Sherry Boschert

SAN DIEGO – Significant increases in adiposity and insulin resistance quickly became apparent in a 12-week study of low-dose antipsychotics to treat mainly nonpsychotic disorders in 144 children.

Newer, “atypical” antipsychotics increasingly are being used to treat mood and disruptive behavior disorders in children, Dr. John W. Newcomer said at the annual meeting of the American Diabetes Association.

“It’s a topic of increasing concern in a number of state Medicaid” systems, he said. Concerns have been generated in part by data showing premature mortality in people with mental disorders that’s related primarily to cardiovascular disease but also to cardiometabolic risk.

Children in the open-label study were randomized to flexibly dosed treatment with risperidone, olanzapine, or aripiprazole. It was their first use of antipsychotics.

These were “very low doses,” he emphasized. “These are not doses that would be used to treat a psychotic disorder,” said Dr. Newcomer, who led the study while at Washington University, St. Louis. He now is a professor of psychiatry and behavioral sciences at the University of Miami.

The 5-year Metabolic Effects of Antipsychotics in Children (MEAC) study targeted symptoms of aggression and irritability in patients aged 6-18 years. “Typically, they had been suspended from school,” he said.

The main primary diagnosis was treatment-refractory attention deficit hyperactivity disorder (ADHD) in 57% of patients. “This is what clinicians are using these drugs for in this type of public-sector population – kids who fail two or three courses of stimulants who then are looking for some other treatment.”

Other main diagnoses included oppositional defiant disorder in 22%, pervasive developmental disorder in 6%, bipolar disorder in 4%, and major depression in 3%. Smaller proportions of patients were diagnosed with other mood disorders, Asperger’s syndrome, autism, obsessive-compulsive disorder, or Tourette’s syndrome.

Mean doses were 1 mg/day in the 49 patients on risperidone, 6.3 mg/day in the 46 patients on olanzapine, and 6 mg/day in the 49 patients on aripiprazole. Approximately half of patients also were on stable doses of stimulants for ADHD.

Total body percentage of adiposity increased 2.4% after 12 weeks on antipsychotics – slightly less than a standard deviation, and a highly significant change, Dr. Newcomer and his associates reported. Mean total fat increased 2.3 kg, they added.

The percentage body fat increased the most in the youngest children. Greater changes were seen with olanzapine than with risperidone or aripiprazole. About a fourth of patients on risperidone or aripiprazole showed little change in body fat, but three-quarters on those drugs and nearly all patients on olanzapine showed increases.

Whole-body insulin sensitivity decreased approximately from 8 mg/kg per minute to 7 mg/kg per minute, a significant reduction. Olanzapine produced the greatest reduction in whole-body insulin sensitivity.

Importantly, scores for irritability and aggression improved in all groups, he added.

“I’m not a child psychiatrist. I was not terribly sympathetic to this at the beginning” of clinicians’ use of antipsychotics for these indications, said Dr. Newcomer, who chaired the Drug Utilization Review Board for Missouri Medicaid for 14 years. “But I was educated by the psychiatric outcome. There was really profound psychiatric symptom improvement, with kids going back to school and [behaving differently],” he said. The psychiatric response was similar among treatment groups in the study.

As early as 6 weeks after starting therapy, significant changes could be seen on adiposity. Children with the biggest changes in body fat showed effects within the first month of treatment.

Height, weight, waist circumference, body mass index, and BMI percentile were measured at all visits. At baseline and at 12 weeks, investigators performed dual-energy x-ray absorptiometry (DEXA) scans and MRI to assess changes in adiposity, hyperinsulinemic euglycemic clamp with isotopomers to assess changes in insulin sensitivity, plasma sampling (such as oral glucose tolerance test or measuring fasting glucose and lipids), ECG, and psychiatric ratings. At the 6-week follow-up, patients underwent DEXA, oral glucose tolerance testing, and lab measures of fasting status.

A previous nonrandomized study of 272 antipsychotic-naive children and adolescents reported weight gains of 4-8 kg and increases in BMI percentile for patients taking any of four atypical antipsychotics for a median of 11 weeks, compared with a control group (JAMA 2009;302:1811-2).

The study’s design raised concern that the effects could be larger than reported, however, because overweight or obese children were assigned to drugs considered to have the lowest risk for weight gain, Dr. Newcomer said.

In a post-hoc analysis, Dr. Newcomer showed that at the start of the current study, the children had similar rates of overweight or obesity as did children in the general population, but rates were higher in the cohort by the end of the study. The rate of overweight or obese children in the cohort increased from about 33% to 48%.

“I’m personally skeptical about the idea that it’s the psychiatric disorders themselves that are the metabolic challenge, rather than the treatment being the primary effect,” he said.

Medicaid data suggest that 43% of prescriptions for atypical antipsychotics are for indications that are not backed by evidence justifying use, he said. Visits to U.S. physicians that included prescriptions for antipsychotics to patients aged 20 years or younger more than doubled between 1997 and 2002, to a rate greater than 1,400 per 100,000 visits, a separate study reported (Arch Gen. Psych. 2006;63-681).

The National Institutes of Health funded the study. Dr. Newcomer has been a consultant for or received grants from Janssen Pharmaceuticals Inc., Pfizer Inc. , AstraZeneca, Bristol-Myers Squibb, Otsuka Pharmaceutical Co. Ltd., Schering/Merck, Vivus Inc., Obecure Ltd., Biovail Corp., Lundbeck A/S, Sanofi, and Dainippon Sumitomo Pharma Co. Ltd./Sepracor Inc.

SAN DIEGO – Significant increases in adiposity and insulin resistance quickly became apparent in a 12-week study of low-dose antipsychotics to treat mainly nonpsychotic disorders in 144 children.

Newer, “atypical” antipsychotics increasingly are being used to treat mood and disruptive behavior disorders in children, Dr. John W. Newcomer said at the annual meeting of the American Diabetes Association.

“It’s a topic of increasing concern in a number of state Medicaid” systems, he said. Concerns have been generated in part by data showing premature mortality in people with mental disorders that’s related primarily to cardiovascular disease but also to cardiometabolic risk.

Children in the open-label study were randomized to flexibly dosed treatment with risperidone, olanzapine, or aripiprazole. It was their first use of antipsychotics.

These were “very low doses,” he emphasized. “These are not doses that would be used to treat a psychotic disorder,” said Dr. Newcomer, who led the study while at Washington University, St. Louis. He now is a professor of psychiatry and behavioral sciences at the University of Miami.

The 5-year Metabolic Effects of Antipsychotics in Children (MEAC) study targeted symptoms of aggression and irritability in patients aged 6-18 years. “Typically, they had been suspended from school,” he said.

The main primary diagnosis was treatment-refractory attention deficit hyperactivity disorder (ADHD) in 57% of patients. “This is what clinicians are using these drugs for in this type of public-sector population – kids who fail two or three courses of stimulants who then are looking for some other treatment.”

Other main diagnoses included oppositional defiant disorder in 22%, pervasive developmental disorder in 6%, bipolar disorder in 4%, and major depression in 3%. Smaller proportions of patients were diagnosed with other mood disorders, Asperger’s syndrome, autism, obsessive-compulsive disorder, or Tourette’s syndrome.

Mean doses were 1 mg/day in the 49 patients on risperidone, 6.3 mg/day in the 46 patients on olanzapine, and 6 mg/day in the 49 patients on aripiprazole. Approximately half of patients also were on stable doses of stimulants for ADHD.

Total body percentage of adiposity increased 2.4% after 12 weeks on antipsychotics – slightly less than a standard deviation, and a highly significant change, Dr. Newcomer and his associates reported. Mean total fat increased 2.3 kg, they added.

The percentage body fat increased the most in the youngest children. Greater changes were seen with olanzapine than with risperidone or aripiprazole. About a fourth of patients on risperidone or aripiprazole showed little change in body fat, but three-quarters on those drugs and nearly all patients on olanzapine showed increases.

Whole-body insulin sensitivity decreased approximately from 8 mg/kg per minute to 7 mg/kg per minute, a significant reduction. Olanzapine produced the greatest reduction in whole-body insulin sensitivity.

Importantly, scores for irritability and aggression improved in all groups, he added.

“I’m not a child psychiatrist. I was not terribly sympathetic to this at the beginning” of clinicians’ use of antipsychotics for these indications, said Dr. Newcomer, who chaired the Drug Utilization Review Board for Missouri Medicaid for 14 years. “But I was educated by the psychiatric outcome. There was really profound psychiatric symptom improvement, with kids going back to school and [behaving differently],” he said. The psychiatric response was similar among treatment groups in the study.

As early as 6 weeks after starting therapy, significant changes could be seen on adiposity. Children with the biggest changes in body fat showed effects within the first month of treatment.

Height, weight, waist circumference, body mass index, and BMI percentile were measured at all visits. At baseline and at 12 weeks, investigators performed dual-energy x-ray absorptiometry (DEXA) scans and MRI to assess changes in adiposity, hyperinsulinemic euglycemic clamp with isotopomers to assess changes in insulin sensitivity, plasma sampling (such as oral glucose tolerance test or measuring fasting glucose and lipids), ECG, and psychiatric ratings. At the 6-week follow-up, patients underwent DEXA, oral glucose tolerance testing, and lab measures of fasting status.

A previous nonrandomized study of 272 antipsychotic-naive children and adolescents reported weight gains of 4-8 kg and increases in BMI percentile for patients taking any of four atypical antipsychotics for a median of 11 weeks, compared with a control group (JAMA 2009;302:1811-2).

The study’s design raised concern that the effects could be larger than reported, however, because overweight or obese children were assigned to drugs considered to have the lowest risk for weight gain, Dr. Newcomer said.

In a post-hoc analysis, Dr. Newcomer showed that at the start of the current study, the children had similar rates of overweight or obesity as did children in the general population, but rates were higher in the cohort by the end of the study. The rate of overweight or obese children in the cohort increased from about 33% to 48%.

“I’m personally skeptical about the idea that it’s the psychiatric disorders themselves that are the metabolic challenge, rather than the treatment being the primary effect,” he said.

Medicaid data suggest that 43% of prescriptions for atypical antipsychotics are for indications that are not backed by evidence justifying use, he said. Visits to U.S. physicians that included prescriptions for antipsychotics to patients aged 20 years or younger more than doubled between 1997 and 2002, to a rate greater than 1,400 per 100,000 visits, a separate study reported (Arch Gen. Psych. 2006;63-681).

The National Institutes of Health funded the study. Dr. Newcomer has been a consultant for or received grants from Janssen Pharmaceuticals Inc., Pfizer Inc. , AstraZeneca, Bristol-Myers Squibb, Otsuka Pharmaceutical Co. Ltd., Schering/Merck, Vivus Inc., Obecure Ltd., Biovail Corp., Lundbeck A/S, Sanofi, and Dainippon Sumitomo Pharma Co. Ltd./Sepracor Inc.

SAN DIEGO – Significant increases in adiposity and insulin resistance quickly became apparent in a 12-week study of low-dose antipsychotics to treat mainly nonpsychotic disorders in 144 children.

Newer, “atypical” antipsychotics increasingly are being used to treat mood and disruptive behavior disorders in children, Dr. John W. Newcomer said at the annual meeting of the American Diabetes Association.

“It’s a topic of increasing concern in a number of state Medicaid” systems, he said. Concerns have been generated in part by data showing premature mortality in people with mental disorders that’s related primarily to cardiovascular disease but also to cardiometabolic risk.

Children in the open-label study were randomized to flexibly dosed treatment with risperidone, olanzapine, or aripiprazole. It was their first use of antipsychotics.

These were “very low doses,” he emphasized. “These are not doses that would be used to treat a psychotic disorder,” said Dr. Newcomer, who led the study while at Washington University, St. Louis. He now is a professor of psychiatry and behavioral sciences at the University of Miami.

The 5-year Metabolic Effects of Antipsychotics in Children (MEAC) study targeted symptoms of aggression and irritability in patients aged 6-18 years. “Typically, they had been suspended from school,” he said.

The main primary diagnosis was treatment-refractory attention deficit hyperactivity disorder (ADHD) in 57% of patients. “This is what clinicians are using these drugs for in this type of public-sector population – kids who fail two or three courses of stimulants who then are looking for some other treatment.”

Other main diagnoses included oppositional defiant disorder in 22%, pervasive developmental disorder in 6%, bipolar disorder in 4%, and major depression in 3%. Smaller proportions of patients were diagnosed with other mood disorders, Asperger’s syndrome, autism, obsessive-compulsive disorder, or Tourette’s syndrome.

Mean doses were 1 mg/day in the 49 patients on risperidone, 6.3 mg/day in the 46 patients on olanzapine, and 6 mg/day in the 49 patients on aripiprazole. Approximately half of patients also were on stable doses of stimulants for ADHD.

Total body percentage of adiposity increased 2.4% after 12 weeks on antipsychotics – slightly less than a standard deviation, and a highly significant change, Dr. Newcomer and his associates reported. Mean total fat increased 2.3 kg, they added.

The percentage body fat increased the most in the youngest children. Greater changes were seen with olanzapine than with risperidone or aripiprazole. About a fourth of patients on risperidone or aripiprazole showed little change in body fat, but three-quarters on those drugs and nearly all patients on olanzapine showed increases.

Whole-body insulin sensitivity decreased approximately from 8 mg/kg per minute to 7 mg/kg per minute, a significant reduction. Olanzapine produced the greatest reduction in whole-body insulin sensitivity.

Importantly, scores for irritability and aggression improved in all groups, he added.

“I’m not a child psychiatrist. I was not terribly sympathetic to this at the beginning” of clinicians’ use of antipsychotics for these indications, said Dr. Newcomer, who chaired the Drug Utilization Review Board for Missouri Medicaid for 14 years. “But I was educated by the psychiatric outcome. There was really profound psychiatric symptom improvement, with kids going back to school and [behaving differently],” he said. The psychiatric response was similar among treatment groups in the study.

As early as 6 weeks after starting therapy, significant changes could be seen on adiposity. Children with the biggest changes in body fat showed effects within the first month of treatment.

Height, weight, waist circumference, body mass index, and BMI percentile were measured at all visits. At baseline and at 12 weeks, investigators performed dual-energy x-ray absorptiometry (DEXA) scans and MRI to assess changes in adiposity, hyperinsulinemic euglycemic clamp with isotopomers to assess changes in insulin sensitivity, plasma sampling (such as oral glucose tolerance test or measuring fasting glucose and lipids), ECG, and psychiatric ratings. At the 6-week follow-up, patients underwent DEXA, oral glucose tolerance testing, and lab measures of fasting status.

A previous nonrandomized study of 272 antipsychotic-naive children and adolescents reported weight gains of 4-8 kg and increases in BMI percentile for patients taking any of four atypical antipsychotics for a median of 11 weeks, compared with a control group (JAMA 2009;302:1811-2).

The study’s design raised concern that the effects could be larger than reported, however, because overweight or obese children were assigned to drugs considered to have the lowest risk for weight gain, Dr. Newcomer said.

In a post-hoc analysis, Dr. Newcomer showed that at the start of the current study, the children had similar rates of overweight or obesity as did children in the general population, but rates were higher in the cohort by the end of the study. The rate of overweight or obese children in the cohort increased from about 33% to 48%.

“I’m personally skeptical about the idea that it’s the psychiatric disorders themselves that are the metabolic challenge, rather than the treatment being the primary effect,” he said.

Medicaid data suggest that 43% of prescriptions for atypical antipsychotics are for indications that are not backed by evidence justifying use, he said. Visits to U.S. physicians that included prescriptions for antipsychotics to patients aged 20 years or younger more than doubled between 1997 and 2002, to a rate greater than 1,400 per 100,000 visits, a separate study reported (Arch Gen. Psych. 2006;63-681).

The National Institutes of Health funded the study. Dr. Newcomer has been a consultant for or received grants from Janssen Pharmaceuticals Inc., Pfizer Inc. , AstraZeneca, Bristol-Myers Squibb, Otsuka Pharmaceutical Co. Ltd., Schering/Merck, Vivus Inc., Obecure Ltd., Biovail Corp., Lundbeck A/S, Sanofi, and Dainippon Sumitomo Pharma Co. Ltd./Sepracor Inc.

SAN DIEGO – Significant increases in adiposity and insulin resistance quickly became apparent in a 12-week study of low-dose antipsychotics to treat mainly nonpsychotic disorders in 144 children.

Newer, “atypical” antipsychotics increasingly are being used to treat mood and disruptive behavior disorders in children, Dr. John W. Newcomer said at the annual meeting of the American Diabetes Association.

“It’s a topic of increasing concern in a number of state Medicaid” systems, he said. Concerns have been generated in part by data showing premature mortality in people with mental disorders that’s related primarily to cardiovascular disease but also to cardiometabolic risk.

Children in the open-label study were randomized to flexibly dosed treatment with risperidone, olanzapine, or aripiprazole. It was their first use of antipsychotics.

These were “very low doses,” he emphasized. “These are not doses that would be used to treat a psychotic disorder,” said Dr. Newcomer, who led the study while at Washington University, St. Louis. He now is a professor of psychiatry and behavioral sciences at the University of Miami.

The 5-year Metabolic Effects of Antipsychotics in Children (MEAC) study targeted symptoms of aggression and irritability in patients aged 6-18 years. “Typically, they had been suspended from school,” he said.

The main primary diagnosis was treatment-refractory attention deficit hyperactivity disorder (ADHD) in 57% of patients. “This is what clinicians are using these drugs for in this type of public-sector population – kids who fail two or three courses of stimulants who then are looking for some other treatment.”

Other main diagnoses included oppositional defiant disorder in 22%, pervasive developmental disorder in 6%, bipolar disorder in 4%, and major depression in 3%. Smaller proportions of patients were diagnosed with other mood disorders, Asperger’s syndrome, autism, obsessive-compulsive disorder, or Tourette’s syndrome.

Mean doses were 1 mg/day in the 49 patients on risperidone, 6.3 mg/day in the 46 patients on olanzapine, and 6 mg/day in the 49 patients on aripiprazole. Approximately half of patients also were on stable doses of stimulants for ADHD.

Total body percentage of adiposity increased 2.4% after 12 weeks on antipsychotics – slightly less than a standard deviation, and a highly significant change, Dr. Newcomer and his associates reported. Mean total fat increased 2.3 kg, they added.

The percentage body fat increased the most in the youngest children. Greater changes were seen with olanzapine than with risperidone or aripiprazole. About a fourth of patients on risperidone or aripiprazole showed little change in body fat, but three-quarters on those drugs and nearly all patients on olanzapine showed increases.

Whole-body insulin sensitivity decreased approximately from 8 mg/kg per minute to 7 mg/kg per minute, a significant reduction. Olanzapine produced the greatest reduction in whole-body insulin sensitivity.

Importantly, scores for irritability and aggression improved in all groups, he added.

“I’m not a child psychiatrist. I was not terribly sympathetic to this at the beginning” of clinicians’ use of antipsychotics for these indications, said Dr. Newcomer, who chaired the Drug Utilization Review Board for Missouri Medicaid for 14 years. “But I was educated by the psychiatric outcome. There was really profound psychiatric symptom improvement, with kids going back to school and [behaving differently],” he said. The psychiatric response was similar among treatment groups in the study.

As early as 6 weeks after starting therapy, significant changes could be seen on adiposity. Children with the biggest changes in body fat showed effects within the first month of treatment.

Height, weight, waist circumference, body mass index, and BMI percentile were measured at all visits. At baseline and at 12 weeks, investigators performed dual-energy x-ray absorptiometry (DEXA) scans and MRI to assess changes in adiposity, hyperinsulinemic euglycemic clamp with isotopomers to assess changes in insulin sensitivity, plasma sampling (such as oral glucose tolerance test or measuring fasting glucose and lipids), ECG, and psychiatric ratings. At the 6-week follow-up, patients underwent DEXA, oral glucose tolerance testing, and lab measures of fasting status.

A previous nonrandomized study of 272 antipsychotic-naive children and adolescents reported weight gains of 4-8 kg and increases in BMI percentile for patients taking any of four atypical antipsychotics for a median of 11 weeks, compared with a control group (JAMA 2009;302:1811-2).

The study’s design raised concern that the effects could be larger than reported, however, because overweight or obese children were assigned to drugs considered to have the lowest risk for weight gain, Dr. Newcomer said.

In a post-hoc analysis, Dr. Newcomer showed that at the start of the current study, the children had similar rates of overweight or obesity as did children in the general population, but rates were higher in the cohort by the end of the study. The rate of overweight or obese children in the cohort increased from about 33% to 48%.

“I’m personally skeptical about the idea that it’s the psychiatric disorders themselves that are the metabolic challenge, rather than the treatment being the primary effect,” he said.

Medicaid data suggest that 43% of prescriptions for atypical antipsychotics are for indications that are not backed by evidence justifying use, he said. Visits to U.S. physicians that included prescriptions for antipsychotics to patients aged 20 years or younger more than doubled between 1997 and 2002, to a rate greater than 1,400 per 100,000 visits, a separate study reported (Arch Gen. Psych. 2006;63-681).

The National Institutes of Health funded the study. Dr. Newcomer has been a consultant for or received grants from Janssen Pharmaceuticals Inc., Pfizer Inc. , AstraZeneca, Bristol-Myers Squibb, Otsuka Pharmaceutical Co. Ltd., Schering/Merck, Vivus Inc., Obecure Ltd., Biovail Corp., Lundbeck A/S, Sanofi, and Dainippon Sumitomo Pharma Co. Ltd./Sepracor Inc.

SAN DIEGO – Significant increases in adiposity and insulin resistance quickly became apparent in a 12-week study of low-dose antipsychotics to treat mainly nonpsychotic disorders in 144 children.

Newer, “atypical” antipsychotics increasingly are being used to treat mood and disruptive behavior disorders in children, Dr. John W. Newcomer said at the annual meeting of the American Diabetes Association.

“It’s a topic of increasing concern in a number of state Medicaid” systems, he said. Concerns have been generated in part by data showing premature mortality in people with mental disorders that’s related primarily to cardiovascular disease but also to cardiometabolic risk.

Children in the open-label study were randomized to flexibly dosed treatment with risperidone, olanzapine, or aripiprazole. It was their first use of antipsychotics.

These were “very low doses,” he emphasized. “These are not doses that would be used to treat a psychotic disorder,” said Dr. Newcomer, who led the study while at Washington University, St. Louis. He now is a professor of psychiatry and behavioral sciences at the University of Miami.

The 5-year Metabolic Effects of Antipsychotics in Children (MEAC) study targeted symptoms of aggression and irritability in patients aged 6-18 years. “Typically, they had been suspended from school,” he said.

The main primary diagnosis was treatment-refractory attention deficit hyperactivity disorder (ADHD) in 57% of patients. “This is what clinicians are using these drugs for in this type of public-sector population – kids who fail two or three courses of stimulants who then are looking for some other treatment.”

Other main diagnoses included oppositional defiant disorder in 22%, pervasive developmental disorder in 6%, bipolar disorder in 4%, and major depression in 3%. Smaller proportions of patients were diagnosed with other mood disorders, Asperger’s syndrome, autism, obsessive-compulsive disorder, or Tourette’s syndrome.

Mean doses were 1 mg/day in the 49 patients on risperidone, 6.3 mg/day in the 46 patients on olanzapine, and 6 mg/day in the 49 patients on aripiprazole. Approximately half of patients also were on stable doses of stimulants for ADHD.

Total body percentage of adiposity increased 2.4% after 12 weeks on antipsychotics – slightly less than a standard deviation, and a highly significant change, Dr. Newcomer and his associates reported. Mean total fat increased 2.3 kg, they added.

The percentage body fat increased the most in the youngest children. Greater changes were seen with olanzapine than with risperidone or aripiprazole. About a fourth of patients on risperidone or aripiprazole showed little change in body fat, but three-quarters on those drugs and nearly all patients on olanzapine showed increases.

Whole-body insulin sensitivity decreased approximately from 8 mg/kg per minute to 7 mg/kg per minute, a significant reduction. Olanzapine produced the greatest reduction in whole-body insulin sensitivity.

Importantly, scores for irritability and aggression improved in all groups, he added.

“I’m not a child psychiatrist. I was not terribly sympathetic to this at the beginning” of clinicians’ use of antipsychotics for these indications, said Dr. Newcomer, who chaired the Drug Utilization Review Board for Missouri Medicaid for 14 years. “But I was educated by the psychiatric outcome. There was really profound psychiatric symptom improvement, with kids going back to school and [behaving differently],” he said. The psychiatric response was similar among treatment groups in the study.

As early as 6 weeks after starting therapy, significant changes could be seen on adiposity. Children with the biggest changes in body fat showed effects within the first month of treatment.

Height, weight, waist circumference, body mass index, and BMI percentile were measured at all visits. At baseline and at 12 weeks, investigators performed dual-energy x-ray absorptiometry (DEXA) scans and MRI to assess changes in adiposity, hyperinsulinemic euglycemic clamp with isotopomers to assess changes in insulin sensitivity, plasma sampling (such as oral glucose tolerance test or measuring fasting glucose and lipids), ECG, and psychiatric ratings. At the 6-week follow-up, patients underwent DEXA, oral glucose tolerance testing, and lab measures of fasting status.

A previous nonrandomized study of 272 antipsychotic-naive children and adolescents reported weight gains of 4-8 kg and increases in BMI percentile for patients taking any of four atypical antipsychotics for a median of 11 weeks, compared with a control group (JAMA 2009;302:1811-2).

The study’s design raised concern that the effects could be larger than reported, however, because overweight or obese children were assigned to drugs considered to have the lowest risk for weight gain, Dr. Newcomer said.

In a post-hoc analysis, Dr. Newcomer showed that at the start of the current study, the children had similar rates of overweight or obesity as did children in the general population, but rates were higher in the cohort by the end of the study. The rate of overweight or obese children in the cohort increased from about 33% to 48%.

“I’m personally skeptical about the idea that it’s the psychiatric disorders themselves that are the metabolic challenge, rather than the treatment being the primary effect,” he said.

Medicaid data suggest that 43% of prescriptions for atypical antipsychotics are for indications that are not backed by evidence justifying use, he said. Visits to U.S. physicians that included prescriptions for antipsychotics to patients aged 20 years or younger more than doubled between 1997 and 2002, to a rate greater than 1,400 per 100,000 visits, a separate study reported (Arch Gen. Psych. 2006;63-681).

The National Institutes of Health funded the study. Dr. Newcomer has been a consultant for or received grants from Janssen Pharmaceuticals Inc., Pfizer Inc. , AstraZeneca, Bristol-Myers Squibb, Otsuka Pharmaceutical Co. Ltd., Schering/Merck, Vivus Inc., Obecure Ltd., Biovail Corp., Lundbeck A/S, Sanofi, and Dainippon Sumitomo Pharma Co. Ltd./Sepracor Inc.

SAN DIEGO – Significant increases in adiposity and insulin resistance quickly became apparent in a 12-week study of low-dose antipsychotics to treat mainly nonpsychotic disorders in 144 children.

Newer, “atypical” antipsychotics increasingly are being used to treat mood and disruptive behavior disorders in children, Dr. John W. Newcomer said at the annual meeting of the American Diabetes Association.

“It’s a topic of increasing concern in a number of state Medicaid” systems, he said. Concerns have been generated in part by data showing premature mortality in people with mental disorders that’s related primarily to cardiovascular disease but also to cardiometabolic risk.

Children in the open-label study were randomized to flexibly dosed treatment with risperidone, olanzapine, or aripiprazole. It was their first use of antipsychotics.

These were “very low doses,” he emphasized. “These are not doses that would be used to treat a psychotic disorder,” said Dr. Newcomer, who led the study while at Washington University, St. Louis. He now is a professor of psychiatry and behavioral sciences at the University of Miami.

The 5-year Metabolic Effects of Antipsychotics in Children (MEAC) study targeted symptoms of aggression and irritability in patients aged 6-18 years. “Typically, they had been suspended from school,” he said.

The main primary diagnosis was treatment-refractory attention deficit hyperactivity disorder (ADHD) in 57% of patients. “This is what clinicians are using these drugs for in this type of public-sector population – kids who fail two or three courses of stimulants who then are looking for some other treatment.”

Other main diagnoses included oppositional defiant disorder in 22%, pervasive developmental disorder in 6%, bipolar disorder in 4%, and major depression in 3%. Smaller proportions of patients were diagnosed with other mood disorders, Asperger’s syndrome, autism, obsessive-compulsive disorder, or Tourette’s syndrome.

Mean doses were 1 mg/day in the 49 patients on risperidone, 6.3 mg/day in the 46 patients on olanzapine, and 6 mg/day in the 49 patients on aripiprazole. Approximately half of patients also were on stable doses of stimulants for ADHD.

Total body percentage of adiposity increased 2.4% after 12 weeks on antipsychotics – slightly less than a standard deviation, and a highly significant change, Dr. Newcomer and his associates reported. Mean total fat increased 2.3 kg, they added.

The percentage body fat increased the most in the youngest children. Greater changes were seen with olanzapine than with risperidone or aripiprazole. About a fourth of patients on risperidone or aripiprazole showed little change in body fat, but three-quarters on those drugs and nearly all patients on olanzapine showed increases.

Whole-body insulin sensitivity decreased approximately from 8 mg/kg per minute to 7 mg/kg per minute, a significant reduction. Olanzapine produced the greatest reduction in whole-body insulin sensitivity.

Importantly, scores for irritability and aggression improved in all groups, he added.

“I’m not a child psychiatrist. I was not terribly sympathetic to this at the beginning” of clinicians’ use of antipsychotics for these indications, said Dr. Newcomer, who chaired the Drug Utilization Review Board for Missouri Medicaid for 14 years. “But I was educated by the psychiatric outcome. There was really profound psychiatric symptom improvement, with kids going back to school and [behaving differently],” he said. The psychiatric response was similar among treatment groups in the study.

As early as 6 weeks after starting therapy, significant changes could be seen on adiposity. Children with the biggest changes in body fat showed effects within the first month of treatment.

Height, weight, waist circumference, body mass index, and BMI percentile were measured at all visits. At baseline and at 12 weeks, investigators performed dual-energy x-ray absorptiometry (DEXA) scans and MRI to assess changes in adiposity, hyperinsulinemic euglycemic clamp with isotopomers to assess changes in insulin sensitivity, plasma sampling (such as oral glucose tolerance test or measuring fasting glucose and lipids), ECG, and psychiatric ratings. At the 6-week follow-up, patients underwent DEXA, oral glucose tolerance testing, and lab measures of fasting status.

A previous nonrandomized study of 272 antipsychotic-naive children and adolescents reported weight gains of 4-8 kg and increases in BMI percentile for patients taking any of four atypical antipsychotics for a median of 11 weeks, compared with a control group (JAMA 2009;302:1811-2).

The study’s design raised concern that the effects could be larger than reported, however, because overweight or obese children were assigned to drugs considered to have the lowest risk for weight gain, Dr. Newcomer said.

In a post-hoc analysis, Dr. Newcomer showed that at the start of the current study, the children had similar rates of overweight or obesity as did children in the general population, but rates were higher in the cohort by the end of the study. The rate of overweight or obese children in the cohort increased from about 33% to 48%.

“I’m personally skeptical about the idea that it’s the psychiatric disorders themselves that are the metabolic challenge, rather than the treatment being the primary effect,” he said.

Medicaid data suggest that 43% of prescriptions for atypical antipsychotics are for indications that are not backed by evidence justifying use, he said. Visits to U.S. physicians that included prescriptions for antipsychotics to patients aged 20 years or younger more than doubled between 1997 and 2002, to a rate greater than 1,400 per 100,000 visits, a separate study reported (Arch Gen. Psych. 2006;63-681).

The National Institutes of Health funded the study. Dr. Newcomer has been a consultant for or received grants from Janssen Pharmaceuticals Inc., Pfizer Inc. , AstraZeneca, Bristol-Myers Squibb, Otsuka Pharmaceutical Co. Ltd., Schering/Merck, Vivus Inc., Obecure Ltd., Biovail Corp., Lundbeck A/S, Sanofi, and Dainippon Sumitomo Pharma Co. Ltd./Sepracor Inc.

SAN DIEGO – Having a hemoglobin A_1c level of 5.7%-6.4% or impaired fasting glucose each predicted a sixfold higher risk for developing diabetes among individuals screened for the disease, and people who meet both criteria are at a 32-fold increased risk for diabetes, compared with normoglycemic individuals, a large longitudinal study found.

Using the two tests together could better identify people who are most likely to progress to diabetes and who could therefore benefit from early interventions, Yoriko Heianza and her associates reported at the annual scientific sessions of the American Diabetes Association. The findings simultaneously were published online (Lancet 2011 [doi:10.1016/S0140-6736(11)60472-8]).

.

The study followed 6,241 Japanese subjects, most of whom were government employees and who did not have diabetes at the time of their annual health screenings between 1997 and 2003, and who had annual exams for the next 4-5 years. During that time, 5% developed diabetes, an incidence similar to that in the general Japanese population.

At the baseline exam, 2,092 (34%) were diagnosed with prediabetes. Of those, nearly 20% were diagnosed with prediabetes solely on the basis of an HBA_1c level of 5.7%-6.4% and 61% were diagnosed solely based on impaired fasting glucose, defined as a fasting plasma glucose concentration of 5.6-6.9 mmol/L. The remaining nearly 20% met both criteria for prediabetes, reported Ms. Heianza of the University of Tsukuba (Japan) Institute of Clinical Medicine and Toranomon Hospital, Tokyo.

Only half of the people who were diagnosed with prediabetes based on HbA_1c level also had impaired fasting glucose, and only 24% of people diagnosed by impaired fasting glucose also met the HbA_1c criterion.

Although the HbA_1c test identified fewer individuals with prediabetes (822) than did impaired fasting glucose (1,680), the predictive power for progression to diabetes was similar between tests. Once diagnosed with prediabetes with either test, the risk for developing diabetes was six-fold higher than in normoglycemic individuals, after adjusting for the effects of age, sex, and other factors.

Meeting both criteria significantly increased the risk of developing diabetes to a level 32 times higher than in normoglycemic participants. The predictive power of using both tests is multiplied rather than simply additive, the investigators suggested.

The discordance between prediabetes diagnoses made by either HbA_1c level or impaired fasting glucose in this study was similar to results from the U.S. National Health and Nutrition Examination Survey (NHANES), they added. In the current study, 19.7% met the HbA_1c criterion for prediabetes without having impaired fasting glucose, compared with 17% in the NHANES data. In NHANES, the HbA_1c test had a 27% sensitivity and a 93% specificity for diagnosing prediabetes, compared with a sensitivity of 21% and a specificity of 91% in the Japanese cohort.

Subjects in the Japanese study ranged in age from 24-82 years, with a mean age of 50 years; 75% were men.

Differences in baseline characteristics made up different cardiovascular risk profiles between individuals diagnosed with prediabetes solely based on HbA_1c level or impaired fasting glucose. People diagnosed with prediabetes solely on the HbA_1c criterion were more likely to be female and older, and less likely to be hypertensive or obese. They also had lower levels of triglyceride, uric acid, and HDL cholesterol.

The investigators reported having no conflicts of interest. The study was funded in part by Japan’s Ministry of Health, Labor and Welfare.

SAN DIEGO – Having a hemoglobin A_1c level of 5.7%-6.4% or impaired fasting glucose each predicted a sixfold higher risk for developing diabetes among individuals screened for the disease, and people who meet both criteria are at a 32-fold increased risk for diabetes, compared with normoglycemic individuals, a large longitudinal study found.

Using the two tests together could better identify people who are most likely to progress to diabetes and who could therefore benefit from early interventions, Yoriko Heianza and her associates reported at the annual scientific sessions of the American Diabetes Association. The findings simultaneously were published online (Lancet 2011 [doi:10.1016/S0140-6736(11)60472-8]).

.

The study followed 6,241 Japanese subjects, most of whom were government employees and who did not have diabetes at the time of their annual health screenings between 1997 and 2003, and who had annual exams for the next 4-5 years. During that time, 5% developed diabetes, an incidence similar to that in the general Japanese population.

At the baseline exam, 2,092 (34%) were diagnosed with prediabetes. Of those, nearly 20% were diagnosed with prediabetes solely on the basis of an HBA_1c level of 5.7%-6.4% and 61% were diagnosed solely based on impaired fasting glucose, defined as a fasting plasma glucose concentration of 5.6-6.9 mmol/L. The remaining nearly 20% met both criteria for prediabetes, reported Ms. Heianza of the University of Tsukuba (Japan) Institute of Clinical Medicine and Toranomon Hospital, Tokyo.

Only half of the people who were diagnosed with prediabetes based on HbA_1c level also had impaired fasting glucose, and only 24% of people diagnosed by impaired fasting glucose also met the HbA_1c criterion.

Although the HbA_1c test identified fewer individuals with prediabetes (822) than did impaired fasting glucose (1,680), the predictive power for progression to diabetes was similar between tests. Once diagnosed with prediabetes with either test, the risk for developing diabetes was six-fold higher than in normoglycemic individuals, after adjusting for the effects of age, sex, and other factors.

Meeting both criteria significantly increased the risk of developing diabetes to a level 32 times higher than in normoglycemic participants. The predictive power of using both tests is multiplied rather than simply additive, the investigators suggested.

The discordance between prediabetes diagnoses made by either HbA_1c level or impaired fasting glucose in this study was similar to results from the U.S. National Health and Nutrition Examination Survey (NHANES), they added. In the current study, 19.7% met the HbA_1c criterion for prediabetes without having impaired fasting glucose, compared with 17% in the NHANES data. In NHANES, the HbA_1c test had a 27% sensitivity and a 93% specificity for diagnosing prediabetes, compared with a sensitivity of 21% and a specificity of 91% in the Japanese cohort.

Subjects in the Japanese study ranged in age from 24-82 years, with a mean age of 50 years; 75% were men.

Differences in baseline characteristics made up different cardiovascular risk profiles between individuals diagnosed with prediabetes solely based on HbA_1c level or impaired fasting glucose. People diagnosed with prediabetes solely on the HbA_1c criterion were more likely to be female and older, and less likely to be hypertensive or obese. They also had lower levels of triglyceride, uric acid, and HDL cholesterol.

The investigators reported having no conflicts of interest. The study was funded in part by Japan’s Ministry of Health, Labor and Welfare.

SAN DIEGO – Having a hemoglobin A_1c level of 5.7%-6.4% or impaired fasting glucose each predicted a sixfold higher risk for developing diabetes among individuals screened for the disease, and people who meet both criteria are at a 32-fold increased risk for diabetes, compared with normoglycemic individuals, a large longitudinal study found.

Using the two tests together could better identify people who are most likely to progress to diabetes and who could therefore benefit from early interventions, Yoriko Heianza and her associates reported at the annual scientific sessions of the American Diabetes Association. The findings simultaneously were published online (Lancet 2011 [doi:10.1016/S0140-6736(11)60472-8]).

.

The study followed 6,241 Japanese subjects, most of whom were government employees and who did not have diabetes at the time of their annual health screenings between 1997 and 2003, and who had annual exams for the next 4-5 years. During that time, 5% developed diabetes, an incidence similar to that in the general Japanese population.

At the baseline exam, 2,092 (34%) were diagnosed with prediabetes. Of those, nearly 20% were diagnosed with prediabetes solely on the basis of an HBA_1c level of 5.7%-6.4% and 61% were diagnosed solely based on impaired fasting glucose, defined as a fasting plasma glucose concentration of 5.6-6.9 mmol/L. The remaining nearly 20% met both criteria for prediabetes, reported Ms. Heianza of the University of Tsukuba (Japan) Institute of Clinical Medicine and Toranomon Hospital, Tokyo.

Only half of the people who were diagnosed with prediabetes based on HbA_1c level also had impaired fasting glucose, and only 24% of people diagnosed by impaired fasting glucose also met the HbA_1c criterion.

Although the HbA_1c test identified fewer individuals with prediabetes (822) than did impaired fasting glucose (1,680), the predictive power for progression to diabetes was similar between tests. Once diagnosed with prediabetes with either test, the risk for developing diabetes was six-fold higher than in normoglycemic individuals, after adjusting for the effects of age, sex, and other factors.

Meeting both criteria significantly increased the risk of developing diabetes to a level 32 times higher than in normoglycemic participants. The predictive power of using both tests is multiplied rather than simply additive, the investigators suggested.

The discordance between prediabetes diagnoses made by either HbA_1c level or impaired fasting glucose in this study was similar to results from the U.S. National Health and Nutrition Examination Survey (NHANES), they added. In the current study, 19.7% met the HbA_1c criterion for prediabetes without having impaired fasting glucose, compared with 17% in the NHANES data. In NHANES, the HbA_1c test had a 27% sensitivity and a 93% specificity for diagnosing prediabetes, compared with a sensitivity of 21% and a specificity of 91% in the Japanese cohort.

Subjects in the Japanese study ranged in age from 24-82 years, with a mean age of 50 years; 75% were men.

Differences in baseline characteristics made up different cardiovascular risk profiles between individuals diagnosed with prediabetes solely based on HbA_1c level or impaired fasting glucose. People diagnosed with prediabetes solely on the HbA_1c criterion were more likely to be female and older, and less likely to be hypertensive or obese. They also had lower levels of triglyceride, uric acid, and HDL cholesterol.

The investigators reported having no conflicts of interest. The study was funded in part by Japan’s Ministry of Health, Labor and Welfare.

SAN DIEGO – Having a hemoglobin A_1c level of 5.7%-6.4% or impaired fasting glucose each predicted a sixfold higher risk for developing diabetes among individuals screened for the disease, and people who meet both criteria are at a 32-fold increased risk for diabetes, compared with normoglycemic individuals, a large longitudinal study found.

Using the two tests together could better identify people who are most likely to progress to diabetes and who could therefore benefit from early interventions, Yoriko Heianza and her associates reported at the annual scientific sessions of the American Diabetes Association. The findings simultaneously were published online (Lancet 2011 [doi:10.1016/S0140-6736(11)60472-8]).

.

The study followed 6,241 Japanese subjects, most of whom were government employees and who did not have diabetes at the time of their annual health screenings between 1997 and 2003, and who had annual exams for the next 4-5 years. During that time, 5% developed diabetes, an incidence similar to that in the general Japanese population.

At the baseline exam, 2,092 (34%) were diagnosed with prediabetes. Of those, nearly 20% were diagnosed with prediabetes solely on the basis of an HBA_1c level of 5.7%-6.4% and 61% were diagnosed solely based on impaired fasting glucose, defined as a fasting plasma glucose concentration of 5.6-6.9 mmol/L. The remaining nearly 20% met both criteria for prediabetes, reported Ms. Heianza of the University of Tsukuba (Japan) Institute of Clinical Medicine and Toranomon Hospital, Tokyo.

Only half of the people who were diagnosed with prediabetes based on HbA_1c level also had impaired fasting glucose, and only 24% of people diagnosed by impaired fasting glucose also met the HbA_1c criterion.

Although the HbA_1c test identified fewer individuals with prediabetes (822) than did impaired fasting glucose (1,680), the predictive power for progression to diabetes was similar between tests. Once diagnosed with prediabetes with either test, the risk for developing diabetes was six-fold higher than in normoglycemic individuals, after adjusting for the effects of age, sex, and other factors.

Meeting both criteria significantly increased the risk of developing diabetes to a level 32 times higher than in normoglycemic participants. The predictive power of using both tests is multiplied rather than simply additive, the investigators suggested.

The discordance between prediabetes diagnoses made by either HbA_1c level or impaired fasting glucose in this study was similar to results from the U.S. National Health and Nutrition Examination Survey (NHANES), they added. In the current study, 19.7% met the HbA_1c criterion for prediabetes without having impaired fasting glucose, compared with 17% in the NHANES data. In NHANES, the HbA_1c test had a 27% sensitivity and a 93% specificity for diagnosing prediabetes, compared with a sensitivity of 21% and a specificity of 91% in the Japanese cohort.

Subjects in the Japanese study ranged in age from 24-82 years, with a mean age of 50 years; 75% were men.

Differences in baseline characteristics made up different cardiovascular risk profiles between individuals diagnosed with prediabetes solely based on HbA_1c level or impaired fasting glucose. People diagnosed with prediabetes solely on the HbA_1c criterion were more likely to be female and older, and less likely to be hypertensive or obese. They also had lower levels of triglyceride, uric acid, and HDL cholesterol.

The investigators reported having no conflicts of interest. The study was funded in part by Japan’s Ministry of Health, Labor and Welfare.

SAN DIEGO – Having a hemoglobin A_1c level of 5.7%-6.4% or impaired fasting glucose each predicted a sixfold higher risk for developing diabetes among individuals screened for the disease, and people who meet both criteria are at a 32-fold increased risk for diabetes, compared with normoglycemic individuals, a large longitudinal study found.

Using the two tests together could better identify people who are most likely to progress to diabetes and who could therefore benefit from early interventions, Yoriko Heianza and her associates reported at the annual scientific sessions of the American Diabetes Association. The findings simultaneously were published online (Lancet 2011 [doi:10.1016/S0140-6736(11)60472-8]).

.

The study followed 6,241 Japanese subjects, most of whom were government employees and who did not have diabetes at the time of their annual health screenings between 1997 and 2003, and who had annual exams for the next 4-5 years. During that time, 5% developed diabetes, an incidence similar to that in the general Japanese population.

At the baseline exam, 2,092 (34%) were diagnosed with prediabetes. Of those, nearly 20% were diagnosed with prediabetes solely on the basis of an HBA_1c level of 5.7%-6.4% and 61% were diagnosed solely based on impaired fasting glucose, defined as a fasting plasma glucose concentration of 5.6-6.9 mmol/L. The remaining nearly 20% met both criteria for prediabetes, reported Ms. Heianza of the University of Tsukuba (Japan) Institute of Clinical Medicine and Toranomon Hospital, Tokyo.

Only half of the people who were diagnosed with prediabetes based on HbA_1c level also had impaired fasting glucose, and only 24% of people diagnosed by impaired fasting glucose also met the HbA_1c criterion.

Although the HbA_1c test identified fewer individuals with prediabetes (822) than did impaired fasting glucose (1,680), the predictive power for progression to diabetes was similar between tests. Once diagnosed with prediabetes with either test, the risk for developing diabetes was six-fold higher than in normoglycemic individuals, after adjusting for the effects of age, sex, and other factors.

Meeting both criteria significantly increased the risk of developing diabetes to a level 32 times higher than in normoglycemic participants. The predictive power of using both tests is multiplied rather than simply additive, the investigators suggested.

The discordance between prediabetes diagnoses made by either HbA_1c level or impaired fasting glucose in this study was similar to results from the U.S. National Health and Nutrition Examination Survey (NHANES), they added. In the current study, 19.7% met the HbA_1c criterion for prediabetes without having impaired fasting glucose, compared with 17% in the NHANES data. In NHANES, the HbA_1c test had a 27% sensitivity and a 93% specificity for diagnosing prediabetes, compared with a sensitivity of 21% and a specificity of 91% in the Japanese cohort.

Subjects in the Japanese study ranged in age from 24-82 years, with a mean age of 50 years; 75% were men.

Differences in baseline characteristics made up different cardiovascular risk profiles between individuals diagnosed with prediabetes solely based on HbA_1c level or impaired fasting glucose. People diagnosed with prediabetes solely on the HbA_1c criterion were more likely to be female and older, and less likely to be hypertensive or obese. They also had lower levels of triglyceride, uric acid, and HDL cholesterol.

The investigators reported having no conflicts of interest. The study was funded in part by Japan’s Ministry of Health, Labor and Welfare.

SAN DIEGO – Having a hemoglobin A_1c level of 5.7%-6.4% or impaired fasting glucose each predicted a sixfold higher risk for developing diabetes among individuals screened for the disease, and people who meet both criteria are at a 32-fold increased risk for diabetes, compared with normoglycemic individuals, a large longitudinal study found.

Using the two tests together could better identify people who are most likely to progress to diabetes and who could therefore benefit from early interventions, Yoriko Heianza and her associates reported at the annual scientific sessions of the American Diabetes Association. The findings simultaneously were published online (Lancet 2011 [doi:10.1016/S0140-6736(11)60472-8]).

.

The study followed 6,241 Japanese subjects, most of whom were government employees and who did not have diabetes at the time of their annual health screenings between 1997 and 2003, and who had annual exams for the next 4-5 years. During that time, 5% developed diabetes, an incidence similar to that in the general Japanese population.

At the baseline exam, 2,092 (34%) were diagnosed with prediabetes. Of those, nearly 20% were diagnosed with prediabetes solely on the basis of an HBA_1c level of 5.7%-6.4% and 61% were diagnosed solely based on impaired fasting glucose, defined as a fasting plasma glucose concentration of 5.6-6.9 mmol/L. The remaining nearly 20% met both criteria for prediabetes, reported Ms. Heianza of the University of Tsukuba (Japan) Institute of Clinical Medicine and Toranomon Hospital, Tokyo.

Only half of the people who were diagnosed with prediabetes based on HbA_1c level also had impaired fasting glucose, and only 24% of people diagnosed by impaired fasting glucose also met the HbA_1c criterion.

Although the HbA_1c test identified fewer individuals with prediabetes (822) than did impaired fasting glucose (1,680), the predictive power for progression to diabetes was similar between tests. Once diagnosed with prediabetes with either test, the risk for developing diabetes was six-fold higher than in normoglycemic individuals, after adjusting for the effects of age, sex, and other factors.

Meeting both criteria significantly increased the risk of developing diabetes to a level 32 times higher than in normoglycemic participants. The predictive power of using both tests is multiplied rather than simply additive, the investigators suggested.

The discordance between prediabetes diagnoses made by either HbA_1c level or impaired fasting glucose in this study was similar to results from the U.S. National Health and Nutrition Examination Survey (NHANES), they added. In the current study, 19.7% met the HbA_1c criterion for prediabetes without having impaired fasting glucose, compared with 17% in the NHANES data. In NHANES, the HbA_1c test had a 27% sensitivity and a 93% specificity for diagnosing prediabetes, compared with a sensitivity of 21% and a specificity of 91% in the Japanese cohort.

Subjects in the Japanese study ranged in age from 24-82 years, with a mean age of 50 years; 75% were men.

Differences in baseline characteristics made up different cardiovascular risk profiles between individuals diagnosed with prediabetes solely based on HbA_1c level or impaired fasting glucose. People diagnosed with prediabetes solely on the HbA_1c criterion were more likely to be female and older, and less likely to be hypertensive or obese. They also had lower levels of triglyceride, uric acid, and HDL cholesterol.

The investigators reported having no conflicts of interest. The study was funded in part by Japan’s Ministry of Health, Labor and Welfare.

HONOLULU – Concussions in athletes often produce acute and chronic psychiatric symptoms, but there are few data on the epidemiology and treatment of these problems.

That’s beginning to change.

Physicians increasingly are recognizing chronic traumatic encephalopathy and psychiatric symptoms in athletes after traumatic brain injury (TBI). Unfortunately, little is known about the use of psychotropic medications in athletes with or without TBI, eating disorders, depression, anxiety, or other disorders, several speakers said at the annual meeting of the American Psychiatric Association.

Psychiatric sequelae from TBI in particular "is a timely topic, but that doesn’t mean it hasn’t been around a long time," said Dr. Antonia L. Baum, moderator of the session and a sports psychiatrist in Chevy Chase, Md.

Dr. Claudia L. Reardon of the University of Wisconsin, Madison, recently published a review article summarizing the medical literature on the diagnosis and treatment of mental illness in athletes, which she was able to describe in a single presentation at the meeting (Sports Med. 2010;40:961-80).

Psychiatric symptoms can arise in an athlete after TBI for a variety of reasons. Symptoms of attention-deficit/hyperactivity disorder (ADHD), for example, may worsen after a concussion, or the TBI’s damage to specific brain areas might cause psychiatric symptoms. Reaction to the stress of TBI or to stressful life events after the TBI, might lead to psychiatric symptoms, Dr. Reardon said.

Between 20% and 30% of people who suffer concussions develop acute major depressive disorder, and subacute depression or mood liability is seen in others. Insomnia troubles 36%-70% of patients after TBI. Other acute and subacute symptoms after TBI include anxiety, posttraumatic stress disorder, irritability, apathy, personality changes, impulsivity, somatization, and ADHD-like symptoms. In patients with preexisting disorders, concussion may exacerbate symptoms and make them more difficult to treat.

Chronic traumatic encephalopathy (CTE), a neurodegenerative disease, can develop years after recovery from the acute effects of TBI, especially if the brain has insufficient time to recover between serial concussions.

Clinical symptoms of CTE emerge 8 years after serial concussions, around age 43 years on average; but the timing varies widely, Dr. Reardon said. Symptom onset usually is insidious, with slow and steady progression over an average of 18 years, though somewhat faster in football players than in other athletes.

Irritability, anger, apathy, a "punchy" personality, and a so-called "shorter fuse" typify early symptoms of CTE. "Rarely, cognitive difficulties are the first signs to emerge, but usually psychiatric symptoms are what we see first," she said.

People with CTE are more likely to be suicidal, to have an early accidental death, or to overdose on drugs, compared with people without CTE. In later stages of CTE, the neurologic abnormalities appear, such as parkinsonism or speech and gait abnormalities.

Children may be at greater risk than adults for long-term sequelae of TBI, because their brains are still developing, and serious sequelae may be more likely in female than in male athletes, the literature suggests.

Concussions are common not just in "contact" sports such as football and soccer, but in many other sports, even when there’s not a blow to the head. Athletes may have hard contact with floors (gymnastics or wrestling), walls (racquetball), or other objects or people (golf or basketball), she said.

"Traumatic brain injury does set people up for even higher rates of psychiatric conditions, so it’s important to know the baseline rates of these conditions in athletes," Dr. Reardon said.

Eating disorders can be found in up to 60% of female athletes in such sports as running and gymnastics. In male athletes, eating disorders increasingly are being recognized in rowing, wrestling, and other sports, but male bodies tend to recover once the season is over, while females do not.

Abuse of alcohol, stimulants, steroids, and other substances is fairly common in athletes, and TBI can reduce tolerance to alcohol, she noted.

The incidence of major depressive disorder in athletes is probably similar to that in nonathletes, but athletes are at high risk for depression after injury, overtraining, poor performance, or retirement. A few athletes may develop compulsive disorders, but superstitious rituals usually are normal, so "don’t become overly concerned about obsessive-compulsive disorder," she advised.

More Research Data Coming

Physicians, athletes, and sports leagues are beginning to gather sorely needed data on TBI and sequelae in athletes.

"We need to know baseline function to assess any changes" after TBI, said Dr. David A. Baron, professor of psychiatry and director of the Global Center for Exercise, Psychiatry and Sports at the University of Southern California, Los Angeles.

The Glasgow Coma Score may not be sensitive or specific enough to detect many of the problems that sports psychiatrists see, such as early cognitive symptoms, he asserted. "We might be missing some very early clinical findings" by using this most common system for classifying TBI severity, Dr. Baron said.

In 2007, under pressure from politicians and the media, the National Football League for the first time acknowledged that concussions lead to long-term problems and put independent neurologists in charge of return-to-play decisions after TBI, Dr. Baron said. The league started a database to log every concussion for every player. There’s also a new interest in studying the long-term effects of TBI in retired athletes.

William Tsushima, Ph.D. and his son Vincent G. Tsushima, Ph.D., both neuropsychologists in Honolulu, reported that 4 million high school and college athletes have undergone computer-based neuropsychological assessments before sports participation. Each year, 300,000 athletes suffer mild TBI, including 60,000 high school athletes with cognitive and emotional symptoms of TBI. Every player in the National Hockey League now is required to undergo testing before playing.

A study by the Tsushimas in 639 high school athletes found that younger teens recover more slowly than older athletes after concussion, suggesting that more time is needed before allowing younger athletes to return to play.

They used the ImPACT neurocognitive assessment tool, which now comes in a handheld version for use on the field that includes a brief mental status evaluation, Dr. Vincent G. Tsushima said. The device’s makers are working on versions for use with younger ages (5-11 years) and in different languages, he said.

Weigh Rx Choices for Concussion in Athletes

Consider three questions before starting an athlete on a psychiatric medication: Is it safe, especially if the athlete exercises to exhaustion and sweats a lot? Will it affect performance? Is it allowed under antidoping guidelines?

Results of studies of psychiatric medications in athletes may not be generalizable, cautioned Dr. Reardon. They typically involve only one or two doses rather than long-term use.

One of the most common measures of effects on performance is grip strength. "How readily can you extrapolate that to the athlete who is an Olympic 400-meter dasher?" asked Dr. Reardon, who previously was a 400-meter runner in track and field competitions.

The selective serotonin reuptake inhibitor drugs generally are considered first-line therapy for behavioral and cognitive symptoms of traumatic brain injury (TBI) that do not start resolving within a few weeks of TBI, including anxiety, depression, irritability, poor tolerance of frustration, and even cognitive difficulties in athletes who suffered concussion.

Preliminary data suggest that fluoxetine does not affect athletic performance and has no safety concerns. One study reported that paroxetine inhibited athletic performance, but another found no effects.

Very preliminary data from one study on bupropion suggests it may be performance enhancing if used acutely in hot temperatures, but "we should take very seriously that we should avoid this medication in athletes who suffered recent head injury, given the epileptogenic potential of the drug," she said.

In athletes with TBI, preliminary data suggest avoiding anticholinergics and other anxiolytics or sedative-hypnotic drugs that may cause cognitive slowing, fatigue, or drowsiness. Beta-blockers are banned in archery and probably inhibit performance in endurance sports. Melatonin, used as a sleep aid, seems safe and does not seem to inhibit performance. Avoid benzodiazepines, especially longer-acting ones, which affect performance.

A relatively new area in the treatment of deficits in memory or attention after TBI is "cognitive enhancers, commonly stimulants. This is "a potential recipe for disaster" for athletes who exercise to exhaustion in hot climates, Dr. Reardon warned, because stimulants allow the athlete to exercise harder, to a higher core body temperature without perceiving greater effort. "There are reports of some who dropped dead," she cautioned.

Amantadine, bromocriptine, and to a lesser extent levodopa also increasingly are being used after TBI, but there is little research in athletes. Preliminary interest is growing in using cholinergic augmentation (donepezil, for instance) to treat attention or memory deficits after TBI, Dr. Reardon noted, but not yet in athletes.

Dr. Reardon, Dr. W. Tsushima, and Dr. V. Tsushima said they have no relevant conflicts of interest. Dr. Baron has received financial support from Eli Lilly.

HONOLULU – Concussions in athletes often produce acute and chronic psychiatric symptoms, but there are few data on the epidemiology and treatment of these problems.

That’s beginning to change.

Physicians increasingly are recognizing chronic traumatic encephalopathy and psychiatric symptoms in athletes after traumatic brain injury (TBI). Unfortunately, little is known about the use of psychotropic medications in athletes with or without TBI, eating disorders, depression, anxiety, or other disorders, several speakers said at the annual meeting of the American Psychiatric Association.

Psychiatric sequelae from TBI in particular "is a timely topic, but that doesn’t mean it hasn’t been around a long time," said Dr. Antonia L. Baum, moderator of the session and a sports psychiatrist in Chevy Chase, Md.

Dr. Claudia L. Reardon of the University of Wisconsin, Madison, recently published a review article summarizing the medical literature on the diagnosis and treatment of mental illness in athletes, which she was able to describe in a single presentation at the meeting (Sports Med. 2010;40:961-80).

Psychiatric symptoms can arise in an athlete after TBI for a variety of reasons. Symptoms of attention-deficit/hyperactivity disorder (ADHD), for example, may worsen after a concussion, or the TBI’s damage to specific brain areas might cause psychiatric symptoms. Reaction to the stress of TBI or to stressful life events after the TBI, might lead to psychiatric symptoms, Dr. Reardon said.

Between 20% and 30% of people who suffer concussions develop acute major depressive disorder, and subacute depression or mood liability is seen in others. Insomnia troubles 36%-70% of patients after TBI. Other acute and subacute symptoms after TBI include anxiety, posttraumatic stress disorder, irritability, apathy, personality changes, impulsivity, somatization, and ADHD-like symptoms. In patients with preexisting disorders, concussion may exacerbate symptoms and make them more difficult to treat.

Chronic traumatic encephalopathy (CTE), a neurodegenerative disease, can develop years after recovery from the acute effects of TBI, especially if the brain has insufficient time to recover between serial concussions.

Clinical symptoms of CTE emerge 8 years after serial concussions, around age 43 years on average; but the timing varies widely, Dr. Reardon said. Symptom onset usually is insidious, with slow and steady progression over an average of 18 years, though somewhat faster in football players than in other athletes.

Irritability, anger, apathy, a "punchy" personality, and a so-called "shorter fuse" typify early symptoms of CTE. "Rarely, cognitive difficulties are the first signs to emerge, but usually psychiatric symptoms are what we see first," she said.

People with CTE are more likely to be suicidal, to have an early accidental death, or to overdose on drugs, compared with people without CTE. In later stages of CTE, the neurologic abnormalities appear, such as parkinsonism or speech and gait abnormalities.

Children may be at greater risk than adults for long-term sequelae of TBI, because their brains are still developing, and serious sequelae may be more likely in female than in male athletes, the literature suggests.

Concussions are common not just in "contact" sports such as football and soccer, but in many other sports, even when there’s not a blow to the head. Athletes may have hard contact with floors (gymnastics or wrestling), walls (racquetball), or other objects or people (golf or basketball), she said.

"Traumatic brain injury does set people up for even higher rates of psychiatric conditions, so it’s important to know the baseline rates of these conditions in athletes," Dr. Reardon said.

Eating disorders can be found in up to 60% of female athletes in such sports as running and gymnastics. In male athletes, eating disorders increasingly are being recognized in rowing, wrestling, and other sports, but male bodies tend to recover once the season is over, while females do not.

Abuse of alcohol, stimulants, steroids, and other substances is fairly common in athletes, and TBI can reduce tolerance to alcohol, she noted.

The incidence of major depressive disorder in athletes is probably similar to that in nonathletes, but athletes are at high risk for depression after injury, overtraining, poor performance, or retirement. A few athletes may develop compulsive disorders, but superstitious rituals usually are normal, so "don’t become overly concerned about obsessive-compulsive disorder," she advised.

More Research Data Coming

Physicians, athletes, and sports leagues are beginning to gather sorely needed data on TBI and sequelae in athletes.

"We need to know baseline function to assess any changes" after TBI, said Dr. David A. Baron, professor of psychiatry and director of the Global Center for Exercise, Psychiatry and Sports at the University of Southern California, Los Angeles.

The Glasgow Coma Score may not be sensitive or specific enough to detect many of the problems that sports psychiatrists see, such as early cognitive symptoms, he asserted. "We might be missing some very early clinical findings" by using this most common system for classifying TBI severity, Dr. Baron said.

In 2007, under pressure from politicians and the media, the National Football League for the first time acknowledged that concussions lead to long-term problems and put independent neurologists in charge of return-to-play decisions after TBI, Dr. Baron said. The league started a database to log every concussion for every player. There’s also a new interest in studying the long-term effects of TBI in retired athletes.

William Tsushima, Ph.D. and his son Vincent G. Tsushima, Ph.D., both neuropsychologists in Honolulu, reported that 4 million high school and college athletes have undergone computer-based neuropsychological assessments before sports participation. Each year, 300,000 athletes suffer mild TBI, including 60,000 high school athletes with cognitive and emotional symptoms of TBI. Every player in the National Hockey League now is required to undergo testing before playing.

A study by the Tsushimas in 639 high school athletes found that younger teens recover more slowly than older athletes after concussion, suggesting that more time is needed before allowing younger athletes to return to play.

They used the ImPACT neurocognitive assessment tool, which now comes in a handheld version for use on the field that includes a brief mental status evaluation, Dr. Vincent G. Tsushima said. The device’s makers are working on versions for use with younger ages (5-11 years) and in different languages, he said.

Weigh Rx Choices for Concussion in Athletes

Consider three questions before starting an athlete on a psychiatric medication: Is it safe, especially if the athlete exercises to exhaustion and sweats a lot? Will it affect performance? Is it allowed under antidoping guidelines?

Results of studies of psychiatric medications in athletes may not be generalizable, cautioned Dr. Reardon. They typically involve only one or two doses rather than long-term use.

One of the most common measures of effects on performance is grip strength. "How readily can you extrapolate that to the athlete who is an Olympic 400-meter dasher?" asked Dr. Reardon, who previously was a 400-meter runner in track and field competitions.

The selective serotonin reuptake inhibitor drugs generally are considered first-line therapy for behavioral and cognitive symptoms of traumatic brain injury (TBI) that do not start resolving within a few weeks of TBI, including anxiety, depression, irritability, poor tolerance of frustration, and even cognitive difficulties in athletes who suffered concussion.

Preliminary data suggest that fluoxetine does not affect athletic performance and has no safety concerns. One study reported that paroxetine inhibited athletic performance, but another found no effects.

Very preliminary data from one study on bupropion suggests it may be performance enhancing if used acutely in hot temperatures, but "we should take very seriously that we should avoid this medication in athletes who suffered recent head injury, given the epileptogenic potential of the drug," she said.

In athletes with TBI, preliminary data suggest avoiding anticholinergics and other anxiolytics or sedative-hypnotic drugs that may cause cognitive slowing, fatigue, or drowsiness. Beta-blockers are banned in archery and probably inhibit performance in endurance sports. Melatonin, used as a sleep aid, seems safe and does not seem to inhibit performance. Avoid benzodiazepines, especially longer-acting ones, which affect performance.

A relatively new area in the treatment of deficits in memory or attention after TBI is "cognitive enhancers, commonly stimulants. This is "a potential recipe for disaster" for athletes who exercise to exhaustion in hot climates, Dr. Reardon warned, because stimulants allow the athlete to exercise harder, to a higher core body temperature without perceiving greater effort. "There are reports of some who dropped dead," she cautioned.

Amantadine, bromocriptine, and to a lesser extent levodopa also increasingly are being used after TBI, but there is little research in athletes. Preliminary interest is growing in using cholinergic augmentation (donepezil, for instance) to treat attention or memory deficits after TBI, Dr. Reardon noted, but not yet in athletes.

Dr. Reardon, Dr. W. Tsushima, and Dr. V. Tsushima said they have no relevant conflicts of interest. Dr. Baron has received financial support from Eli Lilly.

HONOLULU – Concussions in athletes often produce acute and chronic psychiatric symptoms, but there are few data on the epidemiology and treatment of these problems.

That’s beginning to change.

Physicians increasingly are recognizing chronic traumatic encephalopathy and psychiatric symptoms in athletes after traumatic brain injury (TBI). Unfortunately, little is known about the use of psychotropic medications in athletes with or without TBI, eating disorders, depression, anxiety, or other disorders, several speakers said at the annual meeting of the American Psychiatric Association.

Psychiatric sequelae from TBI in particular "is a timely topic, but that doesn’t mean it hasn’t been around a long time," said Dr. Antonia L. Baum, moderator of the session and a sports psychiatrist in Chevy Chase, Md.

Dr. Claudia L. Reardon of the University of Wisconsin, Madison, recently published a review article summarizing the medical literature on the diagnosis and treatment of mental illness in athletes, which she was able to describe in a single presentation at the meeting (Sports Med. 2010;40:961-80).

Psychiatric symptoms can arise in an athlete after TBI for a variety of reasons. Symptoms of attention-deficit/hyperactivity disorder (ADHD), for example, may worsen after a concussion, or the TBI’s damage to specific brain areas might cause psychiatric symptoms. Reaction to the stress of TBI or to stressful life events after the TBI, might lead to psychiatric symptoms, Dr. Reardon said.

Between 20% and 30% of people who suffer concussions develop acute major depressive disorder, and subacute depression or mood liability is seen in others. Insomnia troubles 36%-70% of patients after TBI. Other acute and subacute symptoms after TBI include anxiety, posttraumatic stress disorder, irritability, apathy, personality changes, impulsivity, somatization, and ADHD-like symptoms. In patients with preexisting disorders, concussion may exacerbate symptoms and make them more difficult to treat.

Chronic traumatic encephalopathy (CTE), a neurodegenerative disease, can develop years after recovery from the acute effects of TBI, especially if the brain has insufficient time to recover between serial concussions.

Clinical symptoms of CTE emerge 8 years after serial concussions, around age 43 years on average; but the timing varies widely, Dr. Reardon said. Symptom onset usually is insidious, with slow and steady progression over an average of 18 years, though somewhat faster in football players than in other athletes.

Irritability, anger, apathy, a "punchy" personality, and a so-called "shorter fuse" typify early symptoms of CTE. "Rarely, cognitive difficulties are the first signs to emerge, but usually psychiatric symptoms are what we see first," she said.

People with CTE are more likely to be suicidal, to have an early accidental death, or to overdose on drugs, compared with people without CTE. In later stages of CTE, the neurologic abnormalities appear, such as parkinsonism or speech and gait abnormalities.

Children may be at greater risk than adults for long-term sequelae of TBI, because their brains are still developing, and serious sequelae may be more likely in female than in male athletes, the literature suggests.

Concussions are common not just in "contact" sports such as football and soccer, but in many other sports, even when there’s not a blow to the head. Athletes may have hard contact with floors (gymnastics or wrestling), walls (racquetball), or other objects or people (golf or basketball), she said.

"Traumatic brain injury does set people up for even higher rates of psychiatric conditions, so it’s important to know the baseline rates of these conditions in athletes," Dr. Reardon said.

Eating disorders can be found in up to 60% of female athletes in such sports as running and gymnastics. In male athletes, eating disorders increasingly are being recognized in rowing, wrestling, and other sports, but male bodies tend to recover once the season is over, while females do not.

Abuse of alcohol, stimulants, steroids, and other substances is fairly common in athletes, and TBI can reduce tolerance to alcohol, she noted.

The incidence of major depressive disorder in athletes is probably similar to that in nonathletes, but athletes are at high risk for depression after injury, overtraining, poor performance, or retirement. A few athletes may develop compulsive disorders, but superstitious rituals usually are normal, so "don’t become overly concerned about obsessive-compulsive disorder," she advised.

More Research Data Coming

Physicians, athletes, and sports leagues are beginning to gather sorely needed data on TBI and sequelae in athletes.

"We need to know baseline function to assess any changes" after TBI, said Dr. David A. Baron, professor of psychiatry and director of the Global Center for Exercise, Psychiatry and Sports at the University of Southern California, Los Angeles.

The Glasgow Coma Score may not be sensitive or specific enough to detect many of the problems that sports psychiatrists see, such as early cognitive symptoms, he asserted. "We might be missing some very early clinical findings" by using this most common system for classifying TBI severity, Dr. Baron said.

In 2007, under pressure from politicians and the media, the National Football League for the first time acknowledged that concussions lead to long-term problems and put independent neurologists in charge of return-to-play decisions after TBI, Dr. Baron said. The league started a database to log every concussion for every player. There’s also a new interest in studying the long-term effects of TBI in retired athletes.

William Tsushima, Ph.D. and his son Vincent G. Tsushima, Ph.D., both neuropsychologists in Honolulu, reported that 4 million high school and college athletes have undergone computer-based neuropsychological assessments before sports participation. Each year, 300,000 athletes suffer mild TBI, including 60,000 high school athletes with cognitive and emotional symptoms of TBI. Every player in the National Hockey League now is required to undergo testing before playing.

A study by the Tsushimas in 639 high school athletes found that younger teens recover more slowly than older athletes after concussion, suggesting that more time is needed before allowing younger athletes to return to play.

They used the ImPACT neurocognitive assessment tool, which now comes in a handheld version for use on the field that includes a brief mental status evaluation, Dr. Vincent G. Tsushima said. The device’s makers are working on versions for use with younger ages (5-11 years) and in different languages, he said.

Weigh Rx Choices for Concussion in Athletes

Consider three questions before starting an athlete on a psychiatric medication: Is it safe, especially if the athlete exercises to exhaustion and sweats a lot? Will it affect performance? Is it allowed under antidoping guidelines?

Results of studies of psychiatric medications in athletes may not be generalizable, cautioned Dr. Reardon. They typically involve only one or two doses rather than long-term use.

One of the most common measures of effects on performance is grip strength. "How readily can you extrapolate that to the athlete who is an Olympic 400-meter dasher?" asked Dr. Reardon, who previously was a 400-meter runner in track and field competitions.

The selective serotonin reuptake inhibitor drugs generally are considered first-line therapy for behavioral and cognitive symptoms of traumatic brain injury (TBI) that do not start resolving within a few weeks of TBI, including anxiety, depression, irritability, poor tolerance of frustration, and even cognitive difficulties in athletes who suffered concussion.

Preliminary data suggest that fluoxetine does not affect athletic performance and has no safety concerns. One study reported that paroxetine inhibited athletic performance, but another found no effects.

Very preliminary data from one study on bupropion suggests it may be performance enhancing if used acutely in hot temperatures, but "we should take very seriously that we should avoid this medication in athletes who suffered recent head injury, given the epileptogenic potential of the drug," she said.

In athletes with TBI, preliminary data suggest avoiding anticholinergics and other anxiolytics or sedative-hypnotic drugs that may cause cognitive slowing, fatigue, or drowsiness. Beta-blockers are banned in archery and probably inhibit performance in endurance sports. Melatonin, used as a sleep aid, seems safe and does not seem to inhibit performance. Avoid benzodiazepines, especially longer-acting ones, which affect performance.

A relatively new area in the treatment of deficits in memory or attention after TBI is "cognitive enhancers, commonly stimulants. This is "a potential recipe for disaster" for athletes who exercise to exhaustion in hot climates, Dr. Reardon warned, because stimulants allow the athlete to exercise harder, to a higher core body temperature without perceiving greater effort. "There are reports of some who dropped dead," she cautioned.

Amantadine, bromocriptine, and to a lesser extent levodopa also increasingly are being used after TBI, but there is little research in athletes. Preliminary interest is growing in using cholinergic augmentation (donepezil, for instance) to treat attention or memory deficits after TBI, Dr. Reardon noted, but not yet in athletes.

Dr. Reardon, Dr. W. Tsushima, and Dr. V. Tsushima said they have no relevant conflicts of interest. Dr. Baron has received financial support from Eli Lilly.

HONOLULU – Concussions in athletes often produce acute and chronic psychiatric symptoms, but there are few data on the epidemiology and treatment of these problems.

That’s beginning to change.

Physicians increasingly are recognizing chronic traumatic encephalopathy and psychiatric symptoms in athletes after traumatic brain injury (TBI). Unfortunately, little is known about the use of psychotropic medications in athletes with or without TBI, eating disorders, depression, anxiety, or other disorders, several speakers said at the annual meeting of the American Psychiatric Association.

Psychiatric sequelae from TBI in particular "is a timely topic, but that doesn’t mean it hasn’t been around a long time," said Dr. Antonia L. Baum, moderator of the session and a sports psychiatrist in Chevy Chase, Md.

Dr. Claudia L. Reardon of the University of Wisconsin, Madison, recently published a review article summarizing the medical literature on the diagnosis and treatment of mental illness in athletes, which she was able to describe in a single presentation at the meeting (Sports Med. 2010;40:961-80).

Psychiatric symptoms can arise in an athlete after TBI for a variety of reasons. Symptoms of attention-deficit/hyperactivity disorder (ADHD), for example, may worsen after a concussion, or the TBI’s damage to specific brain areas might cause psychiatric symptoms. Reaction to the stress of TBI or to stressful life events after the TBI, might lead to psychiatric symptoms, Dr. Reardon said.

Between 20% and 30% of people who suffer concussions develop acute major depressive disorder, and subacute depression or mood liability is seen in others. Insomnia troubles 36%-70% of patients after TBI. Other acute and subacute symptoms after TBI include anxiety, posttraumatic stress disorder, irritability, apathy, personality changes, impulsivity, somatization, and ADHD-like symptoms. In patients with preexisting disorders, concussion may exacerbate symptoms and make them more difficult to treat.

Chronic traumatic encephalopathy (CTE), a neurodegenerative disease, can develop years after recovery from the acute effects of TBI, especially if the brain has insufficient time to recover between serial concussions.

Clinical symptoms of CTE emerge 8 years after serial concussions, around age 43 years on average; but the timing varies widely, Dr. Reardon said. Symptom onset usually is insidious, with slow and steady progression over an average of 18 years, though somewhat faster in football players than in other athletes.

Irritability, anger, apathy, a "punchy" personality, and a so-called "shorter fuse" typify early symptoms of CTE. "Rarely, cognitive difficulties are the first signs to emerge, but usually psychiatric symptoms are what we see first," she said.

People with CTE are more likely to be suicidal, to have an early accidental death, or to overdose on drugs, compared with people without CTE. In later stages of CTE, the neurologic abnormalities appear, such as parkinsonism or speech and gait abnormalities.

Children may be at greater risk than adults for long-term sequelae of TBI, because their brains are still developing, and serious sequelae may be more likely in female than in male athletes, the literature suggests.

Concussions are common not just in "contact" sports such as football and soccer, but in many other sports, even when there’s not a blow to the head. Athletes may have hard contact with floors (gymnastics or wrestling), walls (racquetball), or other objects or people (golf or basketball), she said.

"Traumatic brain injury does set people up for even higher rates of psychiatric conditions, so it’s important to know the baseline rates of these conditions in athletes," Dr. Reardon said.

Eating disorders can be found in up to 60% of female athletes in such sports as running and gymnastics. In male athletes, eating disorders increasingly are being recognized in rowing, wrestling, and other sports, but male bodies tend to recover once the season is over, while females do not.

Abuse of alcohol, stimulants, steroids, and other substances is fairly common in athletes, and TBI can reduce tolerance to alcohol, she noted.

The incidence of major depressive disorder in athletes is probably similar to that in nonathletes, but athletes are at high risk for depression after injury, overtraining, poor performance, or retirement. A few athletes may develop compulsive disorders, but superstitious rituals usually are normal, so "don’t become overly concerned about obsessive-compulsive disorder," she advised.

More Research Data Coming

Physicians, athletes, and sports leagues are beginning to gather sorely needed data on TBI and sequelae in athletes.

"We need to know baseline function to assess any changes" after TBI, said Dr. David A. Baron, professor of psychiatry and director of the Global Center for Exercise, Psychiatry and Sports at the University of Southern California, Los Angeles.

The Glasgow Coma Score may not be sensitive or specific enough to detect many of the problems that sports psychiatrists see, such as early cognitive symptoms, he asserted. "We might be missing some very early clinical findings" by using this most common system for classifying TBI severity, Dr. Baron said.

In 2007, under pressure from politicians and the media, the National Football League for the first time acknowledged that concussions lead to long-term problems and put independent neurologists in charge of return-to-play decisions after TBI, Dr. Baron said. The league started a database to log every concussion for every player. There’s also a new interest in studying the long-term effects of TBI in retired athletes.

William Tsushima, Ph.D. and his son Vincent G. Tsushima, Ph.D., both neuropsychologists in Honolulu, reported that 4 million high school and college athletes have undergone computer-based neuropsychological assessments before sports participation. Each year, 300,000 athletes suffer mild TBI, including 60,000 high school athletes with cognitive and emotional symptoms of TBI. Every player in the National Hockey League now is required to undergo testing before playing.

A study by the Tsushimas in 639 high school athletes found that younger teens recover more slowly than older athletes after concussion, suggesting that more time is needed before allowing younger athletes to return to play.

They used the ImPACT neurocognitive assessment tool, which now comes in a handheld version for use on the field that includes a brief mental status evaluation, Dr. Vincent G. Tsushima said. The device’s makers are working on versions for use with younger ages (5-11 years) and in different languages, he said.

Weigh Rx Choices for Concussion in Athletes

Consider three questions before starting an athlete on a psychiatric medication: Is it safe, especially if the athlete exercises to exhaustion and sweats a lot? Will it affect performance? Is it allowed under antidoping guidelines?

Results of studies of psychiatric medications in athletes may not be generalizable, cautioned Dr. Reardon. They typically involve only one or two doses rather than long-term use.

One of the most common measures of effects on performance is grip strength. "How readily can you extrapolate that to the athlete who is an Olympic 400-meter dasher?" asked Dr. Reardon, who previously was a 400-meter runner in track and field competitions.

The selective serotonin reuptake inhibitor drugs generally are considered first-line therapy for behavioral and cognitive symptoms of traumatic brain injury (TBI) that do not start resolving within a few weeks of TBI, including anxiety, depression, irritability, poor tolerance of frustration, and even cognitive difficulties in athletes who suffered concussion.

Preliminary data suggest that fluoxetine does not affect athletic performance and has no safety concerns. One study reported that paroxetine inhibited athletic performance, but another found no effects.

Very preliminary data from one study on bupropion suggests it may be performance enhancing if used acutely in hot temperatures, but "we should take very seriously that we should avoid this medication in athletes who suffered recent head injury, given the epileptogenic potential of the drug," she said.

In athletes with TBI, preliminary data suggest avoiding anticholinergics and other anxiolytics or sedative-hypnotic drugs that may cause cognitive slowing, fatigue, or drowsiness. Beta-blockers are banned in archery and probably inhibit performance in endurance sports. Melatonin, used as a sleep aid, seems safe and does not seem to inhibit performance. Avoid benzodiazepines, especially longer-acting ones, which affect performance.

A relatively new area in the treatment of deficits in memory or attention after TBI is "cognitive enhancers, commonly stimulants. This is "a potential recipe for disaster" for athletes who exercise to exhaustion in hot climates, Dr. Reardon warned, because stimulants allow the athlete to exercise harder, to a higher core body temperature without perceiving greater effort. "There are reports of some who dropped dead," she cautioned.

Amantadine, bromocriptine, and to a lesser extent levodopa also increasingly are being used after TBI, but there is little research in athletes. Preliminary interest is growing in using cholinergic augmentation (donepezil, for instance) to treat attention or memory deficits after TBI, Dr. Reardon noted, but not yet in athletes.

Dr. Reardon, Dr. W. Tsushima, and Dr. V. Tsushima said they have no relevant conflicts of interest. Dr. Baron has received financial support from Eli Lilly.

HONOLULU – Concussions in athletes often produce acute and chronic psychiatric symptoms, but there are few data on the epidemiology and treatment of these problems.

That’s beginning to change.

Physicians increasingly are recognizing chronic traumatic encephalopathy and psychiatric symptoms in athletes after traumatic brain injury (TBI). Unfortunately, little is known about the use of psychotropic medications in athletes with or without TBI, eating disorders, depression, anxiety, or other disorders, several speakers said at the annual meeting of the American Psychiatric Association.

Psychiatric sequelae from TBI in particular "is a timely topic, but that doesn’t mean it hasn’t been around a long time," said Dr. Antonia L. Baum, moderator of the session and a sports psychiatrist in Chevy Chase, Md.

Dr. Claudia L. Reardon of the University of Wisconsin, Madison, recently published a review article summarizing the medical literature on the diagnosis and treatment of mental illness in athletes, which she was able to describe in a single presentation at the meeting (Sports Med. 2010;40:961-80).

Psychiatric symptoms can arise in an athlete after TBI for a variety of reasons. Symptoms of attention-deficit/hyperactivity disorder (ADHD), for example, may worsen after a concussion, or the TBI’s damage to specific brain areas might cause psychiatric symptoms. Reaction to the stress of TBI or to stressful life events after the TBI, might lead to psychiatric symptoms, Dr. Reardon said.

Between 20% and 30% of people who suffer concussions develop acute major depressive disorder, and subacute depression or mood liability is seen in others. Insomnia troubles 36%-70% of patients after TBI. Other acute and subacute symptoms after TBI include anxiety, posttraumatic stress disorder, irritability, apathy, personality changes, impulsivity, somatization, and ADHD-like symptoms. In patients with preexisting disorders, concussion may exacerbate symptoms and make them more difficult to treat.

Chronic traumatic encephalopathy (CTE), a neurodegenerative disease, can develop years after recovery from the acute effects of TBI, especially if the brain has insufficient time to recover between serial concussions.

Clinical symptoms of CTE emerge 8 years after serial concussions, around age 43 years on average; but the timing varies widely, Dr. Reardon said. Symptom onset usually is insidious, with slow and steady progression over an average of 18 years, though somewhat faster in football players than in other athletes.

Irritability, anger, apathy, a "punchy" personality, and a so-called "shorter fuse" typify early symptoms of CTE. "Rarely, cognitive difficulties are the first signs to emerge, but usually psychiatric symptoms are what we see first," she said.

People with CTE are more likely to be suicidal, to have an early accidental death, or to overdose on drugs, compared with people without CTE. In later stages of CTE, the neurologic abnormalities appear, such as parkinsonism or speech and gait abnormalities.

Children may be at greater risk than adults for long-term sequelae of TBI, because their brains are still developing, and serious sequelae may be more likely in female than in male athletes, the literature suggests.

Concussions are common not just in "contact" sports such as football and soccer, but in many other sports, even when there’s not a blow to the head. Athletes may have hard contact with floors (gymnastics or wrestling), walls (racquetball), or other objects or people (golf or basketball), she said.

"Traumatic brain injury does set people up for even higher rates of psychiatric conditions, so it’s important to know the baseline rates of these conditions in athletes," Dr. Reardon said.

Eating disorders can be found in up to 60% of female athletes in such sports as running and gymnastics. In male athletes, eating disorders increasingly are being recognized in rowing, wrestling, and other sports, but male bodies tend to recover once the season is over, while females do not.

Abuse of alcohol, stimulants, steroids, and other substances is fairly common in athletes, and TBI can reduce tolerance to alcohol, she noted.

The incidence of major depressive disorder in athletes is probably similar to that in nonathletes, but athletes are at high risk for depression after injury, overtraining, poor performance, or retirement. A few athletes may develop compulsive disorders, but superstitious rituals usually are normal, so "don’t become overly concerned about obsessive-compulsive disorder," she advised.

More Research Data Coming

Physicians, athletes, and sports leagues are beginning to gather sorely needed data on TBI and sequelae in athletes.

"We need to know baseline function to assess any changes" after TBI, said Dr. David A. Baron, professor of psychiatry and director of the Global Center for Exercise, Psychiatry and Sports at the University of Southern California, Los Angeles.

The Glasgow Coma Score may not be sensitive or specific enough to detect many of the problems that sports psychiatrists see, such as early cognitive symptoms, he asserted. "We might be missing some very early clinical findings" by using this most common system for classifying TBI severity, Dr. Baron said.

In 2007, under pressure from politicians and the media, the National Football League for the first time acknowledged that concussions lead to long-term problems and put independent neurologists in charge of return-to-play decisions after TBI, Dr. Baron said. The league started a database to log every concussion for every player. There’s also a new interest in studying the long-term effects of TBI in retired athletes.

William Tsushima, Ph.D. and his son Vincent G. Tsushima, Ph.D., both neuropsychologists in Honolulu, reported that 4 million high school and college athletes have undergone computer-based neuropsychological assessments before sports participation. Each year, 300,000 athletes suffer mild TBI, including 60,000 high school athletes with cognitive and emotional symptoms of TBI. Every player in the National Hockey League now is required to undergo testing before playing.

A study by the Tsushimas in 639 high school athletes found that younger teens recover more slowly than older athletes after concussion, suggesting that more time is needed before allowing younger athletes to return to play.

They used the ImPACT neurocognitive assessment tool, which now comes in a handheld version for use on the field that includes a brief mental status evaluation, Dr. Vincent G. Tsushima said. The device’s makers are working on versions for use with younger ages (5-11 years) and in different languages, he said.

Weigh Rx Choices for Concussion in Athletes

Consider three questions before starting an athlete on a psychiatric medication: Is it safe, especially if the athlete exercises to exhaustion and sweats a lot? Will it affect performance? Is it allowed under antidoping guidelines?

Results of studies of psychiatric medications in athletes may not be generalizable, cautioned Dr. Reardon. They typically involve only one or two doses rather than long-term use.

One of the most common measures of effects on performance is grip strength. "How readily can you extrapolate that to the athlete who is an Olympic 400-meter dasher?" asked Dr. Reardon, who previously was a 400-meter runner in track and field competitions.

The selective serotonin reuptake inhibitor drugs generally are considered first-line therapy for behavioral and cognitive symptoms of traumatic brain injury (TBI) that do not start resolving within a few weeks of TBI, including anxiety, depression, irritability, poor tolerance of frustration, and even cognitive difficulties in athletes who suffered concussion.

Preliminary data suggest that fluoxetine does not affect athletic performance and has no safety concerns. One study reported that paroxetine inhibited athletic performance, but another found no effects.

Very preliminary data from one study on bupropion suggests it may be performance enhancing if used acutely in hot temperatures, but "we should take very seriously that we should avoid this medication in athletes who suffered recent head injury, given the epileptogenic potential of the drug," she said.

In athletes with TBI, preliminary data suggest avoiding anticholinergics and other anxiolytics or sedative-hypnotic drugs that may cause cognitive slowing, fatigue, or drowsiness. Beta-blockers are banned in archery and probably inhibit performance in endurance sports. Melatonin, used as a sleep aid, seems safe and does not seem to inhibit performance. Avoid benzodiazepines, especially longer-acting ones, which affect performance.

A relatively new area in the treatment of deficits in memory or attention after TBI is "cognitive enhancers, commonly stimulants. This is "a potential recipe for disaster" for athletes who exercise to exhaustion in hot climates, Dr. Reardon warned, because stimulants allow the athlete to exercise harder, to a higher core body temperature without perceiving greater effort. "There are reports of some who dropped dead," she cautioned.

Amantadine, bromocriptine, and to a lesser extent levodopa also increasingly are being used after TBI, but there is little research in athletes. Preliminary interest is growing in using cholinergic augmentation (donepezil, for instance) to treat attention or memory deficits after TBI, Dr. Reardon noted, but not yet in athletes.

Dr. Reardon, Dr. W. Tsushima, and Dr. V. Tsushima said they have no relevant conflicts of interest. Dr. Baron has received financial support from Eli Lilly.

HONOLULU – Concussions in athletes often produce acute and chronic psychiatric symptoms, but there are few data on the epidemiology and treatment of these problems.

That’s beginning to change.

Physicians increasingly are recognizing chronic traumatic encephalopathy and psychiatric symptoms in athletes after traumatic brain injury (TBI). Unfortunately, little is known about the use of psychotropic medications in athletes with or without TBI, eating disorders, depression, anxiety, or other disorders, several speakers said at the annual meeting of the American Psychiatric Association.

Psychiatric sequelae from TBI in particular "is a timely topic, but that doesn’t mean it hasn’t been around a long time," said Dr. Antonia L. Baum, moderator of the session and a sports psychiatrist in Chevy Chase, Md.

Dr. Claudia L. Reardon of the University of Wisconsin, Madison, recently published a review article summarizing the medical literature on the diagnosis and treatment of mental illness in athletes, which she was able to describe in a single presentation at the meeting (Sports Med. 2010;40:961-80).

Psychiatric symptoms can arise in an athlete after TBI for a variety of reasons. Symptoms of attention-deficit/hyperactivity disorder (ADHD), for example, may worsen after a concussion, or the TBI’s damage to specific brain areas might cause psychiatric symptoms. Reaction to the stress of TBI or to stressful life events after the TBI, might lead to psychiatric symptoms, Dr. Reardon said.

Between 20% and 30% of people who suffer concussions develop acute major depressive disorder, and subacute depression or mood liability is seen in others. Insomnia troubles 36%-70% of patients after TBI. Other acute and subacute symptoms after TBI include anxiety, posttraumatic stress disorder, irritability, apathy, personality changes, impulsivity, somatization, and ADHD-like symptoms. In patients with preexisting disorders, concussion may exacerbate symptoms and make them more difficult to treat.

Chronic traumatic encephalopathy (CTE), a neurodegenerative disease, can develop years after recovery from the acute effects of TBI, especially if the brain has insufficient time to recover between serial concussions.

Clinical symptoms of CTE emerge 8 years after serial concussions, around age 43 years on average; but the timing varies widely, Dr. Reardon said. Symptom onset usually is insidious, with slow and steady progression over an average of 18 years, though somewhat faster in football players than in other athletes.

Irritability, anger, apathy, a "punchy" personality, and a so-called "shorter fuse" typify early symptoms of CTE. "Rarely, cognitive difficulties are the first signs to emerge, but usually psychiatric symptoms are what we see first," she said.

People with CTE are more likely to be suicidal, to have an early accidental death, or to overdose on drugs, compared with people without CTE. In later stages of CTE, the neurologic abnormalities appear, such as parkinsonism or speech and gait abnormalities.

Children may be at greater risk than adults for long-term sequelae of TBI, because their brains are still developing, and serious sequelae may be more likely in female than in male athletes, the literature suggests.

Concussions are common not just in "contact" sports such as football and soccer, but in many other sports, even when there’s not a blow to the head. Athletes may have hard contact with floors (gymnastics or wrestling), walls (racquetball), or other objects or people (golf or basketball), she said.

"Traumatic brain injury does set people up for even higher rates of psychiatric conditions, so it’s important to know the baseline rates of these conditions in athletes," Dr. Reardon said.

Eating disorders can be found in up to 60% of female athletes in such sports as running and gymnastics. In male athletes, eating disorders increasingly are being recognized in rowing, wrestling, and other sports, but male bodies tend to recover once the season is over, while females do not.

Abuse of alcohol, stimulants, steroids, and other substances is fairly common in athletes, and TBI can reduce tolerance to alcohol, she noted.

The incidence of major depressive disorder in athletes is probably similar to that in nonathletes, but athletes are at high risk for depression after injury, overtraining, poor performance, or retirement. A few athletes may develop compulsive disorders, but superstitious rituals usually are normal, so "don’t become overly concerned about obsessive-compulsive disorder," she advised.

More Research Data Coming

Physicians, athletes, and sports leagues are beginning to gather sorely needed data on TBI and sequelae in athletes.

"We need to know baseline function to assess any changes" after TBI, said Dr. David A. Baron, professor of psychiatry and director of the Global Center for Exercise, Psychiatry and Sports at the University of Southern California, Los Angeles.

The Glasgow Coma Score may not be sensitive or specific enough to detect many of the problems that sports psychiatrists see, such as early cognitive symptoms, he asserted. "We might be missing some very early clinical findings" by using this most common system for classifying TBI severity, Dr. Baron said.

In 2007, under pressure from politicians and the media, the National Football League for the first time acknowledged that concussions lead to long-term problems and put independent neurologists in charge of return-to-play decisions after TBI, Dr. Baron said. The league started a database to log every concussion for every player. There’s also a new interest in studying the long-term effects of TBI in retired athletes.

William Tsushima, Ph.D. and his son Vincent G. Tsushima, Ph.D., both neuropsychologists in Honolulu, reported that 4 million high school and college athletes have undergone computer-based neuropsychological assessments before sports participation. Each year, 300,000 athletes suffer mild TBI, including 60,000 high school athletes with cognitive and emotional symptoms of TBI. Every player in the National Hockey League now is required to undergo testing before playing.

A study by the Tsushimas in 639 high school athletes found that younger teens recover more slowly than older athletes after concussion, suggesting that more time is needed before allowing younger athletes to return to play.

They used the ImPACT neurocognitive assessment tool, which now comes in a handheld version for use on the field that includes a brief mental status evaluation, Dr. Vincent G. Tsushima said. The device’s makers are working on versions for use with younger ages (5-11 years) and in different languages, he said.

Weigh Rx Choices for Concussion in Athletes

Consider three questions before starting an athlete on a psychiatric medication: Is it safe, especially if the athlete exercises to exhaustion and sweats a lot? Will it affect performance? Is it allowed under antidoping guidelines?

Results of studies of psychiatric medications in athletes may not be generalizable, cautioned Dr. Reardon. They typically involve only one or two doses rather than long-term use.

One of the most common measures of effects on performance is grip strength. "How readily can you extrapolate that to the athlete who is an Olympic 400-meter dasher?" asked Dr. Reardon, who previously was a 400-meter runner in track and field competitions.

The selective serotonin reuptake inhibitor drugs generally are considered first-line therapy for behavioral and cognitive symptoms of traumatic brain injury (TBI) that do not start resolving within a few weeks of TBI, including anxiety, depression, irritability, poor tolerance of frustration, and even cognitive difficulties in athletes who suffered concussion.

Preliminary data suggest that fluoxetine does not affect athletic performance and has no safety concerns. One study reported that paroxetine inhibited athletic performance, but another found no effects.

Very preliminary data from one study on bupropion suggests it may be performance enhancing if used acutely in hot temperatures, but "we should take very seriously that we should avoid this medication in athletes who suffered recent head injury, given the epileptogenic potential of the drug," she said.

In athletes with TBI, preliminary data suggest avoiding anticholinergics and other anxiolytics or sedative-hypnotic drugs that may cause cognitive slowing, fatigue, or drowsiness. Beta-blockers are banned in archery and probably inhibit performance in endurance sports. Melatonin, used as a sleep aid, seems safe and does not seem to inhibit performance. Avoid benzodiazepines, especially longer-acting ones, which affect performance.

A relatively new area in the treatment of deficits in memory or attention after TBI is "cognitive enhancers, commonly stimulants. This is "a potential recipe for disaster" for athletes who exercise to exhaustion in hot climates, Dr. Reardon warned, because stimulants allow the athlete to exercise harder, to a higher core body temperature without perceiving greater effort. "There are reports of some who dropped dead," she cautioned.

Amantadine, bromocriptine, and to a lesser extent levodopa also increasingly are being used after TBI, but there is little research in athletes. Preliminary interest is growing in using cholinergic augmentation (donepezil, for instance) to treat attention or memory deficits after TBI, Dr. Reardon noted, but not yet in athletes.

Dr. Reardon, Dr. W. Tsushima, and Dr. V. Tsushima said they have no relevant conflicts of interest. Dr. Baron has received financial support from Eli Lilly.

HONOLULU – Concussions in athletes often produce acute and chronic psychiatric symptoms, but there are few data on the epidemiology and treatment of these problems.

That’s beginning to change.

Physicians increasingly are recognizing chronic traumatic encephalopathy and psychiatric symptoms in athletes after traumatic brain injury (TBI). Unfortunately, little is known about the use of psychotropic medications in athletes with or without TBI, eating disorders, depression, anxiety, or other disorders, several speakers said at the annual meeting of the American Psychiatric Association.

Psychiatric sequelae from TBI in particular "is a timely topic, but that doesn’t mean it hasn’t been around a long time," said Dr. Antonia L. Baum, moderator of the session and a sports psychiatrist in Chevy Chase, Md.

Dr. Claudia L. Reardon of the University of Wisconsin, Madison, recently published a review article summarizing the medical literature on the diagnosis and treatment of mental illness in athletes, which she was able to describe in a single presentation at the meeting (Sports Med. 2010;40:961-80).

Psychiatric symptoms can arise in an athlete after TBI for a variety of reasons. Symptoms of attention-deficit/hyperactivity disorder (ADHD), for example, may worsen after a concussion, or the TBI’s damage to specific brain areas might cause psychiatric symptoms. Reaction to the stress of TBI or to stressful life events after the TBI, might lead to psychiatric symptoms, Dr. Reardon said.

Between 20% and 30% of people who suffer concussions develop acute major depressive disorder, and subacute depression or mood liability is seen in others. Insomnia troubles 36%-70% of patients after TBI. Other acute and subacute symptoms after TBI include anxiety, posttraumatic stress disorder, irritability, apathy, personality changes, impulsivity, somatization, and ADHD-like symptoms. In patients with preexisting disorders, concussion may exacerbate symptoms and make them more difficult to treat.

Chronic traumatic encephalopathy (CTE), a neurodegenerative disease, can develop years after recovery from the acute effects of TBI, especially if the brain has insufficient time to recover between serial concussions.

Clinical symptoms of CTE emerge 8 years after serial concussions, around age 43 years on average; but the timing varies widely, Dr. Reardon said. Symptom onset usually is insidious, with slow and steady progression over an average of 18 years, though somewhat faster in football players than in other athletes.

Irritability, anger, apathy, a "punchy" personality, and a so-called "shorter fuse" typify early symptoms of CTE. "Rarely, cognitive difficulties are the first signs to emerge, but usually psychiatric symptoms are what we see first," she said.

People with CTE are more likely to be suicidal, to have an early accidental death, or to overdose on drugs, compared with people without CTE. In later stages of CTE, the neurologic abnormalities appear, such as parkinsonism or speech and gait abnormalities.

Children may be at greater risk than adults for long-term sequelae of TBI, because their brains are still developing, and serious sequelae may be more likely in female than in male athletes, the literature suggests.

Concussions are common not just in "contact" sports such as football and soccer, but in many other sports, even when there’s not a blow to the head. Athletes may have hard contact with floors (gymnastics or wrestling), walls (racquetball), or other objects or people (golf or basketball), she said.

"Traumatic brain injury does set people up for even higher rates of psychiatric conditions, so it’s important to know the baseline rates of these conditions in athletes," Dr. Reardon said.

Eating disorders can be found in up to 60% of female athletes in such sports as running and gymnastics. In male athletes, eating disorders increasingly are being recognized in rowing, wrestling, and other sports, but male bodies tend to recover once the season is over, while females do not.

Abuse of alcohol, stimulants, steroids, and other substances is fairly common in athletes, and TBI can reduce tolerance to alcohol, she noted.

The incidence of major depressive disorder in athletes is probably similar to that in nonathletes, but athletes are at high risk for depression after injury, overtraining, poor performance, or retirement. A few athletes may develop compulsive disorders, but superstitious rituals usually are normal, so "don’t become overly concerned about obsessive-compulsive disorder," she advised.

More Research Data Coming

Physicians, athletes, and sports leagues are beginning to gather sorely needed data on TBI and sequelae in athletes.

"We need to know baseline function to assess any changes" after TBI, said Dr. David A. Baron, professor of psychiatry and director of the Global Center for Exercise, Psychiatry and Sports at the University of Southern California, Los Angeles.

The Glasgow Coma Score may not be sensitive or specific enough to detect many of the problems that sports psychiatrists see, such as early cognitive symptoms, he asserted. "We might be missing some very early clinical findings" by using this most common system for classifying TBI severity, Dr. Baron said.

In 2007, under pressure from politicians and the media, the National Football League for the first time acknowledged that concussions lead to long-term problems and put independent neurologists in charge of return-to-play decisions after TBI, Dr. Baron said. The league started a database to log every concussion for every player. There’s also a new interest in studying the long-term effects of TBI in retired athletes.

William Tsushima, Ph.D. and his son Vincent G. Tsushima, Ph.D., both neuropsychologists in Honolulu, reported that 4 million high school and college athletes have undergone computer-based neuropsychological assessments before sports participation. Each year, 300,000 athletes suffer mild TBI, including 60,000 high school athletes with cognitive and emotional symptoms of TBI. Every player in the National Hockey League now is required to undergo testing before playing.

A study by the Tsushimas in 639 high school athletes found that younger teens recover more slowly than older athletes after concussion, suggesting that more time is needed before allowing younger athletes to return to play.

They used the ImPACT neurocognitive assessment tool, which now comes in a handheld version for use on the field that includes a brief mental status evaluation, Dr. Vincent G. Tsushima said. The device’s makers are working on versions for use with younger ages (5-11 years) and in different languages, he said.

Weigh Rx Choices for Concussion in Athletes

Consider three questions before starting an athlete on a psychiatric medication: Is it safe, especially if the athlete exercises to exhaustion and sweats a lot? Will it affect performance? Is it allowed under antidoping guidelines?

Results of studies of psychiatric medications in athletes may not be generalizable, cautioned Dr. Reardon. They typically involve only one or two doses rather than long-term use.

One of the most common measures of effects on performance is grip strength. "How readily can you extrapolate that to the athlete who is an Olympic 400-meter dasher?" asked Dr. Reardon, who previously was a 400-meter runner in track and field competitions.

The selective serotonin reuptake inhibitor drugs generally are considered first-line therapy for behavioral and cognitive symptoms of traumatic brain injury (TBI) that do not start resolving within a few weeks of TBI, including anxiety, depression, irritability, poor tolerance of frustration, and even cognitive difficulties in athletes who suffered concussion.

Preliminary data suggest that fluoxetine does not affect athletic performance and has no safety concerns. One study reported that paroxetine inhibited athletic performance, but another found no effects.

Very preliminary data from one study on bupropion suggests it may be performance enhancing if used acutely in hot temperatures, but "we should take very seriously that we should avoid this medication in athletes who suffered recent head injury, given the epileptogenic potential of the drug," she said.

In athletes with TBI, preliminary data suggest avoiding anticholinergics and other anxiolytics or sedative-hypnotic drugs that may cause cognitive slowing, fatigue, or drowsiness. Beta-blockers are banned in archery and probably inhibit performance in endurance sports. Melatonin, used as a sleep aid, seems safe and does not seem to inhibit performance. Avoid benzodiazepines, especially longer-acting ones, which affect performance.

A relatively new area in the treatment of deficits in memory or attention after TBI is "cognitive enhancers, commonly stimulants. This is "a potential recipe for disaster" for athletes who exercise to exhaustion in hot climates, Dr. Reardon warned, because stimulants allow the athlete to exercise harder, to a higher core body temperature without perceiving greater effort. "There are reports of some who dropped dead," she cautioned.

Amantadine, bromocriptine, and to a lesser extent levodopa also increasingly are being used after TBI, but there is little research in athletes. Preliminary interest is growing in using cholinergic augmentation (donepezil, for instance) to treat attention or memory deficits after TBI, Dr. Reardon noted, but not yet in athletes.

Dr. Reardon, Dr. W. Tsushima, and Dr. V. Tsushima said they have no relevant conflicts of interest. Dr. Baron has received financial support from Eli Lilly.

HONOLULU – Concussions in athletes often produce acute and chronic psychiatric symptoms, but there are few data on the epidemiology and treatment of these problems.

That’s beginning to change.

Physicians increasingly are recognizing chronic traumatic encephalopathy and psychiatric symptoms in athletes after traumatic brain injury (TBI). Unfortunately, little is known about the use of psychotropic medications in athletes with or without TBI, eating disorders, depression, anxiety, or other disorders, several speakers said at the annual meeting of the American Psychiatric Association.

Psychiatric sequelae from TBI in particular "is a timely topic, but that doesn’t mean it hasn’t been around a long time," said Dr. Antonia L. Baum, moderator of the session and a sports psychiatrist in Chevy Chase, Md.

Dr. Claudia L. Reardon of the University of Wisconsin, Madison, recently published a review article summarizing the medical literature on the diagnosis and treatment of mental illness in athletes, which she was able to describe in a single presentation at the meeting (Sports Med. 2010;40:961-80).

Psychiatric symptoms can arise in an athlete after TBI for a variety of reasons. Symptoms of attention-deficit/hyperactivity disorder (ADHD), for example, may worsen after a concussion, or the TBI’s damage to specific brain areas might cause psychiatric symptoms. Reaction to the stress of TBI or to stressful life events after the TBI, might lead to psychiatric symptoms, Dr. Reardon said.

Between 20% and 30% of people who suffer concussions develop acute major depressive disorder, and subacute depression or mood liability is seen in others. Insomnia troubles 36%-70% of patients after TBI. Other acute and subacute symptoms after TBI include anxiety, posttraumatic stress disorder, irritability, apathy, personality changes, impulsivity, somatization, and ADHD-like symptoms. In patients with preexisting disorders, concussion may exacerbate symptoms and make them more difficult to treat.

Chronic traumatic encephalopathy (CTE), a neurodegenerative disease, can develop years after recovery from the acute effects of TBI, especially if the brain has insufficient time to recover between serial concussions.

Clinical symptoms of CTE emerge 8 years after serial concussions, around age 43 years on average; but the timing varies widely, Dr. Reardon said. Symptom onset usually is insidious, with slow and steady progression over an average of 18 years, though somewhat faster in football players than in other athletes.

Irritability, anger, apathy, a "punchy" personality, and a so-called "shorter fuse" typify early symptoms of CTE. "Rarely, cognitive difficulties are the first signs to emerge, but usually psychiatric symptoms are what we see first," she said.

People with CTE are more likely to be suicidal, to have an early accidental death, or to overdose on drugs, compared with people without CTE. In later stages of CTE, the neurologic abnormalities appear, such as parkinsonism or speech and gait abnormalities.

Children may be at greater risk than adults for long-term sequelae of TBI, because their brains are still developing, and serious sequelae may be more likely in female than in male athletes, the literature suggests.

Concussions are common not just in "contact" sports such as football and soccer, but in many other sports, even when there’s not a blow to the head. Athletes may have hard contact with floors (gymnastics or wrestling), walls (racquetball), or other objects or people (golf or basketball), she said.

"Traumatic brain injury does set people up for even higher rates of psychiatric conditions, so it’s important to know the baseline rates of these conditions in athletes," Dr. Reardon said.

Eating disorders can be found in up to 60% of female athletes in such sports as running and gymnastics. In male athletes, eating disorders increasingly are being recognized in rowing, wrestling, and other sports, but male bodies tend to recover once the season is over, while females do not.

Abuse of alcohol, stimulants, steroids, and other substances is fairly common in athletes, and TBI can reduce tolerance to alcohol, she noted.

The incidence of major depressive disorder in athletes is probably similar to that in nonathletes, but athletes are at high risk for depression after injury, overtraining, poor performance, or retirement. A few athletes may develop compulsive disorders, but superstitious rituals usually are normal, so "don’t become overly concerned about obsessive-compulsive disorder," she advised.

More Research Data Coming

Physicians, athletes, and sports leagues are beginning to gather sorely needed data on TBI and sequelae in athletes.

"We need to know baseline function to assess any changes" after TBI, said Dr. David A. Baron, professor of psychiatry and director of the Global Center for Exercise, Psychiatry and Sports at the University of Southern California, Los Angeles.

The Glasgow Coma Score may not be sensitive or specific enough to detect many of the problems that sports psychiatrists see, such as early cognitive symptoms, he asserted. "We might be missing some very early clinical findings" by using this most common system for classifying TBI severity, Dr. Baron said.

In 2007, under pressure from politicians and the media, the National Football League for the first time acknowledged that concussions lead to long-term problems and put independent neurologists in charge of return-to-play decisions after TBI, Dr. Baron said. The league started a database to log every concussion for every player. There’s also a new interest in studying the long-term effects of TBI in retired athletes.

William Tsushima, Ph.D. and his son Vincent G. Tsushima, Ph.D., both neuropsychologists in Honolulu, reported that 4 million high school and college athletes have undergone computer-based neuropsychological assessments before sports participation. Each year, 300,000 athletes suffer mild TBI, including 60,000 high school athletes with cognitive and emotional symptoms of TBI. Every player in the National Hockey League now is required to undergo testing before playing.

A study by the Tsushimas in 639 high school athletes found that younger teens recover more slowly than older athletes after concussion, suggesting that more time is needed before allowing younger athletes to return to play.

They used the ImPACT neurocognitive assessment tool, which now comes in a handheld version for use on the field that includes a brief mental status evaluation, Dr. Vincent G. Tsushima said. The device’s makers are working on versions for use with younger ages (5-11 years) and in different languages, he said.

Weigh Rx Choices for Concussion in Athletes

Consider three questions before starting an athlete on a psychiatric medication: Is it safe, especially if the athlete exercises to exhaustion and sweats a lot? Will it affect performance? Is it allowed under antidoping guidelines?

Results of studies of psychiatric medications in athletes may not be generalizable, cautioned Dr. Reardon. They typically involve only one or two doses rather than long-term use.

One of the most common measures of effects on performance is grip strength. "How readily can you extrapolate that to the athlete who is an Olympic 400-meter dasher?" asked Dr. Reardon, who previously was a 400-meter runner in track and field competitions.

The selective serotonin reuptake inhibitor drugs generally are considered first-line therapy for behavioral and cognitive symptoms of traumatic brain injury (TBI) that do not start resolving within a few weeks of TBI, including anxiety, depression, irritability, poor tolerance of frustration, and even cognitive difficulties in athletes who suffered concussion.

Preliminary data suggest that fluoxetine does not affect athletic performance and has no safety concerns. One study reported that paroxetine inhibited athletic performance, but another found no effects.

Very preliminary data from one study on bupropion suggests it may be performance enhancing if used acutely in hot temperatures, but "we should take very seriously that we should avoid this medication in athletes who suffered recent head injury, given the epileptogenic potential of the drug," she said.

In athletes with TBI, preliminary data suggest avoiding anticholinergics and other anxiolytics or sedative-hypnotic drugs that may cause cognitive slowing, fatigue, or drowsiness. Beta-blockers are banned in archery and probably inhibit performance in endurance sports. Melatonin, used as a sleep aid, seems safe and does not seem to inhibit performance. Avoid benzodiazepines, especially longer-acting ones, which affect performance.

A relatively new area in the treatment of deficits in memory or attention after TBI is "cognitive enhancers, commonly stimulants. This is "a potential recipe for disaster" for athletes who exercise to exhaustion in hot climates, Dr. Reardon warned, because stimulants allow the athlete to exercise harder, to a higher core body temperature without perceiving greater effort. "There are reports of some who dropped dead," she cautioned.

Amantadine, bromocriptine, and to a lesser extent levodopa also increasingly are being used after TBI, but there is little research in athletes. Preliminary interest is growing in using cholinergic augmentation (donepezil, for instance) to treat attention or memory deficits after TBI, Dr. Reardon noted, but not yet in athletes.

Dr. Reardon, Dr. W. Tsushima, and Dr. V. Tsushima said they have no relevant conflicts of interest. Dr. Baron has received financial support from Eli Lilly.

HONOLULU – Concussions in athletes often produce acute and chronic psychiatric symptoms, but there are few data on the epidemiology and treatment of these problems.

That’s beginning to change.

Physicians increasingly are recognizing chronic traumatic encephalopathy and psychiatric symptoms in athletes after traumatic brain injury (TBI). Unfortunately, little is known about the use of psychotropic medications in athletes with or without TBI, eating disorders, depression, anxiety, or other disorders, several speakers said at the annual meeting of the American Psychiatric Association.

Psychiatric sequelae from TBI in particular "is a timely topic, but that doesn’t mean it hasn’t been around a long time," said Dr. Antonia L. Baum, moderator of the session and a sports psychiatrist in Chevy Chase, Md.

Dr. Claudia L. Reardon of the University of Wisconsin, Madison, recently published a review article summarizing the medical literature on the diagnosis and treatment of mental illness in athletes, which she was able to describe in a single presentation at the meeting (Sports Med. 2010;40:961-80).

Psychiatric symptoms can arise in an athlete after TBI for a variety of reasons. Symptoms of attention-deficit/hyperactivity disorder (ADHD), for example, may worsen after a concussion, or the TBI’s damage to specific brain areas might cause psychiatric symptoms. Reaction to the stress of TBI or to stressful life events after the TBI, might lead to psychiatric symptoms, Dr. Reardon said.

Between 20% and 30% of people who suffer concussions develop acute major depressive disorder, and subacute depression or mood liability is seen in others. Insomnia troubles 36%-70% of patients after TBI. Other acute and subacute symptoms after TBI include anxiety, posttraumatic stress disorder, irritability, apathy, personality changes, impulsivity, somatization, and ADHD-like symptoms. In patients with preexisting disorders, concussion may exacerbate symptoms and make them more difficult to treat.

Chronic traumatic encephalopathy (CTE), a neurodegenerative disease, can develop years after recovery from the acute effects of TBI, especially if the brain has insufficient time to recover between serial concussions.

Clinical symptoms of CTE emerge 8 years after serial concussions, around age 43 years on average; but the timing varies widely, Dr. Reardon said. Symptom onset usually is insidious, with slow and steady progression over an average of 18 years, though somewhat faster in football players than in other athletes.

Irritability, anger, apathy, a "punchy" personality, and a so-called "shorter fuse" typify early symptoms of CTE. "Rarely, cognitive difficulties are the first signs to emerge, but usually psychiatric symptoms are what we see first," she said.

People with CTE are more likely to be suicidal, to have an early accidental death, or to overdose on drugs, compared with people without CTE. In later stages of CTE, the neurologic abnormalities appear, such as parkinsonism or speech and gait abnormalities.

Children may be at greater risk than adults for long-term sequelae of TBI, because their brains are still developing, and serious sequelae may be more likely in female than in male athletes, the literature suggests.

Concussions are common not just in "contact" sports such as football and soccer, but in many other sports, even when there’s not a blow to the head. Athletes may have hard contact with floors (gymnastics or wrestling), walls (racquetball), or other objects or people (golf or basketball), she said.

"Traumatic brain injury does set people up for even higher rates of psychiatric conditions, so it’s important to know the baseline rates of these conditions in athletes," Dr. Reardon said.

Eating disorders can be found in up to 60% of female athletes in such sports as running and gymnastics. In male athletes, eating disorders increasingly are being recognized in rowing, wrestling, and other sports, but male bodies tend to recover once the season is over, while females do not.

Abuse of alcohol, stimulants, steroids, and other substances is fairly common in athletes, and TBI can reduce tolerance to alcohol, she noted.

The incidence of major depressive disorder in athletes is probably similar to that in nonathletes, but athletes are at high risk for depression after injury, overtraining, poor performance, or retirement. A few athletes may develop compulsive disorders, but superstitious rituals usually are normal, so "don’t become overly concerned about obsessive-compulsive disorder," she advised.

More Research Data Coming

Physicians, athletes, and sports leagues are beginning to gather sorely needed data on TBI and sequelae in athletes.

"We need to know baseline function to assess any changes" after TBI, said Dr. David A. Baron, professor of psychiatry and director of the Global Center for Exercise, Psychiatry and Sports at the University of Southern California, Los Angeles.

The Glasgow Coma Score may not be sensitive or specific enough to detect many of the problems that sports psychiatrists see, such as early cognitive symptoms, he asserted. "We might be missing some very early clinical findings" by using this most common system for classifying TBI severity, Dr. Baron said.

In 2007, under pressure from politicians and the media, the National Football League for the first time acknowledged that concussions lead to long-term problems and put independent neurologists in charge of return-to-play decisions after TBI, Dr. Baron said. The league started a database to log every concussion for every player. There’s also a new interest in studying the long-term effects of TBI in retired athletes.

William Tsushima, Ph.D. and his son Vincent G. Tsushima, Ph.D., both neuropsychologists in Honolulu, reported that 4 million high school and college athletes have undergone computer-based neuropsychological assessments before sports participation. Each year, 300,000 athletes suffer mild TBI, including 60,000 high school athletes with cognitive and emotional symptoms of TBI. Every player in the National Hockey League now is required to undergo testing before playing.

A study by the Tsushimas in 639 high school athletes found that younger teens recover more slowly than older athletes after concussion, suggesting that more time is needed before allowing younger athletes to return to play.

They used the ImPACT neurocognitive assessment tool, which now comes in a handheld version for use on the field that includes a brief mental status evaluation, Dr. Vincent G. Tsushima said. The device’s makers are working on versions for use with younger ages (5-11 years) and in different languages, he said.

Weigh Rx Choices for Concussion in Athletes

Consider three questions before starting an athlete on a psychiatric medication: Is it safe, especially if the athlete exercises to exhaustion and sweats a lot? Will it affect performance? Is it allowed under antidoping guidelines?

Results of studies of psychiatric medications in athletes may not be generalizable, cautioned Dr. Reardon. They typically involve only one or two doses rather than long-term use.

One of the most common measures of effects on performance is grip strength. "How readily can you extrapolate that to the athlete who is an Olympic 400-meter dasher?" asked Dr. Reardon, who previously was a 400-meter runner in track and field competitions.

The selective serotonin reuptake inhibitor drugs generally are considered first-line therapy for behavioral and cognitive symptoms of traumatic brain injury (TBI) that do not start resolving within a few weeks of TBI, including anxiety, depression, irritability, poor tolerance of frustration, and even cognitive difficulties in athletes who suffered concussion.

Preliminary data suggest that fluoxetine does not affect athletic performance and has no safety concerns. One study reported that paroxetine inhibited athletic performance, but another found no effects.

Very preliminary data from one study on bupropion suggests it may be performance enhancing if used acutely in hot temperatures, but "we should take very seriously that we should avoid this medication in athletes who suffered recent head injury, given the epileptogenic potential of the drug," she said.

In athletes with TBI, preliminary data suggest avoiding anticholinergics and other anxiolytics or sedative-hypnotic drugs that may cause cognitive slowing, fatigue, or drowsiness. Beta-blockers are banned in archery and probably inhibit performance in endurance sports. Melatonin, used as a sleep aid, seems safe and does not seem to inhibit performance. Avoid benzodiazepines, especially longer-acting ones, which affect performance.

A relatively new area in the treatment of deficits in memory or attention after TBI is "cognitive enhancers, commonly stimulants. This is "a potential recipe for disaster" for athletes who exercise to exhaustion in hot climates, Dr. Reardon warned, because stimulants allow the athlete to exercise harder, to a higher core body temperature without perceiving greater effort. "There are reports of some who dropped dead," she cautioned.

Amantadine, bromocriptine, and to a lesser extent levodopa also increasingly are being used after TBI, but there is little research in athletes. Preliminary interest is growing in using cholinergic augmentation (donepezil, for instance) to treat attention or memory deficits after TBI, Dr. Reardon noted, but not yet in athletes.

Dr. Reardon, Dr. W. Tsushima, and Dr. V. Tsushima said they have no relevant conflicts of interest. Dr. Baron has received financial support from Eli Lilly.

LAS VEGAS – Preoperative scrubs before nail avulsion fail to reduce postoperative infection, recent data suggest.

However, studies have identified best practices for reducing bacterial counts – such as irrigating after nail plate avulsion though there is no evidence that the measures reduce postoperative infection rates.

Photo credit: Dr. Nathaniel J. Jellinek

"Every study that has looked at rates of colonization or recolonization after your scrub showed significant bacterial presence. As good as our scrubs are, they're probably not good enough," Dr. Nathaniel J. Jellinek said at the annual meeting of the American College of Mohs Surgery.

A recent study measured bacterial counts after a 7-minute surgical scrub and again after avulsion of the nail plate. The bacterial counts were essentially the same. "It's as if the surgical scrub didn't do any good," said Dr. Jellinek, who was not involved in the study (Dermatol. Surg. 2010;36:1258-65).

The investigators then irrigated the nail bed with saline, which reduced bacterial counts by 95%. That's "an easy thing to do intraoperatively that you might consider for your practice," said Dr. Jellinek of the department of dermatology at Brown University, Providence, R.I.

Studies published mainly in the podiatric and orthopedic literature show that postoperative infection rates are higher after nail surgery than after skin surgery. Rates of bacterial colonization before and after surgical preparation of nails make the term "sterile surgery" inaccurate for these procedures, which might better be considered clean-contaminated or even contaminated surgery, he said in an interview after his presentation.

Photo credit: Dr. Nathaniel J. Jellinek

Other studies have shown that applying alcohol and chlorhexidine may be superior to chloroxylenol and povidone-iodine to reduce bacterial counts before nail surgery. Bacterial persistence and recolonization also can be reduced by the use of bristled brushes, soaked gauze pads, scrubbing to the interdigital webs, and repeat scrubs.

"At this point, it's all hypothetical whether it decreases infection. But we know that infection rates are unacceptably high, so it can only help if you decrease the bacterial count," Dr. Jellinek said.

He has added multiple prophylactic measures to his practice, where he performs a lot of nail surgery.

First, Dr. Jellinek informs the patient that the nail is a dirty site, he reviews wound care, and educates the patient to pay attention to risk factors for infection and avoid putting fingers or toes in dirty places.

He recommends strict sterile preoperative and intraoperative techniques. A nurse or medical assistant should scrub the surgical area for several minutes. "We're talking not 10 or 30 seconds, but 2, 3, 5 minutes," he said.

The scrub should use multiple agents. He prefers using a bristle brush to scrub with chlorhexidine, gauze pads soaked in 70% isopropyl alcohol, and maybe even povidone-iodine paint. He lets all that sit, and applies a sterile glove over the digit, hand, or foot after the scrub.

During surgery, once the nail plate is avulsed, he recommends either performing a repeat scrub or at least irrigating the nail bed with sterile saline.

Dr. Jellinek said recent data have lowered his threshold for using prophylactic antibiotics. He has come to appreciate that nail infections may be caused by different organisms than those that cause most skin infections and require different antibiotics for treatment.

As a result, "I actually have very few nail infections, but I can't pinpoint which of those five or six things that I've done give me those results," he said.

Studies of prophylactic measures to avoid postoperative nail infections include:

• Preoperative skin and nail preparation of the foot: Comparison of the efficacy of 4 different methods in reducing bacterial load (J. Am. Acad. Dermatol. 2009;61:986-92).

• Chlorhexidine Provides Superior Skin Decontamination in Foot and Ankle Surgery: A Prospective Randomized Study (Clin. Orthop. Relat. Res. 2005;438:204-8).

• Preoperative Skin Preparation of the Foot and Ankle: Bristles and Alcohol Are Better (J. Bone Joint Surg. 2005;87:986-92).

• Efficacy of Surgical Preparation in Solutions in Foot and Ankle Surgery (J. Bone Joint Surg. 2005;87:980-5).

Dr. Jellinek said he had no relevant financial disclosures.

LAS VEGAS – Preoperative scrubs before nail avulsion fail to reduce postoperative infection, recent data suggest.

However, studies have identified best practices for reducing bacterial counts – such as irrigating after nail plate avulsion though there is no evidence that the measures reduce postoperative infection rates.

Photo credit: Dr. Nathaniel J. Jellinek

"Every study that has looked at rates of colonization or recolonization after your scrub showed significant bacterial presence. As good as our scrubs are, they're probably not good enough," Dr. Nathaniel J. Jellinek said at the annual meeting of the American College of Mohs Surgery.

A recent study measured bacterial counts after a 7-minute surgical scrub and again after avulsion of the nail plate. The bacterial counts were essentially the same. "It's as if the surgical scrub didn't do any good," said Dr. Jellinek, who was not involved in the study (Dermatol. Surg. 2010;36:1258-65).

The investigators then irrigated the nail bed with saline, which reduced bacterial counts by 95%. That's "an easy thing to do intraoperatively that you might consider for your practice," said Dr. Jellinek of the department of dermatology at Brown University, Providence, R.I.

Studies published mainly in the podiatric and orthopedic literature show that postoperative infection rates are higher after nail surgery than after skin surgery. Rates of bacterial colonization before and after surgical preparation of nails make the term "sterile surgery" inaccurate for these procedures, which might better be considered clean-contaminated or even contaminated surgery, he said in an interview after his presentation.

Photo credit: Dr. Nathaniel J. Jellinek

Other studies have shown that applying alcohol and chlorhexidine may be superior to chloroxylenol and povidone-iodine to reduce bacterial counts before nail surgery. Bacterial persistence and recolonization also can be reduced by the use of bristled brushes, soaked gauze pads, scrubbing to the interdigital webs, and repeat scrubs.

"At this point, it's all hypothetical whether it decreases infection. But we know that infection rates are unacceptably high, so it can only help if you decrease the bacterial count," Dr. Jellinek said.

He has added multiple prophylactic measures to his practice, where he performs a lot of nail surgery.

First, Dr. Jellinek informs the patient that the nail is a dirty site, he reviews wound care, and educates the patient to pay attention to risk factors for infection and avoid putting fingers or toes in dirty places.

He recommends strict sterile preoperative and intraoperative techniques. A nurse or medical assistant should scrub the surgical area for several minutes. "We're talking not 10 or 30 seconds, but 2, 3, 5 minutes," he said.

The scrub should use multiple agents. He prefers using a bristle brush to scrub with chlorhexidine, gauze pads soaked in 70% isopropyl alcohol, and maybe even povidone-iodine paint. He lets all that sit, and applies a sterile glove over the digit, hand, or foot after the scrub.

During surgery, once the nail plate is avulsed, he recommends either performing a repeat scrub or at least irrigating the nail bed with sterile saline.

Dr. Jellinek said recent data have lowered his threshold for using prophylactic antibiotics. He has come to appreciate that nail infections may be caused by different organisms than those that cause most skin infections and require different antibiotics for treatment.

As a result, "I actually have very few nail infections, but I can't pinpoint which of those five or six things that I've done give me those results," he said.

Studies of prophylactic measures to avoid postoperative nail infections include:

• Preoperative skin and nail preparation of the foot: Comparison of the efficacy of 4 different methods in reducing bacterial load (J. Am. Acad. Dermatol. 2009;61:986-92).

• Chlorhexidine Provides Superior Skin Decontamination in Foot and Ankle Surgery: A Prospective Randomized Study (Clin. Orthop. Relat. Res. 2005;438:204-8).

• Preoperative Skin Preparation of the Foot and Ankle: Bristles and Alcohol Are Better (J. Bone Joint Surg. 2005;87:986-92).

• Efficacy of Surgical Preparation in Solutions in Foot and Ankle Surgery (J. Bone Joint Surg. 2005;87:980-5).

Dr. Jellinek said he had no relevant financial disclosures.

LAS VEGAS – Preoperative scrubs before nail avulsion fail to reduce postoperative infection, recent data suggest.

However, studies have identified best practices for reducing bacterial counts – such as irrigating after nail plate avulsion though there is no evidence that the measures reduce postoperative infection rates.

Photo credit: Dr. Nathaniel J. Jellinek

"Every study that has looked at rates of colonization or recolonization after your scrub showed significant bacterial presence. As good as our scrubs are, they're probably not good enough," Dr. Nathaniel J. Jellinek said at the annual meeting of the American College of Mohs Surgery.

A recent study measured bacterial counts after a 7-minute surgical scrub and again after avulsion of the nail plate. The bacterial counts were essentially the same. "It's as if the surgical scrub didn't do any good," said Dr. Jellinek, who was not involved in the study (Dermatol. Surg. 2010;36:1258-65).

The investigators then irrigated the nail bed with saline, which reduced bacterial counts by 95%. That's "an easy thing to do intraoperatively that you might consider for your practice," said Dr. Jellinek of the department of dermatology at Brown University, Providence, R.I.

Studies published mainly in the podiatric and orthopedic literature show that postoperative infection rates are higher after nail surgery than after skin surgery. Rates of bacterial colonization before and after surgical preparation of nails make the term "sterile surgery" inaccurate for these procedures, which might better be considered clean-contaminated or even contaminated surgery, he said in an interview after his presentation.

Photo credit: Dr. Nathaniel J. Jellinek

Other studies have shown that applying alcohol and chlorhexidine may be superior to chloroxylenol and povidone-iodine to reduce bacterial counts before nail surgery. Bacterial persistence and recolonization also can be reduced by the use of bristled brushes, soaked gauze pads, scrubbing to the interdigital webs, and repeat scrubs.

"At this point, it's all hypothetical whether it decreases infection. But we know that infection rates are unacceptably high, so it can only help if you decrease the bacterial count," Dr. Jellinek said.

He has added multiple prophylactic measures to his practice, where he performs a lot of nail surgery.

First, Dr. Jellinek informs the patient that the nail is a dirty site, he reviews wound care, and educates the patient to pay attention to risk factors for infection and avoid putting fingers or toes in dirty places.

He recommends strict sterile preoperative and intraoperative techniques. A nurse or medical assistant should scrub the surgical area for several minutes. "We're talking not 10 or 30 seconds, but 2, 3, 5 minutes," he said.

The scrub should use multiple agents. He prefers using a bristle brush to scrub with chlorhexidine, gauze pads soaked in 70% isopropyl alcohol, and maybe even povidone-iodine paint. He lets all that sit, and applies a sterile glove over the digit, hand, or foot after the scrub.

During surgery, once the nail plate is avulsed, he recommends either performing a repeat scrub or at least irrigating the nail bed with sterile saline.

Dr. Jellinek said recent data have lowered his threshold for using prophylactic antibiotics. He has come to appreciate that nail infections may be caused by different organisms than those that cause most skin infections and require different antibiotics for treatment.

As a result, "I actually have very few nail infections, but I can't pinpoint which of those five or six things that I've done give me those results," he said.

Studies of prophylactic measures to avoid postoperative nail infections include:

• Preoperative skin and nail preparation of the foot: Comparison of the efficacy of 4 different methods in reducing bacterial load (J. Am. Acad. Dermatol. 2009;61:986-92).

• Chlorhexidine Provides Superior Skin Decontamination in Foot and Ankle Surgery: A Prospective Randomized Study (Clin. Orthop. Relat. Res. 2005;438:204-8).

• Preoperative Skin Preparation of the Foot and Ankle: Bristles and Alcohol Are Better (J. Bone Joint Surg. 2005;87:986-92).

• Efficacy of Surgical Preparation in Solutions in Foot and Ankle Surgery (J. Bone Joint Surg. 2005;87:980-5).

Dr. Jellinek said he had no relevant financial disclosures.

LAS VEGAS – A perioperative hemorrhage in a patient undergoing Mohs surgery is a bloody mess, but a thrombosis causing a stroke is a catastrophe.

"Bleeding is overemphasized in our specialty, because it's dramatic. But it is very inconsequential in contrast to thrombosis, which is probably underappreciated," Dr. Clark C. Otley said at the annual meeting of the American College of Mohs Surgery.

Photo credit: Courtesy Dr. Clark C. Otley 

He reviewed the literature on the risks for hemorrhage in patients on anticoagulant therapy who undergo Mohs surgery and the risks for thrombosis in patients who stop their anticoagulant therapy before Mohs.

"The bottom line is that bleeding happens, but nobody dies. That's in contrast to the thrombotic data, where people do die," said Dr. Otley, professor of dermatology at the Mayo Clinic, Rochester, Minn.

The consequences of a thrombotic episode are so much greater than the impact of a hemorrhagic complication that he recommended continuing medically necessary anticoagulants in most cases. "Take extra care with clopidogrel plus aspirin and with warfarin. Taking patients off these, especially if they have a fresh stent, is not the right thing to do," he said.

A survey of 168 American College of Mohs Surgery members in 2003 gathered reports of thrombotic complications within 3 days of Mohs surgery in 46 patients who had stopped anticoagulant therapy, Dr. Otley noted. These included stroke in 24 patients, transient ischemic attack in 8, MI in 5, cerebral emboli or death in 3 patients each, pulmonary embolus in 2, and blindness in 1 patient (J. Am. Acad. Dermatol 2003;48:233-7).

A separate survey of more than 270 dermasurgeons in 2005 found thrombotic complications in 126 patients who stopped anticoagulants for Mohs surgery, including stroke in 39 patients, transient ischemic attack in 25, MI in 19, unstable angina in 17, death in 15, deep venous thrombosis in 7, and pulmonary embolus in 4 patients (Dermatol. Surg. 2007;33:1189-97).

Case reports are emerging of thrombotic episodes in patients on newer anticoagulants who stop therapy for cutaneous surgery. For instance, he noted, a patient who stopped ticlopidine and aspirin developed a deep venous thrombosis. A patient who stopped clopidogrel and ardeparin thrombosed a prosthetic valve. A patient who stopped clopidogrel and aspirin had an MI.

These problems typically present as emergencies, which the Mohs surgeon may not see, Dr. Otley noted. "You may have had more patients experience this than you know about," he said.

Most of the data on the risk of hemorrhagic complications in patients undergoing superficial cutaneous surgery while on anticoagulants focus on traditional agents such as warfarin, aspirin, and NSAIDs, with some data on heparin. Little or no data exist on the risks with newer, more potent anticoagulants.

A total of 10 of 11 studies of patients on warfarin, aspirin, or NSAIDs found no increased risk of perioperative severe hemorrhagic complications, Dr. Otley said. One study of 21 patients on warfarin found an increased risk of complications including persistent bleeding, hematoma, infection, or graft loss. The most severe complication observed in any of the 11 studies was hematoma.

A meta-analysis of the data found a significantly increased risk if moderate and severe hemorrhagic complications were combined as an outcome, but not for severe complications alone, he noted (Dermatol. Surg. 2008;34:160-5).

Clopidogrel (Plavix) is new enough that there is little consensus on how to manage patients on this potent anticoagulant during cutaneous surgery. "This is the one that we’re seeing a ton of patients on," Dr. Otley said. "If your patient has a fresh stent, you would be insane to take that patient off this medication."

Patients on clopidogrel usually are on other anticoagulants, too. Data suggest there is a significant 28-fold higher risk of severe hemorrhagic complications in patients on any clopidogrel-containing regimen, compared with patients not taking anticoagulants, and a significant eightfold higher risk in patients on clopidogrel plus aspirin, compared with patients on aspirin alone. If you compare patients on clopidogrel with patients not on anticoagulant therapy, the difference in risk for severe hemorrhagic complications is not significant, probably due to the small number of patients on clopidogrel alone, he said.

"Nobody has died of hemorrhagic complications, to my knowledge," while having cutaneous surgery on clopidogrel. However, stopping the drug increases the risk of death from thrombotic complications, Dr. Otley said.

There are no data yet on cutaneous surgery complications in patients on dabigatran, "the new kid on the block," and a drug that "you're going to be hearing a lot about," he said. Dabigatran is as effective as warfarin for preventing stroke in high-risk patients.

If patients scheduled for Mohs surgery are on dabigatran, "I'd probably have them continue it unless your hematologist says otherwise," Dr. Otley said. He urged Mohs surgeons to start collecting data on any complications in patients on dabigatran.

To prevent bleeding complications from Mohs surgery, pay attention to hematologic parameters and monitor blood pressure. Hypertension is the leading cause of excessive intraoperative bleeding, he said. Administer sedatives for anxiolysis, use epinephrine as needed, apply pressure dressings, and put in a drain if you think a patient is going to bleed. Use blood products if needed.

In the OR, dislodge temporary clots, eliminate dead space, apply pressure dressings, and use other techniques for secondary prevention of bleeding complications, he advised. "There's no better time to have someone bleed than while you have them open, so rub all those clots off and recoagulate," he said.

Patients with hemorrhagic complications often apologize to Dr. Otley, thinking they did something that caused the bleeding. "I can guarantee you thrombotic patients will not be apologizing to you," he said.

Dr. Otley said he has no relevant conflicts of interest.

LAS VEGAS – A perioperative hemorrhage in a patient undergoing Mohs surgery is a bloody mess, but a thrombosis causing a stroke is a catastrophe.

"Bleeding is overemphasized in our specialty, because it's dramatic. But it is very inconsequential in contrast to thrombosis, which is probably underappreciated," Dr. Clark C. Otley said at the annual meeting of the American College of Mohs Surgery.

Photo credit: Courtesy Dr. Clark C. Otley 

He reviewed the literature on the risks for hemorrhage in patients on anticoagulant therapy who undergo Mohs surgery and the risks for thrombosis in patients who stop their anticoagulant therapy before Mohs.

"The bottom line is that bleeding happens, but nobody dies. That's in contrast to the thrombotic data, where people do die," said Dr. Otley, professor of dermatology at the Mayo Clinic, Rochester, Minn.

The consequences of a thrombotic episode are so much greater than the impact of a hemorrhagic complication that he recommended continuing medically necessary anticoagulants in most cases. "Take extra care with clopidogrel plus aspirin and with warfarin. Taking patients off these, especially if they have a fresh stent, is not the right thing to do," he said.

A survey of 168 American College of Mohs Surgery members in 2003 gathered reports of thrombotic complications within 3 days of Mohs surgery in 46 patients who had stopped anticoagulant therapy, Dr. Otley noted. These included stroke in 24 patients, transient ischemic attack in 8, MI in 5, cerebral emboli or death in 3 patients each, pulmonary embolus in 2, and blindness in 1 patient (J. Am. Acad. Dermatol 2003;48:233-7).

A separate survey of more than 270 dermasurgeons in 2005 found thrombotic complications in 126 patients who stopped anticoagulants for Mohs surgery, including stroke in 39 patients, transient ischemic attack in 25, MI in 19, unstable angina in 17, death in 15, deep venous thrombosis in 7, and pulmonary embolus in 4 patients (Dermatol. Surg. 2007;33:1189-97).

Case reports are emerging of thrombotic episodes in patients on newer anticoagulants who stop therapy for cutaneous surgery. For instance, he noted, a patient who stopped ticlopidine and aspirin developed a deep venous thrombosis. A patient who stopped clopidogrel and ardeparin thrombosed a prosthetic valve. A patient who stopped clopidogrel and aspirin had an MI.

These problems typically present as emergencies, which the Mohs surgeon may not see, Dr. Otley noted. "You may have had more patients experience this than you know about," he said.

Most of the data on the risk of hemorrhagic complications in patients undergoing superficial cutaneous surgery while on anticoagulants focus on traditional agents such as warfarin, aspirin, and NSAIDs, with some data on heparin. Little or no data exist on the risks with newer, more potent anticoagulants.

A total of 10 of 11 studies of patients on warfarin, aspirin, or NSAIDs found no increased risk of perioperative severe hemorrhagic complications, Dr. Otley said. One study of 21 patients on warfarin found an increased risk of complications including persistent bleeding, hematoma, infection, or graft loss. The most severe complication observed in any of the 11 studies was hematoma.

A meta-analysis of the data found a significantly increased risk if moderate and severe hemorrhagic complications were combined as an outcome, but not for severe complications alone, he noted (Dermatol. Surg. 2008;34:160-5).

Clopidogrel (Plavix) is new enough that there is little consensus on how to manage patients on this potent anticoagulant during cutaneous surgery. "This is the one that we’re seeing a ton of patients on," Dr. Otley said. "If your patient has a fresh stent, you would be insane to take that patient off this medication."

Patients on clopidogrel usually are on other anticoagulants, too. Data suggest there is a significant 28-fold higher risk of severe hemorrhagic complications in patients on any clopidogrel-containing regimen, compared with patients not taking anticoagulants, and a significant eightfold higher risk in patients on clopidogrel plus aspirin, compared with patients on aspirin alone. If you compare patients on clopidogrel with patients not on anticoagulant therapy, the difference in risk for severe hemorrhagic complications is not significant, probably due to the small number of patients on clopidogrel alone, he said.

"Nobody has died of hemorrhagic complications, to my knowledge," while having cutaneous surgery on clopidogrel. However, stopping the drug increases the risk of death from thrombotic complications, Dr. Otley said.

There are no data yet on cutaneous surgery complications in patients on dabigatran, "the new kid on the block," and a drug that "you're going to be hearing a lot about," he said. Dabigatran is as effective as warfarin for preventing stroke in high-risk patients.

If patients scheduled for Mohs surgery are on dabigatran, "I'd probably have them continue it unless your hematologist says otherwise," Dr. Otley said. He urged Mohs surgeons to start collecting data on any complications in patients on dabigatran.

To prevent bleeding complications from Mohs surgery, pay attention to hematologic parameters and monitor blood pressure. Hypertension is the leading cause of excessive intraoperative bleeding, he said. Administer sedatives for anxiolysis, use epinephrine as needed, apply pressure dressings, and put in a drain if you think a patient is going to bleed. Use blood products if needed.

In the OR, dislodge temporary clots, eliminate dead space, apply pressure dressings, and use other techniques for secondary prevention of bleeding complications, he advised. "There's no better time to have someone bleed than while you have them open, so rub all those clots off and recoagulate," he said.

Patients with hemorrhagic complications often apologize to Dr. Otley, thinking they did something that caused the bleeding. "I can guarantee you thrombotic patients will not be apologizing to you," he said.

Dr. Otley said he has no relevant conflicts of interest.

LAS VEGAS – A perioperative hemorrhage in a patient undergoing Mohs surgery is a bloody mess, but a thrombosis causing a stroke is a catastrophe.

"Bleeding is overemphasized in our specialty, because it's dramatic. But it is very inconsequential in contrast to thrombosis, which is probably underappreciated," Dr. Clark C. Otley said at the annual meeting of the American College of Mohs Surgery.

Photo credit: Courtesy Dr. Clark C. Otley 

He reviewed the literature on the risks for hemorrhage in patients on anticoagulant therapy who undergo Mohs surgery and the risks for thrombosis in patients who stop their anticoagulant therapy before Mohs.

"The bottom line is that bleeding happens, but nobody dies. That's in contrast to the thrombotic data, where people do die," said Dr. Otley, professor of dermatology at the Mayo Clinic, Rochester, Minn.

The consequences of a thrombotic episode are so much greater than the impact of a hemorrhagic complication that he recommended continuing medically necessary anticoagulants in most cases. "Take extra care with clopidogrel plus aspirin and with warfarin. Taking patients off these, especially if they have a fresh stent, is not the right thing to do," he said.

A survey of 168 American College of Mohs Surgery members in 2003 gathered reports of thrombotic complications within 3 days of Mohs surgery in 46 patients who had stopped anticoagulant therapy, Dr. Otley noted. These included stroke in 24 patients, transient ischemic attack in 8, MI in 5, cerebral emboli or death in 3 patients each, pulmonary embolus in 2, and blindness in 1 patient (J. Am. Acad. Dermatol 2003;48:233-7).

A separate survey of more than 270 dermasurgeons in 2005 found thrombotic complications in 126 patients who stopped anticoagulants for Mohs surgery, including stroke in 39 patients, transient ischemic attack in 25, MI in 19, unstable angina in 17, death in 15, deep venous thrombosis in 7, and pulmonary embolus in 4 patients (Dermatol. Surg. 2007;33:1189-97).

Case reports are emerging of thrombotic episodes in patients on newer anticoagulants who stop therapy for cutaneous surgery. For instance, he noted, a patient who stopped ticlopidine and aspirin developed a deep venous thrombosis. A patient who stopped clopidogrel and ardeparin thrombosed a prosthetic valve. A patient who stopped clopidogrel and aspirin had an MI.

These problems typically present as emergencies, which the Mohs surgeon may not see, Dr. Otley noted. "You may have had more patients experience this than you know about," he said.

Most of the data on the risk of hemorrhagic complications in patients undergoing superficial cutaneous surgery while on anticoagulants focus on traditional agents such as warfarin, aspirin, and NSAIDs, with some data on heparin. Little or no data exist on the risks with newer, more potent anticoagulants.

A total of 10 of 11 studies of patients on warfarin, aspirin, or NSAIDs found no increased risk of perioperative severe hemorrhagic complications, Dr. Otley said. One study of 21 patients on warfarin found an increased risk of complications including persistent bleeding, hematoma, infection, or graft loss. The most severe complication observed in any of the 11 studies was hematoma.

A meta-analysis of the data found a significantly increased risk if moderate and severe hemorrhagic complications were combined as an outcome, but not for severe complications alone, he noted (Dermatol. Surg. 2008;34:160-5).

Clopidogrel (Plavix) is new enough that there is little consensus on how to manage patients on this potent anticoagulant during cutaneous surgery. "This is the one that we’re seeing a ton of patients on," Dr. Otley said. "If your patient has a fresh stent, you would be insane to take that patient off this medication."

Patients on clopidogrel usually are on other anticoagulants, too. Data suggest there is a significant 28-fold higher risk of severe hemorrhagic complications in patients on any clopidogrel-containing regimen, compared with patients not taking anticoagulants, and a significant eightfold higher risk in patients on clopidogrel plus aspirin, compared with patients on aspirin alone. If you compare patients on clopidogrel with patients not on anticoagulant therapy, the difference in risk for severe hemorrhagic complications is not significant, probably due to the small number of patients on clopidogrel alone, he said.

"Nobody has died of hemorrhagic complications, to my knowledge," while having cutaneous surgery on clopidogrel. However, stopping the drug increases the risk of death from thrombotic complications, Dr. Otley said.

There are no data yet on cutaneous surgery complications in patients on dabigatran, "the new kid on the block," and a drug that "you're going to be hearing a lot about," he said. Dabigatran is as effective as warfarin for preventing stroke in high-risk patients.

If patients scheduled for Mohs surgery are on dabigatran, "I'd probably have them continue it unless your hematologist says otherwise," Dr. Otley said. He urged Mohs surgeons to start collecting data on any complications in patients on dabigatran.

To prevent bleeding complications from Mohs surgery, pay attention to hematologic parameters and monitor blood pressure. Hypertension is the leading cause of excessive intraoperative bleeding, he said. Administer sedatives for anxiolysis, use epinephrine as needed, apply pressure dressings, and put in a drain if you think a patient is going to bleed. Use blood products if needed.

In the OR, dislodge temporary clots, eliminate dead space, apply pressure dressings, and use other techniques for secondary prevention of bleeding complications, he advised. "There's no better time to have someone bleed than while you have them open, so rub all those clots off and recoagulate," he said.

Patients with hemorrhagic complications often apologize to Dr. Otley, thinking they did something that caused the bleeding. "I can guarantee you thrombotic patients will not be apologizing to you," he said.

Dr. Otley said he has no relevant conflicts of interest.

HONOLULU – Ginkgo biloba and simvastatin were not helpful in patients with relapsing-remitting multiple sclerosis in separate randomized controlled trials.

Treatment with ginkgo at 120 mg twice a day for 12 weeks produced no significant, short-term improvements in cognitive function in a study of 121 patients. The addition of simvastatin (Zocor) to interferon therapy for multiple sclerosis in a separate study did not significantly reduce the annualized relapse rate after 1–3 years, investigators reported at the meeting.

In the first study, both the ginkgo and placebo groups had improved average scores on a battery of neuropsychological tests. There were no significant differences between groups in scores on the Paced Auditory Serial Addition Test, the California Verbal Learning Test II, the Controlled Oral Word Association Test, or the Stroop Color–Word Test, said Dr. Jesus Lovera of Louisiana State University, New Orleans.

The two groups also did not differ significantly in secondary outcomes (including perceived cognitive deficits, family reports of cognitive deficits, fatigue, or depression) or in rates of adverse events. In the ginkgo group, one patient had an MI and one developed a severe depressive episode requiring hospitalization, but these were not attributed to ginkgo.

While the study found no short-term cognitive benefits from ginkgo, it did not assess any potential long-term benefits, Dr. Lovera said. There are no approved treatments for impairment of cognition in people with multiple sclerosis, which affects 40%-50% of patients.

Dr. Per Soelberg Sørensen and his associates reported in a separate presentation on a study of 307 treatment-naive patients who were starting treatment with interferon-beta-1a (IFN-beta-1a, Avonex) for relapsing-remitting multiple sclerosis. They were randomized to add-on therapy with either placebo or 80 mg/day of simvastatin (40 mg/day in the first month) for 1–3 years. Patients were followed clinically every 3 months and brain MRIs were conducted at baseline and after 1 year of treatment. At least 1 year of follow-up was completed by 136 patients in the simvastatin group and 132 in the placebo group.

In the study, the annualized documented relapse rate was 31% higher in the simvastatin group (0.19) compared with the placebo group (0.14), but the difference was not statistically significant, said Dr. Sørensen of the Danish Multiple Sclerosis Center in the Rigshospitalet, Copenhagen.

The annualized total rate of documented and undocumented relapses was 15% higher in the simvastatin group (0.44), compared with the placebo group (0.38). Patients who received simvastatin had more new or enlarging T2 lesions on MRI than did those who received placebo (3 vs. 2.5). These and other measures were not statistically significant differences between groups, but suggested a trend toward more disease activity in the simvastatin group compared with placebo, Dr. Sørensen said.

Based on the findings of this multicenter study, simvastatin cannot be recommended as an add-on to IFN-beta-1a therapy for relapsing multiple sclerosis, but patients taking statins for treatment of hypercholesterolemia or to prevent cardiovascular disease should not be discouraged from taking them during IFN-beta-1a therapy, Dr. Sørensen said.

Dr. Lovera and two of his associates disclosed financial relationships with EMD Serono, Teva Pharmaceuticals, Biogen Idec, and/or Pfizer. The ginkgo and placebo were provided by Dr. Willmar Schwabe GmbH, Karlsruhe, Germany. The U.S. Department of Veterans Affairs funded his study.

Dr. Sørensen and multiple associates disclosed financial relationships with Biogen Idec, Merck Serono, Teva Neuroscience, Genmab, Novartis, Bayer Schering, and/or Sanofi-Aventis. The study was funded by Biogen Idec.

There was a trend toward more disease activity in the simvastatin group, compared with placebo.

Source DR. SØRENSEN

HONOLULU – Ginkgo biloba and simvastatin were not helpful in patients with relapsing-remitting multiple sclerosis in separate randomized controlled trials.

Treatment with ginkgo at 120 mg twice a day for 12 weeks produced no significant, short-term improvements in cognitive function in a study of 121 patients. The addition of simvastatin (Zocor) to interferon therapy for multiple sclerosis in a separate study did not significantly reduce the annualized relapse rate after 1–3 years, investigators reported at the meeting.

In the first study, both the ginkgo and placebo groups had improved average scores on a battery of neuropsychological tests. There were no significant differences between groups in scores on the Paced Auditory Serial Addition Test, the California Verbal Learning Test II, the Controlled Oral Word Association Test, or the Stroop Color–Word Test, said Dr. Jesus Lovera of Louisiana State University, New Orleans.

The two groups also did not differ significantly in secondary outcomes (including perceived cognitive deficits, family reports of cognitive deficits, fatigue, or depression) or in rates of adverse events. In the ginkgo group, one patient had an MI and one developed a severe depressive episode requiring hospitalization, but these were not attributed to ginkgo.

While the study found no short-term cognitive benefits from ginkgo, it did not assess any potential long-term benefits, Dr. Lovera said. There are no approved treatments for impairment of cognition in people with multiple sclerosis, which affects 40%-50% of patients.

Dr. Per Soelberg Sørensen and his associates reported in a separate presentation on a study of 307 treatment-naive patients who were starting treatment with interferon-beta-1a (IFN-beta-1a, Avonex) for relapsing-remitting multiple sclerosis. They were randomized to add-on therapy with either placebo or 80 mg/day of simvastatin (40 mg/day in the first month) for 1–3 years. Patients were followed clinically every 3 months and brain MRIs were conducted at baseline and after 1 year of treatment. At least 1 year of follow-up was completed by 136 patients in the simvastatin group and 132 in the placebo group.

In the study, the annualized documented relapse rate was 31% higher in the simvastatin group (0.19) compared with the placebo group (0.14), but the difference was not statistically significant, said Dr. Sørensen of the Danish Multiple Sclerosis Center in the Rigshospitalet, Copenhagen.

The annualized total rate of documented and undocumented relapses was 15% higher in the simvastatin group (0.44), compared with the placebo group (0.38). Patients who received simvastatin had more new or enlarging T2 lesions on MRI than did those who received placebo (3 vs. 2.5). These and other measures were not statistically significant differences between groups, but suggested a trend toward more disease activity in the simvastatin group compared with placebo, Dr. Sørensen said.

Based on the findings of this multicenter study, simvastatin cannot be recommended as an add-on to IFN-beta-1a therapy for relapsing multiple sclerosis, but patients taking statins for treatment of hypercholesterolemia or to prevent cardiovascular disease should not be discouraged from taking them during IFN-beta-1a therapy, Dr. Sørensen said.

Dr. Lovera and two of his associates disclosed financial relationships with EMD Serono, Teva Pharmaceuticals, Biogen Idec, and/or Pfizer. The ginkgo and placebo were provided by Dr. Willmar Schwabe GmbH, Karlsruhe, Germany. The U.S. Department of Veterans Affairs funded his study.

Dr. Sørensen and multiple associates disclosed financial relationships with Biogen Idec, Merck Serono, Teva Neuroscience, Genmab, Novartis, Bayer Schering, and/or Sanofi-Aventis. The study was funded by Biogen Idec.

There was a trend toward more disease activity in the simvastatin group, compared with placebo.

Source DR. SØRENSEN

HONOLULU – Ginkgo biloba and simvastatin were not helpful in patients with relapsing-remitting multiple sclerosis in separate randomized controlled trials.

Treatment with ginkgo at 120 mg twice a day for 12 weeks produced no significant, short-term improvements in cognitive function in a study of 121 patients. The addition of simvastatin (Zocor) to interferon therapy for multiple sclerosis in a separate study did not significantly reduce the annualized relapse rate after 1–3 years, investigators reported at the meeting.

In the first study, both the ginkgo and placebo groups had improved average scores on a battery of neuropsychological tests. There were no significant differences between groups in scores on the Paced Auditory Serial Addition Test, the California Verbal Learning Test II, the Controlled Oral Word Association Test, or the Stroop Color–Word Test, said Dr. Jesus Lovera of Louisiana State University, New Orleans.

The two groups also did not differ significantly in secondary outcomes (including perceived cognitive deficits, family reports of cognitive deficits, fatigue, or depression) or in rates of adverse events. In the ginkgo group, one patient had an MI and one developed a severe depressive episode requiring hospitalization, but these were not attributed to ginkgo.

While the study found no short-term cognitive benefits from ginkgo, it did not assess any potential long-term benefits, Dr. Lovera said. There are no approved treatments for impairment of cognition in people with multiple sclerosis, which affects 40%-50% of patients.

Dr. Per Soelberg Sørensen and his associates reported in a separate presentation on a study of 307 treatment-naive patients who were starting treatment with interferon-beta-1a (IFN-beta-1a, Avonex) for relapsing-remitting multiple sclerosis. They were randomized to add-on therapy with either placebo or 80 mg/day of simvastatin (40 mg/day in the first month) for 1–3 years. Patients were followed clinically every 3 months and brain MRIs were conducted at baseline and after 1 year of treatment. At least 1 year of follow-up was completed by 136 patients in the simvastatin group and 132 in the placebo group.

In the study, the annualized documented relapse rate was 31% higher in the simvastatin group (0.19) compared with the placebo group (0.14), but the difference was not statistically significant, said Dr. Sørensen of the Danish Multiple Sclerosis Center in the Rigshospitalet, Copenhagen.

The annualized total rate of documented and undocumented relapses was 15% higher in the simvastatin group (0.44), compared with the placebo group (0.38). Patients who received simvastatin had more new or enlarging T2 lesions on MRI than did those who received placebo (3 vs. 2.5). These and other measures were not statistically significant differences between groups, but suggested a trend toward more disease activity in the simvastatin group compared with placebo, Dr. Sørensen said.

Based on the findings of this multicenter study, simvastatin cannot be recommended as an add-on to IFN-beta-1a therapy for relapsing multiple sclerosis, but patients taking statins for treatment of hypercholesterolemia or to prevent cardiovascular disease should not be discouraged from taking them during IFN-beta-1a therapy, Dr. Sørensen said.

Dr. Lovera and two of his associates disclosed financial relationships with EMD Serono, Teva Pharmaceuticals, Biogen Idec, and/or Pfizer. The ginkgo and placebo were provided by Dr. Willmar Schwabe GmbH, Karlsruhe, Germany. The U.S. Department of Veterans Affairs funded his study.

Dr. Sørensen and multiple associates disclosed financial relationships with Biogen Idec, Merck Serono, Teva Neuroscience, Genmab, Novartis, Bayer Schering, and/or Sanofi-Aventis. The study was funded by Biogen Idec.

There was a trend toward more disease activity in the simvastatin group, compared with placebo.

Source DR. SØRENSEN