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Anomalous Motor Learning May Be Specific to Children With Autism
Children with autism rely heavily on proprioception, unlike children with other developmental motor impairments or typically developing children.
PROVIDENCE, RI—Children with autism spectrum disorder form a representation of internal models that places an unusually strong reliance on proprioception, according to research presented at the 39th National Meeting of the Child Neurology Society.
“This anomalous motor learning is specific to autism spectrum disorder, rather than a general deficit of all populations with developmental motor impairments, as children with ADHD did not generalize differently than typically developing children,” reported Stewart H. Mostofsky, MD, research scientist at the Kennedy Krieger Institute and Associate Professor of Neurology, Johns Hopkins University School of Medicine, Baltimore, and colleagues. “Our results suggest that autism-associated impairment in understanding actions of others may be a consequence of the fact that in learning to perform actions, children with autism place a greater than normal reliance on their own proprioception while discounting the visual consequences of their actions.”
The researchers analyzed 25 children with autism (mean age, 10.31), 16 with ADHD (mean age, 10.66), and 39 typically developing children (mean age, 10.82). As part of a game, each child held the handle of a robotic arm, trying to capture animals that had escaped from a zoo. An animal would appear at a target location 8 cm away; if the child reached the target in time, the animal was captured and the child was given a point.
“Analyses revealed that all groups were able to effectively adapt their arm movement,” stated Dr. Mostofsky’s group. “However, generalization patterns were markedly different. There was a significant interaction between diagnostic group and relative generalization to targets 2 and 3. Posthoc analyses revealed this difference was due to significantly greater generalization of the autism group in the intrinsic (proprioceptive) coordinate system as compared to typically developing children. In contrast, there was no significant difference in generalization between ADHD and typically developing children.”
Regression analyses revealed that among all groups, generalization in the intrinsic (proprioceptive) coordinate system (ie, to target 3) was a significant predictor of social ability, such that greater social impairment was predicted by increased force for target 3, noted Dr. Mostofsky and colleagues. “Further,” the researchers concluded, “for the children with autism, increased force for target 3 predicted impaired social interaction. In addition, increased generalization to target 3 also predicted impaired imitation ability, as assessed on a praxis examination, as well as impairment in motor control.”
Children with autism rely heavily on proprioception, unlike children with other developmental motor impairments or typically developing children.
PROVIDENCE, RI—Children with autism spectrum disorder form a representation of internal models that places an unusually strong reliance on proprioception, according to research presented at the 39th National Meeting of the Child Neurology Society.
“This anomalous motor learning is specific to autism spectrum disorder, rather than a general deficit of all populations with developmental motor impairments, as children with ADHD did not generalize differently than typically developing children,” reported Stewart H. Mostofsky, MD, research scientist at the Kennedy Krieger Institute and Associate Professor of Neurology, Johns Hopkins University School of Medicine, Baltimore, and colleagues. “Our results suggest that autism-associated impairment in understanding actions of others may be a consequence of the fact that in learning to perform actions, children with autism place a greater than normal reliance on their own proprioception while discounting the visual consequences of their actions.”
The researchers analyzed 25 children with autism (mean age, 10.31), 16 with ADHD (mean age, 10.66), and 39 typically developing children (mean age, 10.82). As part of a game, each child held the handle of a robotic arm, trying to capture animals that had escaped from a zoo. An animal would appear at a target location 8 cm away; if the child reached the target in time, the animal was captured and the child was given a point.
“Analyses revealed that all groups were able to effectively adapt their arm movement,” stated Dr. Mostofsky’s group. “However, generalization patterns were markedly different. There was a significant interaction between diagnostic group and relative generalization to targets 2 and 3. Posthoc analyses revealed this difference was due to significantly greater generalization of the autism group in the intrinsic (proprioceptive) coordinate system as compared to typically developing children. In contrast, there was no significant difference in generalization between ADHD and typically developing children.”
Regression analyses revealed that among all groups, generalization in the intrinsic (proprioceptive) coordinate system (ie, to target 3) was a significant predictor of social ability, such that greater social impairment was predicted by increased force for target 3, noted Dr. Mostofsky and colleagues. “Further,” the researchers concluded, “for the children with autism, increased force for target 3 predicted impaired social interaction. In addition, increased generalization to target 3 also predicted impaired imitation ability, as assessed on a praxis examination, as well as impairment in motor control.”
Children with autism rely heavily on proprioception, unlike children with other developmental motor impairments or typically developing children.
PROVIDENCE, RI—Children with autism spectrum disorder form a representation of internal models that places an unusually strong reliance on proprioception, according to research presented at the 39th National Meeting of the Child Neurology Society.
“This anomalous motor learning is specific to autism spectrum disorder, rather than a general deficit of all populations with developmental motor impairments, as children with ADHD did not generalize differently than typically developing children,” reported Stewart H. Mostofsky, MD, research scientist at the Kennedy Krieger Institute and Associate Professor of Neurology, Johns Hopkins University School of Medicine, Baltimore, and colleagues. “Our results suggest that autism-associated impairment in understanding actions of others may be a consequence of the fact that in learning to perform actions, children with autism place a greater than normal reliance on their own proprioception while discounting the visual consequences of their actions.”
The researchers analyzed 25 children with autism (mean age, 10.31), 16 with ADHD (mean age, 10.66), and 39 typically developing children (mean age, 10.82). As part of a game, each child held the handle of a robotic arm, trying to capture animals that had escaped from a zoo. An animal would appear at a target location 8 cm away; if the child reached the target in time, the animal was captured and the child was given a point.
“Analyses revealed that all groups were able to effectively adapt their arm movement,” stated Dr. Mostofsky’s group. “However, generalization patterns were markedly different. There was a significant interaction between diagnostic group and relative generalization to targets 2 and 3. Posthoc analyses revealed this difference was due to significantly greater generalization of the autism group in the intrinsic (proprioceptive) coordinate system as compared to typically developing children. In contrast, there was no significant difference in generalization between ADHD and typically developing children.”
Regression analyses revealed that among all groups, generalization in the intrinsic (proprioceptive) coordinate system (ie, to target 3) was a significant predictor of social ability, such that greater social impairment was predicted by increased force for target 3, noted Dr. Mostofsky and colleagues. “Further,” the researchers concluded, “for the children with autism, increased force for target 3 predicted impaired social interaction. In addition, increased generalization to target 3 also predicted impaired imitation ability, as assessed on a praxis examination, as well as impairment in motor control.”
Self-Monitoring of Glucose in Diabetes
Despite therapeutic advances in diabetes management, the majority of patients with diabetes are unable to achieve glycemic targets proven to reduce the burden of the disease. This burden not only involves the quality of life of patients with diabetes who experience the complications of this disease; it also includes the burden to society. One out of every five health care dollars is spent on caring for someone with diabetes—the majority on treating the complications.1
Major barriers to patients’ ability to achieve glycemic goals include the need to make behavioral changes, lack of awareness of glycemic levels, and fear of hypoglycemia.2
Q: Is self-monitoring of blood glucose worthwhile in diabetes?
Studies have shown a benefit from self-monitoring of blood glucose (SMBG) in patients using insulin but not in those taking oral antidiabetic drugs. However, the American Diabetes Association recommends that patients with diabetes monitor their glucose once daily if they are being treated with noninsulin therapy and at least three times daily if they are taking insulin.3
Guidelines from the American Association of Clinical Endocrinologists (AACE) state that patients taking noninsulin or once-daily insulin therapy who have not achieved A1C targets should monitor at least twice daily, while those at target should monitor at least once daily. Those taking multiple daily injections should perform SMBG at least three times per day. If patients experience frequent hypoglycemia, AACE suggests monitoring glucose more often.4
The A1C test provides the “big picture,” the average daily glucose level during the previous 90 to 120 days, and correlates with end-organ impact. It does not identify glycemic variability, hypoglycemia, or hyperglycemia.
By contrast, SMBG patterns provide day-to-day data that can be used to select and manage glucose control programs and ultimately optimize a patient’s A1C. SMBG provides a measure of the specific pharmacologic impact of medications and, through feedback, allows design and implementation of physiologic insulin-replacement programs.
One example of SMBG is to have patients monitor glucose in pairs (ie, pick a meal each day and do a premeal and two-hour postmeal reading) and ask them to keep a log or download the data from their meter in the office. This type of monitoring can be enlightening and self-empowering for the patient in that it can provide valuable information regarding the glycemic response to the particular meal.
Intensive glycemic management has been shown to reduce the incidence and progression of diabetic complications. However, it is associated with an increase in severe hypoglycemia. This is worrisome for both patients and providers, as severe hypoglycemia has been associated with an increase in risk for mortality. SMBG can assist patients in understanding how their lifestyle affects their diabetes, as well as identifying hypoglycemia for those who may have hypoglycemia unawareness (ie, who lack the relevant symptoms).
Q: What is continuous glucose monitoring (CGM)?
CGM devices give real-time readouts of current glucose levels. They utilize a subcutaneous sensor that is inserted in the abdomen and worn for 3 to 7 days (depending on which device is used). The sensor sends an electronic signal to a receiver worn by the patient.
There are three major CGM devices that have been approved by the FDA and are available for both personal and professional use. Health care providers can purchase the units and have patients wear them for retrospective analysis; this is a reimbursable expense. All available CGM devices measure glucose values in the interstitial fluid. The sensor reads electrical current produced by the same glucose-oxidase reaction that is utilized by glucose meters that patients use to perform fingersticks for home monitoring.
Currently available CGM systems need to be calibrated at least twice daily. Sensor calibration entails the pairing of the fingerstick value with the sensor value from the interstitial space. Calibration confirms sensor accuracy during various points by “teaching” the sensor the glucose value that corresponds with the electrical current signal.
There is a known physiologic lag time that occurs between fingerstick and sensor values. This lag time is typically up to 15 minutes but is increased with rapidly changing glucose values.
Q: What are the benefits of CGM?
Recent studies have shown CGM can improve A1C without increasing the incidence of hypoglycemia.5
CGM systems have both low and high glucose threshold alarms that can be set to alert once the threshold is reached. The newest generation devices can also predict hypoglycemia or hyperglycemia by tracking rate of change, and users can be alerted to a potential event. This would then allow them to take appropriate action, such as consuming food or carbohydrates or taking insulin as necessary. (Before taking any action, the glucose should first be confirmed by SMBG.)
Software programs allow for review of glucose data, which can assist in identifying trends not appreciated by typical SMBG testing (such as nocturnal hypoglycemia and meal-time excursions). This allows for adjustment of insulin regimens to reduce the incidence of these events.
Q: Can CGM replace SMBG?
While CGM can provide much more detail regarding glucose trends and patterns, it is not a replacement for SMBG. CGM should not be used as a replacement for SMBG to dose insulin for meal- or activity-related adjustments. All dosing decisions should be based on the SMBG.
Currently, CGM is indicated for patients 18 or older, in conjunction with SMBG for the purpose of improving glycemic control:
• to identify and aid in management of glycemic patterns not recognized with typical SMBG
• to prevent glycemic excursions of hypoglycemia and hyperglycemia.
Its use is supported by ADA and AACE guidelines for glucose monitoring.
Q: Who would benefit from CGM?
Suitable candidates for CGM include those with a high degree of glycemic variability, those with hypoglycemic unawareness, shift workers, patients who use insulin pumps, athletes, and women who are planning to become or are pregnant. Patients should work closely with their health care team and perform regular SMBG.
It has been suggested that patients need comprehensive training and follow-up visits to fully understand the large amount of data that they can be confronted with, in order to fully benefit from these devices.6 While the accuracy is improving, there are a few limitations to this technology, including false alarms. Studies have also shown a positive correlation between sensor wear time (hours per week) and greater reductions in A1C.5
Conclusion
Glucose monitoring is a necessary tool—for patients as well as providers—that assists in identifying how patients’ lifestyles affect their diabetes.
1. American Diabetes Association. Economic costs of diabetes in the US in 2007. Diabetes Care. 2008;31(3):596-615.
2. Hirsch IB, Armstrong D, Bergenstal RM, et al. Clinical application of emerging sensor technologies in diabetes management: consensus guidelines for continuous glucose monitoring (CGM). Diabetes Technol Ther. 2008;10(4):232-246.
3. American Diabetes Association. Standards of medical care in diabetes—2011. Diabetes Care. 2010;34(suppl 1):S11-S61.
4. American Association of Clinical Endocrinologists. Medical guidelines for clinical practice for the management of diabetes mellitus. Endocrin Prac. 2007;13(suppl 1):1-68.
5. Bergenstal RM, Tamberlane WV, Ahmann A, et al; STAR 3 Study Group. Effectiveness of sensor-augmented insulin-pump therapy in type 1 diabetes. N Engl J Med. 2010;363(4):311-320.
6. Fabiato K, Buse J, Duclos M, et al. Clinical experience with continuous glucose monitoring in adults. Diabetes Technol Ther. 2009;11(suppl 1):S93-S103.
Despite therapeutic advances in diabetes management, the majority of patients with diabetes are unable to achieve glycemic targets proven to reduce the burden of the disease. This burden not only involves the quality of life of patients with diabetes who experience the complications of this disease; it also includes the burden to society. One out of every five health care dollars is spent on caring for someone with diabetes—the majority on treating the complications.1
Major barriers to patients’ ability to achieve glycemic goals include the need to make behavioral changes, lack of awareness of glycemic levels, and fear of hypoglycemia.2
Q: Is self-monitoring of blood glucose worthwhile in diabetes?
Studies have shown a benefit from self-monitoring of blood glucose (SMBG) in patients using insulin but not in those taking oral antidiabetic drugs. However, the American Diabetes Association recommends that patients with diabetes monitor their glucose once daily if they are being treated with noninsulin therapy and at least three times daily if they are taking insulin.3
Guidelines from the American Association of Clinical Endocrinologists (AACE) state that patients taking noninsulin or once-daily insulin therapy who have not achieved A1C targets should monitor at least twice daily, while those at target should monitor at least once daily. Those taking multiple daily injections should perform SMBG at least three times per day. If patients experience frequent hypoglycemia, AACE suggests monitoring glucose more often.4
The A1C test provides the “big picture,” the average daily glucose level during the previous 90 to 120 days, and correlates with end-organ impact. It does not identify glycemic variability, hypoglycemia, or hyperglycemia.
By contrast, SMBG patterns provide day-to-day data that can be used to select and manage glucose control programs and ultimately optimize a patient’s A1C. SMBG provides a measure of the specific pharmacologic impact of medications and, through feedback, allows design and implementation of physiologic insulin-replacement programs.
One example of SMBG is to have patients monitor glucose in pairs (ie, pick a meal each day and do a premeal and two-hour postmeal reading) and ask them to keep a log or download the data from their meter in the office. This type of monitoring can be enlightening and self-empowering for the patient in that it can provide valuable information regarding the glycemic response to the particular meal.
Intensive glycemic management has been shown to reduce the incidence and progression of diabetic complications. However, it is associated with an increase in severe hypoglycemia. This is worrisome for both patients and providers, as severe hypoglycemia has been associated with an increase in risk for mortality. SMBG can assist patients in understanding how their lifestyle affects their diabetes, as well as identifying hypoglycemia for those who may have hypoglycemia unawareness (ie, who lack the relevant symptoms).
Q: What is continuous glucose monitoring (CGM)?
CGM devices give real-time readouts of current glucose levels. They utilize a subcutaneous sensor that is inserted in the abdomen and worn for 3 to 7 days (depending on which device is used). The sensor sends an electronic signal to a receiver worn by the patient.
There are three major CGM devices that have been approved by the FDA and are available for both personal and professional use. Health care providers can purchase the units and have patients wear them for retrospective analysis; this is a reimbursable expense. All available CGM devices measure glucose values in the interstitial fluid. The sensor reads electrical current produced by the same glucose-oxidase reaction that is utilized by glucose meters that patients use to perform fingersticks for home monitoring.
Currently available CGM systems need to be calibrated at least twice daily. Sensor calibration entails the pairing of the fingerstick value with the sensor value from the interstitial space. Calibration confirms sensor accuracy during various points by “teaching” the sensor the glucose value that corresponds with the electrical current signal.
There is a known physiologic lag time that occurs between fingerstick and sensor values. This lag time is typically up to 15 minutes but is increased with rapidly changing glucose values.
Q: What are the benefits of CGM?
Recent studies have shown CGM can improve A1C without increasing the incidence of hypoglycemia.5
CGM systems have both low and high glucose threshold alarms that can be set to alert once the threshold is reached. The newest generation devices can also predict hypoglycemia or hyperglycemia by tracking rate of change, and users can be alerted to a potential event. This would then allow them to take appropriate action, such as consuming food or carbohydrates or taking insulin as necessary. (Before taking any action, the glucose should first be confirmed by SMBG.)
Software programs allow for review of glucose data, which can assist in identifying trends not appreciated by typical SMBG testing (such as nocturnal hypoglycemia and meal-time excursions). This allows for adjustment of insulin regimens to reduce the incidence of these events.
Q: Can CGM replace SMBG?
While CGM can provide much more detail regarding glucose trends and patterns, it is not a replacement for SMBG. CGM should not be used as a replacement for SMBG to dose insulin for meal- or activity-related adjustments. All dosing decisions should be based on the SMBG.
Currently, CGM is indicated for patients 18 or older, in conjunction with SMBG for the purpose of improving glycemic control:
• to identify and aid in management of glycemic patterns not recognized with typical SMBG
• to prevent glycemic excursions of hypoglycemia and hyperglycemia.
Its use is supported by ADA and AACE guidelines for glucose monitoring.
Q: Who would benefit from CGM?
Suitable candidates for CGM include those with a high degree of glycemic variability, those with hypoglycemic unawareness, shift workers, patients who use insulin pumps, athletes, and women who are planning to become or are pregnant. Patients should work closely with their health care team and perform regular SMBG.
It has been suggested that patients need comprehensive training and follow-up visits to fully understand the large amount of data that they can be confronted with, in order to fully benefit from these devices.6 While the accuracy is improving, there are a few limitations to this technology, including false alarms. Studies have also shown a positive correlation between sensor wear time (hours per week) and greater reductions in A1C.5
Conclusion
Glucose monitoring is a necessary tool—for patients as well as providers—that assists in identifying how patients’ lifestyles affect their diabetes.
Despite therapeutic advances in diabetes management, the majority of patients with diabetes are unable to achieve glycemic targets proven to reduce the burden of the disease. This burden not only involves the quality of life of patients with diabetes who experience the complications of this disease; it also includes the burden to society. One out of every five health care dollars is spent on caring for someone with diabetes—the majority on treating the complications.1
Major barriers to patients’ ability to achieve glycemic goals include the need to make behavioral changes, lack of awareness of glycemic levels, and fear of hypoglycemia.2
Q: Is self-monitoring of blood glucose worthwhile in diabetes?
Studies have shown a benefit from self-monitoring of blood glucose (SMBG) in patients using insulin but not in those taking oral antidiabetic drugs. However, the American Diabetes Association recommends that patients with diabetes monitor their glucose once daily if they are being treated with noninsulin therapy and at least three times daily if they are taking insulin.3
Guidelines from the American Association of Clinical Endocrinologists (AACE) state that patients taking noninsulin or once-daily insulin therapy who have not achieved A1C targets should monitor at least twice daily, while those at target should monitor at least once daily. Those taking multiple daily injections should perform SMBG at least three times per day. If patients experience frequent hypoglycemia, AACE suggests monitoring glucose more often.4
The A1C test provides the “big picture,” the average daily glucose level during the previous 90 to 120 days, and correlates with end-organ impact. It does not identify glycemic variability, hypoglycemia, or hyperglycemia.
By contrast, SMBG patterns provide day-to-day data that can be used to select and manage glucose control programs and ultimately optimize a patient’s A1C. SMBG provides a measure of the specific pharmacologic impact of medications and, through feedback, allows design and implementation of physiologic insulin-replacement programs.
One example of SMBG is to have patients monitor glucose in pairs (ie, pick a meal each day and do a premeal and two-hour postmeal reading) and ask them to keep a log or download the data from their meter in the office. This type of monitoring can be enlightening and self-empowering for the patient in that it can provide valuable information regarding the glycemic response to the particular meal.
Intensive glycemic management has been shown to reduce the incidence and progression of diabetic complications. However, it is associated with an increase in severe hypoglycemia. This is worrisome for both patients and providers, as severe hypoglycemia has been associated with an increase in risk for mortality. SMBG can assist patients in understanding how their lifestyle affects their diabetes, as well as identifying hypoglycemia for those who may have hypoglycemia unawareness (ie, who lack the relevant symptoms).
Q: What is continuous glucose monitoring (CGM)?
CGM devices give real-time readouts of current glucose levels. They utilize a subcutaneous sensor that is inserted in the abdomen and worn for 3 to 7 days (depending on which device is used). The sensor sends an electronic signal to a receiver worn by the patient.
There are three major CGM devices that have been approved by the FDA and are available for both personal and professional use. Health care providers can purchase the units and have patients wear them for retrospective analysis; this is a reimbursable expense. All available CGM devices measure glucose values in the interstitial fluid. The sensor reads electrical current produced by the same glucose-oxidase reaction that is utilized by glucose meters that patients use to perform fingersticks for home monitoring.
Currently available CGM systems need to be calibrated at least twice daily. Sensor calibration entails the pairing of the fingerstick value with the sensor value from the interstitial space. Calibration confirms sensor accuracy during various points by “teaching” the sensor the glucose value that corresponds with the electrical current signal.
There is a known physiologic lag time that occurs between fingerstick and sensor values. This lag time is typically up to 15 minutes but is increased with rapidly changing glucose values.
Q: What are the benefits of CGM?
Recent studies have shown CGM can improve A1C without increasing the incidence of hypoglycemia.5
CGM systems have both low and high glucose threshold alarms that can be set to alert once the threshold is reached. The newest generation devices can also predict hypoglycemia or hyperglycemia by tracking rate of change, and users can be alerted to a potential event. This would then allow them to take appropriate action, such as consuming food or carbohydrates or taking insulin as necessary. (Before taking any action, the glucose should first be confirmed by SMBG.)
Software programs allow for review of glucose data, which can assist in identifying trends not appreciated by typical SMBG testing (such as nocturnal hypoglycemia and meal-time excursions). This allows for adjustment of insulin regimens to reduce the incidence of these events.
Q: Can CGM replace SMBG?
While CGM can provide much more detail regarding glucose trends and patterns, it is not a replacement for SMBG. CGM should not be used as a replacement for SMBG to dose insulin for meal- or activity-related adjustments. All dosing decisions should be based on the SMBG.
Currently, CGM is indicated for patients 18 or older, in conjunction with SMBG for the purpose of improving glycemic control:
• to identify and aid in management of glycemic patterns not recognized with typical SMBG
• to prevent glycemic excursions of hypoglycemia and hyperglycemia.
Its use is supported by ADA and AACE guidelines for glucose monitoring.
Q: Who would benefit from CGM?
Suitable candidates for CGM include those with a high degree of glycemic variability, those with hypoglycemic unawareness, shift workers, patients who use insulin pumps, athletes, and women who are planning to become or are pregnant. Patients should work closely with their health care team and perform regular SMBG.
It has been suggested that patients need comprehensive training and follow-up visits to fully understand the large amount of data that they can be confronted with, in order to fully benefit from these devices.6 While the accuracy is improving, there are a few limitations to this technology, including false alarms. Studies have also shown a positive correlation between sensor wear time (hours per week) and greater reductions in A1C.5
Conclusion
Glucose monitoring is a necessary tool—for patients as well as providers—that assists in identifying how patients’ lifestyles affect their diabetes.
1. American Diabetes Association. Economic costs of diabetes in the US in 2007. Diabetes Care. 2008;31(3):596-615.
2. Hirsch IB, Armstrong D, Bergenstal RM, et al. Clinical application of emerging sensor technologies in diabetes management: consensus guidelines for continuous glucose monitoring (CGM). Diabetes Technol Ther. 2008;10(4):232-246.
3. American Diabetes Association. Standards of medical care in diabetes—2011. Diabetes Care. 2010;34(suppl 1):S11-S61.
4. American Association of Clinical Endocrinologists. Medical guidelines for clinical practice for the management of diabetes mellitus. Endocrin Prac. 2007;13(suppl 1):1-68.
5. Bergenstal RM, Tamberlane WV, Ahmann A, et al; STAR 3 Study Group. Effectiveness of sensor-augmented insulin-pump therapy in type 1 diabetes. N Engl J Med. 2010;363(4):311-320.
6. Fabiato K, Buse J, Duclos M, et al. Clinical experience with continuous glucose monitoring in adults. Diabetes Technol Ther. 2009;11(suppl 1):S93-S103.
1. American Diabetes Association. Economic costs of diabetes in the US in 2007. Diabetes Care. 2008;31(3):596-615.
2. Hirsch IB, Armstrong D, Bergenstal RM, et al. Clinical application of emerging sensor technologies in diabetes management: consensus guidelines for continuous glucose monitoring (CGM). Diabetes Technol Ther. 2008;10(4):232-246.
3. American Diabetes Association. Standards of medical care in diabetes—2011. Diabetes Care. 2010;34(suppl 1):S11-S61.
4. American Association of Clinical Endocrinologists. Medical guidelines for clinical practice for the management of diabetes mellitus. Endocrin Prac. 2007;13(suppl 1):1-68.
5. Bergenstal RM, Tamberlane WV, Ahmann A, et al; STAR 3 Study Group. Effectiveness of sensor-augmented insulin-pump therapy in type 1 diabetes. N Engl J Med. 2010;363(4):311-320.
6. Fabiato K, Buse J, Duclos M, et al. Clinical experience with continuous glucose monitoring in adults. Diabetes Technol Ther. 2009;11(suppl 1):S93-S103.
Erratum (2010;86:239-240)
Pityriasis Alba Revisited: Perspectives on an Enigmatic Disorder of Childhood
Drug testing is inexpensive? Not always, says this doc
As a recently retired physician who worked in family practice, palliative care, and occupational medicine for more than 30 years, I read “Is it time to drug test your chronic pain patient?” (J Fam Pract. 2010;59:628-633) with interest. I myself suffer from arthritis in the neck and low back, for which a medical school colleague prescribed a very low dose of hydrocodone prn several years ago. I believe my resident physician may have read your article right before my last office visit; he suggested a drug screen was appropriate for me because hydrocodone is a “high-risk” medication.
I understood, of course, and readily agreed. After all, I did thousands of these screens during my years of practice—at a cost of about $5 per test. The authors of your article apparently did not research the average retail cost of the test, stating only that it is “inexpensive.” Imagine my surprise when I saw the bill—$676 for the drug screen alone. My insurer readily paid its portion of the “allowable” charge ($434).
The medication itself is wonderful; it helps keep me functioning and costs me about 8 cents per pill, so I won’t complain too much. But I suspect that most of your readers would be surprised by the true cost of this “inexpensive” test at a major medical school.
Mack Tyner, MD
Gainesville, Fla
As a recently retired physician who worked in family practice, palliative care, and occupational medicine for more than 30 years, I read “Is it time to drug test your chronic pain patient?” (J Fam Pract. 2010;59:628-633) with interest. I myself suffer from arthritis in the neck and low back, for which a medical school colleague prescribed a very low dose of hydrocodone prn several years ago. I believe my resident physician may have read your article right before my last office visit; he suggested a drug screen was appropriate for me because hydrocodone is a “high-risk” medication.
I understood, of course, and readily agreed. After all, I did thousands of these screens during my years of practice—at a cost of about $5 per test. The authors of your article apparently did not research the average retail cost of the test, stating only that it is “inexpensive.” Imagine my surprise when I saw the bill—$676 for the drug screen alone. My insurer readily paid its portion of the “allowable” charge ($434).
The medication itself is wonderful; it helps keep me functioning and costs me about 8 cents per pill, so I won’t complain too much. But I suspect that most of your readers would be surprised by the true cost of this “inexpensive” test at a major medical school.
Mack Tyner, MD
Gainesville, Fla
As a recently retired physician who worked in family practice, palliative care, and occupational medicine for more than 30 years, I read “Is it time to drug test your chronic pain patient?” (J Fam Pract. 2010;59:628-633) with interest. I myself suffer from arthritis in the neck and low back, for which a medical school colleague prescribed a very low dose of hydrocodone prn several years ago. I believe my resident physician may have read your article right before my last office visit; he suggested a drug screen was appropriate for me because hydrocodone is a “high-risk” medication.
I understood, of course, and readily agreed. After all, I did thousands of these screens during my years of practice—at a cost of about $5 per test. The authors of your article apparently did not research the average retail cost of the test, stating only that it is “inexpensive.” Imagine my surprise when I saw the bill—$676 for the drug screen alone. My insurer readily paid its portion of the “allowable” charge ($434).
The medication itself is wonderful; it helps keep me functioning and costs me about 8 cents per pill, so I won’t complain too much. But I suspect that most of your readers would be surprised by the true cost of this “inexpensive” test at a major medical school.
Mack Tyner, MD
Gainesville, Fla
Changes to the CPT code set and Medicare billing
The Current Procedural Terminology (CPT) code set for 2011 includes several changes of interest to ObGyns. These include 1) guideline clarifications regarding wound debridement and obstetric care codes; 2) new codes for subsequent observation care; micro-remodeling of the bladder neck; insertion of a vaginal after-loading device; and 3) a lab code for detecting amniotic fluid in cervicovaginal secretions (using the AmniSure kit).
There is also a new code for vaccine counseling that will have an impact on you if your practice offers the human papillomavirus (HPV) vaccine to patients younger than 19 years.
There are changes to Medicare this year that you should take note of if you care for these patients, particularly in the area of preventive visit billing.
CPT and Medicare changes both took effect on January 1. The Health Insurance Portability and Accountability Act (HIPAA) requires that insurers accepted the new codes on that date.
Changes to the CPT code set
OBSERVATION CARE
One of the biggest headaches for medical practices has been standardized coding and billing for observation care that lasts more than 1 day. In the past, payers accepted a problem E/M for Day 2 of observation care, or instructed practices to code an unlisted E/M service. Now, you may report all care rendered in the observation setting with the addition of three new codes for subsequent care:
99244 Subsequent observation care, per day, for the evaluation and management of a patient, which requires at least 2 of these 3 key components: problem focused interval history, problem focused examination; medical decision making that is straightforward or of low complexity. Counseling and/or coordination of care with other providers or agencies are provided consistent with the nature of the problem(s) and the patient’s and/or family’s needs. Usually, the patient is stable, recovering, or improving. Physicians typically spend 15 minutes at the bedside and on the patient’s hospital floor or unit.
99225 Subsequent observation care, per day, for the evaluation and management of a patient, which requires at least 2 of these 3 key components: an expanded problem focused interval history; an expanded problem focused examination; medical decision making of moderate complexity. Counseling and/or coordination of care with other providers or agencies are provided consistent with the nature of the problem(s) and the patient’s and/or family’s needs. Usually, the patient is responding inadequately to therapy or has developed a minor complication. Physicians typically spend 25 minutes at the bedside and on the patient’s hospital floor or unit.
99226 Subsequent observation care, per day, for the evaluation and management of a patient, which requires at least 2 of these 3 key components: a detailed interval history; a detailed examination; medical decision making of high complexity. Counseling and/or coordination of care with other providers or agencies are provided consistent with the nature of the problem(s) and the patient’s and/or family’s needs. Usually, the patient is unstable or has developed a significant complication or a significant new problem. Physicians typically spend 35 minutes at the bedside and on the patient’s hospital floor or unit.
Note that each of these codes 1) “suggests” the status of the patient for each level of billing, and 2) includes a typical time. This means that, unlike the observation care admission codes or the observation admission/same-day discharge codes, time that is spent with the patient, or on the unit, may be used to select the code—if you document 1) the requirement that more than 50% of the typical time was spent on counseling or coordination of care, or both, and 2) a detailed description of this activity.
Codes for wound debridement were given a facelift with the addition of a new guideline that addresses both surgical and medical debridement. The surgical debridement codes, (11042–11047) are now reported on the basis of the depth of tissue removed and the surface area of the wound. This means that codes 11040 and 11041 were deleted to make room for new and revised codes.
This change will mean that, when you report these codes, you will need to document more information to bill. It’s also understood that coding separately for debridement of dermis or epidermis at the same time you code for debriding underlying structures would be inappropriate.
CPT has also indicated that active wound management codes 97597 and 97598 can now be reported by physicians or nonphysician providers as long as the provider has direct (one-on-one) contact. These codes should be reported for skin-surface debridement only.
The new and revised codes (some of which have been published in CPT in nonsequential order) are:
11042 Debridement, subcutaneous tissue (includes epidermis and dermis, if performed); first 20 sq cm or less
+11045 (new add-on code reported with 11042 only) each additional 20 sq cm or part thereof
11043 Debridement, muscle and/or facia (includes epidermis, dermis, and subcutaneous tissue, if performed); first 20 sq cm or less
+11046 (new add-on code reported with 11043 only) each additional 20 sq cm or part thereof
11044 Debridement, bone (includes epidermis, dermis, subcutaneous tissue, muscle and/or fascia, if performed); first 20 sq cm or less
+11047 (new add-on code reported with 11044 only) each additional 20 sq cm or part thereof
97597 Debridement (e.g., high pressure waterjet with/without suction, sharp selective debridement with scissors, scalpel and forceps), open wound, (e.g., fibrin, devitalized epidermis and/or dermis, exudate, debris, biofilm), including topical application(s), wound assessment, use of a whirlpool, when performed and instruction(s) for ongoing care, per session, total wound(s) surface area; first 20 sq cm or less
+95798 (add-on code reported with 97597 only) Each additional 20 sq cm, or part thereof.
TRANSURETHRAL RADIOFREQUENCY
Category III code 0193T, which described transurethral radiofrequency micro-remodeling for stress urinary incontinence, has been deleted and converted to a Category I CPT code, 53860 (Transurethral radiofrequency micro-remodeling of the female bladder neck and proximal urethra for stress urinary incontinence). The procedure includes a periurethral block and flushing the bladder with a lidocaine slurry, and can be performed in the office.
In all, the procedure requires nine treatment cycles during the session, but the code is billed only once. Catheterization and measurement of a voiding sample after the procedure are included in the code.
AFTERLOADING DEVICES FOR CLINICAL BRACHYTHERAPY
CPT revised—slightly—existing code 57155, and added code 57156 (Insertion of a vaginal radiation afterloading apparatus for clinical brachytherapy).
- Code 57155 was revised to clarify that only a single tandem is inserted into the uterus. There had been confusion earlier in this regard.
- The new code describes a procedure that may also include dilation of the vaginal canal to remove postradiation adhesions. That procedure also involves 1) placement of bladder and rectal catheters and 2) radiographic imaging to confirm placement, which are not coded separately.
CLARIFICATION OF OBSTETRIC GUIDELINES
Been having problems with payers and their interpretation of the delivery only, postpartum only, and delivery with postpartum care codes? CPT has, at last, clarified what you can, and cannot, bill in those circumstances. (Keep in mind, however, that you may not unbundle these procedures if more extensive care is provided: Most payers want you to bill the global OB care code that includes antepartum, intrapartum, and postpartum care.)
In some cases (such as Medicaid), the payer stipulates that only the physician who actually performed the delivery may bill for it, even if the delivering physician is covering for, or is a member of, the same group practice as the primary attending of record. The “delivery-only” codes should be reported when 1) an unaffiliated physician has delivered the baby but will not be providing any outpatient postpartum care or 2) the payer has specified this method of billing for the covering or affiliated provider.
CPT has clarified that delivery-only codes (59409, 59514, or 59612, 59620) include admission to the hospital, the admission history and physical exam, uncomplicated labor and delivery (including delivery of the placenta, or use of forceps or vacuum extraction). These codes do not include inpatient rounding or discharge day care after delivery (and, of course, include no outpatient postpartum care). When, as the delivering physician, you also provide inpatient postdelivery care, therefore, you may additionally bill subsequent hospital care codes and discharge day management codes (99231-99233, 99238-99239).
If the unaffiliated physician performs the delivery and also intends on providing outpatient postpartum care, the CPT codes for delivery with postpartum are to be reported (59410, 59515, 59614, 59622). In addition to the delivery, these codes include all inpatient and outpatient postpartum care. And finally, for those physicians who are only providing outpatient postpartum care, the code 59430, Postpartum care only, should be reported.
PLACENTAL ALPHA MICROGLOBULIN-1
A new code, 84112 (Placental alpha microglobulin-1 [PAMG-11], cervicovaginal secretion, qualitative), has been added to allow the clinical laboratory to bill for this immunoassay that detects amniotic fluid in the secretions. Physician work involves collection of the specimen but, under CPT rules, collection is included as part of any E/M service.
Note: An existing code for this test that is used by Blue Cross/Blue Shield payers (S3628) remains valid in 2011.
HPV VACCINE COUNSELING
Before January 1, 2011, if you counseled a patient about the HPV vaccine, you could report preventive counseling codes, such as 99401–99404, in addition to the vaccine administration code, 90471 (Immunization administration, 1 vaccine). Now, however, you have a new code for counseling and vaccine administration for a patient who is younger than 19 years—the age group most likely to be counseled about this vaccine. When you see, and counsel, such a patient before administering the vaccine, on the same date of service, code 90460 (Immunization administration through 18 years of age via any route of administration, with counseling by physician or other qualified health care profession; first vaccine/toxoid component), and 90649 for the quadrivalent or 90650 for the bivalent HPV vaccine.
If your patient is 19 years or older and requires counseling, continue to bill 99401– 99404 for counseling, with 90471 for immunization and 90649 or 90650 for the vaccine. Keep in mind: Whether you report 90460 or the 9940X codes, you are required to document the content of the counseling. Codes 9940X also require documentation of the duration of counseling.
INFLUENZA VACCINE
New codes have been established for the flu vaccine, but you won’t be using them: They are intended to address future pandemic strains of influenza. This year’s vaccine contains the H1N1 strain, but is coded as the normal seasonal flu vaccine, based on the type given:
90656 (preservative-free)
90658 (split virus)
90660 (intranasal)
90662 (enhanced vaccine for patients older than 65 years).
Changes to Medicare billing
Some of the coding and billing changes this year that have an impact on ObGyn practice come from the Centers of Medicare and Medicaid Services (CMS) and the Affordable Care Act.
TIMELY FILING
The Affordable Care Act calls for a reduction in the maximum time period for submission of Medicare fee-for-service claims. Before January 1, a provider had 15 to 27 months to submit first-time claims to Medicare. Now, these claims must be filed within a calendar year of the date of service. Exceptions can be made for retroactive entitlement or in situations in which there is a secondary payer.
PAYMENTS TO CERTIFIED NURSE MIDWIVES
Next, more good news—if you employ a certified nurse midwife (CNM) in your practice. Before January 1, Medicare reimbursed direct billing from a CNM at only 65% of the Medicare Physician Fee Schedule. Now, a CNM is paid the same as a physician when she (he) bills under her own number.
In the past, some practices billed for the services of a CNM under “incident to” rules, to capture the physician payment—but this also meant that the CNM could not see a new patient. Under the change I’m describing, all CNMs can bill Medicare directly; see new patients; and be paid the same as the physician is paid. In addition, CNMs are no longer required to be supervised by a physician when they perform diagnostic tests that fall under the scope of their practice.
ANNUAL WELLNESS VISIT
The Affordable Care Act extended preventive coverage to Medicare beneficiaries in the form of an annual wellness visit. The two new codes here have been valued based on a level 4-problem new and established E/M service:
G0438 Annual wellness visit, including personalized prevention plan services, first visit
G0439 Annual wellness visit, including personalized prevention plan services, subsequent visit
Payment for the initial visit is made only beginning the second year the patient is eligible for Medicare Part B—during the first year of coverage, only the Initial Preventive Physical Examination (IPPE) (the “Welcome to Medicare”) exam will be covered.
CMS has stated that only one physician will be paid for the initial visit; when the patient returns to the same or a new physician in the third year, only a subsequent visit will be paid. It is, therefore, important that this information be conveyed to any new physician who sees the patient.
The annual codes can be billed in addition to any other preventive service, such as G0101 or Q0091; no modifier is needed for this combination. Medicare has waived both the copayment and the deductible for the annual wellness visit, as well as all Medicare-covered preventive services that have been recommended with a grade of “A” (“strongly recommends”) or “B” (“recommends”) by the US Preventive Services Task Force.
The annual wellness visit requires seven elements at a minimum (i.e., you may document and perform more elements than this, but not fewer):
- Establish or update the patient’s medical and family history
- List her current medical providers and suppliers and all prescribed medications
- Record measurements of height, weight, body mass index (initial visit only), blood pressure, and other routine measurements
- Detect any cognitive impairment
- Establish or update a screening schedule for the next 5 to 10 years, including screenings appropriate for the general population, and any additional screenings that may be appropriate because of her particular risk factors
- Review the patient’s 1) potential (i.e., risk factors) for depression, based on use of an appropriate screening instrument, and 2) functional ability and level of safety based on direct observation or screening questions
- Furnish 1) personalized health advice and 2) refer her appropriately to health education or preventive services.
CMS has also indicated that, although they will pay for a problem E/M service and the annual wellness visit on the same date of service with a modifier -25 added to the E/M service, they expect this type of billing to be rare—because of the nature of the wellness visit, which is time-intensive. They also expect that, given these requirements, the patient will not be billed additionally for a noncovered preventive service.
We want to hear from you! Tell us what you think.
The Current Procedural Terminology (CPT) code set for 2011 includes several changes of interest to ObGyns. These include 1) guideline clarifications regarding wound debridement and obstetric care codes; 2) new codes for subsequent observation care; micro-remodeling of the bladder neck; insertion of a vaginal after-loading device; and 3) a lab code for detecting amniotic fluid in cervicovaginal secretions (using the AmniSure kit).
There is also a new code for vaccine counseling that will have an impact on you if your practice offers the human papillomavirus (HPV) vaccine to patients younger than 19 years.
There are changes to Medicare this year that you should take note of if you care for these patients, particularly in the area of preventive visit billing.
CPT and Medicare changes both took effect on January 1. The Health Insurance Portability and Accountability Act (HIPAA) requires that insurers accepted the new codes on that date.
Changes to the CPT code set
OBSERVATION CARE
One of the biggest headaches for medical practices has been standardized coding and billing for observation care that lasts more than 1 day. In the past, payers accepted a problem E/M for Day 2 of observation care, or instructed practices to code an unlisted E/M service. Now, you may report all care rendered in the observation setting with the addition of three new codes for subsequent care:
99244 Subsequent observation care, per day, for the evaluation and management of a patient, which requires at least 2 of these 3 key components: problem focused interval history, problem focused examination; medical decision making that is straightforward or of low complexity. Counseling and/or coordination of care with other providers or agencies are provided consistent with the nature of the problem(s) and the patient’s and/or family’s needs. Usually, the patient is stable, recovering, or improving. Physicians typically spend 15 minutes at the bedside and on the patient’s hospital floor or unit.
99225 Subsequent observation care, per day, for the evaluation and management of a patient, which requires at least 2 of these 3 key components: an expanded problem focused interval history; an expanded problem focused examination; medical decision making of moderate complexity. Counseling and/or coordination of care with other providers or agencies are provided consistent with the nature of the problem(s) and the patient’s and/or family’s needs. Usually, the patient is responding inadequately to therapy or has developed a minor complication. Physicians typically spend 25 minutes at the bedside and on the patient’s hospital floor or unit.
99226 Subsequent observation care, per day, for the evaluation and management of a patient, which requires at least 2 of these 3 key components: a detailed interval history; a detailed examination; medical decision making of high complexity. Counseling and/or coordination of care with other providers or agencies are provided consistent with the nature of the problem(s) and the patient’s and/or family’s needs. Usually, the patient is unstable or has developed a significant complication or a significant new problem. Physicians typically spend 35 minutes at the bedside and on the patient’s hospital floor or unit.
Note that each of these codes 1) “suggests” the status of the patient for each level of billing, and 2) includes a typical time. This means that, unlike the observation care admission codes or the observation admission/same-day discharge codes, time that is spent with the patient, or on the unit, may be used to select the code—if you document 1) the requirement that more than 50% of the typical time was spent on counseling or coordination of care, or both, and 2) a detailed description of this activity.
Codes for wound debridement were given a facelift with the addition of a new guideline that addresses both surgical and medical debridement. The surgical debridement codes, (11042–11047) are now reported on the basis of the depth of tissue removed and the surface area of the wound. This means that codes 11040 and 11041 were deleted to make room for new and revised codes.
This change will mean that, when you report these codes, you will need to document more information to bill. It’s also understood that coding separately for debridement of dermis or epidermis at the same time you code for debriding underlying structures would be inappropriate.
CPT has also indicated that active wound management codes 97597 and 97598 can now be reported by physicians or nonphysician providers as long as the provider has direct (one-on-one) contact. These codes should be reported for skin-surface debridement only.
The new and revised codes (some of which have been published in CPT in nonsequential order) are:
11042 Debridement, subcutaneous tissue (includes epidermis and dermis, if performed); first 20 sq cm or less
+11045 (new add-on code reported with 11042 only) each additional 20 sq cm or part thereof
11043 Debridement, muscle and/or facia (includes epidermis, dermis, and subcutaneous tissue, if performed); first 20 sq cm or less
+11046 (new add-on code reported with 11043 only) each additional 20 sq cm or part thereof
11044 Debridement, bone (includes epidermis, dermis, subcutaneous tissue, muscle and/or fascia, if performed); first 20 sq cm or less
+11047 (new add-on code reported with 11044 only) each additional 20 sq cm or part thereof
97597 Debridement (e.g., high pressure waterjet with/without suction, sharp selective debridement with scissors, scalpel and forceps), open wound, (e.g., fibrin, devitalized epidermis and/or dermis, exudate, debris, biofilm), including topical application(s), wound assessment, use of a whirlpool, when performed and instruction(s) for ongoing care, per session, total wound(s) surface area; first 20 sq cm or less
+95798 (add-on code reported with 97597 only) Each additional 20 sq cm, or part thereof.
TRANSURETHRAL RADIOFREQUENCY
Category III code 0193T, which described transurethral radiofrequency micro-remodeling for stress urinary incontinence, has been deleted and converted to a Category I CPT code, 53860 (Transurethral radiofrequency micro-remodeling of the female bladder neck and proximal urethra for stress urinary incontinence). The procedure includes a periurethral block and flushing the bladder with a lidocaine slurry, and can be performed in the office.
In all, the procedure requires nine treatment cycles during the session, but the code is billed only once. Catheterization and measurement of a voiding sample after the procedure are included in the code.
AFTERLOADING DEVICES FOR CLINICAL BRACHYTHERAPY
CPT revised—slightly—existing code 57155, and added code 57156 (Insertion of a vaginal radiation afterloading apparatus for clinical brachytherapy).
- Code 57155 was revised to clarify that only a single tandem is inserted into the uterus. There had been confusion earlier in this regard.
- The new code describes a procedure that may also include dilation of the vaginal canal to remove postradiation adhesions. That procedure also involves 1) placement of bladder and rectal catheters and 2) radiographic imaging to confirm placement, which are not coded separately.
CLARIFICATION OF OBSTETRIC GUIDELINES
Been having problems with payers and their interpretation of the delivery only, postpartum only, and delivery with postpartum care codes? CPT has, at last, clarified what you can, and cannot, bill in those circumstances. (Keep in mind, however, that you may not unbundle these procedures if more extensive care is provided: Most payers want you to bill the global OB care code that includes antepartum, intrapartum, and postpartum care.)
In some cases (such as Medicaid), the payer stipulates that only the physician who actually performed the delivery may bill for it, even if the delivering physician is covering for, or is a member of, the same group practice as the primary attending of record. The “delivery-only” codes should be reported when 1) an unaffiliated physician has delivered the baby but will not be providing any outpatient postpartum care or 2) the payer has specified this method of billing for the covering or affiliated provider.
CPT has clarified that delivery-only codes (59409, 59514, or 59612, 59620) include admission to the hospital, the admission history and physical exam, uncomplicated labor and delivery (including delivery of the placenta, or use of forceps or vacuum extraction). These codes do not include inpatient rounding or discharge day care after delivery (and, of course, include no outpatient postpartum care). When, as the delivering physician, you also provide inpatient postdelivery care, therefore, you may additionally bill subsequent hospital care codes and discharge day management codes (99231-99233, 99238-99239).
If the unaffiliated physician performs the delivery and also intends on providing outpatient postpartum care, the CPT codes for delivery with postpartum are to be reported (59410, 59515, 59614, 59622). In addition to the delivery, these codes include all inpatient and outpatient postpartum care. And finally, for those physicians who are only providing outpatient postpartum care, the code 59430, Postpartum care only, should be reported.
PLACENTAL ALPHA MICROGLOBULIN-1
A new code, 84112 (Placental alpha microglobulin-1 [PAMG-11], cervicovaginal secretion, qualitative), has been added to allow the clinical laboratory to bill for this immunoassay that detects amniotic fluid in the secretions. Physician work involves collection of the specimen but, under CPT rules, collection is included as part of any E/M service.
Note: An existing code for this test that is used by Blue Cross/Blue Shield payers (S3628) remains valid in 2011.
HPV VACCINE COUNSELING
Before January 1, 2011, if you counseled a patient about the HPV vaccine, you could report preventive counseling codes, such as 99401–99404, in addition to the vaccine administration code, 90471 (Immunization administration, 1 vaccine). Now, however, you have a new code for counseling and vaccine administration for a patient who is younger than 19 years—the age group most likely to be counseled about this vaccine. When you see, and counsel, such a patient before administering the vaccine, on the same date of service, code 90460 (Immunization administration through 18 years of age via any route of administration, with counseling by physician or other qualified health care profession; first vaccine/toxoid component), and 90649 for the quadrivalent or 90650 for the bivalent HPV vaccine.
If your patient is 19 years or older and requires counseling, continue to bill 99401– 99404 for counseling, with 90471 for immunization and 90649 or 90650 for the vaccine. Keep in mind: Whether you report 90460 or the 9940X codes, you are required to document the content of the counseling. Codes 9940X also require documentation of the duration of counseling.
INFLUENZA VACCINE
New codes have been established for the flu vaccine, but you won’t be using them: They are intended to address future pandemic strains of influenza. This year’s vaccine contains the H1N1 strain, but is coded as the normal seasonal flu vaccine, based on the type given:
90656 (preservative-free)
90658 (split virus)
90660 (intranasal)
90662 (enhanced vaccine for patients older than 65 years).
Changes to Medicare billing
Some of the coding and billing changes this year that have an impact on ObGyn practice come from the Centers of Medicare and Medicaid Services (CMS) and the Affordable Care Act.
TIMELY FILING
The Affordable Care Act calls for a reduction in the maximum time period for submission of Medicare fee-for-service claims. Before January 1, a provider had 15 to 27 months to submit first-time claims to Medicare. Now, these claims must be filed within a calendar year of the date of service. Exceptions can be made for retroactive entitlement or in situations in which there is a secondary payer.
PAYMENTS TO CERTIFIED NURSE MIDWIVES
Next, more good news—if you employ a certified nurse midwife (CNM) in your practice. Before January 1, Medicare reimbursed direct billing from a CNM at only 65% of the Medicare Physician Fee Schedule. Now, a CNM is paid the same as a physician when she (he) bills under her own number.
In the past, some practices billed for the services of a CNM under “incident to” rules, to capture the physician payment—but this also meant that the CNM could not see a new patient. Under the change I’m describing, all CNMs can bill Medicare directly; see new patients; and be paid the same as the physician is paid. In addition, CNMs are no longer required to be supervised by a physician when they perform diagnostic tests that fall under the scope of their practice.
ANNUAL WELLNESS VISIT
The Affordable Care Act extended preventive coverage to Medicare beneficiaries in the form of an annual wellness visit. The two new codes here have been valued based on a level 4-problem new and established E/M service:
G0438 Annual wellness visit, including personalized prevention plan services, first visit
G0439 Annual wellness visit, including personalized prevention plan services, subsequent visit
Payment for the initial visit is made only beginning the second year the patient is eligible for Medicare Part B—during the first year of coverage, only the Initial Preventive Physical Examination (IPPE) (the “Welcome to Medicare”) exam will be covered.
CMS has stated that only one physician will be paid for the initial visit; when the patient returns to the same or a new physician in the third year, only a subsequent visit will be paid. It is, therefore, important that this information be conveyed to any new physician who sees the patient.
The annual codes can be billed in addition to any other preventive service, such as G0101 or Q0091; no modifier is needed for this combination. Medicare has waived both the copayment and the deductible for the annual wellness visit, as well as all Medicare-covered preventive services that have been recommended with a grade of “A” (“strongly recommends”) or “B” (“recommends”) by the US Preventive Services Task Force.
The annual wellness visit requires seven elements at a minimum (i.e., you may document and perform more elements than this, but not fewer):
- Establish or update the patient’s medical and family history
- List her current medical providers and suppliers and all prescribed medications
- Record measurements of height, weight, body mass index (initial visit only), blood pressure, and other routine measurements
- Detect any cognitive impairment
- Establish or update a screening schedule for the next 5 to 10 years, including screenings appropriate for the general population, and any additional screenings that may be appropriate because of her particular risk factors
- Review the patient’s 1) potential (i.e., risk factors) for depression, based on use of an appropriate screening instrument, and 2) functional ability and level of safety based on direct observation or screening questions
- Furnish 1) personalized health advice and 2) refer her appropriately to health education or preventive services.
CMS has also indicated that, although they will pay for a problem E/M service and the annual wellness visit on the same date of service with a modifier -25 added to the E/M service, they expect this type of billing to be rare—because of the nature of the wellness visit, which is time-intensive. They also expect that, given these requirements, the patient will not be billed additionally for a noncovered preventive service.
We want to hear from you! Tell us what you think.
The Current Procedural Terminology (CPT) code set for 2011 includes several changes of interest to ObGyns. These include 1) guideline clarifications regarding wound debridement and obstetric care codes; 2) new codes for subsequent observation care; micro-remodeling of the bladder neck; insertion of a vaginal after-loading device; and 3) a lab code for detecting amniotic fluid in cervicovaginal secretions (using the AmniSure kit).
There is also a new code for vaccine counseling that will have an impact on you if your practice offers the human papillomavirus (HPV) vaccine to patients younger than 19 years.
There are changes to Medicare this year that you should take note of if you care for these patients, particularly in the area of preventive visit billing.
CPT and Medicare changes both took effect on January 1. The Health Insurance Portability and Accountability Act (HIPAA) requires that insurers accepted the new codes on that date.
Changes to the CPT code set
OBSERVATION CARE
One of the biggest headaches for medical practices has been standardized coding and billing for observation care that lasts more than 1 day. In the past, payers accepted a problem E/M for Day 2 of observation care, or instructed practices to code an unlisted E/M service. Now, you may report all care rendered in the observation setting with the addition of three new codes for subsequent care:
99244 Subsequent observation care, per day, for the evaluation and management of a patient, which requires at least 2 of these 3 key components: problem focused interval history, problem focused examination; medical decision making that is straightforward or of low complexity. Counseling and/or coordination of care with other providers or agencies are provided consistent with the nature of the problem(s) and the patient’s and/or family’s needs. Usually, the patient is stable, recovering, or improving. Physicians typically spend 15 minutes at the bedside and on the patient’s hospital floor or unit.
99225 Subsequent observation care, per day, for the evaluation and management of a patient, which requires at least 2 of these 3 key components: an expanded problem focused interval history; an expanded problem focused examination; medical decision making of moderate complexity. Counseling and/or coordination of care with other providers or agencies are provided consistent with the nature of the problem(s) and the patient’s and/or family’s needs. Usually, the patient is responding inadequately to therapy or has developed a minor complication. Physicians typically spend 25 minutes at the bedside and on the patient’s hospital floor or unit.
99226 Subsequent observation care, per day, for the evaluation and management of a patient, which requires at least 2 of these 3 key components: a detailed interval history; a detailed examination; medical decision making of high complexity. Counseling and/or coordination of care with other providers or agencies are provided consistent with the nature of the problem(s) and the patient’s and/or family’s needs. Usually, the patient is unstable or has developed a significant complication or a significant new problem. Physicians typically spend 35 minutes at the bedside and on the patient’s hospital floor or unit.
Note that each of these codes 1) “suggests” the status of the patient for each level of billing, and 2) includes a typical time. This means that, unlike the observation care admission codes or the observation admission/same-day discharge codes, time that is spent with the patient, or on the unit, may be used to select the code—if you document 1) the requirement that more than 50% of the typical time was spent on counseling or coordination of care, or both, and 2) a detailed description of this activity.
Codes for wound debridement were given a facelift with the addition of a new guideline that addresses both surgical and medical debridement. The surgical debridement codes, (11042–11047) are now reported on the basis of the depth of tissue removed and the surface area of the wound. This means that codes 11040 and 11041 were deleted to make room for new and revised codes.
This change will mean that, when you report these codes, you will need to document more information to bill. It’s also understood that coding separately for debridement of dermis or epidermis at the same time you code for debriding underlying structures would be inappropriate.
CPT has also indicated that active wound management codes 97597 and 97598 can now be reported by physicians or nonphysician providers as long as the provider has direct (one-on-one) contact. These codes should be reported for skin-surface debridement only.
The new and revised codes (some of which have been published in CPT in nonsequential order) are:
11042 Debridement, subcutaneous tissue (includes epidermis and dermis, if performed); first 20 sq cm or less
+11045 (new add-on code reported with 11042 only) each additional 20 sq cm or part thereof
11043 Debridement, muscle and/or facia (includes epidermis, dermis, and subcutaneous tissue, if performed); first 20 sq cm or less
+11046 (new add-on code reported with 11043 only) each additional 20 sq cm or part thereof
11044 Debridement, bone (includes epidermis, dermis, subcutaneous tissue, muscle and/or fascia, if performed); first 20 sq cm or less
+11047 (new add-on code reported with 11044 only) each additional 20 sq cm or part thereof
97597 Debridement (e.g., high pressure waterjet with/without suction, sharp selective debridement with scissors, scalpel and forceps), open wound, (e.g., fibrin, devitalized epidermis and/or dermis, exudate, debris, biofilm), including topical application(s), wound assessment, use of a whirlpool, when performed and instruction(s) for ongoing care, per session, total wound(s) surface area; first 20 sq cm or less
+95798 (add-on code reported with 97597 only) Each additional 20 sq cm, or part thereof.
TRANSURETHRAL RADIOFREQUENCY
Category III code 0193T, which described transurethral radiofrequency micro-remodeling for stress urinary incontinence, has been deleted and converted to a Category I CPT code, 53860 (Transurethral radiofrequency micro-remodeling of the female bladder neck and proximal urethra for stress urinary incontinence). The procedure includes a periurethral block and flushing the bladder with a lidocaine slurry, and can be performed in the office.
In all, the procedure requires nine treatment cycles during the session, but the code is billed only once. Catheterization and measurement of a voiding sample after the procedure are included in the code.
AFTERLOADING DEVICES FOR CLINICAL BRACHYTHERAPY
CPT revised—slightly—existing code 57155, and added code 57156 (Insertion of a vaginal radiation afterloading apparatus for clinical brachytherapy).
- Code 57155 was revised to clarify that only a single tandem is inserted into the uterus. There had been confusion earlier in this regard.
- The new code describes a procedure that may also include dilation of the vaginal canal to remove postradiation adhesions. That procedure also involves 1) placement of bladder and rectal catheters and 2) radiographic imaging to confirm placement, which are not coded separately.
CLARIFICATION OF OBSTETRIC GUIDELINES
Been having problems with payers and their interpretation of the delivery only, postpartum only, and delivery with postpartum care codes? CPT has, at last, clarified what you can, and cannot, bill in those circumstances. (Keep in mind, however, that you may not unbundle these procedures if more extensive care is provided: Most payers want you to bill the global OB care code that includes antepartum, intrapartum, and postpartum care.)
In some cases (such as Medicaid), the payer stipulates that only the physician who actually performed the delivery may bill for it, even if the delivering physician is covering for, or is a member of, the same group practice as the primary attending of record. The “delivery-only” codes should be reported when 1) an unaffiliated physician has delivered the baby but will not be providing any outpatient postpartum care or 2) the payer has specified this method of billing for the covering or affiliated provider.
CPT has clarified that delivery-only codes (59409, 59514, or 59612, 59620) include admission to the hospital, the admission history and physical exam, uncomplicated labor and delivery (including delivery of the placenta, or use of forceps or vacuum extraction). These codes do not include inpatient rounding or discharge day care after delivery (and, of course, include no outpatient postpartum care). When, as the delivering physician, you also provide inpatient postdelivery care, therefore, you may additionally bill subsequent hospital care codes and discharge day management codes (99231-99233, 99238-99239).
If the unaffiliated physician performs the delivery and also intends on providing outpatient postpartum care, the CPT codes for delivery with postpartum are to be reported (59410, 59515, 59614, 59622). In addition to the delivery, these codes include all inpatient and outpatient postpartum care. And finally, for those physicians who are only providing outpatient postpartum care, the code 59430, Postpartum care only, should be reported.
PLACENTAL ALPHA MICROGLOBULIN-1
A new code, 84112 (Placental alpha microglobulin-1 [PAMG-11], cervicovaginal secretion, qualitative), has been added to allow the clinical laboratory to bill for this immunoassay that detects amniotic fluid in the secretions. Physician work involves collection of the specimen but, under CPT rules, collection is included as part of any E/M service.
Note: An existing code for this test that is used by Blue Cross/Blue Shield payers (S3628) remains valid in 2011.
HPV VACCINE COUNSELING
Before January 1, 2011, if you counseled a patient about the HPV vaccine, you could report preventive counseling codes, such as 99401–99404, in addition to the vaccine administration code, 90471 (Immunization administration, 1 vaccine). Now, however, you have a new code for counseling and vaccine administration for a patient who is younger than 19 years—the age group most likely to be counseled about this vaccine. When you see, and counsel, such a patient before administering the vaccine, on the same date of service, code 90460 (Immunization administration through 18 years of age via any route of administration, with counseling by physician or other qualified health care profession; first vaccine/toxoid component), and 90649 for the quadrivalent or 90650 for the bivalent HPV vaccine.
If your patient is 19 years or older and requires counseling, continue to bill 99401– 99404 for counseling, with 90471 for immunization and 90649 or 90650 for the vaccine. Keep in mind: Whether you report 90460 or the 9940X codes, you are required to document the content of the counseling. Codes 9940X also require documentation of the duration of counseling.
INFLUENZA VACCINE
New codes have been established for the flu vaccine, but you won’t be using them: They are intended to address future pandemic strains of influenza. This year’s vaccine contains the H1N1 strain, but is coded as the normal seasonal flu vaccine, based on the type given:
90656 (preservative-free)
90658 (split virus)
90660 (intranasal)
90662 (enhanced vaccine for patients older than 65 years).
Changes to Medicare billing
Some of the coding and billing changes this year that have an impact on ObGyn practice come from the Centers of Medicare and Medicaid Services (CMS) and the Affordable Care Act.
TIMELY FILING
The Affordable Care Act calls for a reduction in the maximum time period for submission of Medicare fee-for-service claims. Before January 1, a provider had 15 to 27 months to submit first-time claims to Medicare. Now, these claims must be filed within a calendar year of the date of service. Exceptions can be made for retroactive entitlement or in situations in which there is a secondary payer.
PAYMENTS TO CERTIFIED NURSE MIDWIVES
Next, more good news—if you employ a certified nurse midwife (CNM) in your practice. Before January 1, Medicare reimbursed direct billing from a CNM at only 65% of the Medicare Physician Fee Schedule. Now, a CNM is paid the same as a physician when she (he) bills under her own number.
In the past, some practices billed for the services of a CNM under “incident to” rules, to capture the physician payment—but this also meant that the CNM could not see a new patient. Under the change I’m describing, all CNMs can bill Medicare directly; see new patients; and be paid the same as the physician is paid. In addition, CNMs are no longer required to be supervised by a physician when they perform diagnostic tests that fall under the scope of their practice.
ANNUAL WELLNESS VISIT
The Affordable Care Act extended preventive coverage to Medicare beneficiaries in the form of an annual wellness visit. The two new codes here have been valued based on a level 4-problem new and established E/M service:
G0438 Annual wellness visit, including personalized prevention plan services, first visit
G0439 Annual wellness visit, including personalized prevention plan services, subsequent visit
Payment for the initial visit is made only beginning the second year the patient is eligible for Medicare Part B—during the first year of coverage, only the Initial Preventive Physical Examination (IPPE) (the “Welcome to Medicare”) exam will be covered.
CMS has stated that only one physician will be paid for the initial visit; when the patient returns to the same or a new physician in the third year, only a subsequent visit will be paid. It is, therefore, important that this information be conveyed to any new physician who sees the patient.
The annual codes can be billed in addition to any other preventive service, such as G0101 or Q0091; no modifier is needed for this combination. Medicare has waived both the copayment and the deductible for the annual wellness visit, as well as all Medicare-covered preventive services that have been recommended with a grade of “A” (“strongly recommends”) or “B” (“recommends”) by the US Preventive Services Task Force.
The annual wellness visit requires seven elements at a minimum (i.e., you may document and perform more elements than this, but not fewer):
- Establish or update the patient’s medical and family history
- List her current medical providers and suppliers and all prescribed medications
- Record measurements of height, weight, body mass index (initial visit only), blood pressure, and other routine measurements
- Detect any cognitive impairment
- Establish or update a screening schedule for the next 5 to 10 years, including screenings appropriate for the general population, and any additional screenings that may be appropriate because of her particular risk factors
- Review the patient’s 1) potential (i.e., risk factors) for depression, based on use of an appropriate screening instrument, and 2) functional ability and level of safety based on direct observation or screening questions
- Furnish 1) personalized health advice and 2) refer her appropriately to health education or preventive services.
CMS has also indicated that, although they will pay for a problem E/M service and the annual wellness visit on the same date of service with a modifier -25 added to the E/M service, they expect this type of billing to be rare—because of the nature of the wellness visit, which is time-intensive. They also expect that, given these requirements, the patient will not be billed additionally for a noncovered preventive service.
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IN THIS ARTICLE
Would a colonoscopy have made a difference? ... Suicide blamed on failure to diagnose bipolar disorder
Would a colonoscopy have made a difference?
ABDOMINAL PAIN, BURNING AND CRAMPING, and inability to eat led a 31-year-old man to visit his primary care physician. A nurse practitioner (NP) examined the man, prescribed ranitidine, and gave him an appointment for a complete physical the following month.
The patient’s history, as provided during the physical exam, included tobacco chewing, high coffee intake, and occasional abdominal pain and increased stools. He said that his mother had been diagnosed with colon cancer at 54 years of age. Neither a rectal exam nor colonoscopy was performed.
The NP substituted pantoprazole for ranitidine and ordered an upper gastrointestinal series with contrast to rule out gastritis or an ulcer. The results were negative. They were given to the primary care physician, who never saw the patient or reviewed his chart.
A month later, the patient saw a nurse for continued problems eating, despite symptom relief on pantoprazole. The nurse stuck with a diagnosis of gastritis and told the patient to follow up in 6 months and to call if problems arose.
Four months later, the patient returned complaining of worsening stomach cramps and burning. The NP changed his medication to lansoprazole and set up an appointment in 3 months with a gastroenterologist.
The patient returned a month afterward reporting increasing pain and loose stools. The GI consult was moved to an earlier date after discussion with the primary care physician, but the patient went to an emergency room before the scheduled consultation.
An abdominal computed tomography scan and colonoscopy revealed near obstruction of the right side of the colon by a stage IV tumor and metastasis to the peritoneum and lymph nodes. The patient underwent immediate surgery, followed by chemotherapy, more surgery, and a cingulotomy for pain relief. He died about 2 years later.
PLAINTIFF’S CLAIM The NP should have performed a rectal exam, obtained stool for occult blood tests, or ordered a colonoscopy. The patient’s chances of survival would have been better if he’d been diagnosed and treated earlier.
THE DEFENSE The patient didn’t need a colonoscopy; his tobacco chewing and excessive coffee drinking explained his eating difficulties. The NP was properly supervised and there was no independent duty to review individual patient charts and sign off on them regularly. The patient was already at stage IV when he was seen initially; nothing could have changed the treatment or outcome.
VERDICT $4.65 million Massachusetts verdict.
COMMENT Regardless of the medical facts of this case, supervision of staff and other health professionals is tricky. Clear job descriptions, protocols for care, and expectations for consultation will help avoid legal pitfalls.
Suicide blamed on failure to diagnose bipolar disorder
A 29-YEAR-OLD WOMAN spent about 6 months under the care of a psychiatrist, during which time she was diagnosed with severe depression. The psychiatrist prescribed a series of selective serotonin reuptake inhibitors (SSRIs). The patient took the medications as prescribed but eventually committed suicide.
PLAINTIFF’S CLAIM The psychiatrist misdiagnosed the patient; the patient’s depression was one symptom of bipolar disorder. The US Food and Drug Administration has warned that SSRIs increase the risk of suicide in patients with bipolar disorder.
THE DEFENSE The last time the psychiatrist saw the patient was more than 30 days before her death; the diagnosis of depression was correct.
VERDICT $175,000 Michigan settlement.
COMMENT Every patient with depressive features should be screened for bipolar disorder. As this case illustrates, the medical and legal consequences can be profound.
Would a colonoscopy have made a difference?
ABDOMINAL PAIN, BURNING AND CRAMPING, and inability to eat led a 31-year-old man to visit his primary care physician. A nurse practitioner (NP) examined the man, prescribed ranitidine, and gave him an appointment for a complete physical the following month.
The patient’s history, as provided during the physical exam, included tobacco chewing, high coffee intake, and occasional abdominal pain and increased stools. He said that his mother had been diagnosed with colon cancer at 54 years of age. Neither a rectal exam nor colonoscopy was performed.
The NP substituted pantoprazole for ranitidine and ordered an upper gastrointestinal series with contrast to rule out gastritis or an ulcer. The results were negative. They were given to the primary care physician, who never saw the patient or reviewed his chart.
A month later, the patient saw a nurse for continued problems eating, despite symptom relief on pantoprazole. The nurse stuck with a diagnosis of gastritis and told the patient to follow up in 6 months and to call if problems arose.
Four months later, the patient returned complaining of worsening stomach cramps and burning. The NP changed his medication to lansoprazole and set up an appointment in 3 months with a gastroenterologist.
The patient returned a month afterward reporting increasing pain and loose stools. The GI consult was moved to an earlier date after discussion with the primary care physician, but the patient went to an emergency room before the scheduled consultation.
An abdominal computed tomography scan and colonoscopy revealed near obstruction of the right side of the colon by a stage IV tumor and metastasis to the peritoneum and lymph nodes. The patient underwent immediate surgery, followed by chemotherapy, more surgery, and a cingulotomy for pain relief. He died about 2 years later.
PLAINTIFF’S CLAIM The NP should have performed a rectal exam, obtained stool for occult blood tests, or ordered a colonoscopy. The patient’s chances of survival would have been better if he’d been diagnosed and treated earlier.
THE DEFENSE The patient didn’t need a colonoscopy; his tobacco chewing and excessive coffee drinking explained his eating difficulties. The NP was properly supervised and there was no independent duty to review individual patient charts and sign off on them regularly. The patient was already at stage IV when he was seen initially; nothing could have changed the treatment or outcome.
VERDICT $4.65 million Massachusetts verdict.
COMMENT Regardless of the medical facts of this case, supervision of staff and other health professionals is tricky. Clear job descriptions, protocols for care, and expectations for consultation will help avoid legal pitfalls.
Suicide blamed on failure to diagnose bipolar disorder
A 29-YEAR-OLD WOMAN spent about 6 months under the care of a psychiatrist, during which time she was diagnosed with severe depression. The psychiatrist prescribed a series of selective serotonin reuptake inhibitors (SSRIs). The patient took the medications as prescribed but eventually committed suicide.
PLAINTIFF’S CLAIM The psychiatrist misdiagnosed the patient; the patient’s depression was one symptom of bipolar disorder. The US Food and Drug Administration has warned that SSRIs increase the risk of suicide in patients with bipolar disorder.
THE DEFENSE The last time the psychiatrist saw the patient was more than 30 days before her death; the diagnosis of depression was correct.
VERDICT $175,000 Michigan settlement.
COMMENT Every patient with depressive features should be screened for bipolar disorder. As this case illustrates, the medical and legal consequences can be profound.
Would a colonoscopy have made a difference?
ABDOMINAL PAIN, BURNING AND CRAMPING, and inability to eat led a 31-year-old man to visit his primary care physician. A nurse practitioner (NP) examined the man, prescribed ranitidine, and gave him an appointment for a complete physical the following month.
The patient’s history, as provided during the physical exam, included tobacco chewing, high coffee intake, and occasional abdominal pain and increased stools. He said that his mother had been diagnosed with colon cancer at 54 years of age. Neither a rectal exam nor colonoscopy was performed.
The NP substituted pantoprazole for ranitidine and ordered an upper gastrointestinal series with contrast to rule out gastritis or an ulcer. The results were negative. They were given to the primary care physician, who never saw the patient or reviewed his chart.
A month later, the patient saw a nurse for continued problems eating, despite symptom relief on pantoprazole. The nurse stuck with a diagnosis of gastritis and told the patient to follow up in 6 months and to call if problems arose.
Four months later, the patient returned complaining of worsening stomach cramps and burning. The NP changed his medication to lansoprazole and set up an appointment in 3 months with a gastroenterologist.
The patient returned a month afterward reporting increasing pain and loose stools. The GI consult was moved to an earlier date after discussion with the primary care physician, but the patient went to an emergency room before the scheduled consultation.
An abdominal computed tomography scan and colonoscopy revealed near obstruction of the right side of the colon by a stage IV tumor and metastasis to the peritoneum and lymph nodes. The patient underwent immediate surgery, followed by chemotherapy, more surgery, and a cingulotomy for pain relief. He died about 2 years later.
PLAINTIFF’S CLAIM The NP should have performed a rectal exam, obtained stool for occult blood tests, or ordered a colonoscopy. The patient’s chances of survival would have been better if he’d been diagnosed and treated earlier.
THE DEFENSE The patient didn’t need a colonoscopy; his tobacco chewing and excessive coffee drinking explained his eating difficulties. The NP was properly supervised and there was no independent duty to review individual patient charts and sign off on them regularly. The patient was already at stage IV when he was seen initially; nothing could have changed the treatment or outcome.
VERDICT $4.65 million Massachusetts verdict.
COMMENT Regardless of the medical facts of this case, supervision of staff and other health professionals is tricky. Clear job descriptions, protocols for care, and expectations for consultation will help avoid legal pitfalls.
Suicide blamed on failure to diagnose bipolar disorder
A 29-YEAR-OLD WOMAN spent about 6 months under the care of a psychiatrist, during which time she was diagnosed with severe depression. The psychiatrist prescribed a series of selective serotonin reuptake inhibitors (SSRIs). The patient took the medications as prescribed but eventually committed suicide.
PLAINTIFF’S CLAIM The psychiatrist misdiagnosed the patient; the patient’s depression was one symptom of bipolar disorder. The US Food and Drug Administration has warned that SSRIs increase the risk of suicide in patients with bipolar disorder.
THE DEFENSE The last time the psychiatrist saw the patient was more than 30 days before her death; the diagnosis of depression was correct.
VERDICT $175,000 Michigan settlement.
COMMENT Every patient with depressive features should be screened for bipolar disorder. As this case illustrates, the medical and legal consequences can be profound.
Traumatic brain injury: Pharmacotherapy options for cognitive deficits
Mr. A, age 45, presents to the psychiatry clinic complaining of “ADHD.” He says he is not able to sit through movies and often gets distracted while on his computer at work. He also is having problems in his relationship with his wife; she says having a conversation with him is difficult. He has seen a psychiatrist for depression, which is currently managed by his primary care physician (PCP), who prescribed sertraline, 100 mg/d. Mr. A feels that although his depression is now under control, the medication has had limited effect on improving his concentration.
With further discussion, Mr. A reveals that 6 months ago he was involved in a car accident and suffered a mild traumatic brain injury (TBI). He was hospitalized overnight and was encouraged to follow up with his PCP. During his only follow-up visit, Mr. A told his PCP that he was having difficulty concentrating since the accident. However, because Mr. A has a remote history of alcohol abuse, his physician was reluctant to give him additional medication and referred him to a psychiatrist.
TBI is increasingly common but often overlooked or not treated in the emergency room (ER). Each year at least 1.7 million people experience a TBI; 275,000 are hospitalized and 52,000 die.1 The true incidence likely is greater because patients who do not present to the ER or hospital are not included in most studies, and the often-subtle psychiatric sequelae may preclude patients from seeking mental health treatment.
Psychiatric disorders are common among those who sustain a TBI (Table 1).2 One prospective cohort study found that patients with mild TBI are 2.8 times more likely than other patients to develop a psychiatric disorder.3 Statistics regarding TBI and psychiatric illness often are limited because they rely on self-reports, chart review, or retrospective studies.4
TBI severity can be classified on the basis of Glasgow Coma Scale score and other factors (Table 2).5 The correlation between severity of injury and resulting psychiatric illness or post-concussive symptoms is unclear.6 There is evidence that cognitive defects are associated with decreased function. Cognitive dysfunction also has been associated with disability 10 years after moderate to severe TBI.7 The association between cognitive dysfunction and outcome is more strongly correlated with moderate to severe TBI; there is no clear association in mild TBI.7 Additionally, compared with patients with severe TBI, those with mild TBI were more likely to be employed. At all severity levels, function improves over time. Mild, moderate, and severe TBI have a similar recovery curve.7
Table 1
Psychiatric symptoms: Common among TBI patients
| Psychiatric symptom | Incidence |
|---|---|
| Aggression | 30% |
| Anxiety | 10% to 70% |
| Apathy | 10% |
| Cognitive impairment | 25% to 70% |
| Depression | 25% to 50% |
| Mania | 1% to 10% |
| Psychosis | 3% to 8% |
| TBI: traumatic brain injury | |
| Source: Adapted from reference 2 | |
Table 2
Classifying severity of traumatic brain injury
| Severity | GCS score | LOC duration | PTA* |
|---|---|---|---|
| Mild | 13 to 15 | <30 minutes | <1 hour |
| Moderate | 9 to 12 | 1 to 24 hours | 1 to 24 hours |
| Severe | <8 | >24 hours | >24 hours |
| *Includes loss of memory immediately before or after the accident | |||
| GCS: Glasgow Coma Scale; LOC: loss of consciousness; PTA: posttraumatic amnesia | |||
| Source: Reference 5 | |||
Cognitive dysfunction and TBI
Cognitive dysfunction can be split into 3 categories:
- executive function
- memory
- processing speed.
The incidence of cognitive dysfunction after TBI is unclear. Several methods are used to quantify cognitive dysfunction in TBI patients; it is widely regarded that the Mini-Mental State Exam is not adequate to screen for subtle cognitive deficits.6 However, there is no clear consensus on which tool should be used.5
Off-label pharmacotherapy
There are no FDA-approved medications for treating neuropsychiatric sequelae of TBI. Treatment should be symptom-based and employ the “start low, go slow” approach. Compared with patients without brain injury, TBI patients may experience increased adverse effects from psychotropics but may require standard doses. These patients also may have comorbidities such as seizure disorders, substance abuse, and depression that will affect treatment.2 Different areas of cognitive function respond to different medication classes. Suggested medications include stimulant and nonstimulant catecholaminergic agents and cholinesterase inhibitors (Table 3).8
Executive function responds to non-stimulant catecholaminergics. In a review, Writer and Schillerstrom5 found that TBI patients who received catecholaminergic augmentation showed improved function in 6 of 7 studies. In 2 randomized controlled trials (RCTs) and 4 nonrandomized, placebo-controlled trials, patients with mild to severe TBI showed improved executive function, attention, global cognitive function, memory, language, and/ or arousal with use of bromocriptine, pramipexole, carbidopa/levodopa, or amantadine.5 The greatest improvements were found in executive function. In 1 RCT, 10 patients with mild to severe TBI showed no functional improvement after 2 weeks of treatment.
Amantadine, 200 to 400 mg/d, has been shown to safely improve arousal and cognitive function in patients with moderate to severe TBI when started 3 days to 5 months after injury.9 Amantadine, 400 mg/d, also improves executive function measures without significant benefit in attention or memory in patients with mild to severe TBI 6 months post-injury.10
Memory responds to cholinesterase inhibitors. Memory deficits secondary to TBI affect immediate and delayed memory. The cholinesterase inhibitor donepezil is approved for treating Alzheimer’s disease (AD) in the United States and Canada, and research suggests memory deficits after TBI may be similar to those seen in AD.11 This includes deficits in long-term memory storage, which likely is associated with the cholinergic system.11 Post-mortem studies have found similarities in traumatically injured brains and those of AD patients.11
Three small prospective studies of done-pezil have shown improved memory and attention in TBI patients when cognition is the primary outcome, with 1 small negative open-label trial.7 In a study of 53 patients, Whelan et al12 found that donepezil improved patients’ intelligence quotient and clinician-based assessment of cognition over 2 years. Taverni et al13 found memory improvement in 2 TBI patients within 3 weeks of starting donepezil. These results suggest that donepezil may be used in acute and late phases of memory deficits following mild, moderate, or severe TBI.6 All studies titrated donepezil from 5 to 10 mg/d over several weeks. Dosing guidelines for donepezil in AD suggest 5 mg/d for 4 to 6 weeks, which may be increased to 10 mg/d if needed.8
Rivastigmine (3 to 6 mg/d) has been shown to be effective in mild TBI when started 1 year after injury and safe for 12 to 38 weeks of treatment.14,15 One retrospective cohort study of 111 patients with chronic TBI found no difference among donepezil, rivastigmine, or galantamine, with mean doses of 7.2 mg/d, 10 mg/d, and 2.3 mg/d, respectively.16 Sixty-one percent of patients showed improvement and the remainder had modest or no response. This study suggests that positive response on cognition may be similar among cholinesterase inhibitors. In case reports, physostigmine has offered some benefit17,18; however, cardiovascular and autonomic side effects restrict its use.11 Tacrine is associated with problematic gastrointestinal and hepatic side effects.11
Processing speed responds to stimulant catecholaminergics. Although the incidence of psychiatric illness is not correlated with TBI severity, evidence suggests that speed of processing mediates the relationship between injury severity and functional decline.19 Therefore, aggressively treating these deficits may help improve function.
Methylphenidate improves attention and processing speed after TBI. A review of 7 randomized trials and 2 nonrandomized trials indicated that patients with mild to severe, chronic TBI experienced significantly improved cognitive function after methylphenidate treatment.5 Willmott and Ponsford20 found significant enhancement in information processing speed within 2 weeks of methylphenidate treatment in 40 patients with moderate or severe TBI. Methylphenidate increased the rate of recovery and led to improvement in acute21 and post-acute phases.22 In addition, methylphenidate may improve processing speed even in the absence of significant changes in attention.23
The standard methylphenidate dose used in most studies, 0.3 mg/kg twice daily, is safe and effective. Dosing usually is started at 5 mg/d and titrated to symptomatic relief. Because methylphenidate does not lower the seizure threshold, it is safe for patients at high risk for seizure.24 Methylphenidate also significantly improves attention and speed of processing in pediatric head trauma.25,26
Dextroamphetamine also is used to treat speed of processing dysfunction after TBI, but is less studied than methylphenidate. Dextroamphetamine, 5 to 30 mg/d, was found to effectively treat attention problems that interfered with rehabilitation in patients with severe TBI.27
Table 3
Recommended treatments for mild TBI-related cognitive deficits
| Deficit | First-line medication | Side effects | Contraindications | Other treatments |
|---|---|---|---|---|
| Memory | Donepezil (5 to 10 mg/d) | Diarrhea, nausea, vomiting, muscle cramps, fatigue, anorexia | Hypersensitivity to donepezil or piperidine derivatives | Rivastigmine, galantamine, physostigmine, CDP-choline |
| Speed of processing | Methylphenidate (0.3 mg/kg twice daily) | Headache, insomnia, decreased appetite, nausea, vomiting, anxiety, irritability | Hypersensitivity to methylphenidate, glaucoma, history of Tourette syndrome or tics, use of MAOI within 14 days | Dextroamphetamine |
| Executive function | Amantadine (200 to 400 mg/d) | CNS depression, orthostatic hypotension, peripheral edema, agitation, nausea, anorexia | Hypersensitivity to amantadine | Bromocriptine, pramipexole, carbidopa/levodopa |
| CDP-choline: cytidinediphosphocholine; MAOI: monoamine oxidase inhibitor | ||||
| Source: Reference 8 | ||||
Nonpharmacologic treatments
In addition to pharmacotherapy, nonpharmacologic interventions also should be a mainstay of treatment. Compensatory training and cognitive exercise may improve patients’ cognitive deficits and return some sense of control. Individual and family psychotherapy, including cognitive-behavioral therapy, also may be beneficial.2 Review sources have identified the importance of validating patients’ symptoms and developing a goal-based treatment plan.6
CASE CONTINUED: Improvement with stimulants
Unlike many TBI patients who do not recognize the often-subtle psychiatric sequelae of their injury, Mr. A is aware of his difficulty concentrating, which is temporally linked with his accident. After exploring the association between Mr. A’s symptoms and his injury, his psychiatrist concludes that Mr. A’s cognitive deficits likely are associated with his TBI. Mr. A’s history of alcohol abuse raises concerns about prescribing stimulants. However, after assuring that Mr. A’s depression is well controlled and addressing his risk of substance abuse, his psychiatrist prescribes methylphenidate titrated to 30 mg/d. When he returns to the clinic several weeks later, Mr. A reports improved attention and functioning at work, and continues to follow up with the psychiatrist without requiring changes to his medication regimen.
Related Resource
- Konrad C, Geburek AJ, Rist F, et al. Long-term cognitive and emotional consequences of mild traumatic brain injury. Psychol Med. 2010;22:1-15.
Drug Brand Names
- Amantadine • Symadine, Symmetrel
- Bromocriptine • Parlodel
- Carbidopa/levodopa • Sinemet
- Dextroamphetamine • Dexedrine
- Donepezil • Aricept
- Galantamine • Razadyne
- Methylphenidate • Ritalin, Methylin, others
- Physostigmine • Antilirium
- Pramipexole • Mirapex
- Rivastigmine • Exelon
- Sertraline • Zoloft
- Tacrine • Cognex
Disclosures
Dr. Scher and Ms. Loomis report no financial relationship with any company whose products mentioned in this article or with the manufacturers of competing products.
Dr. McCarron is a speaker for Eli Lilly and Company.
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17. Goldberg E, Gerstman LJ, Mattis S, et al. Selective effects of cholinergic treatment on verbal memory in posttraumatic amnesia. J Clin Neuropsychol. 1982;4(3):219-234.
18. Eames P, Sutton A. Protracted post-traumatic confusional state treated with physostigmine. Brain Inj. 1995;9(7):729-734.
19. Rassovsky Y, Satz P, Alfano MS, et al. Functional outcome in TBI II: verbal memory and information processing speed mediators. J Clin Exp Neuropsychol. 2006;28(4):581-591.
20. Willmott C, Ponsford J. Efficacy of methylphenidate in the rehabilitation of attention following traumatic brain injury: a randomised, crossover, double blind, placebo controlled inpatient trial. J Neurol Neurosurg Psychiatry. 2009;80(5):552-557.
20. Kaelin DL, Cifu DX, Matthies B. Methylphenidate effect on attention deficit in the acutely brain-injured adult. Arch Phys Med Rehabil. 1996;77(1):6-9.
22. Whyte J, Hart T, Vaccaro M, et al. Effects of methylphenidate on attention deficits after traumatic brain injury: a multidimensional, randomized, controlled trial. Am J Phys Med Rehabil. 2004;83(6):401-420.
23. Whyte J, Hart T, Schuster K, et al. Effects of methylphenidate on attentional function after traumatic brain injury. A randomized, placebo-controlled trial. Am J Phys Med Rehabil. 1997;76(6):440-450.
24. Wroblewski BA, Leary JM, Phelan AM, et al. Methylphenidate and seizure frequency in brain injured patients with seizure disorders. J Clin Psychiatry. 1992;53(3):86-89.
25. Mahalick DM, Carmel PW, Greenberg JP, et al. Psychopharmacologic treatment of acquired attention disorders in children with brain injury. Pediatr Neurosurg. 1998;29(3):121-126.
26. Hornyak JE, Nelson VS, Hurvitz EA. The use of methylphenidate in paediatric traumatic brain injury. Pediatr Rehabil. 1997;1(1):15-17.
27. Hornstein A, Lennihan L, Seliger G. Amphetamine in recovery from brain injury. Brain Inj. 1996;10(2):145-148.
Mr. A, age 45, presents to the psychiatry clinic complaining of “ADHD.” He says he is not able to sit through movies and often gets distracted while on his computer at work. He also is having problems in his relationship with his wife; she says having a conversation with him is difficult. He has seen a psychiatrist for depression, which is currently managed by his primary care physician (PCP), who prescribed sertraline, 100 mg/d. Mr. A feels that although his depression is now under control, the medication has had limited effect on improving his concentration.
With further discussion, Mr. A reveals that 6 months ago he was involved in a car accident and suffered a mild traumatic brain injury (TBI). He was hospitalized overnight and was encouraged to follow up with his PCP. During his only follow-up visit, Mr. A told his PCP that he was having difficulty concentrating since the accident. However, because Mr. A has a remote history of alcohol abuse, his physician was reluctant to give him additional medication and referred him to a psychiatrist.
TBI is increasingly common but often overlooked or not treated in the emergency room (ER). Each year at least 1.7 million people experience a TBI; 275,000 are hospitalized and 52,000 die.1 The true incidence likely is greater because patients who do not present to the ER or hospital are not included in most studies, and the often-subtle psychiatric sequelae may preclude patients from seeking mental health treatment.
Psychiatric disorders are common among those who sustain a TBI (Table 1).2 One prospective cohort study found that patients with mild TBI are 2.8 times more likely than other patients to develop a psychiatric disorder.3 Statistics regarding TBI and psychiatric illness often are limited because they rely on self-reports, chart review, or retrospective studies.4
TBI severity can be classified on the basis of Glasgow Coma Scale score and other factors (Table 2).5 The correlation between severity of injury and resulting psychiatric illness or post-concussive symptoms is unclear.6 There is evidence that cognitive defects are associated with decreased function. Cognitive dysfunction also has been associated with disability 10 years after moderate to severe TBI.7 The association between cognitive dysfunction and outcome is more strongly correlated with moderate to severe TBI; there is no clear association in mild TBI.7 Additionally, compared with patients with severe TBI, those with mild TBI were more likely to be employed. At all severity levels, function improves over time. Mild, moderate, and severe TBI have a similar recovery curve.7
Table 1
Psychiatric symptoms: Common among TBI patients
| Psychiatric symptom | Incidence |
|---|---|
| Aggression | 30% |
| Anxiety | 10% to 70% |
| Apathy | 10% |
| Cognitive impairment | 25% to 70% |
| Depression | 25% to 50% |
| Mania | 1% to 10% |
| Psychosis | 3% to 8% |
| TBI: traumatic brain injury | |
| Source: Adapted from reference 2 | |
Table 2
Classifying severity of traumatic brain injury
| Severity | GCS score | LOC duration | PTA* |
|---|---|---|---|
| Mild | 13 to 15 | <30 minutes | <1 hour |
| Moderate | 9 to 12 | 1 to 24 hours | 1 to 24 hours |
| Severe | <8 | >24 hours | >24 hours |
| *Includes loss of memory immediately before or after the accident | |||
| GCS: Glasgow Coma Scale; LOC: loss of consciousness; PTA: posttraumatic amnesia | |||
| Source: Reference 5 | |||
Cognitive dysfunction and TBI
Cognitive dysfunction can be split into 3 categories:
- executive function
- memory
- processing speed.
The incidence of cognitive dysfunction after TBI is unclear. Several methods are used to quantify cognitive dysfunction in TBI patients; it is widely regarded that the Mini-Mental State Exam is not adequate to screen for subtle cognitive deficits.6 However, there is no clear consensus on which tool should be used.5
Off-label pharmacotherapy
There are no FDA-approved medications for treating neuropsychiatric sequelae of TBI. Treatment should be symptom-based and employ the “start low, go slow” approach. Compared with patients without brain injury, TBI patients may experience increased adverse effects from psychotropics but may require standard doses. These patients also may have comorbidities such as seizure disorders, substance abuse, and depression that will affect treatment.2 Different areas of cognitive function respond to different medication classes. Suggested medications include stimulant and nonstimulant catecholaminergic agents and cholinesterase inhibitors (Table 3).8
Executive function responds to non-stimulant catecholaminergics. In a review, Writer and Schillerstrom5 found that TBI patients who received catecholaminergic augmentation showed improved function in 6 of 7 studies. In 2 randomized controlled trials (RCTs) and 4 nonrandomized, placebo-controlled trials, patients with mild to severe TBI showed improved executive function, attention, global cognitive function, memory, language, and/ or arousal with use of bromocriptine, pramipexole, carbidopa/levodopa, or amantadine.5 The greatest improvements were found in executive function. In 1 RCT, 10 patients with mild to severe TBI showed no functional improvement after 2 weeks of treatment.
Amantadine, 200 to 400 mg/d, has been shown to safely improve arousal and cognitive function in patients with moderate to severe TBI when started 3 days to 5 months after injury.9 Amantadine, 400 mg/d, also improves executive function measures without significant benefit in attention or memory in patients with mild to severe TBI 6 months post-injury.10
Memory responds to cholinesterase inhibitors. Memory deficits secondary to TBI affect immediate and delayed memory. The cholinesterase inhibitor donepezil is approved for treating Alzheimer’s disease (AD) in the United States and Canada, and research suggests memory deficits after TBI may be similar to those seen in AD.11 This includes deficits in long-term memory storage, which likely is associated with the cholinergic system.11 Post-mortem studies have found similarities in traumatically injured brains and those of AD patients.11
Three small prospective studies of done-pezil have shown improved memory and attention in TBI patients when cognition is the primary outcome, with 1 small negative open-label trial.7 In a study of 53 patients, Whelan et al12 found that donepezil improved patients’ intelligence quotient and clinician-based assessment of cognition over 2 years. Taverni et al13 found memory improvement in 2 TBI patients within 3 weeks of starting donepezil. These results suggest that donepezil may be used in acute and late phases of memory deficits following mild, moderate, or severe TBI.6 All studies titrated donepezil from 5 to 10 mg/d over several weeks. Dosing guidelines for donepezil in AD suggest 5 mg/d for 4 to 6 weeks, which may be increased to 10 mg/d if needed.8
Rivastigmine (3 to 6 mg/d) has been shown to be effective in mild TBI when started 1 year after injury and safe for 12 to 38 weeks of treatment.14,15 One retrospective cohort study of 111 patients with chronic TBI found no difference among donepezil, rivastigmine, or galantamine, with mean doses of 7.2 mg/d, 10 mg/d, and 2.3 mg/d, respectively.16 Sixty-one percent of patients showed improvement and the remainder had modest or no response. This study suggests that positive response on cognition may be similar among cholinesterase inhibitors. In case reports, physostigmine has offered some benefit17,18; however, cardiovascular and autonomic side effects restrict its use.11 Tacrine is associated with problematic gastrointestinal and hepatic side effects.11
Processing speed responds to stimulant catecholaminergics. Although the incidence of psychiatric illness is not correlated with TBI severity, evidence suggests that speed of processing mediates the relationship between injury severity and functional decline.19 Therefore, aggressively treating these deficits may help improve function.
Methylphenidate improves attention and processing speed after TBI. A review of 7 randomized trials and 2 nonrandomized trials indicated that patients with mild to severe, chronic TBI experienced significantly improved cognitive function after methylphenidate treatment.5 Willmott and Ponsford20 found significant enhancement in information processing speed within 2 weeks of methylphenidate treatment in 40 patients with moderate or severe TBI. Methylphenidate increased the rate of recovery and led to improvement in acute21 and post-acute phases.22 In addition, methylphenidate may improve processing speed even in the absence of significant changes in attention.23
The standard methylphenidate dose used in most studies, 0.3 mg/kg twice daily, is safe and effective. Dosing usually is started at 5 mg/d and titrated to symptomatic relief. Because methylphenidate does not lower the seizure threshold, it is safe for patients at high risk for seizure.24 Methylphenidate also significantly improves attention and speed of processing in pediatric head trauma.25,26
Dextroamphetamine also is used to treat speed of processing dysfunction after TBI, but is less studied than methylphenidate. Dextroamphetamine, 5 to 30 mg/d, was found to effectively treat attention problems that interfered with rehabilitation in patients with severe TBI.27
Table 3
Recommended treatments for mild TBI-related cognitive deficits
| Deficit | First-line medication | Side effects | Contraindications | Other treatments |
|---|---|---|---|---|
| Memory | Donepezil (5 to 10 mg/d) | Diarrhea, nausea, vomiting, muscle cramps, fatigue, anorexia | Hypersensitivity to donepezil or piperidine derivatives | Rivastigmine, galantamine, physostigmine, CDP-choline |
| Speed of processing | Methylphenidate (0.3 mg/kg twice daily) | Headache, insomnia, decreased appetite, nausea, vomiting, anxiety, irritability | Hypersensitivity to methylphenidate, glaucoma, history of Tourette syndrome or tics, use of MAOI within 14 days | Dextroamphetamine |
| Executive function | Amantadine (200 to 400 mg/d) | CNS depression, orthostatic hypotension, peripheral edema, agitation, nausea, anorexia | Hypersensitivity to amantadine | Bromocriptine, pramipexole, carbidopa/levodopa |
| CDP-choline: cytidinediphosphocholine; MAOI: monoamine oxidase inhibitor | ||||
| Source: Reference 8 | ||||
Nonpharmacologic treatments
In addition to pharmacotherapy, nonpharmacologic interventions also should be a mainstay of treatment. Compensatory training and cognitive exercise may improve patients’ cognitive deficits and return some sense of control. Individual and family psychotherapy, including cognitive-behavioral therapy, also may be beneficial.2 Review sources have identified the importance of validating patients’ symptoms and developing a goal-based treatment plan.6
CASE CONTINUED: Improvement with stimulants
Unlike many TBI patients who do not recognize the often-subtle psychiatric sequelae of their injury, Mr. A is aware of his difficulty concentrating, which is temporally linked with his accident. After exploring the association between Mr. A’s symptoms and his injury, his psychiatrist concludes that Mr. A’s cognitive deficits likely are associated with his TBI. Mr. A’s history of alcohol abuse raises concerns about prescribing stimulants. However, after assuring that Mr. A’s depression is well controlled and addressing his risk of substance abuse, his psychiatrist prescribes methylphenidate titrated to 30 mg/d. When he returns to the clinic several weeks later, Mr. A reports improved attention and functioning at work, and continues to follow up with the psychiatrist without requiring changes to his medication regimen.
Related Resource
- Konrad C, Geburek AJ, Rist F, et al. Long-term cognitive and emotional consequences of mild traumatic brain injury. Psychol Med. 2010;22:1-15.
Drug Brand Names
- Amantadine • Symadine, Symmetrel
- Bromocriptine • Parlodel
- Carbidopa/levodopa • Sinemet
- Dextroamphetamine • Dexedrine
- Donepezil • Aricept
- Galantamine • Razadyne
- Methylphenidate • Ritalin, Methylin, others
- Physostigmine • Antilirium
- Pramipexole • Mirapex
- Rivastigmine • Exelon
- Sertraline • Zoloft
- Tacrine • Cognex
Disclosures
Dr. Scher and Ms. Loomis report no financial relationship with any company whose products mentioned in this article or with the manufacturers of competing products.
Dr. McCarron is a speaker for Eli Lilly and Company.
Mr. A, age 45, presents to the psychiatry clinic complaining of “ADHD.” He says he is not able to sit through movies and often gets distracted while on his computer at work. He also is having problems in his relationship with his wife; she says having a conversation with him is difficult. He has seen a psychiatrist for depression, which is currently managed by his primary care physician (PCP), who prescribed sertraline, 100 mg/d. Mr. A feels that although his depression is now under control, the medication has had limited effect on improving his concentration.
With further discussion, Mr. A reveals that 6 months ago he was involved in a car accident and suffered a mild traumatic brain injury (TBI). He was hospitalized overnight and was encouraged to follow up with his PCP. During his only follow-up visit, Mr. A told his PCP that he was having difficulty concentrating since the accident. However, because Mr. A has a remote history of alcohol abuse, his physician was reluctant to give him additional medication and referred him to a psychiatrist.
TBI is increasingly common but often overlooked or not treated in the emergency room (ER). Each year at least 1.7 million people experience a TBI; 275,000 are hospitalized and 52,000 die.1 The true incidence likely is greater because patients who do not present to the ER or hospital are not included in most studies, and the often-subtle psychiatric sequelae may preclude patients from seeking mental health treatment.
Psychiatric disorders are common among those who sustain a TBI (Table 1).2 One prospective cohort study found that patients with mild TBI are 2.8 times more likely than other patients to develop a psychiatric disorder.3 Statistics regarding TBI and psychiatric illness often are limited because they rely on self-reports, chart review, or retrospective studies.4
TBI severity can be classified on the basis of Glasgow Coma Scale score and other factors (Table 2).5 The correlation between severity of injury and resulting psychiatric illness or post-concussive symptoms is unclear.6 There is evidence that cognitive defects are associated with decreased function. Cognitive dysfunction also has been associated with disability 10 years after moderate to severe TBI.7 The association between cognitive dysfunction and outcome is more strongly correlated with moderate to severe TBI; there is no clear association in mild TBI.7 Additionally, compared with patients with severe TBI, those with mild TBI were more likely to be employed. At all severity levels, function improves over time. Mild, moderate, and severe TBI have a similar recovery curve.7
Table 1
Psychiatric symptoms: Common among TBI patients
| Psychiatric symptom | Incidence |
|---|---|
| Aggression | 30% |
| Anxiety | 10% to 70% |
| Apathy | 10% |
| Cognitive impairment | 25% to 70% |
| Depression | 25% to 50% |
| Mania | 1% to 10% |
| Psychosis | 3% to 8% |
| TBI: traumatic brain injury | |
| Source: Adapted from reference 2 | |
Table 2
Classifying severity of traumatic brain injury
| Severity | GCS score | LOC duration | PTA* |
|---|---|---|---|
| Mild | 13 to 15 | <30 minutes | <1 hour |
| Moderate | 9 to 12 | 1 to 24 hours | 1 to 24 hours |
| Severe | <8 | >24 hours | >24 hours |
| *Includes loss of memory immediately before or after the accident | |||
| GCS: Glasgow Coma Scale; LOC: loss of consciousness; PTA: posttraumatic amnesia | |||
| Source: Reference 5 | |||
Cognitive dysfunction and TBI
Cognitive dysfunction can be split into 3 categories:
- executive function
- memory
- processing speed.
The incidence of cognitive dysfunction after TBI is unclear. Several methods are used to quantify cognitive dysfunction in TBI patients; it is widely regarded that the Mini-Mental State Exam is not adequate to screen for subtle cognitive deficits.6 However, there is no clear consensus on which tool should be used.5
Off-label pharmacotherapy
There are no FDA-approved medications for treating neuropsychiatric sequelae of TBI. Treatment should be symptom-based and employ the “start low, go slow” approach. Compared with patients without brain injury, TBI patients may experience increased adverse effects from psychotropics but may require standard doses. These patients also may have comorbidities such as seizure disorders, substance abuse, and depression that will affect treatment.2 Different areas of cognitive function respond to different medication classes. Suggested medications include stimulant and nonstimulant catecholaminergic agents and cholinesterase inhibitors (Table 3).8
Executive function responds to non-stimulant catecholaminergics. In a review, Writer and Schillerstrom5 found that TBI patients who received catecholaminergic augmentation showed improved function in 6 of 7 studies. In 2 randomized controlled trials (RCTs) and 4 nonrandomized, placebo-controlled trials, patients with mild to severe TBI showed improved executive function, attention, global cognitive function, memory, language, and/ or arousal with use of bromocriptine, pramipexole, carbidopa/levodopa, or amantadine.5 The greatest improvements were found in executive function. In 1 RCT, 10 patients with mild to severe TBI showed no functional improvement after 2 weeks of treatment.
Amantadine, 200 to 400 mg/d, has been shown to safely improve arousal and cognitive function in patients with moderate to severe TBI when started 3 days to 5 months after injury.9 Amantadine, 400 mg/d, also improves executive function measures without significant benefit in attention or memory in patients with mild to severe TBI 6 months post-injury.10
Memory responds to cholinesterase inhibitors. Memory deficits secondary to TBI affect immediate and delayed memory. The cholinesterase inhibitor donepezil is approved for treating Alzheimer’s disease (AD) in the United States and Canada, and research suggests memory deficits after TBI may be similar to those seen in AD.11 This includes deficits in long-term memory storage, which likely is associated with the cholinergic system.11 Post-mortem studies have found similarities in traumatically injured brains and those of AD patients.11
Three small prospective studies of done-pezil have shown improved memory and attention in TBI patients when cognition is the primary outcome, with 1 small negative open-label trial.7 In a study of 53 patients, Whelan et al12 found that donepezil improved patients’ intelligence quotient and clinician-based assessment of cognition over 2 years. Taverni et al13 found memory improvement in 2 TBI patients within 3 weeks of starting donepezil. These results suggest that donepezil may be used in acute and late phases of memory deficits following mild, moderate, or severe TBI.6 All studies titrated donepezil from 5 to 10 mg/d over several weeks. Dosing guidelines for donepezil in AD suggest 5 mg/d for 4 to 6 weeks, which may be increased to 10 mg/d if needed.8
Rivastigmine (3 to 6 mg/d) has been shown to be effective in mild TBI when started 1 year after injury and safe for 12 to 38 weeks of treatment.14,15 One retrospective cohort study of 111 patients with chronic TBI found no difference among donepezil, rivastigmine, or galantamine, with mean doses of 7.2 mg/d, 10 mg/d, and 2.3 mg/d, respectively.16 Sixty-one percent of patients showed improvement and the remainder had modest or no response. This study suggests that positive response on cognition may be similar among cholinesterase inhibitors. In case reports, physostigmine has offered some benefit17,18; however, cardiovascular and autonomic side effects restrict its use.11 Tacrine is associated with problematic gastrointestinal and hepatic side effects.11
Processing speed responds to stimulant catecholaminergics. Although the incidence of psychiatric illness is not correlated with TBI severity, evidence suggests that speed of processing mediates the relationship between injury severity and functional decline.19 Therefore, aggressively treating these deficits may help improve function.
Methylphenidate improves attention and processing speed after TBI. A review of 7 randomized trials and 2 nonrandomized trials indicated that patients with mild to severe, chronic TBI experienced significantly improved cognitive function after methylphenidate treatment.5 Willmott and Ponsford20 found significant enhancement in information processing speed within 2 weeks of methylphenidate treatment in 40 patients with moderate or severe TBI. Methylphenidate increased the rate of recovery and led to improvement in acute21 and post-acute phases.22 In addition, methylphenidate may improve processing speed even in the absence of significant changes in attention.23
The standard methylphenidate dose used in most studies, 0.3 mg/kg twice daily, is safe and effective. Dosing usually is started at 5 mg/d and titrated to symptomatic relief. Because methylphenidate does not lower the seizure threshold, it is safe for patients at high risk for seizure.24 Methylphenidate also significantly improves attention and speed of processing in pediatric head trauma.25,26
Dextroamphetamine also is used to treat speed of processing dysfunction after TBI, but is less studied than methylphenidate. Dextroamphetamine, 5 to 30 mg/d, was found to effectively treat attention problems that interfered with rehabilitation in patients with severe TBI.27
Table 3
Recommended treatments for mild TBI-related cognitive deficits
| Deficit | First-line medication | Side effects | Contraindications | Other treatments |
|---|---|---|---|---|
| Memory | Donepezil (5 to 10 mg/d) | Diarrhea, nausea, vomiting, muscle cramps, fatigue, anorexia | Hypersensitivity to donepezil or piperidine derivatives | Rivastigmine, galantamine, physostigmine, CDP-choline |
| Speed of processing | Methylphenidate (0.3 mg/kg twice daily) | Headache, insomnia, decreased appetite, nausea, vomiting, anxiety, irritability | Hypersensitivity to methylphenidate, glaucoma, history of Tourette syndrome or tics, use of MAOI within 14 days | Dextroamphetamine |
| Executive function | Amantadine (200 to 400 mg/d) | CNS depression, orthostatic hypotension, peripheral edema, agitation, nausea, anorexia | Hypersensitivity to amantadine | Bromocriptine, pramipexole, carbidopa/levodopa |
| CDP-choline: cytidinediphosphocholine; MAOI: monoamine oxidase inhibitor | ||||
| Source: Reference 8 | ||||
Nonpharmacologic treatments
In addition to pharmacotherapy, nonpharmacologic interventions also should be a mainstay of treatment. Compensatory training and cognitive exercise may improve patients’ cognitive deficits and return some sense of control. Individual and family psychotherapy, including cognitive-behavioral therapy, also may be beneficial.2 Review sources have identified the importance of validating patients’ symptoms and developing a goal-based treatment plan.6
CASE CONTINUED: Improvement with stimulants
Unlike many TBI patients who do not recognize the often-subtle psychiatric sequelae of their injury, Mr. A is aware of his difficulty concentrating, which is temporally linked with his accident. After exploring the association between Mr. A’s symptoms and his injury, his psychiatrist concludes that Mr. A’s cognitive deficits likely are associated with his TBI. Mr. A’s history of alcohol abuse raises concerns about prescribing stimulants. However, after assuring that Mr. A’s depression is well controlled and addressing his risk of substance abuse, his psychiatrist prescribes methylphenidate titrated to 30 mg/d. When he returns to the clinic several weeks later, Mr. A reports improved attention and functioning at work, and continues to follow up with the psychiatrist without requiring changes to his medication regimen.
Related Resource
- Konrad C, Geburek AJ, Rist F, et al. Long-term cognitive and emotional consequences of mild traumatic brain injury. Psychol Med. 2010;22:1-15.
Drug Brand Names
- Amantadine • Symadine, Symmetrel
- Bromocriptine • Parlodel
- Carbidopa/levodopa • Sinemet
- Dextroamphetamine • Dexedrine
- Donepezil • Aricept
- Galantamine • Razadyne
- Methylphenidate • Ritalin, Methylin, others
- Physostigmine • Antilirium
- Pramipexole • Mirapex
- Rivastigmine • Exelon
- Sertraline • Zoloft
- Tacrine • Cognex
Disclosures
Dr. Scher and Ms. Loomis report no financial relationship with any company whose products mentioned in this article or with the manufacturers of competing products.
Dr. McCarron is a speaker for Eli Lilly and Company.
1. Faul M, Xu L, Wald MM, et al. Traumatic brain injury in the United States; emergency department visits, hospitalizations, and deaths, 2002-2006. Atlanta, GA: Centers for Disease Control and Prevention; 2010. Available at: http://www.cdc.gov/traumaticbraininjury/tbi_ed.html. Accessed December 1, 2010.
2. Vaishnavi S, Rao V, Fann JR. Neuropsychiatric problems after traumatic brain injury: unraveling the silent epidemic. Psychosomatics. 2009;50(3):198-205.
3. Fann JR, Burington B, Leonetti A, et al. Psychiatric illness following traumatic brain injury in an adult health maintenance organization population. Arch Gen Psychiatry. 2004;61(1):53-61.
4. Bryant RA, O’Donnell ML, Creamer M, et al. The psychiatric sequelae of traumatic injury. Am J Psychiatry. 2010;167(3):312-320.
5. Writer BW, Schillerstrom JE. Psychopharmacological treatment for cognitive impairment in survivors of traumatic brain injury: a critical review. J Neuropsychiatry Clin Neurosci. 2009;21(4):362-370.
6. Arciniegas DB, Anderson CA, Topkoff J, et al. Mild traumatic brain injury: a neuropsychiatric approach to diagnosis, evaluation, and treatment. Neuropsychiatr Dis Treat. 2005;1(4):311-327.
7. Sigurdardottir S, Andelic N, Roe C, et al. Cognitive recovery and predictors of functional outcome 1 year after traumatic brain injury. J Int Neuropsychol Soc. 2009;15(5):740-750.
8. Physicians’ desk reference 64th ed. Montvale, NJ: Thomson Reuters; 2010.
9. Sawyer E Mauro LS, Mauro LS, Ohlinger MJ. Amantadine enhancement of arousal and cognition after traumatic brain injury. Ann Pharmacother. 2008;42(2):247-252.
10. Kraus MF, Smith GS, Butters M, et al. Effects of the dopaminergic agent and NMDA receptor antagonist amantadine on cognitive function, cerebral glucose metabolism and D2 receptor availability in chronic traumatic brain injury: a study using positron emission tomography (PET). Brain Inj. 2005;19(7):471-479.
11. Griffin SL, van Reekum R, Masanic C. A review of cholinergic agents in the treatment of neurobehavioral deficits following traumatic brain injury. J Neuropsychiatry Clin Neurosci. 2003;15(1):17-26.
12. Whelan FJ, Walker MS, Schultz SK. Donepezil in the treatment of cognitive dysfunction associated with traumatic brain injury. Ann Clin Psychiatry. 2000;12(3):131-135.
13. Taverni JP, Seliger G, Lichtman SW. Donepezil medicated memory improvement in traumatic brain injury during post acute rehabilitation. Brain Inj. 1998;12(1):77-80.
14. Silver JM, McAllister TW, Arciniegas DB. Depression and cognitive complaints following mild traumatic brain injury. Am J Psychiatry. 2009;166(6):653-661.
15. Silver JM, Koumaras B, Chen M, et al. Effects of rivastigmine on cognitive function in patients with traumatic brain injury. Neurology. 2006;67(5):748-755.
16. Tenovuo O. Central acetylcholinesterase inhibitors in the treatment of chronic traumatic brain injury—clinical experience in 111 patients. Prog Neuropsychopharmacol Biol Psychiatry. 2005;29(1):61-67.
17. Goldberg E, Gerstman LJ, Mattis S, et al. Selective effects of cholinergic treatment on verbal memory in posttraumatic amnesia. J Clin Neuropsychol. 1982;4(3):219-234.
18. Eames P, Sutton A. Protracted post-traumatic confusional state treated with physostigmine. Brain Inj. 1995;9(7):729-734.
19. Rassovsky Y, Satz P, Alfano MS, et al. Functional outcome in TBI II: verbal memory and information processing speed mediators. J Clin Exp Neuropsychol. 2006;28(4):581-591.
20. Willmott C, Ponsford J. Efficacy of methylphenidate in the rehabilitation of attention following traumatic brain injury: a randomised, crossover, double blind, placebo controlled inpatient trial. J Neurol Neurosurg Psychiatry. 2009;80(5):552-557.
20. Kaelin DL, Cifu DX, Matthies B. Methylphenidate effect on attention deficit in the acutely brain-injured adult. Arch Phys Med Rehabil. 1996;77(1):6-9.
22. Whyte J, Hart T, Vaccaro M, et al. Effects of methylphenidate on attention deficits after traumatic brain injury: a multidimensional, randomized, controlled trial. Am J Phys Med Rehabil. 2004;83(6):401-420.
23. Whyte J, Hart T, Schuster K, et al. Effects of methylphenidate on attentional function after traumatic brain injury. A randomized, placebo-controlled trial. Am J Phys Med Rehabil. 1997;76(6):440-450.
24. Wroblewski BA, Leary JM, Phelan AM, et al. Methylphenidate and seizure frequency in brain injured patients with seizure disorders. J Clin Psychiatry. 1992;53(3):86-89.
25. Mahalick DM, Carmel PW, Greenberg JP, et al. Psychopharmacologic treatment of acquired attention disorders in children with brain injury. Pediatr Neurosurg. 1998;29(3):121-126.
26. Hornyak JE, Nelson VS, Hurvitz EA. The use of methylphenidate in paediatric traumatic brain injury. Pediatr Rehabil. 1997;1(1):15-17.
27. Hornstein A, Lennihan L, Seliger G. Amphetamine in recovery from brain injury. Brain Inj. 1996;10(2):145-148.
1. Faul M, Xu L, Wald MM, et al. Traumatic brain injury in the United States; emergency department visits, hospitalizations, and deaths, 2002-2006. Atlanta, GA: Centers for Disease Control and Prevention; 2010. Available at: http://www.cdc.gov/traumaticbraininjury/tbi_ed.html. Accessed December 1, 2010.
2. Vaishnavi S, Rao V, Fann JR. Neuropsychiatric problems after traumatic brain injury: unraveling the silent epidemic. Psychosomatics. 2009;50(3):198-205.
3. Fann JR, Burington B, Leonetti A, et al. Psychiatric illness following traumatic brain injury in an adult health maintenance organization population. Arch Gen Psychiatry. 2004;61(1):53-61.
4. Bryant RA, O’Donnell ML, Creamer M, et al. The psychiatric sequelae of traumatic injury. Am J Psychiatry. 2010;167(3):312-320.
5. Writer BW, Schillerstrom JE. Psychopharmacological treatment for cognitive impairment in survivors of traumatic brain injury: a critical review. J Neuropsychiatry Clin Neurosci. 2009;21(4):362-370.
6. Arciniegas DB, Anderson CA, Topkoff J, et al. Mild traumatic brain injury: a neuropsychiatric approach to diagnosis, evaluation, and treatment. Neuropsychiatr Dis Treat. 2005;1(4):311-327.
7. Sigurdardottir S, Andelic N, Roe C, et al. Cognitive recovery and predictors of functional outcome 1 year after traumatic brain injury. J Int Neuropsychol Soc. 2009;15(5):740-750.
8. Physicians’ desk reference 64th ed. Montvale, NJ: Thomson Reuters; 2010.
9. Sawyer E Mauro LS, Mauro LS, Ohlinger MJ. Amantadine enhancement of arousal and cognition after traumatic brain injury. Ann Pharmacother. 2008;42(2):247-252.
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