PTSD

As symptoms of posttraumatic stress disorder (PTSD) progress, the involved person’s physical and mental health deteriorates.¹ This sparks lifestyle changes that allow them to avoid re-exposure to triggering stimuli; however, it also increases their risk of social isolation. Early clinical investigation has found that patients who experience hyperarousal symptoms of overt PTSD—difficulty sleeping, emotional dyscontrol, hypervigilance, and an enhanced startle response—could benefit from the stress-reducing capacity of glucocorticoids.

Decreased glucocorticoids

After a distressing situation, norepinephrine levels rise acutely.^2,3 This contributes to a protective retention of potentially threatening memories, which is how people learn to avoid danger.

Glucocorticoid secretion enhances a patient’s coping mechanisms by helping them process information in a way that diminishes retrieval of fear-evoking memories.^2,3 Glucocorticoid, also called cortisol, is referred to as a “stress hormone.” Cortisol promotes emotional adaptability following a traumatic event; this action diminishes future, inappropriate retrieval of frightening memories as a physiologic mechanism to help people cope with upsetting situations.³

PTSD pathogenesis involves altered hypothalamic-pituitary-adrenal axis function; sustained stress results in decreased levels of circulating glucocorticoid. This is a consequence of enhanced negative feedback and increased glucocorticoid receptor sensitivity, which is evidenced by results of abnormal dexamethasone suppression tests.¹ Downregulation of corticotropin-releasing hormone (CRH) receptors in the pituitary glands and increased CRH levels have been documented in PTSD patients.^1,4 An association between high CRH levels and an increase in startle response explains the exaggerated startle response observed in patients with PTSD. Higher circulating glucocorticoid has the opposite effect⁴; there is an inverse relationship between the daily level of glucocorticoid and startle amplitude. A low level of circulating glucocorticoid promotes recall of frightening events that results in persistent re-experiencing of traumatic memories.^2,3

Glucocorticoids in PTSD

Glucocorticoid administration reduces psychological and physiological responses to stress.³ Exogenous glucocorticoid administration affects cognition by interacting with serotonin, dopamine, and ã-aminobutyric acid by actions on the amygdala, medial prefrontal cortex, and hippocampus.^2,3 Research among  veterans with and without PTSD recorded a decrease in startle response after administration of a single dose of 20 mg of hydrocortisone.⁴ Results of a large study documented that one dose of hydrocortisone administered at >35 mg can inhibit threatening memories and improve social function.³ Hydrocortisone is linked to anxiolytic effects in healthy persons and patients with social phobia or panic disorder.^3,4 Because treatment of PTSD with antidepressants and benzodiazepines often is ineffective,⁵ glucocorticoids may offer a new pharmacotherapy option. Glucocorticoids have been prescribed as prophylactic agents shortly after an acutely stressful event to prevent development of PTSD.⁴ Hydrocortisone is not FDA-approved to treat PTSD; informed consent, physician discretion, and close monitoring are emphasized.

Glucocorticoid use in mitigating PTSD symptom emergence is under investigation. Research suggests that just one acute dose of hydrocortisone might benefit patients prone to PTSD.^3,4 Further study is needed to establish whether prescribing hydrocortisone is efficacious.

Disclosure

The authors report no financial relationships with any company whose products are mentioned in this article or with manufacturers of competing products.

As symptoms of posttraumatic stress disorder (PTSD) progress, the involved person’s physical and mental health deteriorates.¹ This sparks lifestyle changes that allow them to avoid re-exposure to triggering stimuli; however, it also increases their risk of social isolation. Early clinical investigation has found that patients who experience hyperarousal symptoms of overt PTSD—difficulty sleeping, emotional dyscontrol, hypervigilance, and an enhanced startle response—could benefit from the stress-reducing capacity of glucocorticoids.

Decreased glucocorticoids

After a distressing situation, norepinephrine levels rise acutely.^2,3 This contributes to a protective retention of potentially threatening memories, which is how people learn to avoid danger.

Glucocorticoid secretion enhances a patient’s coping mechanisms by helping them process information in a way that diminishes retrieval of fear-evoking memories.^2,3 Glucocorticoid, also called cortisol, is referred to as a “stress hormone.” Cortisol promotes emotional adaptability following a traumatic event; this action diminishes future, inappropriate retrieval of frightening memories as a physiologic mechanism to help people cope with upsetting situations.³

PTSD pathogenesis involves altered hypothalamic-pituitary-adrenal axis function; sustained stress results in decreased levels of circulating glucocorticoid. This is a consequence of enhanced negative feedback and increased glucocorticoid receptor sensitivity, which is evidenced by results of abnormal dexamethasone suppression tests.¹ Downregulation of corticotropin-releasing hormone (CRH) receptors in the pituitary glands and increased CRH levels have been documented in PTSD patients.^1,4 An association between high CRH levels and an increase in startle response explains the exaggerated startle response observed in patients with PTSD. Higher circulating glucocorticoid has the opposite effect⁴; there is an inverse relationship between the daily level of glucocorticoid and startle amplitude. A low level of circulating glucocorticoid promotes recall of frightening events that results in persistent re-experiencing of traumatic memories.^2,3

Glucocorticoids in PTSD

Glucocorticoid administration reduces psychological and physiological responses to stress.³ Exogenous glucocorticoid administration affects cognition by interacting with serotonin, dopamine, and ã-aminobutyric acid by actions on the amygdala, medial prefrontal cortex, and hippocampus.^2,3 Research among  veterans with and without PTSD recorded a decrease in startle response after administration of a single dose of 20 mg of hydrocortisone.⁴ Results of a large study documented that one dose of hydrocortisone administered at >35 mg can inhibit threatening memories and improve social function.³ Hydrocortisone is linked to anxiolytic effects in healthy persons and patients with social phobia or panic disorder.^3,4 Because treatment of PTSD with antidepressants and benzodiazepines often is ineffective,⁵ glucocorticoids may offer a new pharmacotherapy option. Glucocorticoids have been prescribed as prophylactic agents shortly after an acutely stressful event to prevent development of PTSD.⁴ Hydrocortisone is not FDA-approved to treat PTSD; informed consent, physician discretion, and close monitoring are emphasized.

Glucocorticoid use in mitigating PTSD symptom emergence is under investigation. Research suggests that just one acute dose of hydrocortisone might benefit patients prone to PTSD.^3,4 Further study is needed to establish whether prescribing hydrocortisone is efficacious.

Disclosure

The authors report no financial relationships with any company whose products are mentioned in this article or with manufacturers of competing products.

As symptoms of posttraumatic stress disorder (PTSD) progress, the involved person’s physical and mental health deteriorates.¹ This sparks lifestyle changes that allow them to avoid re-exposure to triggering stimuli; however, it also increases their risk of social isolation. Early clinical investigation has found that patients who experience hyperarousal symptoms of overt PTSD—difficulty sleeping, emotional dyscontrol, hypervigilance, and an enhanced startle response—could benefit from the stress-reducing capacity of glucocorticoids.

Decreased glucocorticoids

After a distressing situation, norepinephrine levels rise acutely.^2,3 This contributes to a protective retention of potentially threatening memories, which is how people learn to avoid danger.

Glucocorticoid secretion enhances a patient’s coping mechanisms by helping them process information in a way that diminishes retrieval of fear-evoking memories.^2,3 Glucocorticoid, also called cortisol, is referred to as a “stress hormone.” Cortisol promotes emotional adaptability following a traumatic event; this action diminishes future, inappropriate retrieval of frightening memories as a physiologic mechanism to help people cope with upsetting situations.³

PTSD pathogenesis involves altered hypothalamic-pituitary-adrenal axis function; sustained stress results in decreased levels of circulating glucocorticoid. This is a consequence of enhanced negative feedback and increased glucocorticoid receptor sensitivity, which is evidenced by results of abnormal dexamethasone suppression tests.¹ Downregulation of corticotropin-releasing hormone (CRH) receptors in the pituitary glands and increased CRH levels have been documented in PTSD patients.^1,4 An association between high CRH levels and an increase in startle response explains the exaggerated startle response observed in patients with PTSD. Higher circulating glucocorticoid has the opposite effect⁴; there is an inverse relationship between the daily level of glucocorticoid and startle amplitude. A low level of circulating glucocorticoid promotes recall of frightening events that results in persistent re-experiencing of traumatic memories.^2,3

Glucocorticoids in PTSD

Glucocorticoid administration reduces psychological and physiological responses to stress.³ Exogenous glucocorticoid administration affects cognition by interacting with serotonin, dopamine, and ã-aminobutyric acid by actions on the amygdala, medial prefrontal cortex, and hippocampus.^2,3 Research among  veterans with and without PTSD recorded a decrease in startle response after administration of a single dose of 20 mg of hydrocortisone.⁴ Results of a large study documented that one dose of hydrocortisone administered at >35 mg can inhibit threatening memories and improve social function.³ Hydrocortisone is linked to anxiolytic effects in healthy persons and patients with social phobia or panic disorder.^3,4 Because treatment of PTSD with antidepressants and benzodiazepines often is ineffective,⁵ glucocorticoids may offer a new pharmacotherapy option. Glucocorticoids have been prescribed as prophylactic agents shortly after an acutely stressful event to prevent development of PTSD.⁴ Hydrocortisone is not FDA-approved to treat PTSD; informed consent, physician discretion, and close monitoring are emphasized.

Glucocorticoid use in mitigating PTSD symptom emergence is under investigation. Research suggests that just one acute dose of hydrocortisone might benefit patients prone to PTSD.^3,4 Further study is needed to establish whether prescribing hydrocortisone is efficacious.

Disclosure

The authors report no financial relationships with any company whose products are mentioned in this article or with manufacturers of competing products.

Current Psychiatry and the American Academy of Clinical Psychiatrists welcomed more than 550 psychiatric practitioners from across the United States and abroad to this annual conference, which was headed by Meeting Chair Richard Balon, MD, and Co-chairs Donald W. Black, MD, and Nagy Youssef, MD, March 27-29, 2014 at the Hilton Chicago in Chicago, Illinois. Attendees earned as many as 10 AMA PRA Category 1 Credits™.

 

Thursday, March 27, 2014

MORNING SESSION

Obsessive-compulsive disorder can be misdiagnosed as psychosis, anxiety, or a sexual disorder. In addition to contamination, patients can present with pathologic doubt, somatic obsessions, or obsessions about taboo or symmetry. Among FDA-approved medications, clomipramine might be more effective than selective serotonin reuptake inhibitors (SSRIs). Exposure response prevention therapy shows better response than pharmacotherapy, but best outcomes are seen with combination therapy. Jon E. Grant, JD, MD, MPH, University of Chicago, also discussed obsessive-compulsive personality disorder, body dysmorphic disorder, hoarding, trichotillomania, and excoriation disorder—as well as changes in DSM-5 that cover this group of disorders.

Patients with schizophrenia are at higher risk of death from cardiac and pulmonary disease than the general population. The quality of care of patients with psychosis generally is poor, because of lack of recognition, time, and resources, as well as systematic barriers to accessing health care. Questions about weight gain, lethargy, infections, and sexual functioning can help the practitioner assess a patient’s general health. When appropriate, Henry A. Nasrallah, MD, St. Louis University School of Medicine, recommends, consider switching antipsychotics, which might reverse adverse metabolic events.

Nonpharmacologic treatment goals include improving sleep, educating patients, providing them with tools for improving sleep, and creating an opportunity for patient-practitioner discussion. Stimulus control and sleep restriction are primary therapeutic techniques to improve sleep quality and reduce non-sleeping time in bed. Thomas Roth, PhD, Henry Ford Hospital, also discussed how to modify sleep hygiene techniques for pediatric, adolescent, and geriatric patients.

Donald W. Black, MD, University of Iowa, says that work groups for DSM-5 were asked to consider dimensionality and culture and gender issues. New diagnostic categories include obsessive-compulsive and related disorders and trauma and stressor-related disorders. Some diagnoses were reformulated or introduced, including autism spectrum disorder and disruptive mood dysregulation disorder. The multi-axial system was discontinued in DSM-5. He also reviewed coding issues.

In a sponsored symposium, Prakash S. Masand, MD, Global Medical Education, Inc., looked at the clinical challenges of addressing all 3 symptom domains that characterize depression (emotional, physical, and cognitive) as an introduction to reviewing the efficacy, mechanism of action, and side effects of vortioxetine (Brintellix), a new serotonergic agent for treating major depressive disorder (MDD). In all studies submitted to the FDA, vortioxetine was found to be superior to placebo, in at least 1 dosage group, for alleviating depressive symptoms and for reducing the risk of depressive recurrence.

 

AFTERNOON SESSION

Oppositional defiant disorder is more common in boys (onset at age 6 to 10) and is associated with inconsistent and neglectful parenting. Treatment modalities, including educational training, anticonvulsants, and lithium, do not have a strong evidence base. Intermittent explosive disorder is characterized by short-lived but frequent behavioral outbursts and often begins in adolescence. Dr. Grant also reviewed the evidence on conduct disorder, pyromania, and kleptomania.

Cognitive symptoms of schizophrenia often appear before psychotic symptoms and remain stable across the lifespan. There are no pharmacologic treatments for cognitive deficits in schizophrenia; however, Dr. Nasrallah listed tactics to improve cognitive function, including regular aerobic exercise. These cognitive deficits can be categorized as neurocognitive (memory, learning, executive function) and social (social skills, theory of mind, social cues) and contribute to functional decline and often prevent patients from working and going to school. Dr. Nasrallah described how bipolar disorder (BD) overlaps with schizophrenia in terms of cognitive dysfunction.

^{Henry Nasrallah, MD}

 

Psychiatric disorders exhibit specific sleep/ wake impairments. Sleep disorders can mimic psychiatric symptoms, such as fatigue, cognitive problems, and depression. Sleep disturbances, including insomnia, obstructive sleep apnea, and decreased need for sleep, often coexist with depression, generalized anxiety disorder, posttraumatic stress disorder, and BD, and insomnia is associated with a greater risk of suicide. With antidepressant treatment, sleep in depressed patients improves but does not normalize. Dr. Roth also reviewed pharmacotherapeutic options and non-drug modalities to improve patients’ sleep.

Antidepressants have no efficacy in treating acute episodes of bipolar depression, and using such agents might yield a poor long-term outcome in BD, according to Robert M. Post, MD, George Washington University School of Medicine, Michael J. Ostacher, MD, MPH, MMSc, Stanford University, and Vivek Singh, MD, University of Texas Health Science Center at San Antonio, in an interactive faculty discussion. For patients with bipolar I disorder, lithium monotherapy or the combination of lithium and valproate is more effective than valproate alone; evidence does not support valproate as a maintenance treatment. When a patient with BD shows partial response, attendees at this sponsored symposium were advised, consider adding psychotherapy and psycho-education. Combining a mood stabilizer and an antipsychotic might be more effective than monotherapy and safer, by allowing lower dosages. The only 3 treatments FDA-approved for bipolar depression are the olanzapine-fluoxetine combination, quetiapine, and lurasidone.

 

 

^{Boaz Levy, PhD, (left) receives the 2014 George Winokur Research Award from Carol S. North, MD, for his article on recovery of cognitive function in patients with co-occuring bipolar disorder and alcohol dependence.}

 

Friday, March 28, 2014

MORNING SESSION

Carmen Pinto, MD, at a sponsored symposium, reviewed the utility and safety of
long-acting injectable (LAI) antipsychotics for treating schizophrenia, with a focus on LAI aripiprazole, a partial HT-receptor agonist/partial HT-receptor antagonist. Four monthly injections (400 mg/injection) of the drug are needed to reach steady state; each injection reaches peak level in 5 to 7 days. LAI aripiprazole has been shown to delay time to relapse due to nonadherence and onset of nonresponse to the drug, and has high patient acceptance—even in those who already stable. Safety and side effects with LAI aripiprazole are the same as seen with the oral formulation.

In multimodal therapy for chronic pain, psychiatrists have a role in assessing
psychiatric comorbidities, coping ability, social functioning, and other life functions, including work and personal relationships. Cognitive-behavioral therapy can be particularly useful for chronic pain by helping patients reframe their pain experiences. Raphael J. Leo, MA, MD, FAPM, University at Buffalo, reviewed non-opioid co-analgesics that can be used for patients with comorbid pain and a substance use disorder. If opioids are necessary, consider “weak” or long-acting opioids. Monitor patients for aberrant, drug-seeking behavior.

In the second part of his overview, Dr. Black highlighted specific changes to DSM-5 of particular concern to clinicians. New chapters were created and disorders were consolidated, he explained, such as autism spectrum disorder, somatic symptom disorder, and major neurocognitive disorder. New diagnoses include hoarding disorder and binge eating disorder. Subtypes of schizophrenia were dropped. Pathologic gambling was renamed gambling disorder and gender dysphoria is now called gender identity disorder. The bereavement exclusion of a major depressive episode was dropped.

Antidepressants are effective in mitigating pain in neuropathy, headache, fibromyalgia, and chronic musculoskeletal pain, and have been advocated for other pain syndromes. Selection of an antidepressant depends on the type of pain condition, comorbid depression or anxiety, tolerability, and medical comorbidities. Dr. Leo presented prescribing strategies for tricyclics, serotoninnorepinephrine
reuptake inhibitors, SSRIs, and other antidepressants.

Treating of BD in geriatric patients becomes complicated because therapeutic choices are narrowed and response to therapy is less successful with age, according to George T. Grossberg, MD, St. Louis University. Rapid cycling tends to be the norm in geriatric BD patients. Look for agitation and irritability, rather than full-blown mania; grandiose delusions; psychiatric comorbidity, especially anxiety disorder; and sexually inappropriate behavior. Pharmacotherapeutic options include: mood stabilizers, atypical antipsychotics, and antidepressants (specifically, bupropion and SSRIs—not TCAs, venlafaxine, or duloxetine—and over the short term only). Consider divalproex for mania and hypomania, used cautiously because of its adverse side-effect potential.

 

^{George T. Grossberg, MD}

AFTERNOON SESSION

Often, BD is misdiagnosed as unipolar depression, or the correct diagnosis of BD is delayed, according to Gustavo Alva, MD, ATP Clinical Research. Comorbid substance use disorder or an anxiety disorder is common. Comorbid cardiovascular disease brings a greater risk of mortality in patients with BD than suicide. Approximately two-thirds of patients with BD are taking adjunctive medications; however, antidepressants are no more effective than placebo in treating bipolar depression. At this sponsored symposium, Vladimir Maletic, MD, University of South Carolina, described a 6-week trial in which lurasidone plus lithium or divalporex was more effective in reducing depression, as measured by MADRS, than placebo plus lithium or  akathisia, somnolence, and extrapyramidal symptoms.

When assessing an older patient with psychosis, first establish the cause of the symptoms, such as Alzheimer’s disease, affective disorder, substance use, or hallucinations associated with grief. Older patients with schizophrenia who have been taking typical antipsychotics for years might benefit from a switch to an atypical or a dosage reduction. Dr. Grossberg recommends considering antipsychotics for older patients when symptoms cause severe emotional distress that does not respond to other interventions or an acute episode that poses a safety risk for patients or others. Choose an antipsychotic based on side effects, and “start low and go slow,” when possible. The goal is to reduce agitation and distress—not necessarily to resolve psychotic symptoms.

Anita H. Clayton, MD, University of Virginia Health System, provided a review of sexual function from puberty through midlife and older years. Social factors play a role in sexual satisfaction, such as gender expectations, religious beliefs, and the influence of reporting in the media. Sexual dysfunction becomes worse in men after age 29; in women, the rate of sexual dysfunction appears to be consistent across the lifespan. Cardiovascular disease is a significant risk factor for sexual dysfunction in men, but not in women. Sexual function and depression have a bidirectional relationship; sexual dysfunction may be a symptom or cause of depression and antidepressants may affect desire and function. Medications, including psychotropics, oral contraceptives, and opioids, can cause sexual dysfunction.

 

Providers often are reluctant to bring up sexual issues with their patients, Dr. Clayton says, but patients often want to talk about their sexual problems. In reproductive-age women, look for hypoactive sexual desire disorder and pain. In men, assess for erectile dysfunction or premature ejaculation. Inquire about every phase of the sexual response cycle. When managing sexual dysfunction, aim to minimize contributing factors such as illness or medication, consider FDA-approved medications, encourage a healthy lifestyle, and employ psychological interventions when appropriate. In patients with antidepressant-associated sexual dysfunction, consider switching medications or adding an antidote, such as bupropion, buspirone, or sildenafil.

 

Saturday, March 29, 2014

MORNING SESSION

Because of the lack of double-blind, placebo-controlled trials, the risks of untreated depression vs the risks of antidepressant use in pregnancy are unclear. Marlene P. Freeman, MD, Massachusetts General Hospital, described the limited, long-term data on tricyclics and fluoxetine. Some studies have shown a small risk of birth defects with SSRIs; others did not find an association. For moderate or severe depression, use antidepressants at the lowest dosage and try non-medication options, such as psychotherapy and complementary and alternative medicine. During the third trimester, women may need a higher dosage to maintain therapeutic drug levels. Data indicates that folic acid use during pregnancy is associated with a decreased risk of autism and schizophrenia.

James W. Jefferson, MD, University of Wisconsin School of Medicine and Public Health, recommends ruling out medical conditions, such as cancer, that might be causing your patients’ fatigue or depression. Many medications, including over-the-counter agents and supplements, can cause fatigue. Bupropion was more effective than placebo and SSRIs in treating depressed patients with sleepiness and fatigue. Adding a psychostimulant to an SSRI does not have a significantly better effect than placebo on depressive symptoms. Adjunctive modafanil may improve depression and fatigue. Data for dopamine agonists are limited.

Lithium should be used with caution in pregnant women because of the risk of congenital malformations. Dr. Freeman also discussed the potential risks to the fetus with the mother’s use of valproate and lamotrigine (with the latter, a small increase in oral clefting). High-potency typical antipsychotics are considered safe; low-potency drugs have a higher risk of major malformations. For atypicals, the risk of malformations appears minimal; newborns might display extrapyramidal effects and withdrawal symptoms. Infants exposed to psychostimulants may have lower birth weight, but are not at increased risk of birth defects.

Dr. Jefferson reviewed the efficacy, pharmacokinetics, and adverse effects of vilazodone, levomilnacipran, and vortioxetine, which are antidepressants new to the market. Dr. Jefferson recommends reading package inserts to become familiar with new drugs. He also described studies of medications that were not FDA-approved, including edivoxetine, quetiapine XR monotherapy for MDD, and agomelatine. Agents under investigation include onabotulinumtoxin A injections, ketamine, and lanicemine.

Katherine E. Burdick, PhD, Mount Sinai School of Medicine, defined cognitive domains. First-episode MDD patients perform worse in psychomotor speed and attention than healthy controls. Late-onset depression (after age 60) is associated with worse performance on processing speed and verbal memory. Cognitive deficits in depressed patients range from mild to moderate and are influenced by symptom status and duration of illness. Treating cognitive deficits begins with prevention. Cholinesterase inhibitors are not effective for improving cognition in MDD. Antidepressants, including SSRIs, do not adequately treat cognitive deficits, Roger S. McIntyre, MD, FRCPC, University of Toronto, explained.

 

Current Psychiatry and the American Academy of Clinical Psychiatrists welcomed more than 550 psychiatric practitioners from across the United States and abroad to this annual conference, which was headed by Meeting Chair Richard Balon, MD, and Co-chairs Donald W. Black, MD, and Nagy Youssef, MD, March 27-29, 2014 at the Hilton Chicago in Chicago, Illinois. Attendees earned as many as 10 AMA PRA Category 1 Credits™.

 

Thursday, March 27, 2014

MORNING SESSION

Obsessive-compulsive disorder can be misdiagnosed as psychosis, anxiety, or a sexual disorder. In addition to contamination, patients can present with pathologic doubt, somatic obsessions, or obsessions about taboo or symmetry. Among FDA-approved medications, clomipramine might be more effective than selective serotonin reuptake inhibitors (SSRIs). Exposure response prevention therapy shows better response than pharmacotherapy, but best outcomes are seen with combination therapy. Jon E. Grant, JD, MD, MPH, University of Chicago, also discussed obsessive-compulsive personality disorder, body dysmorphic disorder, hoarding, trichotillomania, and excoriation disorder—as well as changes in DSM-5 that cover this group of disorders.

Patients with schizophrenia are at higher risk of death from cardiac and pulmonary disease than the general population. The quality of care of patients with psychosis generally is poor, because of lack of recognition, time, and resources, as well as systematic barriers to accessing health care. Questions about weight gain, lethargy, infections, and sexual functioning can help the practitioner assess a patient’s general health. When appropriate, Henry A. Nasrallah, MD, St. Louis University School of Medicine, recommends, consider switching antipsychotics, which might reverse adverse metabolic events.

Nonpharmacologic treatment goals include improving sleep, educating patients, providing them with tools for improving sleep, and creating an opportunity for patient-practitioner discussion. Stimulus control and sleep restriction are primary therapeutic techniques to improve sleep quality and reduce non-sleeping time in bed. Thomas Roth, PhD, Henry Ford Hospital, also discussed how to modify sleep hygiene techniques for pediatric, adolescent, and geriatric patients.

Donald W. Black, MD, University of Iowa, says that work groups for DSM-5 were asked to consider dimensionality and culture and gender issues. New diagnostic categories include obsessive-compulsive and related disorders and trauma and stressor-related disorders. Some diagnoses were reformulated or introduced, including autism spectrum disorder and disruptive mood dysregulation disorder. The multi-axial system was discontinued in DSM-5. He also reviewed coding issues.

In a sponsored symposium, Prakash S. Masand, MD, Global Medical Education, Inc., looked at the clinical challenges of addressing all 3 symptom domains that characterize depression (emotional, physical, and cognitive) as an introduction to reviewing the efficacy, mechanism of action, and side effects of vortioxetine (Brintellix), a new serotonergic agent for treating major depressive disorder (MDD). In all studies submitted to the FDA, vortioxetine was found to be superior to placebo, in at least 1 dosage group, for alleviating depressive symptoms and for reducing the risk of depressive recurrence.

 

AFTERNOON SESSION

Oppositional defiant disorder is more common in boys (onset at age 6 to 10) and is associated with inconsistent and neglectful parenting. Treatment modalities, including educational training, anticonvulsants, and lithium, do not have a strong evidence base. Intermittent explosive disorder is characterized by short-lived but frequent behavioral outbursts and often begins in adolescence. Dr. Grant also reviewed the evidence on conduct disorder, pyromania, and kleptomania.

Cognitive symptoms of schizophrenia often appear before psychotic symptoms and remain stable across the lifespan. There are no pharmacologic treatments for cognitive deficits in schizophrenia; however, Dr. Nasrallah listed tactics to improve cognitive function, including regular aerobic exercise. These cognitive deficits can be categorized as neurocognitive (memory, learning, executive function) and social (social skills, theory of mind, social cues) and contribute to functional decline and often prevent patients from working and going to school. Dr. Nasrallah described how bipolar disorder (BD) overlaps with schizophrenia in terms of cognitive dysfunction.

^{Henry Nasrallah, MD}

 

Psychiatric disorders exhibit specific sleep/ wake impairments. Sleep disorders can mimic psychiatric symptoms, such as fatigue, cognitive problems, and depression. Sleep disturbances, including insomnia, obstructive sleep apnea, and decreased need for sleep, often coexist with depression, generalized anxiety disorder, posttraumatic stress disorder, and BD, and insomnia is associated with a greater risk of suicide. With antidepressant treatment, sleep in depressed patients improves but does not normalize. Dr. Roth also reviewed pharmacotherapeutic options and non-drug modalities to improve patients’ sleep.

Antidepressants have no efficacy in treating acute episodes of bipolar depression, and using such agents might yield a poor long-term outcome in BD, according to Robert M. Post, MD, George Washington University School of Medicine, Michael J. Ostacher, MD, MPH, MMSc, Stanford University, and Vivek Singh, MD, University of Texas Health Science Center at San Antonio, in an interactive faculty discussion. For patients with bipolar I disorder, lithium monotherapy or the combination of lithium and valproate is more effective than valproate alone; evidence does not support valproate as a maintenance treatment. When a patient with BD shows partial response, attendees at this sponsored symposium were advised, consider adding psychotherapy and psycho-education. Combining a mood stabilizer and an antipsychotic might be more effective than monotherapy and safer, by allowing lower dosages. The only 3 treatments FDA-approved for bipolar depression are the olanzapine-fluoxetine combination, quetiapine, and lurasidone.

 

 

^{Boaz Levy, PhD, (left) receives the 2014 George Winokur Research Award from Carol S. North, MD, for his article on recovery of cognitive function in patients with co-occuring bipolar disorder and alcohol dependence.}

 

Friday, March 28, 2014

MORNING SESSION

Carmen Pinto, MD, at a sponsored symposium, reviewed the utility and safety of
long-acting injectable (LAI) antipsychotics for treating schizophrenia, with a focus on LAI aripiprazole, a partial HT-receptor agonist/partial HT-receptor antagonist. Four monthly injections (400 mg/injection) of the drug are needed to reach steady state; each injection reaches peak level in 5 to 7 days. LAI aripiprazole has been shown to delay time to relapse due to nonadherence and onset of nonresponse to the drug, and has high patient acceptance—even in those who already stable. Safety and side effects with LAI aripiprazole are the same as seen with the oral formulation.

In multimodal therapy for chronic pain, psychiatrists have a role in assessing
psychiatric comorbidities, coping ability, social functioning, and other life functions, including work and personal relationships. Cognitive-behavioral therapy can be particularly useful for chronic pain by helping patients reframe their pain experiences. Raphael J. Leo, MA, MD, FAPM, University at Buffalo, reviewed non-opioid co-analgesics that can be used for patients with comorbid pain and a substance use disorder. If opioids are necessary, consider “weak” or long-acting opioids. Monitor patients for aberrant, drug-seeking behavior.

In the second part of his overview, Dr. Black highlighted specific changes to DSM-5 of particular concern to clinicians. New chapters were created and disorders were consolidated, he explained, such as autism spectrum disorder, somatic symptom disorder, and major neurocognitive disorder. New diagnoses include hoarding disorder and binge eating disorder. Subtypes of schizophrenia were dropped. Pathologic gambling was renamed gambling disorder and gender dysphoria is now called gender identity disorder. The bereavement exclusion of a major depressive episode was dropped.

Antidepressants are effective in mitigating pain in neuropathy, headache, fibromyalgia, and chronic musculoskeletal pain, and have been advocated for other pain syndromes. Selection of an antidepressant depends on the type of pain condition, comorbid depression or anxiety, tolerability, and medical comorbidities. Dr. Leo presented prescribing strategies for tricyclics, serotoninnorepinephrine
reuptake inhibitors, SSRIs, and other antidepressants.

Treating of BD in geriatric patients becomes complicated because therapeutic choices are narrowed and response to therapy is less successful with age, according to George T. Grossberg, MD, St. Louis University. Rapid cycling tends to be the norm in geriatric BD patients. Look for agitation and irritability, rather than full-blown mania; grandiose delusions; psychiatric comorbidity, especially anxiety disorder; and sexually inappropriate behavior. Pharmacotherapeutic options include: mood stabilizers, atypical antipsychotics, and antidepressants (specifically, bupropion and SSRIs—not TCAs, venlafaxine, or duloxetine—and over the short term only). Consider divalproex for mania and hypomania, used cautiously because of its adverse side-effect potential.

 

^{George T. Grossberg, MD}

AFTERNOON SESSION

Often, BD is misdiagnosed as unipolar depression, or the correct diagnosis of BD is delayed, according to Gustavo Alva, MD, ATP Clinical Research. Comorbid substance use disorder or an anxiety disorder is common. Comorbid cardiovascular disease brings a greater risk of mortality in patients with BD than suicide. Approximately two-thirds of patients with BD are taking adjunctive medications; however, antidepressants are no more effective than placebo in treating bipolar depression. At this sponsored symposium, Vladimir Maletic, MD, University of South Carolina, described a 6-week trial in which lurasidone plus lithium or divalporex was more effective in reducing depression, as measured by MADRS, than placebo plus lithium or  akathisia, somnolence, and extrapyramidal symptoms.

When assessing an older patient with psychosis, first establish the cause of the symptoms, such as Alzheimer’s disease, affective disorder, substance use, or hallucinations associated with grief. Older patients with schizophrenia who have been taking typical antipsychotics for years might benefit from a switch to an atypical or a dosage reduction. Dr. Grossberg recommends considering antipsychotics for older patients when symptoms cause severe emotional distress that does not respond to other interventions or an acute episode that poses a safety risk for patients or others. Choose an antipsychotic based on side effects, and “start low and go slow,” when possible. The goal is to reduce agitation and distress—not necessarily to resolve psychotic symptoms.

Anita H. Clayton, MD, University of Virginia Health System, provided a review of sexual function from puberty through midlife and older years. Social factors play a role in sexual satisfaction, such as gender expectations, religious beliefs, and the influence of reporting in the media. Sexual dysfunction becomes worse in men after age 29; in women, the rate of sexual dysfunction appears to be consistent across the lifespan. Cardiovascular disease is a significant risk factor for sexual dysfunction in men, but not in women. Sexual function and depression have a bidirectional relationship; sexual dysfunction may be a symptom or cause of depression and antidepressants may affect desire and function. Medications, including psychotropics, oral contraceptives, and opioids, can cause sexual dysfunction.

 

Providers often are reluctant to bring up sexual issues with their patients, Dr. Clayton says, but patients often want to talk about their sexual problems. In reproductive-age women, look for hypoactive sexual desire disorder and pain. In men, assess for erectile dysfunction or premature ejaculation. Inquire about every phase of the sexual response cycle. When managing sexual dysfunction, aim to minimize contributing factors such as illness or medication, consider FDA-approved medications, encourage a healthy lifestyle, and employ psychological interventions when appropriate. In patients with antidepressant-associated sexual dysfunction, consider switching medications or adding an antidote, such as bupropion, buspirone, or sildenafil.

 

Saturday, March 29, 2014

MORNING SESSION

Because of the lack of double-blind, placebo-controlled trials, the risks of untreated depression vs the risks of antidepressant use in pregnancy are unclear. Marlene P. Freeman, MD, Massachusetts General Hospital, described the limited, long-term data on tricyclics and fluoxetine. Some studies have shown a small risk of birth defects with SSRIs; others did not find an association. For moderate or severe depression, use antidepressants at the lowest dosage and try non-medication options, such as psychotherapy and complementary and alternative medicine. During the third trimester, women may need a higher dosage to maintain therapeutic drug levels. Data indicates that folic acid use during pregnancy is associated with a decreased risk of autism and schizophrenia.

James W. Jefferson, MD, University of Wisconsin School of Medicine and Public Health, recommends ruling out medical conditions, such as cancer, that might be causing your patients’ fatigue or depression. Many medications, including over-the-counter agents and supplements, can cause fatigue. Bupropion was more effective than placebo and SSRIs in treating depressed patients with sleepiness and fatigue. Adding a psychostimulant to an SSRI does not have a significantly better effect than placebo on depressive symptoms. Adjunctive modafanil may improve depression and fatigue. Data for dopamine agonists are limited.

Lithium should be used with caution in pregnant women because of the risk of congenital malformations. Dr. Freeman also discussed the potential risks to the fetus with the mother’s use of valproate and lamotrigine (with the latter, a small increase in oral clefting). High-potency typical antipsychotics are considered safe; low-potency drugs have a higher risk of major malformations. For atypicals, the risk of malformations appears minimal; newborns might display extrapyramidal effects and withdrawal symptoms. Infants exposed to psychostimulants may have lower birth weight, but are not at increased risk of birth defects.

Dr. Jefferson reviewed the efficacy, pharmacokinetics, and adverse effects of vilazodone, levomilnacipran, and vortioxetine, which are antidepressants new to the market. Dr. Jefferson recommends reading package inserts to become familiar with new drugs. He also described studies of medications that were not FDA-approved, including edivoxetine, quetiapine XR monotherapy for MDD, and agomelatine. Agents under investigation include onabotulinumtoxin A injections, ketamine, and lanicemine.

Katherine E. Burdick, PhD, Mount Sinai School of Medicine, defined cognitive domains. First-episode MDD patients perform worse in psychomotor speed and attention than healthy controls. Late-onset depression (after age 60) is associated with worse performance on processing speed and verbal memory. Cognitive deficits in depressed patients range from mild to moderate and are influenced by symptom status and duration of illness. Treating cognitive deficits begins with prevention. Cholinesterase inhibitors are not effective for improving cognition in MDD. Antidepressants, including SSRIs, do not adequately treat cognitive deficits, Roger S. McIntyre, MD, FRCPC, University of Toronto, explained.

 

Current Psychiatry and the American Academy of Clinical Psychiatrists welcomed more than 550 psychiatric practitioners from across the United States and abroad to this annual conference, which was headed by Meeting Chair Richard Balon, MD, and Co-chairs Donald W. Black, MD, and Nagy Youssef, MD, March 27-29, 2014 at the Hilton Chicago in Chicago, Illinois. Attendees earned as many as 10 AMA PRA Category 1 Credits™.

 

Thursday, March 27, 2014

MORNING SESSION

Obsessive-compulsive disorder can be misdiagnosed as psychosis, anxiety, or a sexual disorder. In addition to contamination, patients can present with pathologic doubt, somatic obsessions, or obsessions about taboo or symmetry. Among FDA-approved medications, clomipramine might be more effective than selective serotonin reuptake inhibitors (SSRIs). Exposure response prevention therapy shows better response than pharmacotherapy, but best outcomes are seen with combination therapy. Jon E. Grant, JD, MD, MPH, University of Chicago, also discussed obsessive-compulsive personality disorder, body dysmorphic disorder, hoarding, trichotillomania, and excoriation disorder—as well as changes in DSM-5 that cover this group of disorders.

Patients with schizophrenia are at higher risk of death from cardiac and pulmonary disease than the general population. The quality of care of patients with psychosis generally is poor, because of lack of recognition, time, and resources, as well as systematic barriers to accessing health care. Questions about weight gain, lethargy, infections, and sexual functioning can help the practitioner assess a patient’s general health. When appropriate, Henry A. Nasrallah, MD, St. Louis University School of Medicine, recommends, consider switching antipsychotics, which might reverse adverse metabolic events.

Nonpharmacologic treatment goals include improving sleep, educating patients, providing them with tools for improving sleep, and creating an opportunity for patient-practitioner discussion. Stimulus control and sleep restriction are primary therapeutic techniques to improve sleep quality and reduce non-sleeping time in bed. Thomas Roth, PhD, Henry Ford Hospital, also discussed how to modify sleep hygiene techniques for pediatric, adolescent, and geriatric patients.

Donald W. Black, MD, University of Iowa, says that work groups for DSM-5 were asked to consider dimensionality and culture and gender issues. New diagnostic categories include obsessive-compulsive and related disorders and trauma and stressor-related disorders. Some diagnoses were reformulated or introduced, including autism spectrum disorder and disruptive mood dysregulation disorder. The multi-axial system was discontinued in DSM-5. He also reviewed coding issues.

In a sponsored symposium, Prakash S. Masand, MD, Global Medical Education, Inc., looked at the clinical challenges of addressing all 3 symptom domains that characterize depression (emotional, physical, and cognitive) as an introduction to reviewing the efficacy, mechanism of action, and side effects of vortioxetine (Brintellix), a new serotonergic agent for treating major depressive disorder (MDD). In all studies submitted to the FDA, vortioxetine was found to be superior to placebo, in at least 1 dosage group, for alleviating depressive symptoms and for reducing the risk of depressive recurrence.

 

AFTERNOON SESSION

Oppositional defiant disorder is more common in boys (onset at age 6 to 10) and is associated with inconsistent and neglectful parenting. Treatment modalities, including educational training, anticonvulsants, and lithium, do not have a strong evidence base. Intermittent explosive disorder is characterized by short-lived but frequent behavioral outbursts and often begins in adolescence. Dr. Grant also reviewed the evidence on conduct disorder, pyromania, and kleptomania.

Cognitive symptoms of schizophrenia often appear before psychotic symptoms and remain stable across the lifespan. There are no pharmacologic treatments for cognitive deficits in schizophrenia; however, Dr. Nasrallah listed tactics to improve cognitive function, including regular aerobic exercise. These cognitive deficits can be categorized as neurocognitive (memory, learning, executive function) and social (social skills, theory of mind, social cues) and contribute to functional decline and often prevent patients from working and going to school. Dr. Nasrallah described how bipolar disorder (BD) overlaps with schizophrenia in terms of cognitive dysfunction.

^{Henry Nasrallah, MD}

 

Psychiatric disorders exhibit specific sleep/ wake impairments. Sleep disorders can mimic psychiatric symptoms, such as fatigue, cognitive problems, and depression. Sleep disturbances, including insomnia, obstructive sleep apnea, and decreased need for sleep, often coexist with depression, generalized anxiety disorder, posttraumatic stress disorder, and BD, and insomnia is associated with a greater risk of suicide. With antidepressant treatment, sleep in depressed patients improves but does not normalize. Dr. Roth also reviewed pharmacotherapeutic options and non-drug modalities to improve patients’ sleep.

Antidepressants have no efficacy in treating acute episodes of bipolar depression, and using such agents might yield a poor long-term outcome in BD, according to Robert M. Post, MD, George Washington University School of Medicine, Michael J. Ostacher, MD, MPH, MMSc, Stanford University, and Vivek Singh, MD, University of Texas Health Science Center at San Antonio, in an interactive faculty discussion. For patients with bipolar I disorder, lithium monotherapy or the combination of lithium and valproate is more effective than valproate alone; evidence does not support valproate as a maintenance treatment. When a patient with BD shows partial response, attendees at this sponsored symposium were advised, consider adding psychotherapy and psycho-education. Combining a mood stabilizer and an antipsychotic might be more effective than monotherapy and safer, by allowing lower dosages. The only 3 treatments FDA-approved for bipolar depression are the olanzapine-fluoxetine combination, quetiapine, and lurasidone.

 

 

^{Boaz Levy, PhD, (left) receives the 2014 George Winokur Research Award from Carol S. North, MD, for his article on recovery of cognitive function in patients with co-occuring bipolar disorder and alcohol dependence.}

 

Friday, March 28, 2014

MORNING SESSION

Carmen Pinto, MD, at a sponsored symposium, reviewed the utility and safety of
long-acting injectable (LAI) antipsychotics for treating schizophrenia, with a focus on LAI aripiprazole, a partial HT-receptor agonist/partial HT-receptor antagonist. Four monthly injections (400 mg/injection) of the drug are needed to reach steady state; each injection reaches peak level in 5 to 7 days. LAI aripiprazole has been shown to delay time to relapse due to nonadherence and onset of nonresponse to the drug, and has high patient acceptance—even in those who already stable. Safety and side effects with LAI aripiprazole are the same as seen with the oral formulation.

In multimodal therapy for chronic pain, psychiatrists have a role in assessing
psychiatric comorbidities, coping ability, social functioning, and other life functions, including work and personal relationships. Cognitive-behavioral therapy can be particularly useful for chronic pain by helping patients reframe their pain experiences. Raphael J. Leo, MA, MD, FAPM, University at Buffalo, reviewed non-opioid co-analgesics that can be used for patients with comorbid pain and a substance use disorder. If opioids are necessary, consider “weak” or long-acting opioids. Monitor patients for aberrant, drug-seeking behavior.

In the second part of his overview, Dr. Black highlighted specific changes to DSM-5 of particular concern to clinicians. New chapters were created and disorders were consolidated, he explained, such as autism spectrum disorder, somatic symptom disorder, and major neurocognitive disorder. New diagnoses include hoarding disorder and binge eating disorder. Subtypes of schizophrenia were dropped. Pathologic gambling was renamed gambling disorder and gender dysphoria is now called gender identity disorder. The bereavement exclusion of a major depressive episode was dropped.

Antidepressants are effective in mitigating pain in neuropathy, headache, fibromyalgia, and chronic musculoskeletal pain, and have been advocated for other pain syndromes. Selection of an antidepressant depends on the type of pain condition, comorbid depression or anxiety, tolerability, and medical comorbidities. Dr. Leo presented prescribing strategies for tricyclics, serotoninnorepinephrine
reuptake inhibitors, SSRIs, and other antidepressants.

Treating of BD in geriatric patients becomes complicated because therapeutic choices are narrowed and response to therapy is less successful with age, according to George T. Grossberg, MD, St. Louis University. Rapid cycling tends to be the norm in geriatric BD patients. Look for agitation and irritability, rather than full-blown mania; grandiose delusions; psychiatric comorbidity, especially anxiety disorder; and sexually inappropriate behavior. Pharmacotherapeutic options include: mood stabilizers, atypical antipsychotics, and antidepressants (specifically, bupropion and SSRIs—not TCAs, venlafaxine, or duloxetine—and over the short term only). Consider divalproex for mania and hypomania, used cautiously because of its adverse side-effect potential.

 

^{George T. Grossberg, MD}

AFTERNOON SESSION

Often, BD is misdiagnosed as unipolar depression, or the correct diagnosis of BD is delayed, according to Gustavo Alva, MD, ATP Clinical Research. Comorbid substance use disorder or an anxiety disorder is common. Comorbid cardiovascular disease brings a greater risk of mortality in patients with BD than suicide. Approximately two-thirds of patients with BD are taking adjunctive medications; however, antidepressants are no more effective than placebo in treating bipolar depression. At this sponsored symposium, Vladimir Maletic, MD, University of South Carolina, described a 6-week trial in which lurasidone plus lithium or divalporex was more effective in reducing depression, as measured by MADRS, than placebo plus lithium or  akathisia, somnolence, and extrapyramidal symptoms.

When assessing an older patient with psychosis, first establish the cause of the symptoms, such as Alzheimer’s disease, affective disorder, substance use, or hallucinations associated with grief. Older patients with schizophrenia who have been taking typical antipsychotics for years might benefit from a switch to an atypical or a dosage reduction. Dr. Grossberg recommends considering antipsychotics for older patients when symptoms cause severe emotional distress that does not respond to other interventions or an acute episode that poses a safety risk for patients or others. Choose an antipsychotic based on side effects, and “start low and go slow,” when possible. The goal is to reduce agitation and distress—not necessarily to resolve psychotic symptoms.

Anita H. Clayton, MD, University of Virginia Health System, provided a review of sexual function from puberty through midlife and older years. Social factors play a role in sexual satisfaction, such as gender expectations, religious beliefs, and the influence of reporting in the media. Sexual dysfunction becomes worse in men after age 29; in women, the rate of sexual dysfunction appears to be consistent across the lifespan. Cardiovascular disease is a significant risk factor for sexual dysfunction in men, but not in women. Sexual function and depression have a bidirectional relationship; sexual dysfunction may be a symptom or cause of depression and antidepressants may affect desire and function. Medications, including psychotropics, oral contraceptives, and opioids, can cause sexual dysfunction.

 

Providers often are reluctant to bring up sexual issues with their patients, Dr. Clayton says, but patients often want to talk about their sexual problems. In reproductive-age women, look for hypoactive sexual desire disorder and pain. In men, assess for erectile dysfunction or premature ejaculation. Inquire about every phase of the sexual response cycle. When managing sexual dysfunction, aim to minimize contributing factors such as illness or medication, consider FDA-approved medications, encourage a healthy lifestyle, and employ psychological interventions when appropriate. In patients with antidepressant-associated sexual dysfunction, consider switching medications or adding an antidote, such as bupropion, buspirone, or sildenafil.

 

Saturday, March 29, 2014

MORNING SESSION

Because of the lack of double-blind, placebo-controlled trials, the risks of untreated depression vs the risks of antidepressant use in pregnancy are unclear. Marlene P. Freeman, MD, Massachusetts General Hospital, described the limited, long-term data on tricyclics and fluoxetine. Some studies have shown a small risk of birth defects with SSRIs; others did not find an association. For moderate or severe depression, use antidepressants at the lowest dosage and try non-medication options, such as psychotherapy and complementary and alternative medicine. During the third trimester, women may need a higher dosage to maintain therapeutic drug levels. Data indicates that folic acid use during pregnancy is associated with a decreased risk of autism and schizophrenia.

James W. Jefferson, MD, University of Wisconsin School of Medicine and Public Health, recommends ruling out medical conditions, such as cancer, that might be causing your patients’ fatigue or depression. Many medications, including over-the-counter agents and supplements, can cause fatigue. Bupropion was more effective than placebo and SSRIs in treating depressed patients with sleepiness and fatigue. Adding a psychostimulant to an SSRI does not have a significantly better effect than placebo on depressive symptoms. Adjunctive modafanil may improve depression and fatigue. Data for dopamine agonists are limited.

Lithium should be used with caution in pregnant women because of the risk of congenital malformations. Dr. Freeman also discussed the potential risks to the fetus with the mother’s use of valproate and lamotrigine (with the latter, a small increase in oral clefting). High-potency typical antipsychotics are considered safe; low-potency drugs have a higher risk of major malformations. For atypicals, the risk of malformations appears minimal; newborns might display extrapyramidal effects and withdrawal symptoms. Infants exposed to psychostimulants may have lower birth weight, but are not at increased risk of birth defects.

Dr. Jefferson reviewed the efficacy, pharmacokinetics, and adverse effects of vilazodone, levomilnacipran, and vortioxetine, which are antidepressants new to the market. Dr. Jefferson recommends reading package inserts to become familiar with new drugs. He also described studies of medications that were not FDA-approved, including edivoxetine, quetiapine XR monotherapy for MDD, and agomelatine. Agents under investigation include onabotulinumtoxin A injections, ketamine, and lanicemine.

Katherine E. Burdick, PhD, Mount Sinai School of Medicine, defined cognitive domains. First-episode MDD patients perform worse in psychomotor speed and attention than healthy controls. Late-onset depression (after age 60) is associated with worse performance on processing speed and verbal memory. Cognitive deficits in depressed patients range from mild to moderate and are influenced by symptom status and duration of illness. Treating cognitive deficits begins with prevention. Cholinesterase inhibitors are not effective for improving cognition in MDD. Antidepressants, including SSRIs, do not adequately treat cognitive deficits, Roger S. McIntyre, MD, FRCPC, University of Toronto, explained.

 

Current Psychiatry and the American Academy of Clinical Psychiatrists were pleased to host more than 550 psychiatric practitioners for this conference, led by Meeting Chair Richard Balon, MD, and Meeting Co-Chairs Donald W. Black, MD, and Nagy Youssef, MD, April 4-6, 2013 at the Swissôtel in Chicago, IL. Attendees could earn up to 18 AMA PRA Category 1 Credits^™.

THURSDAY, APRIL 4, 2013

MORNING SESSIONS

Evidence-based medicine and treatment guidelines may not address complex patients with treatment-resistant depression (TRD). Andrew A. Nierenberg, MD, Massachusetts General Hospital, reviewed newer medications for TRD, including olanzapine-fluoxetine combination, ketamine, riluzole, and L-methylfolate; however, use of these medications requires careful consideration of risks and benefits.

Many FDA-approved drugs have a “black-box” warning, but still are widely used. Henry A. Nasrallah, MD, University of Cincinnati, reviewed black-box warnings for antipsychotics, antidepressants, mood stabilizers, benzodiazepines, stimulants, opiates, and hypnotics and offered strategies on how to incorporate these warnings into clinical practice.

Dr. Nierenberg discussed the outcomes of 3 published medication effectiveness studies for bipolar disorder (BD)—STEP-BD, BALANCE, and LiTMUS—and one currently underway, CHOICE. These studies examined monotherapy and combination therapy with antidepressants, anticonvulsants, antipsychotics, and psychosocial interventions.

Although there is an association between psychosis and violence, most psychotic patients are not violent. Rajiv Tandon, MD, University of Florida, reviewed modifiable and nonmodifiable risk factors for violence, key clinical questions to consider, and scales to use when assessing a patient’s risk of violence.

AFTERNOON SESSIONS

Measuring biomarkers can augment other clinical methods to help identify metabolic, structural, and functional brain changes associated with preclinical stages of cognitive disorders. James Ellison, MD, MPH, McLean Hospital, Harvard Medical School, explained how biomarkers can improve the differential diagnosis of memory impairments and aid in identifying different types of dementia.

Donald W. Black, MD, (right) receives the 2013 George Winokur Research
Award from Carol S. North, MD, for his article on pathological gambling

Case-control studies have found a strong association between schizophrenia and type II diabetes, which contributes to higher mortality among schizophrenia patients. Along with vigilant metabolic monitoring, Dr. Tandon recommended a therapeutic approach that includes changing antipsychotics, prescribing metformin, suggesting lifestyle interventions, and treating comorbid conditions.

Depressed older adults may report anxiety, hopelessness, anhedonia, or somatic symptoms, rather than sadness. Depressive symptoms may be associated with vascular disease or cognitive impairment. Dr. Ellison reviewed psychotherapeutic and pharmacologic treatments for older depressed patients.

FRIDAY, APRIL 5, 2013

MORNING SESSIONS

Many strategies exist for treating patients with TRD; adding an atypical antipsychotic has the best evidence, but there are tolerability considerations. Dr. Nierenberg suggested using a combination of treatments.

Pregnancy is inherently risky for women who take antipsychotics. In all patients of childbearing potential, take a thorough reproductive history and ask about contraception use. Marlene P. Freeman, MD, Massachusetts General Hospital, explained that psychotropics with unfavorable FDA pregnancy ratings may be among first-line choices.

George T. Grossberg, MD, (left) speaks with attendees

Clinical symptoms, cognitive deficits, psychiatric comorbidities, genetic factors, neuroimaging features, and pharmacotherapy may overlap considerably between schizophrenia and BD. Dr. Nasrallah described clinical features that differentiate the 2 disorders.

Cognitive enhancers can improve activities of daily living, behavior, and cognition in patients with Alzheimer’s disease. George T. Grossberg, MD, St. Louis University, reviewed the evidence for acetylcholinesterase inhibitors, the NMDA receptor antagonist memantine, combination therapy, and atypical antipsychotics.

Dietary consultation for older patients might help delay or decrease their risk of dementia. Patients should consume omega-3 fatty acids, whole grains, fresh fruits and vegetables, beans, legumes, and certain spices. Dr. Grossberg also suggested patients engage in physical and mental exercises, social and spiritual activities, and stress reduction, and control cardiovascular risk factors.

AFTERNOON SESSIONS

Many women experience anxiety during pregnancy, and the risk is highest during the first trimester. Dr. Freeman reviewed prevalence, diagnosis, and treatment of panic disorder, generalized anxiety disorder, obsessive-compulsive disorder, and posttraumatic stress disorder during pregnancy and postpartum.

Kathleen Brady, MD, PhD, Medical University of South Carolina, explained how methylenedioxypyrovalerone, also known as bath salts, and other designer drugs are not detectable on standard urine drug screens. Agitation, tachycardia, combative behavior, hyperthermia, and hallucinations have been reported.

Kathleen Brady, MD, MPH

Alcohol abuse and depression are highly comorbid and are associated with higher suicidality, more severe symptoms, and poorer treatment response than either disorder alone. Depressive symptoms often are seen during alcohol withdrawal, and may resolve with abstinence. Dr. Brady reviewed the evidence for treating depressed alcoholics with antidepressants, medications targeting alcohol dependence such as disulfiram and naltrexone, and psychotherapy.

Ralph Aquila, MD, Columbia College of Physicians and Surgeons, discussed risk factors for and consequences of treatment nonadherence in patients with schizophrenia. Leslie L. Citrome, MD, MPH, New York Medical College, covered strategies to improve adherence, including identifying and addressing barriers to adherence for individual patients, improving the therapeutic alliance, and considering long-acting injectable antipsychotics.

 

SATURDAY, APRIL 6, 2013

MORNING SESSIONS

Forty-six percent of depressed patients will stop pharmacotherapy before they have a chance to respond. To minimize short-term side effects, Andrew J. Cutler, MD, Florida Clinical Research Center, suggested educating patients and slowly titrating medications; options for reducing long-term side effects or residual symptoms include switching or augmenting pharmacotherapy.

When treating patients addicted to opioids, outcome measures go beyond general health to obtaining employment and reducing criminal activity. Pharmacotherapy options include methadone maintenance therapy, oral and injectable naltrexone, and oral, sublingual, and implantable buprenorphine. Walter Ling, MD, David Geffen School of Medicine at UCLA, described factors that may improve patient outcomes.

Geriatric BD is relatively common in clinical settings, but there is a lack of evidence-based clinical practice guidelines. James W. Jefferson, MD, University of Wisconsin School of Medicine and Public Health, recommended choosing a treatment based on the illness phase and balancing the benefit of certain pharmacotherapies against short- and long-term risks.

Most medications for treating alcohol dependence work by modulating functions of opioids, glutamate, GABA, and serotonin. Dr. Ling reviewed the evidence base, dosing guidelines, and clinical recommendations for disulfiram, oral and injectable naltrexone, and acamprosate, which are FDA-approved for treating alcohol dependence. He also recommended combining medications with nonpharmacologic treatments, such as 12-step programs.

Most people who die by suicide deny suicide ideation at their last mental health visit. Risk factors for suicide include family history of suicide, childhood or adult trauma, substance abuse, stressful life events, chronic illness, and psychiatric disorders. Dr. Jefferson described suicide rating and tracking scales and encouraged clinicians to document suicide risk evaluations.

AFTERNOON SESSION

Roger S. McIntyre, MD, FRCPCRobert M.A. Hirschfeld, MD, University of Texas Medical Branch, discussed how the concept of allostatic load—bodily “wear and tear” that emerges with sustained allostatic states—may help explain cognitive and physical decline associated with BD. Roger S. McIntyre, MD, FRCPC, University of Toronto, emphasized that BD is a progressive disorder and comorbidities such as metabolic problems may promote this progression. Terence A. Ketter, MD, Stanford School of Medicine, covered new developments in BD treatment, including certain second-generation antipsychotics, dopaminergic neurotransmission enhancers, mood stabilizers, adjunctive antidepressants, and adjunctive psychotherapy.

Current Psychiatry and the American Academy of Clinical Psychiatrists were pleased to host more than 550 psychiatric practitioners for this conference, led by Meeting Chair Richard Balon, MD, and Meeting Co-Chairs Donald W. Black, MD, and Nagy Youssef, MD, April 4-6, 2013 at the Swissôtel in Chicago, IL. Attendees could earn up to 18 AMA PRA Category 1 Credits^™.

THURSDAY, APRIL 4, 2013

MORNING SESSIONS

Evidence-based medicine and treatment guidelines may not address complex patients with treatment-resistant depression (TRD). Andrew A. Nierenberg, MD, Massachusetts General Hospital, reviewed newer medications for TRD, including olanzapine-fluoxetine combination, ketamine, riluzole, and L-methylfolate; however, use of these medications requires careful consideration of risks and benefits.

Many FDA-approved drugs have a “black-box” warning, but still are widely used. Henry A. Nasrallah, MD, University of Cincinnati, reviewed black-box warnings for antipsychotics, antidepressants, mood stabilizers, benzodiazepines, stimulants, opiates, and hypnotics and offered strategies on how to incorporate these warnings into clinical practice.

Dr. Nierenberg discussed the outcomes of 3 published medication effectiveness studies for bipolar disorder (BD)—STEP-BD, BALANCE, and LiTMUS—and one currently underway, CHOICE. These studies examined monotherapy and combination therapy with antidepressants, anticonvulsants, antipsychotics, and psychosocial interventions.

Although there is an association between psychosis and violence, most psychotic patients are not violent. Rajiv Tandon, MD, University of Florida, reviewed modifiable and nonmodifiable risk factors for violence, key clinical questions to consider, and scales to use when assessing a patient’s risk of violence.

AFTERNOON SESSIONS

Measuring biomarkers can augment other clinical methods to help identify metabolic, structural, and functional brain changes associated with preclinical stages of cognitive disorders. James Ellison, MD, MPH, McLean Hospital, Harvard Medical School, explained how biomarkers can improve the differential diagnosis of memory impairments and aid in identifying different types of dementia.

Donald W. Black, MD, (right) receives the 2013 George Winokur Research
Award from Carol S. North, MD, for his article on pathological gambling

Case-control studies have found a strong association between schizophrenia and type II diabetes, which contributes to higher mortality among schizophrenia patients. Along with vigilant metabolic monitoring, Dr. Tandon recommended a therapeutic approach that includes changing antipsychotics, prescribing metformin, suggesting lifestyle interventions, and treating comorbid conditions.

Depressed older adults may report anxiety, hopelessness, anhedonia, or somatic symptoms, rather than sadness. Depressive symptoms may be associated with vascular disease or cognitive impairment. Dr. Ellison reviewed psychotherapeutic and pharmacologic treatments for older depressed patients.

FRIDAY, APRIL 5, 2013

MORNING SESSIONS

Many strategies exist for treating patients with TRD; adding an atypical antipsychotic has the best evidence, but there are tolerability considerations. Dr. Nierenberg suggested using a combination of treatments.

Pregnancy is inherently risky for women who take antipsychotics. In all patients of childbearing potential, take a thorough reproductive history and ask about contraception use. Marlene P. Freeman, MD, Massachusetts General Hospital, explained that psychotropics with unfavorable FDA pregnancy ratings may be among first-line choices.

George T. Grossberg, MD, (left) speaks with attendees

Clinical symptoms, cognitive deficits, psychiatric comorbidities, genetic factors, neuroimaging features, and pharmacotherapy may overlap considerably between schizophrenia and BD. Dr. Nasrallah described clinical features that differentiate the 2 disorders.

Cognitive enhancers can improve activities of daily living, behavior, and cognition in patients with Alzheimer’s disease. George T. Grossberg, MD, St. Louis University, reviewed the evidence for acetylcholinesterase inhibitors, the NMDA receptor antagonist memantine, combination therapy, and atypical antipsychotics.

Dietary consultation for older patients might help delay or decrease their risk of dementia. Patients should consume omega-3 fatty acids, whole grains, fresh fruits and vegetables, beans, legumes, and certain spices. Dr. Grossberg also suggested patients engage in physical and mental exercises, social and spiritual activities, and stress reduction, and control cardiovascular risk factors.

AFTERNOON SESSIONS

Many women experience anxiety during pregnancy, and the risk is highest during the first trimester. Dr. Freeman reviewed prevalence, diagnosis, and treatment of panic disorder, generalized anxiety disorder, obsessive-compulsive disorder, and posttraumatic stress disorder during pregnancy and postpartum.

Kathleen Brady, MD, PhD, Medical University of South Carolina, explained how methylenedioxypyrovalerone, also known as bath salts, and other designer drugs are not detectable on standard urine drug screens. Agitation, tachycardia, combative behavior, hyperthermia, and hallucinations have been reported.

Kathleen Brady, MD, MPH

Alcohol abuse and depression are highly comorbid and are associated with higher suicidality, more severe symptoms, and poorer treatment response than either disorder alone. Depressive symptoms often are seen during alcohol withdrawal, and may resolve with abstinence. Dr. Brady reviewed the evidence for treating depressed alcoholics with antidepressants, medications targeting alcohol dependence such as disulfiram and naltrexone, and psychotherapy.

Ralph Aquila, MD, Columbia College of Physicians and Surgeons, discussed risk factors for and consequences of treatment nonadherence in patients with schizophrenia. Leslie L. Citrome, MD, MPH, New York Medical College, covered strategies to improve adherence, including identifying and addressing barriers to adherence for individual patients, improving the therapeutic alliance, and considering long-acting injectable antipsychotics.

 

SATURDAY, APRIL 6, 2013

MORNING SESSIONS

Forty-six percent of depressed patients will stop pharmacotherapy before they have a chance to respond. To minimize short-term side effects, Andrew J. Cutler, MD, Florida Clinical Research Center, suggested educating patients and slowly titrating medications; options for reducing long-term side effects or residual symptoms include switching or augmenting pharmacotherapy.

When treating patients addicted to opioids, outcome measures go beyond general health to obtaining employment and reducing criminal activity. Pharmacotherapy options include methadone maintenance therapy, oral and injectable naltrexone, and oral, sublingual, and implantable buprenorphine. Walter Ling, MD, David Geffen School of Medicine at UCLA, described factors that may improve patient outcomes.

Geriatric BD is relatively common in clinical settings, but there is a lack of evidence-based clinical practice guidelines. James W. Jefferson, MD, University of Wisconsin School of Medicine and Public Health, recommended choosing a treatment based on the illness phase and balancing the benefit of certain pharmacotherapies against short- and long-term risks.

Most medications for treating alcohol dependence work by modulating functions of opioids, glutamate, GABA, and serotonin. Dr. Ling reviewed the evidence base, dosing guidelines, and clinical recommendations for disulfiram, oral and injectable naltrexone, and acamprosate, which are FDA-approved for treating alcohol dependence. He also recommended combining medications with nonpharmacologic treatments, such as 12-step programs.

Most people who die by suicide deny suicide ideation at their last mental health visit. Risk factors for suicide include family history of suicide, childhood or adult trauma, substance abuse, stressful life events, chronic illness, and psychiatric disorders. Dr. Jefferson described suicide rating and tracking scales and encouraged clinicians to document suicide risk evaluations.

AFTERNOON SESSION

Roger S. McIntyre, MD, FRCPCRobert M.A. Hirschfeld, MD, University of Texas Medical Branch, discussed how the concept of allostatic load—bodily “wear and tear” that emerges with sustained allostatic states—may help explain cognitive and physical decline associated with BD. Roger S. McIntyre, MD, FRCPC, University of Toronto, emphasized that BD is a progressive disorder and comorbidities such as metabolic problems may promote this progression. Terence A. Ketter, MD, Stanford School of Medicine, covered new developments in BD treatment, including certain second-generation antipsychotics, dopaminergic neurotransmission enhancers, mood stabilizers, adjunctive antidepressants, and adjunctive psychotherapy.

Current Psychiatry and the American Academy of Clinical Psychiatrists were pleased to host more than 550 psychiatric practitioners for this conference, led by Meeting Chair Richard Balon, MD, and Meeting Co-Chairs Donald W. Black, MD, and Nagy Youssef, MD, April 4-6, 2013 at the Swissôtel in Chicago, IL. Attendees could earn up to 18 AMA PRA Category 1 Credits^™.

THURSDAY, APRIL 4, 2013

MORNING SESSIONS

Evidence-based medicine and treatment guidelines may not address complex patients with treatment-resistant depression (TRD). Andrew A. Nierenberg, MD, Massachusetts General Hospital, reviewed newer medications for TRD, including olanzapine-fluoxetine combination, ketamine, riluzole, and L-methylfolate; however, use of these medications requires careful consideration of risks and benefits.

Many FDA-approved drugs have a “black-box” warning, but still are widely used. Henry A. Nasrallah, MD, University of Cincinnati, reviewed black-box warnings for antipsychotics, antidepressants, mood stabilizers, benzodiazepines, stimulants, opiates, and hypnotics and offered strategies on how to incorporate these warnings into clinical practice.

Dr. Nierenberg discussed the outcomes of 3 published medication effectiveness studies for bipolar disorder (BD)—STEP-BD, BALANCE, and LiTMUS—and one currently underway, CHOICE. These studies examined monotherapy and combination therapy with antidepressants, anticonvulsants, antipsychotics, and psychosocial interventions.

Although there is an association between psychosis and violence, most psychotic patients are not violent. Rajiv Tandon, MD, University of Florida, reviewed modifiable and nonmodifiable risk factors for violence, key clinical questions to consider, and scales to use when assessing a patient’s risk of violence.

AFTERNOON SESSIONS

Measuring biomarkers can augment other clinical methods to help identify metabolic, structural, and functional brain changes associated with preclinical stages of cognitive disorders. James Ellison, MD, MPH, McLean Hospital, Harvard Medical School, explained how biomarkers can improve the differential diagnosis of memory impairments and aid in identifying different types of dementia.

Donald W. Black, MD, (right) receives the 2013 George Winokur Research
Award from Carol S. North, MD, for his article on pathological gambling

Case-control studies have found a strong association between schizophrenia and type II diabetes, which contributes to higher mortality among schizophrenia patients. Along with vigilant metabolic monitoring, Dr. Tandon recommended a therapeutic approach that includes changing antipsychotics, prescribing metformin, suggesting lifestyle interventions, and treating comorbid conditions.

Depressed older adults may report anxiety, hopelessness, anhedonia, or somatic symptoms, rather than sadness. Depressive symptoms may be associated with vascular disease or cognitive impairment. Dr. Ellison reviewed psychotherapeutic and pharmacologic treatments for older depressed patients.

FRIDAY, APRIL 5, 2013

MORNING SESSIONS

Many strategies exist for treating patients with TRD; adding an atypical antipsychotic has the best evidence, but there are tolerability considerations. Dr. Nierenberg suggested using a combination of treatments.

Pregnancy is inherently risky for women who take antipsychotics. In all patients of childbearing potential, take a thorough reproductive history and ask about contraception use. Marlene P. Freeman, MD, Massachusetts General Hospital, explained that psychotropics with unfavorable FDA pregnancy ratings may be among first-line choices.

George T. Grossberg, MD, (left) speaks with attendees

Clinical symptoms, cognitive deficits, psychiatric comorbidities, genetic factors, neuroimaging features, and pharmacotherapy may overlap considerably between schizophrenia and BD. Dr. Nasrallah described clinical features that differentiate the 2 disorders.

Cognitive enhancers can improve activities of daily living, behavior, and cognition in patients with Alzheimer’s disease. George T. Grossberg, MD, St. Louis University, reviewed the evidence for acetylcholinesterase inhibitors, the NMDA receptor antagonist memantine, combination therapy, and atypical antipsychotics.

Dietary consultation for older patients might help delay or decrease their risk of dementia. Patients should consume omega-3 fatty acids, whole grains, fresh fruits and vegetables, beans, legumes, and certain spices. Dr. Grossberg also suggested patients engage in physical and mental exercises, social and spiritual activities, and stress reduction, and control cardiovascular risk factors.

AFTERNOON SESSIONS

Many women experience anxiety during pregnancy, and the risk is highest during the first trimester. Dr. Freeman reviewed prevalence, diagnosis, and treatment of panic disorder, generalized anxiety disorder, obsessive-compulsive disorder, and posttraumatic stress disorder during pregnancy and postpartum.

Kathleen Brady, MD, PhD, Medical University of South Carolina, explained how methylenedioxypyrovalerone, also known as bath salts, and other designer drugs are not detectable on standard urine drug screens. Agitation, tachycardia, combative behavior, hyperthermia, and hallucinations have been reported.

Kathleen Brady, MD, MPH

Alcohol abuse and depression are highly comorbid and are associated with higher suicidality, more severe symptoms, and poorer treatment response than either disorder alone. Depressive symptoms often are seen during alcohol withdrawal, and may resolve with abstinence. Dr. Brady reviewed the evidence for treating depressed alcoholics with antidepressants, medications targeting alcohol dependence such as disulfiram and naltrexone, and psychotherapy.

Ralph Aquila, MD, Columbia College of Physicians and Surgeons, discussed risk factors for and consequences of treatment nonadherence in patients with schizophrenia. Leslie L. Citrome, MD, MPH, New York Medical College, covered strategies to improve adherence, including identifying and addressing barriers to adherence for individual patients, improving the therapeutic alliance, and considering long-acting injectable antipsychotics.

 

SATURDAY, APRIL 6, 2013

MORNING SESSIONS

Forty-six percent of depressed patients will stop pharmacotherapy before they have a chance to respond. To minimize short-term side effects, Andrew J. Cutler, MD, Florida Clinical Research Center, suggested educating patients and slowly titrating medications; options for reducing long-term side effects or residual symptoms include switching or augmenting pharmacotherapy.

When treating patients addicted to opioids, outcome measures go beyond general health to obtaining employment and reducing criminal activity. Pharmacotherapy options include methadone maintenance therapy, oral and injectable naltrexone, and oral, sublingual, and implantable buprenorphine. Walter Ling, MD, David Geffen School of Medicine at UCLA, described factors that may improve patient outcomes.

Geriatric BD is relatively common in clinical settings, but there is a lack of evidence-based clinical practice guidelines. James W. Jefferson, MD, University of Wisconsin School of Medicine and Public Health, recommended choosing a treatment based on the illness phase and balancing the benefit of certain pharmacotherapies against short- and long-term risks.

Most medications for treating alcohol dependence work by modulating functions of opioids, glutamate, GABA, and serotonin. Dr. Ling reviewed the evidence base, dosing guidelines, and clinical recommendations for disulfiram, oral and injectable naltrexone, and acamprosate, which are FDA-approved for treating alcohol dependence. He also recommended combining medications with nonpharmacologic treatments, such as 12-step programs.

Most people who die by suicide deny suicide ideation at their last mental health visit. Risk factors for suicide include family history of suicide, childhood or adult trauma, substance abuse, stressful life events, chronic illness, and psychiatric disorders. Dr. Jefferson described suicide rating and tracking scales and encouraged clinicians to document suicide risk evaluations.

AFTERNOON SESSION

Roger S. McIntyre, MD, FRCPCRobert M.A. Hirschfeld, MD, University of Texas Medical Branch, discussed how the concept of allostatic load—bodily “wear and tear” that emerges with sustained allostatic states—may help explain cognitive and physical decline associated with BD. Roger S. McIntyre, MD, FRCPC, University of Toronto, emphasized that BD is a progressive disorder and comorbidities such as metabolic problems may promote this progression. Terence A. Ketter, MD, Stanford School of Medicine, covered new developments in BD treatment, including certain second-generation antipsychotics, dopaminergic neurotransmission enhancers, mood stabilizers, adjunctive antidepressants, and adjunctive psychotherapy.

A survey from the National Institute of Child Health and Human Development estimated that 20% of 6th through 10th graders admitted to bullying their classmates.¹ In addition to an increased risk for personal injury, bullied children are more likely to report low self-esteem and emotional problems² and often experience loneliness.¹ In contrast, children who bully suffer in their school performance¹ and are more likely to engage in drug use³ and violence⁴ later in life. Child psychiatrists often see both bullies and their victims.

Evidence-based recommendations are available to help educators improve the school climate⁵ and identify children who are at an increased risk for bullying,⁶ but research supporting specific clinical strategies for managing a child who bullies is limited. Establishing rapport and engaging a bully often is challenging; these difficulties further complicate assessment and successful management of such children.

We present the mnemonic MEAN to help clinicians assess and understand children who bully.

Model. Discuss, demonstrate, and practice models of alternative social skills and behaviors, including active listening, being open to others’ views, accepting failure, controlling impulses, developing problem-solving techniques, and treating others with respect.

Empathize. Encourage children who bully to explore their feelings about themselves—which may uncover poor self-esteem, anger, or guilt—and acknowledge the hurt they cause others by bullying. Focusing on the pain they inflict on others in the context of personal experiences of pain that likely is driving their aggression may enable bullies to empathize with their victims.

Assess. Help the bully assess the costs and benefits of his or her behavior. Point out what the bully stands to gain from ending his or her aggressive behavior, which likely already has resulted in lost recesses, after school detentions, missed sports practices, and the loss of privileges at home. Most importantly, assess and treat any underlying psychopathology, including mood and anxiety disorders.

Nurture. Aid the bully in identifying his or her prosocial strengths to build self-esteem and thereby reduce the need to commit aggressive acts as a means of gaining a sense of control or personal security. Disarm the child with your genuine concern for his or her well-being.

Using these psychotherapeutic techniques may enhance establishing rapport with a child who bullies and may improve outcomes.

Disclosures

Dr. Kepple reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Dr. Madaan receives grant or research support from Eli Lilly and Company, Forest Pharmaceuticals, Merck, Otsuka, Pfizer Inc., and Shire.

A survey from the National Institute of Child Health and Human Development estimated that 20% of 6th through 10th graders admitted to bullying their classmates.¹ In addition to an increased risk for personal injury, bullied children are more likely to report low self-esteem and emotional problems² and often experience loneliness.¹ In contrast, children who bully suffer in their school performance¹ and are more likely to engage in drug use³ and violence⁴ later in life. Child psychiatrists often see both bullies and their victims.

Evidence-based recommendations are available to help educators improve the school climate⁵ and identify children who are at an increased risk for bullying,⁶ but research supporting specific clinical strategies for managing a child who bullies is limited. Establishing rapport and engaging a bully often is challenging; these difficulties further complicate assessment and successful management of such children.

We present the mnemonic MEAN to help clinicians assess and understand children who bully.

Model. Discuss, demonstrate, and practice models of alternative social skills and behaviors, including active listening, being open to others’ views, accepting failure, controlling impulses, developing problem-solving techniques, and treating others with respect.

Empathize. Encourage children who bully to explore their feelings about themselves—which may uncover poor self-esteem, anger, or guilt—and acknowledge the hurt they cause others by bullying. Focusing on the pain they inflict on others in the context of personal experiences of pain that likely is driving their aggression may enable bullies to empathize with their victims.

Assess. Help the bully assess the costs and benefits of his or her behavior. Point out what the bully stands to gain from ending his or her aggressive behavior, which likely already has resulted in lost recesses, after school detentions, missed sports practices, and the loss of privileges at home. Most importantly, assess and treat any underlying psychopathology, including mood and anxiety disorders.

Nurture. Aid the bully in identifying his or her prosocial strengths to build self-esteem and thereby reduce the need to commit aggressive acts as a means of gaining a sense of control or personal security. Disarm the child with your genuine concern for his or her well-being.

Using these psychotherapeutic techniques may enhance establishing rapport with a child who bullies and may improve outcomes.

Disclosures

Dr. Kepple reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Dr. Madaan receives grant or research support from Eli Lilly and Company, Forest Pharmaceuticals, Merck, Otsuka, Pfizer Inc., and Shire.

A survey from the National Institute of Child Health and Human Development estimated that 20% of 6th through 10th graders admitted to bullying their classmates.¹ In addition to an increased risk for personal injury, bullied children are more likely to report low self-esteem and emotional problems² and often experience loneliness.¹ In contrast, children who bully suffer in their school performance¹ and are more likely to engage in drug use³ and violence⁴ later in life. Child psychiatrists often see both bullies and their victims.

Evidence-based recommendations are available to help educators improve the school climate⁵ and identify children who are at an increased risk for bullying,⁶ but research supporting specific clinical strategies for managing a child who bullies is limited. Establishing rapport and engaging a bully often is challenging; these difficulties further complicate assessment and successful management of such children.

We present the mnemonic MEAN to help clinicians assess and understand children who bully.

Model. Discuss, demonstrate, and practice models of alternative social skills and behaviors, including active listening, being open to others’ views, accepting failure, controlling impulses, developing problem-solving techniques, and treating others with respect.

Empathize. Encourage children who bully to explore their feelings about themselves—which may uncover poor self-esteem, anger, or guilt—and acknowledge the hurt they cause others by bullying. Focusing on the pain they inflict on others in the context of personal experiences of pain that likely is driving their aggression may enable bullies to empathize with their victims.

Assess. Help the bully assess the costs and benefits of his or her behavior. Point out what the bully stands to gain from ending his or her aggressive behavior, which likely already has resulted in lost recesses, after school detentions, missed sports practices, and the loss of privileges at home. Most importantly, assess and treat any underlying psychopathology, including mood and anxiety disorders.

Nurture. Aid the bully in identifying his or her prosocial strengths to build self-esteem and thereby reduce the need to commit aggressive acts as a means of gaining a sense of control or personal security. Disarm the child with your genuine concern for his or her well-being.

Using these psychotherapeutic techniques may enhance establishing rapport with a child who bullies and may improve outcomes.

Disclosures

Dr. Kepple reports no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Dr. Madaan receives grant or research support from Eli Lilly and Company, Forest Pharmaceuticals, Merck, Otsuka, Pfizer Inc., and Shire.

In the aftermath of a school shooting, parents and teachers may seek a psychiatrist’s advice on how to best discuss these incidents with children. We offer guidelines on what to tell concerned parents, educators, and other adults who may interact with children affected by a school shooting.

6 tips for interacting with children

1. Talk about the event. Instruct adults to ask children to share their feelings about the incident and to show genuine interest in listening to the child’s thoughts and point of view. Adults shouldn’t pretend the event hasn’t occurred or isn’t serious. Children may be more worried if they think adults are too afraid to tell them what is happening. It is important to gently correct any misinformation older students may have received via social media.¹

2. Reinforce that home is a safe haven. Overwhelming emotions and uncertainty can bring about a sense of insecurity in children. Children may come home seeking a safe environment. Advise parents to plan a night where family members participate in a favorite family activity.¹ Tell parents to remind their children that trust-worthy adults—parents, emergency workers, police, firefighters, doctors, and the military—are helping provide safety, comfort, and support.²

3. Limit television time. If children are exposed to the news, parents should watch it with them briefly, but avoid letting children rewatch the same event repetitively. Constant exposure to the event may heighten a child’s anxiety and fears.

4. Maintain a normal routine. Tell parents they should maintain, as best they can, their normal routine for dinner, homework, chores, and bedtime, but to remain flexible.² Children may have a hard time concentrating on schoolwork or falling asleep. Advise parents to spend extra time reading or playing quiet games with their children, particularly at bedtime. These activities are calming, foster a sense of closeness and security, and reinforce a feeling of normalcy.

5. Encourage emotions. Instruct parents to explain to their children that all feelings are okay and normal, and to let children talk about their feelings and help put them into perspective.¹ Children may need help in expressing these feelings, so be patient. If an incident happened at the child’s school, teachers and administrators may conduct group sessions to help children express their concerns about being back in school.

6. Seek creativity or spirituality. Encourage parents and other adults to provide a creative outlet for children, such as making get well cards or sending letters to the survivors and their families. Writing thank you letters to doctors, nurses, fire-fighters, and police officers also may be comforting.^1,2 Suggest that parents encourage their children to pray or think hopeful thoughts for the victims and their families.

2 tips for interacting with adults

7. Recommend they take care of themselves. Explain to adult caregivers that because children learn by observing, they shouldn’t ignore their own feelings of anxiety, grief, and anger. By expressing their emotions in a productive manner, adults will be better able to support their children. Encourage adults to talk to friends, family, religious leaders, or mental health counselors.

8. Advise adults to be alert for children who may need professional help. Tell them to be vigilant when monitoring a child’s emotional state. Children who may benefit from mental health counseling after a tragedy may exhibit warning signs, such as changes in behavior, appetite, and sleep patterns, which may indicate the child is experiencing grief, anxiety, or discomfort.

Remind adults to be aware of children who are at greater risk for mental health issues, including those who are already struggling with other recent traumatic experiences—past traumatic experiences, personal loss, depression, or other mental illness.¹ Be particularly observant for children who may be at risk of suicide.^1,2 Professional counseling may be needed for a child who is experiencing an emotional reaction that lasts >1 month and is impacting his or her daily functioning.¹

Disclosure

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

In the aftermath of a school shooting, parents and teachers may seek a psychiatrist’s advice on how to best discuss these incidents with children. We offer guidelines on what to tell concerned parents, educators, and other adults who may interact with children affected by a school shooting.

6 tips for interacting with children

1. Talk about the event. Instruct adults to ask children to share their feelings about the incident and to show genuine interest in listening to the child’s thoughts and point of view. Adults shouldn’t pretend the event hasn’t occurred or isn’t serious. Children may be more worried if they think adults are too afraid to tell them what is happening. It is important to gently correct any misinformation older students may have received via social media.¹

2. Reinforce that home is a safe haven. Overwhelming emotions and uncertainty can bring about a sense of insecurity in children. Children may come home seeking a safe environment. Advise parents to plan a night where family members participate in a favorite family activity.¹ Tell parents to remind their children that trust-worthy adults—parents, emergency workers, police, firefighters, doctors, and the military—are helping provide safety, comfort, and support.²

3. Limit television time. If children are exposed to the news, parents should watch it with them briefly, but avoid letting children rewatch the same event repetitively. Constant exposure to the event may heighten a child’s anxiety and fears.

4. Maintain a normal routine. Tell parents they should maintain, as best they can, their normal routine for dinner, homework, chores, and bedtime, but to remain flexible.² Children may have a hard time concentrating on schoolwork or falling asleep. Advise parents to spend extra time reading or playing quiet games with their children, particularly at bedtime. These activities are calming, foster a sense of closeness and security, and reinforce a feeling of normalcy.

5. Encourage emotions. Instruct parents to explain to their children that all feelings are okay and normal, and to let children talk about their feelings and help put them into perspective.¹ Children may need help in expressing these feelings, so be patient. If an incident happened at the child’s school, teachers and administrators may conduct group sessions to help children express their concerns about being back in school.

6. Seek creativity or spirituality. Encourage parents and other adults to provide a creative outlet for children, such as making get well cards or sending letters to the survivors and their families. Writing thank you letters to doctors, nurses, fire-fighters, and police officers also may be comforting.^1,2 Suggest that parents encourage their children to pray or think hopeful thoughts for the victims and their families.

2 tips for interacting with adults

7. Recommend they take care of themselves. Explain to adult caregivers that because children learn by observing, they shouldn’t ignore their own feelings of anxiety, grief, and anger. By expressing their emotions in a productive manner, adults will be better able to support their children. Encourage adults to talk to friends, family, religious leaders, or mental health counselors.

8. Advise adults to be alert for children who may need professional help. Tell them to be vigilant when monitoring a child’s emotional state. Children who may benefit from mental health counseling after a tragedy may exhibit warning signs, such as changes in behavior, appetite, and sleep patterns, which may indicate the child is experiencing grief, anxiety, or discomfort.

Remind adults to be aware of children who are at greater risk for mental health issues, including those who are already struggling with other recent traumatic experiences—past traumatic experiences, personal loss, depression, or other mental illness.¹ Be particularly observant for children who may be at risk of suicide.^1,2 Professional counseling may be needed for a child who is experiencing an emotional reaction that lasts >1 month and is impacting his or her daily functioning.¹

Disclosure

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

In the aftermath of a school shooting, parents and teachers may seek a psychiatrist’s advice on how to best discuss these incidents with children. We offer guidelines on what to tell concerned parents, educators, and other adults who may interact with children affected by a school shooting.

6 tips for interacting with children

1. Talk about the event. Instruct adults to ask children to share their feelings about the incident and to show genuine interest in listening to the child’s thoughts and point of view. Adults shouldn’t pretend the event hasn’t occurred or isn’t serious. Children may be more worried if they think adults are too afraid to tell them what is happening. It is important to gently correct any misinformation older students may have received via social media.¹

2. Reinforce that home is a safe haven. Overwhelming emotions and uncertainty can bring about a sense of insecurity in children. Children may come home seeking a safe environment. Advise parents to plan a night where family members participate in a favorite family activity.¹ Tell parents to remind their children that trust-worthy adults—parents, emergency workers, police, firefighters, doctors, and the military—are helping provide safety, comfort, and support.²

3. Limit television time. If children are exposed to the news, parents should watch it with them briefly, but avoid letting children rewatch the same event repetitively. Constant exposure to the event may heighten a child’s anxiety and fears.

4. Maintain a normal routine. Tell parents they should maintain, as best they can, their normal routine for dinner, homework, chores, and bedtime, but to remain flexible.² Children may have a hard time concentrating on schoolwork or falling asleep. Advise parents to spend extra time reading or playing quiet games with their children, particularly at bedtime. These activities are calming, foster a sense of closeness and security, and reinforce a feeling of normalcy.

5. Encourage emotions. Instruct parents to explain to their children that all feelings are okay and normal, and to let children talk about their feelings and help put them into perspective.¹ Children may need help in expressing these feelings, so be patient. If an incident happened at the child’s school, teachers and administrators may conduct group sessions to help children express their concerns about being back in school.

6. Seek creativity or spirituality. Encourage parents and other adults to provide a creative outlet for children, such as making get well cards or sending letters to the survivors and their families. Writing thank you letters to doctors, nurses, fire-fighters, and police officers also may be comforting.^1,2 Suggest that parents encourage their children to pray or think hopeful thoughts for the victims and their families.

2 tips for interacting with adults

7. Recommend they take care of themselves. Explain to adult caregivers that because children learn by observing, they shouldn’t ignore their own feelings of anxiety, grief, and anger. By expressing their emotions in a productive manner, adults will be better able to support their children. Encourage adults to talk to friends, family, religious leaders, or mental health counselors.

8. Advise adults to be alert for children who may need professional help. Tell them to be vigilant when monitoring a child’s emotional state. Children who may benefit from mental health counseling after a tragedy may exhibit warning signs, such as changes in behavior, appetite, and sleep patterns, which may indicate the child is experiencing grief, anxiety, or discomfort.

Remind adults to be aware of children who are at greater risk for mental health issues, including those who are already struggling with other recent traumatic experiences—past traumatic experiences, personal loss, depression, or other mental illness.¹ Be particularly observant for children who may be at risk of suicide.^1,2 Professional counseling may be needed for a child who is experiencing an emotional reaction that lasts >1 month and is impacting his or her daily functioning.¹

Disclosure

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Re-experiencing a previous life-threatening stress through nightmares or recurrent memories is a hallmark of posttraumatic stress disorder (PTSD). In the United States, the lifetime risk of PTSD is 10.1% and the 12-month prevalence is 3.7%.¹ The selective serotonin reuptake inhibitors (SSRIs) sertraline and paroxetine are FDA-approved for treating PTSD; clinicians commonly use any SSRI for this disorder. Although SSRIs can alleviate many PTSD symptoms, at times patients experience only a partial response, which necessitates other interventions.

Rationale for using topiramate

The anticonvulsant topiramate blocks voltage-sensitive sodium channels, augments γ-aminobutyric acid type A, antagonizes the glutamate receptor, and inhibits carbonic anhydrase. Researchers have hypothesized that limbic nuclei become sensitized and “kindled” after exposure to a traumatic event. Anticonvulsants such as topiramate may help mitigate stress-activated kindling in PTSD.^2,3

What does the evidence say?

Although less compelling than double-blind, placebo-controlled trials, small open-label studies and some case reports indicate a potential role for topiramate in PTSD for specific populations.^4,5 In an 8-week open- label study, Alderman et al⁶ found adjunctive topiramate led to a statistically significant reduction in Clinician-Administered PTSD Scale (CAPS) scores and nightmares in 43 male veterans with combat-related PTSD. There was a nonsignificant decrease in high-risk alcohol use.

In a 2002 retrospective case series, Berlant et al⁷ found topiramate as monotherapy or adjunctive therapy reduced nightmares in 35 patients with chronic, non-combat PTSD. Nightmares decreased in 79% of patients and flashbacks decreased in 86%, with symptom improvement in a median of 4 days. Limitations of this study included lack of placebo control, a low number of participants, and a high dropout rate (9/35).

Two years later, Berlant⁸ used the PTSD Checklist-Civilian version (PCL-C) to assess response to topiramate in an open-label study of 33 patients with chronic, non-hallucinatory PTSD. Twenty-eight patients used topiramate as add-on therapy. PCL-C scores decreased by ≥30% in 77% of patients in 4 weeks, with a median dose of 50 mg/d and a median response time of 9 days.

In a double-blind, placebo-controlled trial, Tucker et al⁹ assessed 38 civilian patients who took topiramate monotherapy for PTSD. Using the CAPS, researchers concluded that topiramate reduced re-experiencing symptoms, but the effect was not statistically significant.⁹

Lindley et al¹⁰ conducted a randomized, double-blind, placebo-controlled trial to study the effect of add-on topiramate in 40 patients with chronic, combat-related PTSD. Because many patients in this study had a history of depression and substance use disorders, topiramate was added to antidepressants; no anticonvulsants, antipsychotics, or benzodiazepines were used. Similar to previous studies, researchers found no statistically significant effect on PTSD symptom severity or global symptom improvement. However, the small number of participants and a high dropout rate limited this study.¹⁰

In a 12-week, double-blind, placebo-controlled study of 35 men and women age 18 to 62 with PTSD, Yeh et al¹¹ found that topiramate (mean dose: 102.94 mg/d) lead to a statistically significant overall CAPS score reduction, with significant improvements in re-experiencing symptoms, such as nightmares.

Our opinion

FDA-approved treatments such as SSRIs should be the first pharmacologic intervention for PTSD. If a patient’s response is partial or inadequate, consider additional treatment options. For patients with persistent re-experiencing symptoms, evidence and experience with prazosin and trazodone are more robust than that for topiramate.¹²

Using topiramate to reduce re-experiencing symptoms such as nightmares in PTSD is not supported by statistically significant evidence from double-blind, placebo- controlled trials. However, numerous open-label studies and case reports suggest that there may be a role for topiramate in PTSD patients who do not respond to other treatments. Data indicate that topiramate may be helpful for PTSD patients who have high-risk alcohol use⁶ or migraine headaches.¹³ Because some patients who take topiramate lose weight, the medication may be useful for PTSD patients who are overweight.¹³

Disclosure

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Related Resource

• U.S. Department of Veterans Affairs. Nightmares and PTSD. www.ptsd.va.gov/public/pages/nightmares.asp.

Drug Brand Names

• Paroxetine • Paxil
• Sertraline • Zoloft
• Prazosin • Minipress
• Topiramate • Topamax
• Trazodone • Desyrel, Oleptro

Re-experiencing a previous life-threatening stress through nightmares or recurrent memories is a hallmark of posttraumatic stress disorder (PTSD). In the United States, the lifetime risk of PTSD is 10.1% and the 12-month prevalence is 3.7%.¹ The selective serotonin reuptake inhibitors (SSRIs) sertraline and paroxetine are FDA-approved for treating PTSD; clinicians commonly use any SSRI for this disorder. Although SSRIs can alleviate many PTSD symptoms, at times patients experience only a partial response, which necessitates other interventions.

Rationale for using topiramate

The anticonvulsant topiramate blocks voltage-sensitive sodium channels, augments γ-aminobutyric acid type A, antagonizes the glutamate receptor, and inhibits carbonic anhydrase. Researchers have hypothesized that limbic nuclei become sensitized and “kindled” after exposure to a traumatic event. Anticonvulsants such as topiramate may help mitigate stress-activated kindling in PTSD.^2,3

What does the evidence say?

Although less compelling than double-blind, placebo-controlled trials, small open-label studies and some case reports indicate a potential role for topiramate in PTSD for specific populations.^4,5 In an 8-week open- label study, Alderman et al⁶ found adjunctive topiramate led to a statistically significant reduction in Clinician-Administered PTSD Scale (CAPS) scores and nightmares in 43 male veterans with combat-related PTSD. There was a nonsignificant decrease in high-risk alcohol use.

In a 2002 retrospective case series, Berlant et al⁷ found topiramate as monotherapy or adjunctive therapy reduced nightmares in 35 patients with chronic, non-combat PTSD. Nightmares decreased in 79% of patients and flashbacks decreased in 86%, with symptom improvement in a median of 4 days. Limitations of this study included lack of placebo control, a low number of participants, and a high dropout rate (9/35).

Two years later, Berlant⁸ used the PTSD Checklist-Civilian version (PCL-C) to assess response to topiramate in an open-label study of 33 patients with chronic, non-hallucinatory PTSD. Twenty-eight patients used topiramate as add-on therapy. PCL-C scores decreased by ≥30% in 77% of patients in 4 weeks, with a median dose of 50 mg/d and a median response time of 9 days.

In a double-blind, placebo-controlled trial, Tucker et al⁹ assessed 38 civilian patients who took topiramate monotherapy for PTSD. Using the CAPS, researchers concluded that topiramate reduced re-experiencing symptoms, but the effect was not statistically significant.⁹

Lindley et al¹⁰ conducted a randomized, double-blind, placebo-controlled trial to study the effect of add-on topiramate in 40 patients with chronic, combat-related PTSD. Because many patients in this study had a history of depression and substance use disorders, topiramate was added to antidepressants; no anticonvulsants, antipsychotics, or benzodiazepines were used. Similar to previous studies, researchers found no statistically significant effect on PTSD symptom severity or global symptom improvement. However, the small number of participants and a high dropout rate limited this study.¹⁰

In a 12-week, double-blind, placebo-controlled study of 35 men and women age 18 to 62 with PTSD, Yeh et al¹¹ found that topiramate (mean dose: 102.94 mg/d) lead to a statistically significant overall CAPS score reduction, with significant improvements in re-experiencing symptoms, such as nightmares.

Our opinion

FDA-approved treatments such as SSRIs should be the first pharmacologic intervention for PTSD. If a patient’s response is partial or inadequate, consider additional treatment options. For patients with persistent re-experiencing symptoms, evidence and experience with prazosin and trazodone are more robust than that for topiramate.¹²

Using topiramate to reduce re-experiencing symptoms such as nightmares in PTSD is not supported by statistically significant evidence from double-blind, placebo- controlled trials. However, numerous open-label studies and case reports suggest that there may be a role for topiramate in PTSD patients who do not respond to other treatments. Data indicate that topiramate may be helpful for PTSD patients who have high-risk alcohol use⁶ or migraine headaches.¹³ Because some patients who take topiramate lose weight, the medication may be useful for PTSD patients who are overweight.¹³

Disclosure

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Related Resource

• U.S. Department of Veterans Affairs. Nightmares and PTSD. www.ptsd.va.gov/public/pages/nightmares.asp.

Drug Brand Names

• Paroxetine • Paxil
• Sertraline • Zoloft
• Prazosin • Minipress
• Topiramate • Topamax
• Trazodone • Desyrel, Oleptro

Re-experiencing a previous life-threatening stress through nightmares or recurrent memories is a hallmark of posttraumatic stress disorder (PTSD). In the United States, the lifetime risk of PTSD is 10.1% and the 12-month prevalence is 3.7%.¹ The selective serotonin reuptake inhibitors (SSRIs) sertraline and paroxetine are FDA-approved for treating PTSD; clinicians commonly use any SSRI for this disorder. Although SSRIs can alleviate many PTSD symptoms, at times patients experience only a partial response, which necessitates other interventions.

Rationale for using topiramate

The anticonvulsant topiramate blocks voltage-sensitive sodium channels, augments γ-aminobutyric acid type A, antagonizes the glutamate receptor, and inhibits carbonic anhydrase. Researchers have hypothesized that limbic nuclei become sensitized and “kindled” after exposure to a traumatic event. Anticonvulsants such as topiramate may help mitigate stress-activated kindling in PTSD.^2,3

What does the evidence say?

Although less compelling than double-blind, placebo-controlled trials, small open-label studies and some case reports indicate a potential role for topiramate in PTSD for specific populations.^4,5 In an 8-week open- label study, Alderman et al⁶ found adjunctive topiramate led to a statistically significant reduction in Clinician-Administered PTSD Scale (CAPS) scores and nightmares in 43 male veterans with combat-related PTSD. There was a nonsignificant decrease in high-risk alcohol use.

In a 2002 retrospective case series, Berlant et al⁷ found topiramate as monotherapy or adjunctive therapy reduced nightmares in 35 patients with chronic, non-combat PTSD. Nightmares decreased in 79% of patients and flashbacks decreased in 86%, with symptom improvement in a median of 4 days. Limitations of this study included lack of placebo control, a low number of participants, and a high dropout rate (9/35).

Two years later, Berlant⁸ used the PTSD Checklist-Civilian version (PCL-C) to assess response to topiramate in an open-label study of 33 patients with chronic, non-hallucinatory PTSD. Twenty-eight patients used topiramate as add-on therapy. PCL-C scores decreased by ≥30% in 77% of patients in 4 weeks, with a median dose of 50 mg/d and a median response time of 9 days.

In a double-blind, placebo-controlled trial, Tucker et al⁹ assessed 38 civilian patients who took topiramate monotherapy for PTSD. Using the CAPS, researchers concluded that topiramate reduced re-experiencing symptoms, but the effect was not statistically significant.⁹

Lindley et al¹⁰ conducted a randomized, double-blind, placebo-controlled trial to study the effect of add-on topiramate in 40 patients with chronic, combat-related PTSD. Because many patients in this study had a history of depression and substance use disorders, topiramate was added to antidepressants; no anticonvulsants, antipsychotics, or benzodiazepines were used. Similar to previous studies, researchers found no statistically significant effect on PTSD symptom severity or global symptom improvement. However, the small number of participants and a high dropout rate limited this study.¹⁰

In a 12-week, double-blind, placebo-controlled study of 35 men and women age 18 to 62 with PTSD, Yeh et al¹¹ found that topiramate (mean dose: 102.94 mg/d) lead to a statistically significant overall CAPS score reduction, with significant improvements in re-experiencing symptoms, such as nightmares.

Our opinion

FDA-approved treatments such as SSRIs should be the first pharmacologic intervention for PTSD. If a patient’s response is partial or inadequate, consider additional treatment options. For patients with persistent re-experiencing symptoms, evidence and experience with prazosin and trazodone are more robust than that for topiramate.¹²

Using topiramate to reduce re-experiencing symptoms such as nightmares in PTSD is not supported by statistically significant evidence from double-blind, placebo- controlled trials. However, numerous open-label studies and case reports suggest that there may be a role for topiramate in PTSD patients who do not respond to other treatments. Data indicate that topiramate may be helpful for PTSD patients who have high-risk alcohol use⁶ or migraine headaches.¹³ Because some patients who take topiramate lose weight, the medication may be useful for PTSD patients who are overweight.¹³

Disclosure

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Related Resource

• U.S. Department of Veterans Affairs. Nightmares and PTSD. www.ptsd.va.gov/public/pages/nightmares.asp.

Drug Brand Names

• Paroxetine • Paxil
• Sertraline • Zoloft
• Prazosin • Minipress
• Topiramate • Topamax
• Trazodone • Desyrel, Oleptro

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