history of abuse.
The physical examination to determine the presence of FND varies, depending on the functional area of impact (eg, motor, neurological, sensory, speech and swallowing). Pay particular attention to presenting signs and clues, and balance them with the patient’s report (or lack of report). Endeavor to demonstrate positive functional signs, such as a positive Hoover test, which relies on the principle of synergistic muscle contraction. You might see evidence of inconsistency, such as weakness or a change in gait, under observation, that seemingly resolves when the patient is getting on and off the exam table.16Table 215-24 describes areas affected by FND, characteristics of the disorder, and related diagnostic examinations.
Table 315,18,19 reviews validated special exams that can aid in making the diagnosis. Additional special tests are discussed in the literature.15-24 These tests can be helpful in narrowing the differential diagnosis but have not been validated and should be used with caution.
Some clinical signs associated with FND might be affected by other factors, including socioeconomic status, limited access to health care, low health literacy, poor communication skills, and physician bias. Keep these factors in mind during the visit, to avoid contributing further to health disparities among groups of patients affected by these problems.
Continue to: CASE
CASE
The work-up over the next month for Mr. D includes numerous studies, all yielding results that are negative or within normal limits: visual acuity; electrocardiography and an event monitor; laboratory testing (including a complete blood count, comprehensive metabolic panel, thyroid-stimulating hormone, creatine kinase, erythrocyte sedimentation rate, C-reactive protein, vitamin B12, folate, and vitamin D); magnetic resonance imaging of the brain and lumbar spine; lumbar puncture; and electromyography.
The score on the 9-item Patient Health Questionnaire for depression is 4 (severity: “none or minimal”); on the 7-item Generalized Anxiety Disorder scale, 0 (“no anxiety disorder”).
Referral. A neurology work-up of headache, lower extremity weakness, and unsteady gait to address several diagnostic possibilities, including migraine and multiple sclerosis, is within normal limits. A cardiology work-up of palpitations is negative for arrhythmias and other concerning findings.
Mr. D declines psychiatric and psychological evaluations.
Building a differential diagnosisis a formidable task
The differential diagnosis of FND is vast. It includes neurological, physiological, and psychiatric symptoms and disorders; somatization; and malingering (Table 4).6 Any disorder or condition in these areas that is in the differential diagnosis can be precipitated or exacerbated by stress; most, however, do not involve loss of physical function.12 In addition, the diagnosis of an FND does not necessarily exclude an organic disorder.
A patient’s presentation becomes complicated—and more difficult to treat—when functional symptoms and an unrelated underlying or early-stage neurological condition coexist. For example, a patient with epilepsy might also have dissociative seizures atop their organic disorder. Neurological disease is considered a risk factor for an overlying FND—just as the risk of depression or anxiety runs concurrently with other chronic diseases.14
Focus on clinical signs to narrow the differential. A thorough social and medical history and physical examination, as discussed earlier, help narrow the differential diagnosis of organic and medically unexplained disorders. Well-defined imaging or laboratory protocols do not exist to guide physicians to a definitive diagnosis, however.
Continue to: Psychiatric conditions
Psychiatric conditions can coexist with the diagnosis of FND, but might be unrelated. A systematic review of the literature showed that 17% to 42% of patients with FND had a concurrent anxiety disorder. Depression disorders were co-diagnosed in 19% to 71% of patients with FND; dissociative and personality disorders were noted, as well.25 However, coexisting psychiatric diagnosis might more likely be associated with distress from the presenting functional neurological symptoms, not linked to the FND diagnosis itself.12 This shift in understanding is reflected in the description of FND in the DSM-5.11
CASE
Mr. D reports debilitating headaches at return office visits. Trials of abortive triptans provide no relief; neither do control medications (beta-blockers, coenzyme Q10, magnesium, onabotulinumtoxinA [Botox], topiramate, and valproate). Lower-extremity weakness and unsteadiness are managed with supportive devices, including a cane, and physical therapy.
Importance of establishing a multidisciplinary approach
The complexity of FND lends itself to a multidisciplinary approach during evaluation and, eventually, for treatment. The assessment and diagnostic intervention that you provide, along with the contributions of consulted specialists (including neurology, physical and occupational therapy, psychiatry, psychology, and other mental health professionals) establishes a team-based approach that can increase the patient’s sense of support and reduce excessive testing and unnecessary medications, surgeries, and other treatments.26
Family physicians are in the ideal position to recognize the patient’s functional capacity and the quality of symptoms and to provide timely referral (eg, to Neurology and Psychiatry) for confirmation of the diagnosis and then treatment.
Evidence-based treatment options include:
- psychotherapy, with an emphasis on cognitive behavioral therapy
- physical therapy
- psychopharmacology
- promising combinations of physical and psychological treatment to improve long-term functionality.27
A promising diagnostic tool
The most significant update in the FND literature is on functional neuroimaging for assessing the disorder. Early findings suggest an intricate relationship between mind and body regarding the pathological distortion in FND. And, there is clear evidence that neuroimaging—specifically, functional magnetic resonance imaging—shows changes in brain activity that correspond to the patient’s symptom report. That said, imaging is not the recommended standard of care in the initial work-up of FND because of its cost and the fact that the diagnosis is principally a clinical undertaking.17,28
Call to action
Offer a generous ear. Begin the diagnostic pursuit by listening carefully and fully to the patient’s complaints, without arriving at a diagnosis with unwarranted bias or haste. This endeavor might require support from other clinical staff (eg, nurses, social workers, case managers) because the diagnostic process can be arduous and lengthy.
Continue to: Convey the diagnosis with sensitivity
Convey the diagnosis with sensitivity. Inquire about the patient’s perceptions and impairments to best personalize your diagnostic explanations. Delivery of the diagnosis might affect the patient’s acceptance and compliance with further testing and treatment of what is generally a persistent and treatment-resistant disorder; poor delivery of diagnostic information can impair the patient–physician relationship and increase the risk of disjointed care. Many patients find that improved patient–physician communication is therapeutic.29
Let the patient know that you’re taking her seriously. Validate patient concerns with a nonstigmatizing diagnostic label; discuss the diagnostic parameters and cause of symptoms in layman’s terms; and emphasize the potential for reversibility.30 Some patients are not satisfied with having a diagnosis of FND until they are reassured with normal results of testing and provided with referral; even then, some seek further reassurance.
Key tenets of managing care for patients who have been given a diagnosis of FND include:
- nonjudgmental, positive regard
- meaningful expression of empathy
- multidisciplinary coordination
- avoidance of unnecessary testing and harmful treatments
- descriptive and contextual explanations of the diagnosis.
Last, keep in mind that the course of treatment for FND is potentially prolonged and multilayered.
CASE
After many visits with his family physician and the neurology and cardiology specialists, as well as an extensive work-up, the physician approaches Mr. D with the possibility of a diagnosis of FND and proposes a multidisciplinary plan that includes:
- a course of physical and occupational therapy
- development of individualized cognitive behavioral tools
- weekly personal and marital counseling
- initiation of a selective serotonin reuptake inhibitor for anxiety
- monthly visits with his family physician.
Months after his return from deployment for evaluation and treatment, Mr. D is able to return to military duty. He reports that his quality of life has improved.
CORRESPONDENCE
Roselyn W. Clemente Fuentes, MD, FAAFP, Eglin Family Medicine Residency, 307 Boatner Road, Eglin AFB, FL 32547; roselynjan.w.fuentes.mil@mail.mil.
CASE
John D,* a 25-year-old patient with an otherwise unremarkable medical history, describes 2 months of daily headache, lower-extremity weakness, and unsteady gait that began fairly suddenly during his first deployment in the US Army. He explains that these symptoms affected his ability to perform his duties and necessitated an early return stateside for evaluation and treatment.
Mr. D denies precipitating trauma or unusual environmental exposures. He reports that, stateside now, symptoms continue to affect his ability to work and attend to personal and family responsibilities.
Asked about stressors, Mr. D notes the birth of his first child approximately 3 months ago, while he was deployed, and marital stressors. He denies suicidal or homicidal ideation.
* The patient’s name has been changed to protect his identity.
The challenge of identifying and managing FND
A functional neurological disorder (FND) is a constellation of psychological, physiological, and neurological symptoms, without an identifiable organic etiology, a conscious decision, or secondary gain for the patient,1 that adversely impacts functioning in 1 or more significant life domains.
Given the high throughput of patients in primary care practices, family physicians can expect to encounter suspected cases of FND in their practices. Regrettably, however, a lack of familiarity with the disorder and its related problems (eg, nonorganic paralysis, sensory loss, nonepileptic seizures, and abnormal movements) can add as much as $20,000 in excess direct and indirect costs of care for every such patient.1 In this article, we synthesize the recent literature on FND so that family physicians can expand their acumen in understanding, identifying, and evaluating patients whose presentation suggests FND.
An underrecognized entity
A precise estimate of the prevalence of FND is difficult to determine because the disorder is underrecognized and misdiagnosed and because it is often accompanied by the confounding of psychological and physiological comorbidities. A 2012 study estimated the annual incidence of FND to be 4 to 12 cases for every 100,000 people2; in primary care and outpatient neurology settings, prevalence is 6% to 22% of all patients.3,4 Stone and colleagues identified functional neurological symptoms as the second most common reason for outpatient neurology consultation,5 with 1 nonepileptic seizure patient seen for every 6 epileptic patients, and functional weakness presenting at the same rate as multiple sclerosis.6
Continue to: Demographics of patients with FND...
Demographics of patients with FND vary, depending on presenting neurological symptoms and disorder subtype. Existing data indicate a correlation between FND and younger age, female sex, physical disability,7 and a history of abuse or trauma.3,8 A challenge in concretely ascertaining the prevalence of FND is that conditions such as fibromyalgia, chronic pelvic pain, globus hystericus, and nonepileptic seizures can also be characterized as medically unexplained functional disorders, even within the network of neurology care.4
Misdiagnosis and bias are not uncommon
Ambiguity in classifying and evaluating FND can affect physicians’ perceptions, assessment, and care of patients with suggestive presenting symptoms. A major early challenge in diagnosing FND is the inconsistency of characterizing terminology (pseudoneurological, somatic, dissociative, conversion, psychogenic, hysterical, factitious, functional, medically unexplained9,10) and definitions in the literature. Neurological symptoms of unidentifiable organic cause can greatly diminish quality of life4; FND is a scientifically and clinically useful diagnosis for many combinations of nonrandomly co-occurring symptoms and clinical signs.
The pitfall of misdiagnosis. Remain cautious about making a diagnosis of FND by exclusion, which might yield an incorrect or false-negative finding because of an atypical presentation. It is important to avoid misdiagnosis by prematurely closing the differential diagnosis; instead, keep in mind that a medically unexplained diagnosis might be better explained by conducting a robust social and medical history and obtaining additional or collateral data, or both, along with appropriate consultation.4,9
Misdiagnosis can lead to a circuitous and costly work-up, with the potential to increase the patient’s distress. You can reduce this burden with early recognition of FND and centralized management of multidisciplinary care, which are more likely to lead to an accurate and timely diagnosis—paramount to empowering patients with access to the correct information and meaningful support needed to enhance treatment and self-care.9
Bias, haste, and dismissal are unproductive. Even with a clear definition of FND, it is not uncommon for a physician to rapidly assess a patient’s clinical signs, make a diagnosis of “unknown etiology,” or openly question the veracity of complaints. Furthermore, be aware of inadvertently characterizing FND using the prefix “pseudo” or the term “hysterical,” which can be psychologically discomforting for many patients, who legitimately experience inexplicable symptoms. Such pejoratives can lead to stigmatizing and misleading assessments and treatment paths4—courses of action that can cause early and, possibly, irreparable harm to the patient–physician relationship and increase the patient’s inclination to go “doctor-shopping,” with associated loss of continuity of care.
Why is it difficult to diagnose FND?
The latest (5th) edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) describes conversion, somatoform disorder, and FND synonymously.DSM-5 diagnostic criteria for conversion disorderare11:
- a specified type of symptom or deficit of altered voluntary motor or sensory function (eg, weakness, difficulty swallowing, slurred speech, seizures)
- clinical evidence of the incompatibility of the symptom or deficit and any recognized neurological or medical disorder
- incapability of better explaining the symptom or deficit as another medical or mental disorder.
- The symptom or deficit causes distress or impairment that (1) is clinically significant in occupational, social, or other important areas of function or (2) warrants medical evaluation.
The overarching feature of these criteria is the inconsistency of symptoms with recognized neurological, physiological, or psychiatric conditions. Although identification of psychological factors can help clarify and provide a treatment direction, such identification is not essential for making a diagnosis of FND. Malingering does not need to be refuted as part of establishing the diagnosis.12
Continue to: In contrast...
In contrast, the World Health Organization’s ICD-10 Classification of Mental and Behavioural Disorders groups diagnostic criteria for FND among the dissociative disorders13:
- Clinical features are specified for the individual dissociative disorder (motor, sensory, convulsions, mixed).
- Evidence is absent of a physical disorder that might explain symptoms.
- Evidence of psychological causation is present in clear temporal association with stressful events and problems or disturbed relationships, even if the patient denies such association.
Note the emphasis on psychological causation and exclusion of purposeful simulation of symptoms, as opposed to a primarily unconscious disconnection from the patient’s body or environment.
ICD-10 guidelines acknowledge the difficulty of finding definitive evidence of a psychological cause and recommend provisional diagnosis of FND if psychological factors are not readily apparent.14 Of note, many patients with FND are affected psychologically by their condition, with an impact on mood, behaviors, and interpersonal interactions, although not necessarily to a clinically diagnostic degree. Therefore, a psychiatric diagnosis alone is not a necessary precursor for the diagnosis of an FND.
CASE
History. Mr. D’s history is positive for light alcohol consumption (“2 or 3 cans of beer on weekends”) and chewing tobacco (he reports stopping 6 months earlier) and negative for substance abuse. The family history is positive for maternal hypertension and paternal suicide when the patient was 10 years old (no other known paternal history).
Physical findings. The review of systems is positive for intermittent palpitations, lower-extremity weakness causing unsteady gait, and generalized headache.
Vital signs are within normal limits, including blood pressure (120/82 mm Hg) and heart rate (110 beats/min). The patient is not in acute distress; he is awake, alert, and oriented × 3. No murmurs are heard; lungs are clear bilaterally to auscultation. There is no tenderness on abdominal palpation, and no hepatomegaly or splenomegaly; bowel sounds are normal. No significant bruising or lacerations are noted.
Neurology exam. Cranial nerves II-XII are intact. Pupils are equal and reactive to light. Reflexes are 2+ bilaterally. Muscle strength and tone are normal; no tremors are noted. Babinski signs are normal. A Romberg test is positive (swaying).
Continue to: Mr. D has an antalgic gait...
Mr. D has an antalgic gait with significant swaying (without falling); bent posture; and unsteadiness that requires a cane. However, he is able to get up and off the exam table without assistance, and to propel himself, by rolling a chair forward and backward, without difficulty.
Conducting a diagnostic examination
Taking the history. Certain clues can aid in the diagnosis of FND (TABLE 1).15 For example, the patient might have been seen in multiple specialty practices for a multitude of vague symptoms indicative of potentially related conditions (eg, chronic fatigue, allergies and sensitivities, fibromyalgia, and other chronic pain). The history might include repeated surgeries to investigate those symptoms (eg, laparoscopy, or hysterectomy at an early age). Taking time and care to explore all clinical clues, patient reports, and collateral data are therefore key to making an accurate diagnosis.
Note any discrepancies between the severity of reported symptoms and functional ability. A technique that can help elucidate a complex or ambiguous medical presentation is to ask the patient to list all their symptoms at the beginning of the interview. This has threefold benefit: You get a broad picture of the problem; the patient is unburdened of their concerns and experiences your validation; and a long list of symptoms can be an early clue to a diagnosis of FND.
Other helpful questions to determine the impact of symptoms on the patient’s well-being include inquiries about16:
- functional impairment
- onset and course of symptoms
- potential causal or correlating events
- dissociative episodes
- previous diagnoses and treatments
- the patient’s perceptions of, and emotional response to, their illness
- a history of abuse.
The physical examination to determine the presence of FND varies, depending on the functional area of impact (eg, motor, neurological, sensory, speech and swallowing). Pay particular attention to presenting signs and clues, and balance them with the patient’s report (or lack of report). Endeavor to demonstrate positive functional signs, such as a positive Hoover test, which relies on the principle of synergistic muscle contraction. You might see evidence of inconsistency, such as weakness or a change in gait, under observation, that seemingly resolves when the patient is getting on and off the exam table.16Table 215-24 describes areas affected by FND, characteristics of the disorder, and related diagnostic examinations.
Table 315,18,19 reviews validated special exams that can aid in making the diagnosis. Additional special tests are discussed in the literature.15-24 These tests can be helpful in narrowing the differential diagnosis but have not been validated and should be used with caution.
Some clinical signs associated with FND might be affected by other factors, including socioeconomic status, limited access to health care, low health literacy, poor communication skills, and physician bias. Keep these factors in mind during the visit, to avoid contributing further to health disparities among groups of patients affected by these problems.
Continue to: CASE
CASE
The work-up over the next month for Mr. D includes numerous studies, all yielding results that are negative or within normal limits: visual acuity; electrocardiography and an event monitor; laboratory testing (including a complete blood count, comprehensive metabolic panel, thyroid-stimulating hormone, creatine kinase, erythrocyte sedimentation rate, C-reactive protein, vitamin B12, folate, and vitamin D); magnetic resonance imaging of the brain and lumbar spine; lumbar puncture; and electromyography.
The score on the 9-item Patient Health Questionnaire for depression is 4 (severity: “none or minimal”); on the 7-item Generalized Anxiety Disorder scale, 0 (“no anxiety disorder”).
Referral. A neurology work-up of headache, lower extremity weakness, and unsteady gait to address several diagnostic possibilities, including migraine and multiple sclerosis, is within normal limits. A cardiology work-up of palpitations is negative for arrhythmias and other concerning findings.
Mr. D declines psychiatric and psychological evaluations.
Building a differential diagnosisis a formidable task
The differential diagnosis of FND is vast. It includes neurological, physiological, and psychiatric symptoms and disorders; somatization; and malingering (Table 4).6 Any disorder or condition in these areas that is in the differential diagnosis can be precipitated or exacerbated by stress; most, however, do not involve loss of physical function.12 In addition, the diagnosis of an FND does not necessarily exclude an organic disorder.
A patient’s presentation becomes complicated—and more difficult to treat—when functional symptoms and an unrelated underlying or early-stage neurological condition coexist. For example, a patient with epilepsy might also have dissociative seizures atop their organic disorder. Neurological disease is considered a risk factor for an overlying FND—just as the risk of depression or anxiety runs concurrently with other chronic diseases.14
Focus on clinical signs to narrow the differential. A thorough social and medical history and physical examination, as discussed earlier, help narrow the differential diagnosis of organic and medically unexplained disorders. Well-defined imaging or laboratory protocols do not exist to guide physicians to a definitive diagnosis, however.
Continue to: Psychiatric conditions
Psychiatric conditions can coexist with the diagnosis of FND, but might be unrelated. A systematic review of the literature showed that 17% to 42% of patients with FND had a concurrent anxiety disorder. Depression disorders were co-diagnosed in 19% to 71% of patients with FND; dissociative and personality disorders were noted, as well.25 However, coexisting psychiatric diagnosis might more likely be associated with distress from the presenting functional neurological symptoms, not linked to the FND diagnosis itself.12 This shift in understanding is reflected in the description of FND in the DSM-5.11
CASE
Mr. D reports debilitating headaches at return office visits. Trials of abortive triptans provide no relief; neither do control medications (beta-blockers, coenzyme Q10, magnesium, onabotulinumtoxinA [Botox], topiramate, and valproate). Lower-extremity weakness and unsteadiness are managed with supportive devices, including a cane, and physical therapy.
Importance of establishing a multidisciplinary approach
The complexity of FND lends itself to a multidisciplinary approach during evaluation and, eventually, for treatment. The assessment and diagnostic intervention that you provide, along with the contributions of consulted specialists (including neurology, physical and occupational therapy, psychiatry, psychology, and other mental health professionals) establishes a team-based approach that can increase the patient’s sense of support and reduce excessive testing and unnecessary medications, surgeries, and other treatments.26
Family physicians are in the ideal position to recognize the patient’s functional capacity and the quality of symptoms and to provide timely referral (eg, to Neurology and Psychiatry) for confirmation of the diagnosis and then treatment.
Evidence-based treatment options include:
- psychotherapy, with an emphasis on cognitive behavioral therapy
- physical therapy
- psychopharmacology
- promising combinations of physical and psychological treatment to improve long-term functionality.27
A promising diagnostic tool
The most significant update in the FND literature is on functional neuroimaging for assessing the disorder. Early findings suggest an intricate relationship between mind and body regarding the pathological distortion in FND. And, there is clear evidence that neuroimaging—specifically, functional magnetic resonance imaging—shows changes in brain activity that correspond to the patient’s symptom report. That said, imaging is not the recommended standard of care in the initial work-up of FND because of its cost and the fact that the diagnosis is principally a clinical undertaking.17,28
Call to action
Offer a generous ear. Begin the diagnostic pursuit by listening carefully and fully to the patient’s complaints, without arriving at a diagnosis with unwarranted bias or haste. This endeavor might require support from other clinical staff (eg, nurses, social workers, case managers) because the diagnostic process can be arduous and lengthy.
Continue to: Convey the diagnosis with sensitivity
Convey the diagnosis with sensitivity. Inquire about the patient’s perceptions and impairments to best personalize your diagnostic explanations. Delivery of the diagnosis might affect the patient’s acceptance and compliance with further testing and treatment of what is generally a persistent and treatment-resistant disorder; poor delivery of diagnostic information can impair the patient–physician relationship and increase the risk of disjointed care. Many patients find that improved patient–physician communication is therapeutic.29
Let the patient know that you’re taking her seriously. Validate patient concerns with a nonstigmatizing diagnostic label; discuss the diagnostic parameters and cause of symptoms in layman’s terms; and emphasize the potential for reversibility.30 Some patients are not satisfied with having a diagnosis of FND until they are reassured with normal results of testing and provided with referral; even then, some seek further reassurance.
Key tenets of managing care for patients who have been given a diagnosis of FND include:
- nonjudgmental, positive regard
- meaningful expression of empathy
- multidisciplinary coordination
- avoidance of unnecessary testing and harmful treatments
- descriptive and contextual explanations of the diagnosis.
Last, keep in mind that the course of treatment for FND is potentially prolonged and multilayered.
CASE
After many visits with his family physician and the neurology and cardiology specialists, as well as an extensive work-up, the physician approaches Mr. D with the possibility of a diagnosis of FND and proposes a multidisciplinary plan that includes:
- a course of physical and occupational therapy
- development of individualized cognitive behavioral tools
- weekly personal and marital counseling
- initiation of a selective serotonin reuptake inhibitor for anxiety
- monthly visits with his family physician.
Months after his return from deployment for evaluation and treatment, Mr. D is able to return to military duty. He reports that his quality of life has improved.
CORRESPONDENCE
Roselyn W. Clemente Fuentes, MD, FAAFP, Eglin Family Medicine Residency, 307 Boatner Road, Eglin AFB, FL 32547; roselynjan.w.fuentes.mil@mail.mil.
1. Konnopka A, Schaefert R, Heinrich S, et al. Economics of medically unexplained symptoms: a systematic review of the literature. Psychother Psychosom. 2012;81:265-275.
2. Carson AJ, Brown R, David AS, et al; on behalf of UK-FNS. Functional (conversion) neurological symptoms: research since the millennium. J Neurol Neurosurg Psychiatry. 2012;83:842-850.
3. Stone J, Carson A, Duncan R, et al. Who is referred to neurology clinics?—the diagnoses made in 3781 new patients. Clin Neurol Neurosurg. 2010;112:747-751.
4. Evens A, Vendetta L, Krebs K, et al. Medically unexplained neurologic symptoms: a primer for physicians who make the initial encounter. Am J Med. 2015;128:1059-1064.
5. Stone J, Reuber M, Carson A. Functional symptoms in neurology: mimics and chameleons. Pract Neurol. 2013;13:104-113.
6. Stone J, Warlow C, Sharpe M. The symptom of functional weakness: a controlled study of 107 patients. Brain. 2010;133:1537-1551.
7. Carson A, Stone J, Hibberd C, et al. Disability, distress and unemployment in neurology outpatients with symptoms ‘unexplained by organic disease’. J Neurol Neurosurg Psychiatry. 2011;82:810-813.
8. Fink P, Hansen MS, Oxhøj M-L. The prevalence of somatoform disorders among internal medical inpatients. J Psychosom Res. 2004;56:413-418.
9. Thomas LE. Are your patient’s medically unexplained symptoms really “all in her head”? Med Hypotheses. 2012;78:542-547.
10. Ding JM, Kanaan RAA. What should we say to patients with unexplained neurological symptoms? How explanation affects offence. J Psychosom Res. 2016;91:55-60.
11. Diagnostic and Statistical Manual of Mental Disorders (DSM-5). 5th ed. American Psychiatric Association; 2013.
12. Stone J, LaFrance WC Jr, Levenson JL, et al. Issues for DSM-5: Conversion disorder. Am J Psychiatry. 2010;167:626-627.
13. The ICD-10 Classification of Mental and Behavioural Disorders: Clinical Descriptions and Diagnostic Guidelines. World Health Organization; 1994. Accessed January 21, 2021. www.who.int/classifications/icd/en/bluebook.pdf
14. Stone J, Carson A, Duncan R, et al. Which neurological diseases are most likely to be associated with “symptoms unexplained by organic disease.” J Neurol. 2012;259:33-38.
15. Shaibani A, Sabbagh M. Pseudoneurologic syndromes: recognition and diagnosis. Am Fam Physician. 1998;57:2485-2494.
16. Stone J, Carson A, Sharpe M. Functional symptoms and signs in neurology: assessment and diagnosis. J Neurol Neurosurg Psychiatry. 2005;76(suppl 1):i2-i12.
17. Vuilleumier P. Brain circuits implicated in psychogenic paralysis in conversion disorders and hypnosis. Neurophysiol Clin. 2014;44:323-337.
18. McKee K, Glass S, Adams C, et al. The inpatient assessment and management of motor functional neurological disorders: an interdisciplinary perspective. Psychosomatics. 2018;59:358-368.
19. Daum C, Hubschmid M, Aybek S. The value of ‘positive’ clinical signs for weakness, sensory and gait disorders in conversion disorder: a systematic and narrative review. J Neurol Neurosurg Psychiatry. 2014;85:180-190.
20. Brown P, Thompson PD. Electrophysiological aids to the diagnosis of psychogenic jerks, spasms, and tremor. Mov Disord. 2001;16:595-599.
21. Ludwig L, McWhirter L, Williams S, et al. Functional coma. In: Hallett M, Stone J, Carson A, eds. Handbook of Clinical Neurology: Volume 139: Functional Neurologic Disorders. 1st ed. Academic Press; 2016:313.
22. Miller NR, Subramanian PS, Patel VR. Walsh and Hoyt’s Clinical Neuro-ophthalmology. 3rd ed. Wolters Kluwer; 2016:512-513.
23. Takazaki K, Stransky AD, Miller G. Psychogenic nonepileptic seizures: diagnosis, management, and bioethics. Pediatr Neurol. 2016;62:3-8.
24. Sahaya K, Dholakia SA, Sahota PK. Psychogenic non-epileptic seizures: a challenging entity. J Clin Neurosci. 2011;18:1602-1607.
25. Gelauff J, Stone J, Edwards M, et al. The prognosis of functional (psychogenic) motor symptoms: a systematic review. J Neurol Neurosurg Psychiatry. 2014;85:220-226.
26. Kranick SM, Gorrindo T, Hallett M. Psychogenic movement disorders and motor conversion: a roadmap for collaboration between neurology and psychiatry. Psychosomatics. 2011;52:109-116.
27. Edwards MJ, Bhatia KP. Functional (psychogenic) movement disorders: merging mind and brain. Lancet Neurol. 2012;11:250-260.
28. Burgmer M, Kugel H, Pfleiderer B, et al. The mirror neuron system under hypnosis—brain substrates of voluntary and involuntary motor activation in hypnotic paralysis. Cortex. 2013;49:437-445.
29. van Bokhoven MA, Koch H, van der Weijden T, et al. Influence of watchful waiting on satisfaction and anxiety among patients seeking care for unexplained complaints, Ann Fam Med. 2009;7:112-120.
30. Stone J, Carson A, Hallet M. Explanation as treatment for functional neurologic disorders. Handb Clin Neurol. 2016;139:543-553.
1. Konnopka A, Schaefert R, Heinrich S, et al. Economics of medically unexplained symptoms: a systematic review of the literature. Psychother Psychosom. 2012;81:265-275.
2. Carson AJ, Brown R, David AS, et al; on behalf of UK-FNS. Functional (conversion) neurological symptoms: research since the millennium. J Neurol Neurosurg Psychiatry. 2012;83:842-850.
3. Stone J, Carson A, Duncan R, et al. Who is referred to neurology clinics?—the diagnoses made in 3781 new patients. Clin Neurol Neurosurg. 2010;112:747-751.
4. Evens A, Vendetta L, Krebs K, et al. Medically unexplained neurologic symptoms: a primer for physicians who make the initial encounter. Am J Med. 2015;128:1059-1064.
5. Stone J, Reuber M, Carson A. Functional symptoms in neurology: mimics and chameleons. Pract Neurol. 2013;13:104-113.
6. Stone J, Warlow C, Sharpe M. The symptom of functional weakness: a controlled study of 107 patients. Brain. 2010;133:1537-1551.
7. Carson A, Stone J, Hibberd C, et al. Disability, distress and unemployment in neurology outpatients with symptoms ‘unexplained by organic disease’. J Neurol Neurosurg Psychiatry. 2011;82:810-813.
8. Fink P, Hansen MS, Oxhøj M-L. The prevalence of somatoform disorders among internal medical inpatients. J Psychosom Res. 2004;56:413-418.
9. Thomas LE. Are your patient’s medically unexplained symptoms really “all in her head”? Med Hypotheses. 2012;78:542-547.
10. Ding JM, Kanaan RAA. What should we say to patients with unexplained neurological symptoms? How explanation affects offence. J Psychosom Res. 2016;91:55-60.
11. Diagnostic and Statistical Manual of Mental Disorders (DSM-5). 5th ed. American Psychiatric Association; 2013.
12. Stone J, LaFrance WC Jr, Levenson JL, et al. Issues for DSM-5: Conversion disorder. Am J Psychiatry. 2010;167:626-627.
13. The ICD-10 Classification of Mental and Behavioural Disorders: Clinical Descriptions and Diagnostic Guidelines. World Health Organization; 1994. Accessed January 21, 2021. www.who.int/classifications/icd/en/bluebook.pdf
14. Stone J, Carson A, Duncan R, et al. Which neurological diseases are most likely to be associated with “symptoms unexplained by organic disease.” J Neurol. 2012;259:33-38.
15. Shaibani A, Sabbagh M. Pseudoneurologic syndromes: recognition and diagnosis. Am Fam Physician. 1998;57:2485-2494.
16. Stone J, Carson A, Sharpe M. Functional symptoms and signs in neurology: assessment and diagnosis. J Neurol Neurosurg Psychiatry. 2005;76(suppl 1):i2-i12.
17. Vuilleumier P. Brain circuits implicated in psychogenic paralysis in conversion disorders and hypnosis. Neurophysiol Clin. 2014;44:323-337.
18. McKee K, Glass S, Adams C, et al. The inpatient assessment and management of motor functional neurological disorders: an interdisciplinary perspective. Psychosomatics. 2018;59:358-368.
19. Daum C, Hubschmid M, Aybek S. The value of ‘positive’ clinical signs for weakness, sensory and gait disorders in conversion disorder: a systematic and narrative review. J Neurol Neurosurg Psychiatry. 2014;85:180-190.
20. Brown P, Thompson PD. Electrophysiological aids to the diagnosis of psychogenic jerks, spasms, and tremor. Mov Disord. 2001;16:595-599.
21. Ludwig L, McWhirter L, Williams S, et al. Functional coma. In: Hallett M, Stone J, Carson A, eds. Handbook of Clinical Neurology: Volume 139: Functional Neurologic Disorders. 1st ed. Academic Press; 2016:313.
22. Miller NR, Subramanian PS, Patel VR. Walsh and Hoyt’s Clinical Neuro-ophthalmology. 3rd ed. Wolters Kluwer; 2016:512-513.
23. Takazaki K, Stransky AD, Miller G. Psychogenic nonepileptic seizures: diagnosis, management, and bioethics. Pediatr Neurol. 2016;62:3-8.
24. Sahaya K, Dholakia SA, Sahota PK. Psychogenic non-epileptic seizures: a challenging entity. J Clin Neurosci. 2011;18:1602-1607.
25. Gelauff J, Stone J, Edwards M, et al. The prognosis of functional (psychogenic) motor symptoms: a systematic review. J Neurol Neurosurg Psychiatry. 2014;85:220-226.
26. Kranick SM, Gorrindo T, Hallett M. Psychogenic movement disorders and motor conversion: a roadmap for collaboration between neurology and psychiatry. Psychosomatics. 2011;52:109-116.
27. Edwards MJ, Bhatia KP. Functional (psychogenic) movement disorders: merging mind and brain. Lancet Neurol. 2012;11:250-260.
28. Burgmer M, Kugel H, Pfleiderer B, et al. The mirror neuron system under hypnosis—brain substrates of voluntary and involuntary motor activation in hypnotic paralysis. Cortex. 2013;49:437-445.
29. van Bokhoven MA, Koch H, van der Weijden T, et al. Influence of watchful waiting on satisfaction and anxiety among patients seeking care for unexplained complaints, Ann Fam Med. 2009;7:112-120.
30. Stone J, Carson A, Hallet M. Explanation as treatment for functional neurologic disorders. Handb Clin Neurol. 2016;139:543-553.
PRACTICE RECOMMENDATIONS
› Avoid using stigmatizing terminology (eg, adding the prefix “pseudo” or the adjective “hysterical”) to characterize a suspected functional neurological disorder (FND) or a medically unexplained disorder. C
› Refrain from ordering functional magnetic resonance imaging as part of the routine evaluation of suspected FND. C
› Validate the patient‘s concerns with an appropriate diagnostic label; use layman’s terms to discuss the diagnostic parameters of FND and the cause of symptoms; and emphasize treatment possibilities and plans. C
Strength of recommendation (SOR)
A Good-quality patient-oriented evidence
B Inconsistent or limited-quality patient-oriented evidence
C Consensus, usual practice, opinion, disease-oriented evidence, case series
Journal to retract psych paper after plagiarism allegations, editor steps down
A medical journal is retracting a paper after a psychiatrist alleged that the managing editor closely copied and published her withdrawn work and claimed it for his own.
In addition, the managing editor, Gary VandenBos, PhD, has resigned at the journal’s request, according to an email sent to the paper’s original author, psychiatrist Amy Barnhorst, MD, vice chair for community mental health at the University of California, Davis, and coauthor and UC Davis colleague Rocco Pallin, MPH.
Dr. Barnhorst shared emails – from the journal’s publisher, Springer Publishing Company, and from the editor in chief, Morgan Sammons, PhD – with this news organization.
The retraction is the end of a saga that began when Dr. Barnhorst and Dr. Pallin submitted a paper, at Dr. VandenBos’s request, to the Journal of Health Service Psychology, published by Springer.
As previously reported by this news organization, Dr. Barnhorst and Dr. Pallin eventually decided to withdraw the paper and were later notified by Dr. VandenBos that he’d published a similar article under his own authorship. Michael O. Miller, a retired judge who trained as a psychologist, was listed as a coauthor.
The two women – acknowledged experts in the article’s subject matter on how physicians can talk to patients about gun violence – immediately notified Dr. Sammons and Springer Publishing when they saw the published piece, saying they believed it plagiarized their original submission.
According to the e-mail Springer sent to Dr. Barnhorst, the publisher investigated and said that it would “be retracting the article shortly.”
The retraction notice will state: “The Editor in Chief and the authors, Dr. VandenBos and Mr. Miller, have retracted this article, as it significantly overlaps with an unpublished manuscript by Amy Barnhorst and Rocco Pallin.” It also states that “[Dr.] VandenBos accepts full responsibility for the overlap.”
The original article will still be available, but it will be marked as “retracted” and feature a link to the retraction notice.
Dr. Barnhorst, who garnered at least 40,000 likes when she tweeted about the alleged theft of her work, said in an interview that she and Dr. Pallin are “glad to see that the investigation is complete and the retraction has been issued.”
“At least we can now submit it to a new journal in a version that appropriately represents our work and expertise,” said Dr. Barnhorst. “I still have no idea how or why this happened, nor how much of it was intentional and on whose part, but I guess I never will!”
Editor removed
When contacted by this news organization to comment on the retraction and removal of Dr. VandenBos as managing editor, Dr. Sammons said it was not possible because, “I treat such correspondence as confidential.”
Dr. Sammons said he could “confirm that our investigation is reaching its conclusion and my colleagues at Springer Nature would be happy to contact you when we can provide a further update.”
Springer spokesperson Anne Korn also would not comment beyond saying, “The conclusion of our investigation is still in progress and may take a little additional time.”
In the letter sent to Dr. Barnhorst and Dr. Pallin, Dr. Sammons said he had “asked for and accepted the resignation of Dr. VandenBos,” and that the resignation will be announced “in the upcoming print issue of our journal.”
Dr. Sammons said he also notified the dean of the University of Arizona College of Law that Mr. Miller, who held a position at the school, was not aware of the original submission by the two women. Even so, the school suspended Mr. Miller’s academic appointment, according to Dr. Sammons’ letter.
The editor in chief also said that, while “[Dr.] VandenBos’ errors were substantial and had substantial consequences, my investigation did not find any intent to plagiarize your work.”
He apologized again to Dr. Barnhorst and Dr. Pallin, though, adding, “I and my associate editors have initiated a revision of our publications processes to ensure that errors such as the above do not occur in the future, and I apologize again that this lapse affected you and your scholarly work.”
A version of this article first appeared on Medscape.com.
A medical journal is retracting a paper after a psychiatrist alleged that the managing editor closely copied and published her withdrawn work and claimed it for his own.
In addition, the managing editor, Gary VandenBos, PhD, has resigned at the journal’s request, according to an email sent to the paper’s original author, psychiatrist Amy Barnhorst, MD, vice chair for community mental health at the University of California, Davis, and coauthor and UC Davis colleague Rocco Pallin, MPH.
Dr. Barnhorst shared emails – from the journal’s publisher, Springer Publishing Company, and from the editor in chief, Morgan Sammons, PhD – with this news organization.
The retraction is the end of a saga that began when Dr. Barnhorst and Dr. Pallin submitted a paper, at Dr. VandenBos’s request, to the Journal of Health Service Psychology, published by Springer.
As previously reported by this news organization, Dr. Barnhorst and Dr. Pallin eventually decided to withdraw the paper and were later notified by Dr. VandenBos that he’d published a similar article under his own authorship. Michael O. Miller, a retired judge who trained as a psychologist, was listed as a coauthor.
The two women – acknowledged experts in the article’s subject matter on how physicians can talk to patients about gun violence – immediately notified Dr. Sammons and Springer Publishing when they saw the published piece, saying they believed it plagiarized their original submission.
According to the e-mail Springer sent to Dr. Barnhorst, the publisher investigated and said that it would “be retracting the article shortly.”
The retraction notice will state: “The Editor in Chief and the authors, Dr. VandenBos and Mr. Miller, have retracted this article, as it significantly overlaps with an unpublished manuscript by Amy Barnhorst and Rocco Pallin.” It also states that “[Dr.] VandenBos accepts full responsibility for the overlap.”
The original article will still be available, but it will be marked as “retracted” and feature a link to the retraction notice.
Dr. Barnhorst, who garnered at least 40,000 likes when she tweeted about the alleged theft of her work, said in an interview that she and Dr. Pallin are “glad to see that the investigation is complete and the retraction has been issued.”
“At least we can now submit it to a new journal in a version that appropriately represents our work and expertise,” said Dr. Barnhorst. “I still have no idea how or why this happened, nor how much of it was intentional and on whose part, but I guess I never will!”
Editor removed
When contacted by this news organization to comment on the retraction and removal of Dr. VandenBos as managing editor, Dr. Sammons said it was not possible because, “I treat such correspondence as confidential.”
Dr. Sammons said he could “confirm that our investigation is reaching its conclusion and my colleagues at Springer Nature would be happy to contact you when we can provide a further update.”
Springer spokesperson Anne Korn also would not comment beyond saying, “The conclusion of our investigation is still in progress and may take a little additional time.”
In the letter sent to Dr. Barnhorst and Dr. Pallin, Dr. Sammons said he had “asked for and accepted the resignation of Dr. VandenBos,” and that the resignation will be announced “in the upcoming print issue of our journal.”
Dr. Sammons said he also notified the dean of the University of Arizona College of Law that Mr. Miller, who held a position at the school, was not aware of the original submission by the two women. Even so, the school suspended Mr. Miller’s academic appointment, according to Dr. Sammons’ letter.
The editor in chief also said that, while “[Dr.] VandenBos’ errors were substantial and had substantial consequences, my investigation did not find any intent to plagiarize your work.”
He apologized again to Dr. Barnhorst and Dr. Pallin, though, adding, “I and my associate editors have initiated a revision of our publications processes to ensure that errors such as the above do not occur in the future, and I apologize again that this lapse affected you and your scholarly work.”
A version of this article first appeared on Medscape.com.
A medical journal is retracting a paper after a psychiatrist alleged that the managing editor closely copied and published her withdrawn work and claimed it for his own.
In addition, the managing editor, Gary VandenBos, PhD, has resigned at the journal’s request, according to an email sent to the paper’s original author, psychiatrist Amy Barnhorst, MD, vice chair for community mental health at the University of California, Davis, and coauthor and UC Davis colleague Rocco Pallin, MPH.
Dr. Barnhorst shared emails – from the journal’s publisher, Springer Publishing Company, and from the editor in chief, Morgan Sammons, PhD – with this news organization.
The retraction is the end of a saga that began when Dr. Barnhorst and Dr. Pallin submitted a paper, at Dr. VandenBos’s request, to the Journal of Health Service Psychology, published by Springer.
As previously reported by this news organization, Dr. Barnhorst and Dr. Pallin eventually decided to withdraw the paper and were later notified by Dr. VandenBos that he’d published a similar article under his own authorship. Michael O. Miller, a retired judge who trained as a psychologist, was listed as a coauthor.
The two women – acknowledged experts in the article’s subject matter on how physicians can talk to patients about gun violence – immediately notified Dr. Sammons and Springer Publishing when they saw the published piece, saying they believed it plagiarized their original submission.
According to the e-mail Springer sent to Dr. Barnhorst, the publisher investigated and said that it would “be retracting the article shortly.”
The retraction notice will state: “The Editor in Chief and the authors, Dr. VandenBos and Mr. Miller, have retracted this article, as it significantly overlaps with an unpublished manuscript by Amy Barnhorst and Rocco Pallin.” It also states that “[Dr.] VandenBos accepts full responsibility for the overlap.”
The original article will still be available, but it will be marked as “retracted” and feature a link to the retraction notice.
Dr. Barnhorst, who garnered at least 40,000 likes when she tweeted about the alleged theft of her work, said in an interview that she and Dr. Pallin are “glad to see that the investigation is complete and the retraction has been issued.”
“At least we can now submit it to a new journal in a version that appropriately represents our work and expertise,” said Dr. Barnhorst. “I still have no idea how or why this happened, nor how much of it was intentional and on whose part, but I guess I never will!”
Editor removed
When contacted by this news organization to comment on the retraction and removal of Dr. VandenBos as managing editor, Dr. Sammons said it was not possible because, “I treat such correspondence as confidential.”
Dr. Sammons said he could “confirm that our investigation is reaching its conclusion and my colleagues at Springer Nature would be happy to contact you when we can provide a further update.”
Springer spokesperson Anne Korn also would not comment beyond saying, “The conclusion of our investigation is still in progress and may take a little additional time.”
In the letter sent to Dr. Barnhorst and Dr. Pallin, Dr. Sammons said he had “asked for and accepted the resignation of Dr. VandenBos,” and that the resignation will be announced “in the upcoming print issue of our journal.”
Dr. Sammons said he also notified the dean of the University of Arizona College of Law that Mr. Miller, who held a position at the school, was not aware of the original submission by the two women. Even so, the school suspended Mr. Miller’s academic appointment, according to Dr. Sammons’ letter.
The editor in chief also said that, while “[Dr.] VandenBos’ errors were substantial and had substantial consequences, my investigation did not find any intent to plagiarize your work.”
He apologized again to Dr. Barnhorst and Dr. Pallin, though, adding, “I and my associate editors have initiated a revision of our publications processes to ensure that errors such as the above do not occur in the future, and I apologize again that this lapse affected you and your scholarly work.”
A version of this article first appeared on Medscape.com.
PTSD prevalent in survivors of severe COVID-19
Posttraumatic stress disorder may occur in up to a third of patients who recover from severe COVID-19 infection, new research suggests.
A study of more than 300 patients who presented to the emergency department with the virus showed a 30.2% prevalence for PTSD 30-120 days after COVID recovery.
or having persistent medical symptoms after hospitalization.
Additional diagnoses, such as depressive and hypomanic episodes and generalized anxiety disorder (GAD), were also present in some of the survivors.
“Previous coronavirus epidemics were associated with PTSD diagnoses in postillness stages, with meta-analytic findings indicating a prevalence of 32.2%,” write the investigators, led by Delfina Janiri, MD, department of psychiatry, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Rome.
However, data focused specifically on COVID-19 have been “piecemeal,” they add.
The findings were published online Feb. 18 in a research letter in JAMA Psychiatry.
A traumatic event
From April to October 2020, the researchers assessed 381 consecutive patients (100% white; 56.4% men; mean age, 55.3 years) who presented to the ED and subsequently participated in a health check at the Fondazione Policlinico Universitario Agostino Gemelli.
The mean length of stay for the 309 patients hospitalized with severe COVID-19 was 18.4 days.
Results showed that 115 participants (30.2%) had PTSD, based on DSM-5 criteria, and 55.7% of the women had the disorder. Additional diagnoses found in the full patient population included:
- Depressive episodes (17.3%).
- GAD (7%).
- Hypomanic episodes (0.7%).
- Psychotic disorders (0.2%).
Patients with PTSD had higher rates than those without PTSD of a previous history of psychiatric disorders (34.8% vs. 20.7%; P = .003) and of delirium or agitation during hospitalization, as assessed with the Confusion Assessment Method (16.5% vs. 6.4%; P = .002).
In addition, 62.6% of those with PTSD had three or more persistent COVID-19 symptoms vs. 37.2% of their counterparts without PTSD (P < .001).
After logistic regression analyses, significant factors associated with a PTSD diagnosis were persistent medical symptoms (P = .002), delirium or agitation (P = .02), and being female (P = .02).
The investigators note that their results are “in line” with findings reported in research examining other traumatic events. This includes about 30% of Hurricane Katrina survivors who experienced PTSD, as did around 25% of survivors of the 2011 “Great Japan Earthquake and Tsunami.”
Study limitations cited include the “relatively small” size of the patient population, that it focused on only one participating center, and that it didn’t include a control group of non-COVID patients who reported to the ED.
“Further longitudinal studies are needed to tailor therapeutic interventions and prevention strategies,” the researchers write.
Dr. Janiri and four of the five other authors have disclosed no relevant financial relationships. The other author, Gabriele Sani, MD, reported having received personal fees from Angelini Spa, Janssen, and Lundbeck outside the submitted work.
A version of this article first appeared on Medscape.com.
Posttraumatic stress disorder may occur in up to a third of patients who recover from severe COVID-19 infection, new research suggests.
A study of more than 300 patients who presented to the emergency department with the virus showed a 30.2% prevalence for PTSD 30-120 days after COVID recovery.
or having persistent medical symptoms after hospitalization.
Additional diagnoses, such as depressive and hypomanic episodes and generalized anxiety disorder (GAD), were also present in some of the survivors.
“Previous coronavirus epidemics were associated with PTSD diagnoses in postillness stages, with meta-analytic findings indicating a prevalence of 32.2%,” write the investigators, led by Delfina Janiri, MD, department of psychiatry, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Rome.
However, data focused specifically on COVID-19 have been “piecemeal,” they add.
The findings were published online Feb. 18 in a research letter in JAMA Psychiatry.
A traumatic event
From April to October 2020, the researchers assessed 381 consecutive patients (100% white; 56.4% men; mean age, 55.3 years) who presented to the ED and subsequently participated in a health check at the Fondazione Policlinico Universitario Agostino Gemelli.
The mean length of stay for the 309 patients hospitalized with severe COVID-19 was 18.4 days.
Results showed that 115 participants (30.2%) had PTSD, based on DSM-5 criteria, and 55.7% of the women had the disorder. Additional diagnoses found in the full patient population included:
- Depressive episodes (17.3%).
- GAD (7%).
- Hypomanic episodes (0.7%).
- Psychotic disorders (0.2%).
Patients with PTSD had higher rates than those without PTSD of a previous history of psychiatric disorders (34.8% vs. 20.7%; P = .003) and of delirium or agitation during hospitalization, as assessed with the Confusion Assessment Method (16.5% vs. 6.4%; P = .002).
In addition, 62.6% of those with PTSD had three or more persistent COVID-19 symptoms vs. 37.2% of their counterparts without PTSD (P < .001).
After logistic regression analyses, significant factors associated with a PTSD diagnosis were persistent medical symptoms (P = .002), delirium or agitation (P = .02), and being female (P = .02).
The investigators note that their results are “in line” with findings reported in research examining other traumatic events. This includes about 30% of Hurricane Katrina survivors who experienced PTSD, as did around 25% of survivors of the 2011 “Great Japan Earthquake and Tsunami.”
Study limitations cited include the “relatively small” size of the patient population, that it focused on only one participating center, and that it didn’t include a control group of non-COVID patients who reported to the ED.
“Further longitudinal studies are needed to tailor therapeutic interventions and prevention strategies,” the researchers write.
Dr. Janiri and four of the five other authors have disclosed no relevant financial relationships. The other author, Gabriele Sani, MD, reported having received personal fees from Angelini Spa, Janssen, and Lundbeck outside the submitted work.
A version of this article first appeared on Medscape.com.
Posttraumatic stress disorder may occur in up to a third of patients who recover from severe COVID-19 infection, new research suggests.
A study of more than 300 patients who presented to the emergency department with the virus showed a 30.2% prevalence for PTSD 30-120 days after COVID recovery.
or having persistent medical symptoms after hospitalization.
Additional diagnoses, such as depressive and hypomanic episodes and generalized anxiety disorder (GAD), were also present in some of the survivors.
“Previous coronavirus epidemics were associated with PTSD diagnoses in postillness stages, with meta-analytic findings indicating a prevalence of 32.2%,” write the investigators, led by Delfina Janiri, MD, department of psychiatry, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Rome.
However, data focused specifically on COVID-19 have been “piecemeal,” they add.
The findings were published online Feb. 18 in a research letter in JAMA Psychiatry.
A traumatic event
From April to October 2020, the researchers assessed 381 consecutive patients (100% white; 56.4% men; mean age, 55.3 years) who presented to the ED and subsequently participated in a health check at the Fondazione Policlinico Universitario Agostino Gemelli.
The mean length of stay for the 309 patients hospitalized with severe COVID-19 was 18.4 days.
Results showed that 115 participants (30.2%) had PTSD, based on DSM-5 criteria, and 55.7% of the women had the disorder. Additional diagnoses found in the full patient population included:
- Depressive episodes (17.3%).
- GAD (7%).
- Hypomanic episodes (0.7%).
- Psychotic disorders (0.2%).
Patients with PTSD had higher rates than those without PTSD of a previous history of psychiatric disorders (34.8% vs. 20.7%; P = .003) and of delirium or agitation during hospitalization, as assessed with the Confusion Assessment Method (16.5% vs. 6.4%; P = .002).
In addition, 62.6% of those with PTSD had three or more persistent COVID-19 symptoms vs. 37.2% of their counterparts without PTSD (P < .001).
After logistic regression analyses, significant factors associated with a PTSD diagnosis were persistent medical symptoms (P = .002), delirium or agitation (P = .02), and being female (P = .02).
The investigators note that their results are “in line” with findings reported in research examining other traumatic events. This includes about 30% of Hurricane Katrina survivors who experienced PTSD, as did around 25% of survivors of the 2011 “Great Japan Earthquake and Tsunami.”
Study limitations cited include the “relatively small” size of the patient population, that it focused on only one participating center, and that it didn’t include a control group of non-COVID patients who reported to the ED.
“Further longitudinal studies are needed to tailor therapeutic interventions and prevention strategies,” the researchers write.
Dr. Janiri and four of the five other authors have disclosed no relevant financial relationships. The other author, Gabriele Sani, MD, reported having received personal fees from Angelini Spa, Janssen, and Lundbeck outside the submitted work.
A version of this article first appeared on Medscape.com.
Heroes: Nurses’ sacrifice in the age of COVID-19
This past year, the referrals to my private practice have taken a noticeable shift and caused me to pause.
More calls have come from nurses, many who work directly with COVID-19 patients, understandably seeking mental health treatment, or support. Especially in this time, nurses are facing trauma and stress that is unimaginable to many, myself included. Despite the collective efforts we have made as a society to recognize their work, I do not think we have given enough consideration to the enormous sacrifice nurses are currently undertaking to save our collective psyche.
As physicians and mental health providers, we have a glimpse into the complexities and stressors of medical treatment. In our line of work, we support patients with trauma on a regular basis. We feel deeply connected to patients, some of whom we have treated until the end of their lives. Despite that, I am not sure that I, or anyone, can truly comprehend what nurses face in today’s climate of care.
There is no denying that doctors are of value to our system, but our service has limits; nurses and doctors operate as two sides to a shared coin. As doctors, we diagnose and prescribe, while nurses explain and dispense. As doctors, we talk to patients, while nurses comfort them. Imagine spending an entire year working in a hospital diligently wiping endotracheal tubes that are responsible for maintaining someone’s life. Imagine spending an entire year laboring through the heavy task of lifting patients to prone them in a position that may save their lives. Imagine spending an entire year holding the hands of comatose patients in hopes of maintaining a sense of humanity.
And this only begins to describe the tasks bestowed upon nurses. While doctors answer pagers or complete insurance authorization forms, nurses empathize and reassure scared and isolated patients. Imagine spending an entire year updating crying family members who cannot see their loved ones. Imagine spending an entire year explaining and pleading to the outside world that wearing a mask and washing hands would reduce the suffering that takes place inside the hospital walls.
Despite the uncertainties, pressures, and demands, nurses have continued, and will continue, to show up for their patients, shift by shift. It takes a tragic number of deaths for the nurses I see in my practice to share that they have lost count. These numbers reflect people they held to feed, carried to prevent ulcers, wiped for decency, caressed for compassion, probed with IVs and tubes, monitored for signs of life, and warmed with blankets. If love were in any job description, it would fall under that of a nurse.
And we can’t ignore the fact that all the lives lost by COVID-19 had family. Family members who, without ever stepping foot in the hospital, needed a place to be heard, a place to receive explanation, and a place for reassurance. This invaluable place is cultivated by nurses. Through Zoom and phone calls, nurses share messages of hope, love, and fear between patients and family. Through Zoom and phone calls, nurses orchestrate visits and last goodbyes.
There is no denying that we have all been affected by this shared human experience. But the pause we owe our nurses feels long overdue, and of great importance. Nurses need a space to be heard, to be comforted, to be recognized. They come to our practices, trying to contain the world’s angst, while also navigating for themselves what it means to go through what they are going through. They hope that by coming to see us, they will find the strength to go back another day, another week, another month. Sometimes, they come to talk about everything but the job, in hopes that by talking about more mundane problems, they will feel “normal” and reconnected.
I hope that our empathy, congruence, and unconditional positive regard will allow them to feel heard.1 I hope that our warmth, concern, and hopefulness provide a welcoming place to voice sadness, anger, and fears.2 I hope that our processing of traumatic memory, our challenge to avoid inaccurate self-blaming beliefs, and our encouragement to create more thought-out conclusions will allow them to understand what is happening more accurately.3
Yet, I worry. I worry that society hasn’t been particularly successful with helping prior generations of heroes. From war veterans, to Sept. 11, 2001, firefighters, it seems that we have repeated mistakes. My experience with veterans in particular has taught me that for many who are suffering, it feels like society has broken its very fabric by being bystanders to the pain.
But suffering and tragedy are an inevitable part of the human experience that we share. What we can keep sight of is this: As physicians, we work with nurses. We are witnessing firsthand the impossible sacrifice they are taking and the limits of resilience. Let us not be too busy to stop and give recognition where and when it is due. Let us listen and learn from our past, and present, heroes. And let us never forget to extend our own hand to those who make a living extending theirs.
Dr. Badre is a clinical and forensic psychiatrist in San Diego. He holds teaching positions at the University of California, San Diego, and the University of San Diego. He teaches medical education, psychopharmacology, ethics in psychiatry, and correctional care. Dr. Badre can be reached at his website, BadreMD.com.
References
1. Rogers CR. J Consult Psychol. 1957;21(2):95-103.
2. Mallo CJ, Mintz DL. Psychodyn Psychiatry. 2013 Mar;41(1):13-37.
3. Resick PA et al. Cognitive Processing Therapy for PTSD: A Comprehensive Manual. Guilford Publications, 2016.
This past year, the referrals to my private practice have taken a noticeable shift and caused me to pause.
More calls have come from nurses, many who work directly with COVID-19 patients, understandably seeking mental health treatment, or support. Especially in this time, nurses are facing trauma and stress that is unimaginable to many, myself included. Despite the collective efforts we have made as a society to recognize their work, I do not think we have given enough consideration to the enormous sacrifice nurses are currently undertaking to save our collective psyche.
As physicians and mental health providers, we have a glimpse into the complexities and stressors of medical treatment. In our line of work, we support patients with trauma on a regular basis. We feel deeply connected to patients, some of whom we have treated until the end of their lives. Despite that, I am not sure that I, or anyone, can truly comprehend what nurses face in today’s climate of care.
There is no denying that doctors are of value to our system, but our service has limits; nurses and doctors operate as two sides to a shared coin. As doctors, we diagnose and prescribe, while nurses explain and dispense. As doctors, we talk to patients, while nurses comfort them. Imagine spending an entire year working in a hospital diligently wiping endotracheal tubes that are responsible for maintaining someone’s life. Imagine spending an entire year laboring through the heavy task of lifting patients to prone them in a position that may save their lives. Imagine spending an entire year holding the hands of comatose patients in hopes of maintaining a sense of humanity.
And this only begins to describe the tasks bestowed upon nurses. While doctors answer pagers or complete insurance authorization forms, nurses empathize and reassure scared and isolated patients. Imagine spending an entire year updating crying family members who cannot see their loved ones. Imagine spending an entire year explaining and pleading to the outside world that wearing a mask and washing hands would reduce the suffering that takes place inside the hospital walls.
Despite the uncertainties, pressures, and demands, nurses have continued, and will continue, to show up for their patients, shift by shift. It takes a tragic number of deaths for the nurses I see in my practice to share that they have lost count. These numbers reflect people they held to feed, carried to prevent ulcers, wiped for decency, caressed for compassion, probed with IVs and tubes, monitored for signs of life, and warmed with blankets. If love were in any job description, it would fall under that of a nurse.
And we can’t ignore the fact that all the lives lost by COVID-19 had family. Family members who, without ever stepping foot in the hospital, needed a place to be heard, a place to receive explanation, and a place for reassurance. This invaluable place is cultivated by nurses. Through Zoom and phone calls, nurses share messages of hope, love, and fear between patients and family. Through Zoom and phone calls, nurses orchestrate visits and last goodbyes.
There is no denying that we have all been affected by this shared human experience. But the pause we owe our nurses feels long overdue, and of great importance. Nurses need a space to be heard, to be comforted, to be recognized. They come to our practices, trying to contain the world’s angst, while also navigating for themselves what it means to go through what they are going through. They hope that by coming to see us, they will find the strength to go back another day, another week, another month. Sometimes, they come to talk about everything but the job, in hopes that by talking about more mundane problems, they will feel “normal” and reconnected.
I hope that our empathy, congruence, and unconditional positive regard will allow them to feel heard.1 I hope that our warmth, concern, and hopefulness provide a welcoming place to voice sadness, anger, and fears.2 I hope that our processing of traumatic memory, our challenge to avoid inaccurate self-blaming beliefs, and our encouragement to create more thought-out conclusions will allow them to understand what is happening more accurately.3
Yet, I worry. I worry that society hasn’t been particularly successful with helping prior generations of heroes. From war veterans, to Sept. 11, 2001, firefighters, it seems that we have repeated mistakes. My experience with veterans in particular has taught me that for many who are suffering, it feels like society has broken its very fabric by being bystanders to the pain.
But suffering and tragedy are an inevitable part of the human experience that we share. What we can keep sight of is this: As physicians, we work with nurses. We are witnessing firsthand the impossible sacrifice they are taking and the limits of resilience. Let us not be too busy to stop and give recognition where and when it is due. Let us listen and learn from our past, and present, heroes. And let us never forget to extend our own hand to those who make a living extending theirs.
Dr. Badre is a clinical and forensic psychiatrist in San Diego. He holds teaching positions at the University of California, San Diego, and the University of San Diego. He teaches medical education, psychopharmacology, ethics in psychiatry, and correctional care. Dr. Badre can be reached at his website, BadreMD.com.
References
1. Rogers CR. J Consult Psychol. 1957;21(2):95-103.
2. Mallo CJ, Mintz DL. Psychodyn Psychiatry. 2013 Mar;41(1):13-37.
3. Resick PA et al. Cognitive Processing Therapy for PTSD: A Comprehensive Manual. Guilford Publications, 2016.
This past year, the referrals to my private practice have taken a noticeable shift and caused me to pause.
More calls have come from nurses, many who work directly with COVID-19 patients, understandably seeking mental health treatment, or support. Especially in this time, nurses are facing trauma and stress that is unimaginable to many, myself included. Despite the collective efforts we have made as a society to recognize their work, I do not think we have given enough consideration to the enormous sacrifice nurses are currently undertaking to save our collective psyche.
As physicians and mental health providers, we have a glimpse into the complexities and stressors of medical treatment. In our line of work, we support patients with trauma on a regular basis. We feel deeply connected to patients, some of whom we have treated until the end of their lives. Despite that, I am not sure that I, or anyone, can truly comprehend what nurses face in today’s climate of care.
There is no denying that doctors are of value to our system, but our service has limits; nurses and doctors operate as two sides to a shared coin. As doctors, we diagnose and prescribe, while nurses explain and dispense. As doctors, we talk to patients, while nurses comfort them. Imagine spending an entire year working in a hospital diligently wiping endotracheal tubes that are responsible for maintaining someone’s life. Imagine spending an entire year laboring through the heavy task of lifting patients to prone them in a position that may save their lives. Imagine spending an entire year holding the hands of comatose patients in hopes of maintaining a sense of humanity.
And this only begins to describe the tasks bestowed upon nurses. While doctors answer pagers or complete insurance authorization forms, nurses empathize and reassure scared and isolated patients. Imagine spending an entire year updating crying family members who cannot see their loved ones. Imagine spending an entire year explaining and pleading to the outside world that wearing a mask and washing hands would reduce the suffering that takes place inside the hospital walls.
Despite the uncertainties, pressures, and demands, nurses have continued, and will continue, to show up for their patients, shift by shift. It takes a tragic number of deaths for the nurses I see in my practice to share that they have lost count. These numbers reflect people they held to feed, carried to prevent ulcers, wiped for decency, caressed for compassion, probed with IVs and tubes, monitored for signs of life, and warmed with blankets. If love were in any job description, it would fall under that of a nurse.
And we can’t ignore the fact that all the lives lost by COVID-19 had family. Family members who, without ever stepping foot in the hospital, needed a place to be heard, a place to receive explanation, and a place for reassurance. This invaluable place is cultivated by nurses. Through Zoom and phone calls, nurses share messages of hope, love, and fear between patients and family. Through Zoom and phone calls, nurses orchestrate visits and last goodbyes.
There is no denying that we have all been affected by this shared human experience. But the pause we owe our nurses feels long overdue, and of great importance. Nurses need a space to be heard, to be comforted, to be recognized. They come to our practices, trying to contain the world’s angst, while also navigating for themselves what it means to go through what they are going through. They hope that by coming to see us, they will find the strength to go back another day, another week, another month. Sometimes, they come to talk about everything but the job, in hopes that by talking about more mundane problems, they will feel “normal” and reconnected.
I hope that our empathy, congruence, and unconditional positive regard will allow them to feel heard.1 I hope that our warmth, concern, and hopefulness provide a welcoming place to voice sadness, anger, and fears.2 I hope that our processing of traumatic memory, our challenge to avoid inaccurate self-blaming beliefs, and our encouragement to create more thought-out conclusions will allow them to understand what is happening more accurately.3
Yet, I worry. I worry that society hasn’t been particularly successful with helping prior generations of heroes. From war veterans, to Sept. 11, 2001, firefighters, it seems that we have repeated mistakes. My experience with veterans in particular has taught me that for many who are suffering, it feels like society has broken its very fabric by being bystanders to the pain.
But suffering and tragedy are an inevitable part of the human experience that we share. What we can keep sight of is this: As physicians, we work with nurses. We are witnessing firsthand the impossible sacrifice they are taking and the limits of resilience. Let us not be too busy to stop and give recognition where and when it is due. Let us listen and learn from our past, and present, heroes. And let us never forget to extend our own hand to those who make a living extending theirs.
Dr. Badre is a clinical and forensic psychiatrist in San Diego. He holds teaching positions at the University of California, San Diego, and the University of San Diego. He teaches medical education, psychopharmacology, ethics in psychiatry, and correctional care. Dr. Badre can be reached at his website, BadreMD.com.
References
1. Rogers CR. J Consult Psychol. 1957;21(2):95-103.
2. Mallo CJ, Mintz DL. Psychodyn Psychiatry. 2013 Mar;41(1):13-37.
3. Resick PA et al. Cognitive Processing Therapy for PTSD: A Comprehensive Manual. Guilford Publications, 2016.
Inflammatory immune findings likely in acute schizophrenia, MDD, bipolar
Researchers have come a long way in understanding the link between acute inflammation and treatment-resistant depression, but more work needs to be done, according to Mark Hyman Rapaport, MD.
“Inflammation has been a hot topic in the past decade, both because of its impact in medical disorders and in psychiatric disorders,” Dr. Rapaport, CEO of the Huntsman Mental Health Institute in Salt Lake City, Utah, said during an annual psychopharmacology update held by the Nevada Psychiatric Association. “We run into difficulty with chronic inflammation, which we see with rheumatic disorders, and when we think of metabolic syndrome and obesity.”
The immune system helps to control energy regulation and neuroendocrine function in acute inflammation and chronic inflammatory diseases. “We see a variety of effects on the central nervous system or liver function or on homeostasis of the body,” said Dr. Rapaport, who also chairs the department of psychiatry at the University of Utah, also in Salt Lake City. “These are all normal and necessary to channel energy to the immune system in order to fight what’s necessary in acute inflammatory response.”
A chronic state of inflammation can result in prolonged allocation of fuels to the immune system, tissue inflammation, and a chronically aberrant immune reaction, he continued. This can cause depressive symptoms/fatigue, anorexia, malnutrition, muscle wasting, cachectic obesity, insulin resistance, dyslipidemia, increased adipose tissue in the proximity of inflammatory lesion, alterations of steroid hormone axes, elevated sympathetic tone, hypertension, decreased parasympathetic tone, inflammation-related anemia, and osteopenia. “So, chronic inflammation has a lot of long-term sequelae that are detrimental,” he said.
Both physical stress and psychological stress also cause an inflammatory state. After looking at the medical literature, Dr. Rapaport and colleagues began to wonder whether inflammation and immune activation associated with psychiatric disorders are attributable to the stress of acute illness. To find out, they performed a meta-analysis of blood cytokine network alterations in psychiatric patients and evaluated comparisons between schizophrenia, bipolar disorder, and depression. A total of three meta-analyses were performed: one of acute/inpatient studies, one on the impact of acute treatment, and one of outpatient studies. The researchers hypothesized that inflammatory and immune findings in psychiatric illnesses were tied to two distinct etiologies: the acute stress of illness and intrinsic immune dysfunction.
The meta-analyses included 68 studies: 40 involving patients with schizophrenia, 18 involving those with major depressive disorder (MDD) and 10 involving those with bipolar disorder. The researchers found that levels of four cytokines were significantly increased in acutely ill patients with schizophrenia, bipolar mania, and MDD, compared with controls: interleukin-6, tumor necrosis factor–alpha (TNF-alpha), soluble IL-2 receptor (sIL-2R), and IL-1 receptor antagonist (IL-1RA). “There has not been a consistent blood panel used across studies, be it within a disorder itself like depression, or across disorders,” Dr. Rapaport noted. “This is a challenge that we face in looking at these data.”
Following treatment of acute illness, IL-6 levels significantly decreased in schizophrenia and MDD, but no significant changes in TNF-alpha levels were observed in patients with schizophrenia or MDD. In addition, sIL-2R levels increase in schizophrenia but remained unchanged in bipolar and MDD, while IL-1RA levels in bipolar mania decreased but remained unchanged in MDD. Meanwhile, assessment of the study’s 24 outpatient studies revealed that levels of IL-6 were significantly increased in outpatients with schizophrenia, euthymic bipolar disorder, and MDD, compared with controls (P < .01 for each). In addition, levels of IL-1 beta and sIL-2R were significantly increased in outpatients with schizophrenia and bipolar disorder.
According to Dr. Rapaport, these meta-analyses suggest that there are likely inflammatory immune findings present in acutely ill patients with MDD, schizophrenia, and bipolar disorder.
“Some of this activation decreases with effective acute treatment of the disorder,” he said. “The data suggest that immune changes are present in a subset of patients with all three disorders.”
“We also need to understand the regulatory role that microglia and astroglia play within the brain,” he said. “We need to identify changes in brain circuitry and function associated with inflammation and other immune changes. We also need to carefully scrutinize publications, understand the assumptions behind the statistics, and carry out more research beyond the protein level.”
He concluded his presentation by calling for research to help clinicians differentiate acute from chronic inflammation. “The study of both is important,” he said. “We need to understand the pathophysiology of immune changes in psychiatric disorders. We need to study both the triggers and pathways to resolution.”
Dr. Rapaport disclosed that he has received research support from the National Institutes of Health, the National Institute of Mental Health, and the National Center for Complementary and Integrative Health.
Researchers have come a long way in understanding the link between acute inflammation and treatment-resistant depression, but more work needs to be done, according to Mark Hyman Rapaport, MD.
“Inflammation has been a hot topic in the past decade, both because of its impact in medical disorders and in psychiatric disorders,” Dr. Rapaport, CEO of the Huntsman Mental Health Institute in Salt Lake City, Utah, said during an annual psychopharmacology update held by the Nevada Psychiatric Association. “We run into difficulty with chronic inflammation, which we see with rheumatic disorders, and when we think of metabolic syndrome and obesity.”
The immune system helps to control energy regulation and neuroendocrine function in acute inflammation and chronic inflammatory diseases. “We see a variety of effects on the central nervous system or liver function or on homeostasis of the body,” said Dr. Rapaport, who also chairs the department of psychiatry at the University of Utah, also in Salt Lake City. “These are all normal and necessary to channel energy to the immune system in order to fight what’s necessary in acute inflammatory response.”
A chronic state of inflammation can result in prolonged allocation of fuels to the immune system, tissue inflammation, and a chronically aberrant immune reaction, he continued. This can cause depressive symptoms/fatigue, anorexia, malnutrition, muscle wasting, cachectic obesity, insulin resistance, dyslipidemia, increased adipose tissue in the proximity of inflammatory lesion, alterations of steroid hormone axes, elevated sympathetic tone, hypertension, decreased parasympathetic tone, inflammation-related anemia, and osteopenia. “So, chronic inflammation has a lot of long-term sequelae that are detrimental,” he said.
Both physical stress and psychological stress also cause an inflammatory state. After looking at the medical literature, Dr. Rapaport and colleagues began to wonder whether inflammation and immune activation associated with psychiatric disorders are attributable to the stress of acute illness. To find out, they performed a meta-analysis of blood cytokine network alterations in psychiatric patients and evaluated comparisons between schizophrenia, bipolar disorder, and depression. A total of three meta-analyses were performed: one of acute/inpatient studies, one on the impact of acute treatment, and one of outpatient studies. The researchers hypothesized that inflammatory and immune findings in psychiatric illnesses were tied to two distinct etiologies: the acute stress of illness and intrinsic immune dysfunction.
The meta-analyses included 68 studies: 40 involving patients with schizophrenia, 18 involving those with major depressive disorder (MDD) and 10 involving those with bipolar disorder. The researchers found that levels of four cytokines were significantly increased in acutely ill patients with schizophrenia, bipolar mania, and MDD, compared with controls: interleukin-6, tumor necrosis factor–alpha (TNF-alpha), soluble IL-2 receptor (sIL-2R), and IL-1 receptor antagonist (IL-1RA). “There has not been a consistent blood panel used across studies, be it within a disorder itself like depression, or across disorders,” Dr. Rapaport noted. “This is a challenge that we face in looking at these data.”
Following treatment of acute illness, IL-6 levels significantly decreased in schizophrenia and MDD, but no significant changes in TNF-alpha levels were observed in patients with schizophrenia or MDD. In addition, sIL-2R levels increase in schizophrenia but remained unchanged in bipolar and MDD, while IL-1RA levels in bipolar mania decreased but remained unchanged in MDD. Meanwhile, assessment of the study’s 24 outpatient studies revealed that levels of IL-6 were significantly increased in outpatients with schizophrenia, euthymic bipolar disorder, and MDD, compared with controls (P < .01 for each). In addition, levels of IL-1 beta and sIL-2R were significantly increased in outpatients with schizophrenia and bipolar disorder.
According to Dr. Rapaport, these meta-analyses suggest that there are likely inflammatory immune findings present in acutely ill patients with MDD, schizophrenia, and bipolar disorder.
“Some of this activation decreases with effective acute treatment of the disorder,” he said. “The data suggest that immune changes are present in a subset of patients with all three disorders.”
“We also need to understand the regulatory role that microglia and astroglia play within the brain,” he said. “We need to identify changes in brain circuitry and function associated with inflammation and other immune changes. We also need to carefully scrutinize publications, understand the assumptions behind the statistics, and carry out more research beyond the protein level.”
He concluded his presentation by calling for research to help clinicians differentiate acute from chronic inflammation. “The study of both is important,” he said. “We need to understand the pathophysiology of immune changes in psychiatric disorders. We need to study both the triggers and pathways to resolution.”
Dr. Rapaport disclosed that he has received research support from the National Institutes of Health, the National Institute of Mental Health, and the National Center for Complementary and Integrative Health.
Researchers have come a long way in understanding the link between acute inflammation and treatment-resistant depression, but more work needs to be done, according to Mark Hyman Rapaport, MD.
“Inflammation has been a hot topic in the past decade, both because of its impact in medical disorders and in psychiatric disorders,” Dr. Rapaport, CEO of the Huntsman Mental Health Institute in Salt Lake City, Utah, said during an annual psychopharmacology update held by the Nevada Psychiatric Association. “We run into difficulty with chronic inflammation, which we see with rheumatic disorders, and when we think of metabolic syndrome and obesity.”
The immune system helps to control energy regulation and neuroendocrine function in acute inflammation and chronic inflammatory diseases. “We see a variety of effects on the central nervous system or liver function or on homeostasis of the body,” said Dr. Rapaport, who also chairs the department of psychiatry at the University of Utah, also in Salt Lake City. “These are all normal and necessary to channel energy to the immune system in order to fight what’s necessary in acute inflammatory response.”
A chronic state of inflammation can result in prolonged allocation of fuels to the immune system, tissue inflammation, and a chronically aberrant immune reaction, he continued. This can cause depressive symptoms/fatigue, anorexia, malnutrition, muscle wasting, cachectic obesity, insulin resistance, dyslipidemia, increased adipose tissue in the proximity of inflammatory lesion, alterations of steroid hormone axes, elevated sympathetic tone, hypertension, decreased parasympathetic tone, inflammation-related anemia, and osteopenia. “So, chronic inflammation has a lot of long-term sequelae that are detrimental,” he said.
Both physical stress and psychological stress also cause an inflammatory state. After looking at the medical literature, Dr. Rapaport and colleagues began to wonder whether inflammation and immune activation associated with psychiatric disorders are attributable to the stress of acute illness. To find out, they performed a meta-analysis of blood cytokine network alterations in psychiatric patients and evaluated comparisons between schizophrenia, bipolar disorder, and depression. A total of three meta-analyses were performed: one of acute/inpatient studies, one on the impact of acute treatment, and one of outpatient studies. The researchers hypothesized that inflammatory and immune findings in psychiatric illnesses were tied to two distinct etiologies: the acute stress of illness and intrinsic immune dysfunction.
The meta-analyses included 68 studies: 40 involving patients with schizophrenia, 18 involving those with major depressive disorder (MDD) and 10 involving those with bipolar disorder. The researchers found that levels of four cytokines were significantly increased in acutely ill patients with schizophrenia, bipolar mania, and MDD, compared with controls: interleukin-6, tumor necrosis factor–alpha (TNF-alpha), soluble IL-2 receptor (sIL-2R), and IL-1 receptor antagonist (IL-1RA). “There has not been a consistent blood panel used across studies, be it within a disorder itself like depression, or across disorders,” Dr. Rapaport noted. “This is a challenge that we face in looking at these data.”
Following treatment of acute illness, IL-6 levels significantly decreased in schizophrenia and MDD, but no significant changes in TNF-alpha levels were observed in patients with schizophrenia or MDD. In addition, sIL-2R levels increase in schizophrenia but remained unchanged in bipolar and MDD, while IL-1RA levels in bipolar mania decreased but remained unchanged in MDD. Meanwhile, assessment of the study’s 24 outpatient studies revealed that levels of IL-6 were significantly increased in outpatients with schizophrenia, euthymic bipolar disorder, and MDD, compared with controls (P < .01 for each). In addition, levels of IL-1 beta and sIL-2R were significantly increased in outpatients with schizophrenia and bipolar disorder.
According to Dr. Rapaport, these meta-analyses suggest that there are likely inflammatory immune findings present in acutely ill patients with MDD, schizophrenia, and bipolar disorder.
“Some of this activation decreases with effective acute treatment of the disorder,” he said. “The data suggest that immune changes are present in a subset of patients with all three disorders.”
“We also need to understand the regulatory role that microglia and astroglia play within the brain,” he said. “We need to identify changes in brain circuitry and function associated with inflammation and other immune changes. We also need to carefully scrutinize publications, understand the assumptions behind the statistics, and carry out more research beyond the protein level.”
He concluded his presentation by calling for research to help clinicians differentiate acute from chronic inflammation. “The study of both is important,” he said. “We need to understand the pathophysiology of immune changes in psychiatric disorders. We need to study both the triggers and pathways to resolution.”
Dr. Rapaport disclosed that he has received research support from the National Institutes of Health, the National Institute of Mental Health, and the National Center for Complementary and Integrative Health.
FROM NPA 2021