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Bipolar patients struggle with emotion regulation across several dimensions
Patients with bipolar and a greater number of comorbidities had greater difficulties in emotion regulation in several categories, including poor acceptance and differentiation of emotion, difficulties with inhibiting impulsive actions, and using appropriate regulation strategies to modulate emotions, than did their nonbipolar peers, according to a small-scale investigation published in Psychiatry Research.
Dr. Tamsyn E. Van Rheenen of Swinburne University, Melbourne, and associates used the Difficulties in Emotion Regulation Scale (DERS) and the General Behaviour Inventory (GBI), a multidimensional measure of difficulties in emotion regulation, to characterize the emotion regulation profile of 50 patients with bipolar disorder, compared with 52 healthy controls. The researchers noticed that impulse control difficulties were a predictor of hypomania propensity, whereas poor access to mood regulation strategies were linked to depression.
“A better understanding of the emotion regulation difficulties experienced by patients with BD can guide the development of new treatment strategies that may ultimately improve outcomes in the disorder. … It is possible that this measure may be efficacious as a diagnostic tool to assess emotion regulation in patients with the disorder,” the authors wrote.
Read the full article in Psychiatry Research here: doi:10.1016/j.psychres.2014.12.001.
Patients with bipolar and a greater number of comorbidities had greater difficulties in emotion regulation in several categories, including poor acceptance and differentiation of emotion, difficulties with inhibiting impulsive actions, and using appropriate regulation strategies to modulate emotions, than did their nonbipolar peers, according to a small-scale investigation published in Psychiatry Research.
Dr. Tamsyn E. Van Rheenen of Swinburne University, Melbourne, and associates used the Difficulties in Emotion Regulation Scale (DERS) and the General Behaviour Inventory (GBI), a multidimensional measure of difficulties in emotion regulation, to characterize the emotion regulation profile of 50 patients with bipolar disorder, compared with 52 healthy controls. The researchers noticed that impulse control difficulties were a predictor of hypomania propensity, whereas poor access to mood regulation strategies were linked to depression.
“A better understanding of the emotion regulation difficulties experienced by patients with BD can guide the development of new treatment strategies that may ultimately improve outcomes in the disorder. … It is possible that this measure may be efficacious as a diagnostic tool to assess emotion regulation in patients with the disorder,” the authors wrote.
Read the full article in Psychiatry Research here: doi:10.1016/j.psychres.2014.12.001.
Patients with bipolar and a greater number of comorbidities had greater difficulties in emotion regulation in several categories, including poor acceptance and differentiation of emotion, difficulties with inhibiting impulsive actions, and using appropriate regulation strategies to modulate emotions, than did their nonbipolar peers, according to a small-scale investigation published in Psychiatry Research.
Dr. Tamsyn E. Van Rheenen of Swinburne University, Melbourne, and associates used the Difficulties in Emotion Regulation Scale (DERS) and the General Behaviour Inventory (GBI), a multidimensional measure of difficulties in emotion regulation, to characterize the emotion regulation profile of 50 patients with bipolar disorder, compared with 52 healthy controls. The researchers noticed that impulse control difficulties were a predictor of hypomania propensity, whereas poor access to mood regulation strategies were linked to depression.
“A better understanding of the emotion regulation difficulties experienced by patients with BD can guide the development of new treatment strategies that may ultimately improve outcomes in the disorder. … It is possible that this measure may be efficacious as a diagnostic tool to assess emotion regulation in patients with the disorder,” the authors wrote.
Read the full article in Psychiatry Research here: doi:10.1016/j.psychres.2014.12.001.
Emotion processing in euthymic bipolar I analyzed
Patients with bipolar disorder I respond to neutral and negative stimuli less accurately than do first-degree relatives of bipolar patients or a control group, Dr. Gianna Sepede and her associates report.
The investigators recruited euthymic bipolar I outpatients, unrelated first-degree relatives of bipolar I subjects, and controls aged 18-55 years. Other than age, the inclusion criteria were right-handedness and an IQ of greater than 70.
Participants were shown colored pictures from the International Affective Picture System. Stimuli generated by a computer were projected over a screen. The participants were told to press a “yes” or “no” button when they were able to see items such as plants and flowers inside neutral or negative pictures on the screen. They were asked to rate the unpleasantness of negative stimuli on a range of 1 (not unpleasant at all) to 9 (extremely unpleasant).
Both the group of first-degree relatives and the control group were about 6% more accurate than was the BD-I group when responding to both neutral and negative stimuli; overall accuracy stood at 87% for the group of relatives and control group and 81% for the BD-I group. In addition, no significant difference was found in response time, with the group of relatives actually having a slightly slower response time than did those in the BD-I group (1,084 milliseconds vs. 1,073 milliseconds vs. 1,036 milliseconds for control group).
A potential explanation for the findings is that “unaffected relatives of BD-I succeeded in maintaining a good “overt” behavioral performance (to correctly identify “targets”) through a high activation of prefrontal areas during neutral stimuli. As a consequence, diminished prefrontal resources were available for the “covert” processing of negative emotions, and occipital regions were hyperactivated to compensate this deficit,” the investigators said, cautioning that this conclusion was still speculative.
Find the full study in Progress in Neuro-Psychopharmacology & Biological Psychiatry (doi: 10.1016/j.pnpbp.2015.01.016).
Patients with bipolar disorder I respond to neutral and negative stimuli less accurately than do first-degree relatives of bipolar patients or a control group, Dr. Gianna Sepede and her associates report.
The investigators recruited euthymic bipolar I outpatients, unrelated first-degree relatives of bipolar I subjects, and controls aged 18-55 years. Other than age, the inclusion criteria were right-handedness and an IQ of greater than 70.
Participants were shown colored pictures from the International Affective Picture System. Stimuli generated by a computer were projected over a screen. The participants were told to press a “yes” or “no” button when they were able to see items such as plants and flowers inside neutral or negative pictures on the screen. They were asked to rate the unpleasantness of negative stimuli on a range of 1 (not unpleasant at all) to 9 (extremely unpleasant).
Both the group of first-degree relatives and the control group were about 6% more accurate than was the BD-I group when responding to both neutral and negative stimuli; overall accuracy stood at 87% for the group of relatives and control group and 81% for the BD-I group. In addition, no significant difference was found in response time, with the group of relatives actually having a slightly slower response time than did those in the BD-I group (1,084 milliseconds vs. 1,073 milliseconds vs. 1,036 milliseconds for control group).
A potential explanation for the findings is that “unaffected relatives of BD-I succeeded in maintaining a good “overt” behavioral performance (to correctly identify “targets”) through a high activation of prefrontal areas during neutral stimuli. As a consequence, diminished prefrontal resources were available for the “covert” processing of negative emotions, and occipital regions were hyperactivated to compensate this deficit,” the investigators said, cautioning that this conclusion was still speculative.
Find the full study in Progress in Neuro-Psychopharmacology & Biological Psychiatry (doi: 10.1016/j.pnpbp.2015.01.016).
Patients with bipolar disorder I respond to neutral and negative stimuli less accurately than do first-degree relatives of bipolar patients or a control group, Dr. Gianna Sepede and her associates report.
The investigators recruited euthymic bipolar I outpatients, unrelated first-degree relatives of bipolar I subjects, and controls aged 18-55 years. Other than age, the inclusion criteria were right-handedness and an IQ of greater than 70.
Participants were shown colored pictures from the International Affective Picture System. Stimuli generated by a computer were projected over a screen. The participants were told to press a “yes” or “no” button when they were able to see items such as plants and flowers inside neutral or negative pictures on the screen. They were asked to rate the unpleasantness of negative stimuli on a range of 1 (not unpleasant at all) to 9 (extremely unpleasant).
Both the group of first-degree relatives and the control group were about 6% more accurate than was the BD-I group when responding to both neutral and negative stimuli; overall accuracy stood at 87% for the group of relatives and control group and 81% for the BD-I group. In addition, no significant difference was found in response time, with the group of relatives actually having a slightly slower response time than did those in the BD-I group (1,084 milliseconds vs. 1,073 milliseconds vs. 1,036 milliseconds for control group).
A potential explanation for the findings is that “unaffected relatives of BD-I succeeded in maintaining a good “overt” behavioral performance (to correctly identify “targets”) through a high activation of prefrontal areas during neutral stimuli. As a consequence, diminished prefrontal resources were available for the “covert” processing of negative emotions, and occipital regions were hyperactivated to compensate this deficit,” the investigators said, cautioning that this conclusion was still speculative.
Find the full study in Progress in Neuro-Psychopharmacology & Biological Psychiatry (doi: 10.1016/j.pnpbp.2015.01.016).
Collaborative care improves functioning, QOL in bipolar
Patients with bipolar disorder who participated in a collaborative care intervention demonstrated more improvement in functioning and quality of life than controls who received care as usual, Dr. Trijntje Y.G. van der Voort and coauthors at the VU University Medical Center department of psychiatry in Amsterdam report.
In an analysis of 138 adult patients with bipolar disorder over 12 months, those randomized to collaborative care showed more improvement in functioning than did patients in the control group, with a small effect size (ES = 0.3; z = -2.5, P = .01). Additionally, patients in the collaborative care group improved more in the physical health domain of quality of life (ES = 0.4; z = 2.5; P = .01), the authors reported.
The findings suggest that collaborative care is “a promising intervention” that could help patients with bipolar disorder improve functioning, physical health, and quality of life, Dr. van der Voort and colleagues said in the report.
Read the full article published in the Journal of Affective Disorders here: doi:10.1016/j.jad.2015.03.005.
Patients with bipolar disorder who participated in a collaborative care intervention demonstrated more improvement in functioning and quality of life than controls who received care as usual, Dr. Trijntje Y.G. van der Voort and coauthors at the VU University Medical Center department of psychiatry in Amsterdam report.
In an analysis of 138 adult patients with bipolar disorder over 12 months, those randomized to collaborative care showed more improvement in functioning than did patients in the control group, with a small effect size (ES = 0.3; z = -2.5, P = .01). Additionally, patients in the collaborative care group improved more in the physical health domain of quality of life (ES = 0.4; z = 2.5; P = .01), the authors reported.
The findings suggest that collaborative care is “a promising intervention” that could help patients with bipolar disorder improve functioning, physical health, and quality of life, Dr. van der Voort and colleagues said in the report.
Read the full article published in the Journal of Affective Disorders here: doi:10.1016/j.jad.2015.03.005.
Patients with bipolar disorder who participated in a collaborative care intervention demonstrated more improvement in functioning and quality of life than controls who received care as usual, Dr. Trijntje Y.G. van der Voort and coauthors at the VU University Medical Center department of psychiatry in Amsterdam report.
In an analysis of 138 adult patients with bipolar disorder over 12 months, those randomized to collaborative care showed more improvement in functioning than did patients in the control group, with a small effect size (ES = 0.3; z = -2.5, P = .01). Additionally, patients in the collaborative care group improved more in the physical health domain of quality of life (ES = 0.4; z = 2.5; P = .01), the authors reported.
The findings suggest that collaborative care is “a promising intervention” that could help patients with bipolar disorder improve functioning, physical health, and quality of life, Dr. van der Voort and colleagues said in the report.
Read the full article published in the Journal of Affective Disorders here: doi:10.1016/j.jad.2015.03.005.
White matter abnormalities could act as bipolar disorder biomarkers
Verbal fluency deficiencies and certain white matter abnormalities are potential biomarkers of bipolar disorder, according to Isabelle E. Bauer, Ph.D., and her associates.
The investigators found that patients with bipolar disorder performed worse on verbal fluency tests than did the healthy control group, and generated fewer S-words and animal names. Meanwhile, patients with bipolar disorder also showed large areas of altered fractional anisotropy, and mean and radial diffusivity (RD) values in several sections of the brain, including the superior and anterior corona radiata and the corpus callosum. Altered RD also was associated with reduced visuomotor capability and progressive demyelination.
“The reported impairment in verbal fluency and changes in [white matter] integrity in fiber tracts connecting to the internal capsule, the corona radiata, and the corpus callosum may serve as cognitive and neural markers of BD [bipolar disorder],” the investigators concluded.
Find the full study in the Journal of Psychiatric Research (2015;62:115-22 [doi: 10.1016/j.jpsychires.2015.01.008]).
Verbal fluency deficiencies and certain white matter abnormalities are potential biomarkers of bipolar disorder, according to Isabelle E. Bauer, Ph.D., and her associates.
The investigators found that patients with bipolar disorder performed worse on verbal fluency tests than did the healthy control group, and generated fewer S-words and animal names. Meanwhile, patients with bipolar disorder also showed large areas of altered fractional anisotropy, and mean and radial diffusivity (RD) values in several sections of the brain, including the superior and anterior corona radiata and the corpus callosum. Altered RD also was associated with reduced visuomotor capability and progressive demyelination.
“The reported impairment in verbal fluency and changes in [white matter] integrity in fiber tracts connecting to the internal capsule, the corona radiata, and the corpus callosum may serve as cognitive and neural markers of BD [bipolar disorder],” the investigators concluded.
Find the full study in the Journal of Psychiatric Research (2015;62:115-22 [doi: 10.1016/j.jpsychires.2015.01.008]).
Verbal fluency deficiencies and certain white matter abnormalities are potential biomarkers of bipolar disorder, according to Isabelle E. Bauer, Ph.D., and her associates.
The investigators found that patients with bipolar disorder performed worse on verbal fluency tests than did the healthy control group, and generated fewer S-words and animal names. Meanwhile, patients with bipolar disorder also showed large areas of altered fractional anisotropy, and mean and radial diffusivity (RD) values in several sections of the brain, including the superior and anterior corona radiata and the corpus callosum. Altered RD also was associated with reduced visuomotor capability and progressive demyelination.
“The reported impairment in verbal fluency and changes in [white matter] integrity in fiber tracts connecting to the internal capsule, the corona radiata, and the corpus callosum may serve as cognitive and neural markers of BD [bipolar disorder],” the investigators concluded.
Find the full study in the Journal of Psychiatric Research (2015;62:115-22 [doi: 10.1016/j.jpsychires.2015.01.008]).
Suicide attempts in bipolar adolescents more common when ADHD present
Adolescents and young adults with bipolar disorder and attention-deficit/hyperactivity disorder had an increased likelihood of attempted suicide, compared with adolescents and young adults with bipolar disorder only (3.0% vs. 1.1%, respectively), according to research published in the Journal of Affective Disorders.
Dr. Wen-Hsuan Lan of Taipei Veterans General Hospital in Taiwan and associates identified 500 adolescents and young adults with bipolar disorder and ADHD between 15 and 24 years old, who were selected from Taiwan’s National Health Insurance Research Database between 2002 and 2008. In addition to exploring the link between ADHD and attempted suicide in patients with bipolar disorder, the researchers also noted that patients with bipolar disorder and ADHD had a higher prevalence of anxiety disorder (25.6% vs. 15.8%; P = .001) and disruptive behavior disorders (13.2% vs. 2.7%; P = .001) than did those with bipolar disorder alone.
“In contrast to the results of these previous studies, our results suggested that ADHD is an independent risk factor for attempted suicide among patients with bipolar disorder after adjustment for demographic factors, anxiety disorder, disruptive behavior disorders, alcohol use disorders, and substance use disorders,” the researchers wrote. Read the entire article here: J. Affect. Disord. 2015;176:171-5.
Adolescents and young adults with bipolar disorder and attention-deficit/hyperactivity disorder had an increased likelihood of attempted suicide, compared with adolescents and young adults with bipolar disorder only (3.0% vs. 1.1%, respectively), according to research published in the Journal of Affective Disorders.
Dr. Wen-Hsuan Lan of Taipei Veterans General Hospital in Taiwan and associates identified 500 adolescents and young adults with bipolar disorder and ADHD between 15 and 24 years old, who were selected from Taiwan’s National Health Insurance Research Database between 2002 and 2008. In addition to exploring the link between ADHD and attempted suicide in patients with bipolar disorder, the researchers also noted that patients with bipolar disorder and ADHD had a higher prevalence of anxiety disorder (25.6% vs. 15.8%; P = .001) and disruptive behavior disorders (13.2% vs. 2.7%; P = .001) than did those with bipolar disorder alone.
“In contrast to the results of these previous studies, our results suggested that ADHD is an independent risk factor for attempted suicide among patients with bipolar disorder after adjustment for demographic factors, anxiety disorder, disruptive behavior disorders, alcohol use disorders, and substance use disorders,” the researchers wrote. Read the entire article here: J. Affect. Disord. 2015;176:171-5.
Adolescents and young adults with bipolar disorder and attention-deficit/hyperactivity disorder had an increased likelihood of attempted suicide, compared with adolescents and young adults with bipolar disorder only (3.0% vs. 1.1%, respectively), according to research published in the Journal of Affective Disorders.
Dr. Wen-Hsuan Lan of Taipei Veterans General Hospital in Taiwan and associates identified 500 adolescents and young adults with bipolar disorder and ADHD between 15 and 24 years old, who were selected from Taiwan’s National Health Insurance Research Database between 2002 and 2008. In addition to exploring the link between ADHD and attempted suicide in patients with bipolar disorder, the researchers also noted that patients with bipolar disorder and ADHD had a higher prevalence of anxiety disorder (25.6% vs. 15.8%; P = .001) and disruptive behavior disorders (13.2% vs. 2.7%; P = .001) than did those with bipolar disorder alone.
“In contrast to the results of these previous studies, our results suggested that ADHD is an independent risk factor for attempted suicide among patients with bipolar disorder after adjustment for demographic factors, anxiety disorder, disruptive behavior disorders, alcohol use disorders, and substance use disorders,” the researchers wrote. Read the entire article here: J. Affect. Disord. 2015;176:171-5.
Benzodiazepine reduction without withdrawal symptoms possible in patients with schizophrenia, bipolar disorder
COLORADO SPRINGS – Patients with schizophrenia and bipolar disorder can reduce or even discontinue their reliance on benzodiazepines when kept to a gradually tapered titration, results of a Danish study have shown.
Benzodiazepines often are prescribed to patients with severe mental illnesses to help relieve comorbid anxiety and insomnia. According to Dr. Lone Baandrup, a researcher at the Center for Neuropsychiatric Schizophrenia Research at the Copenhagen University Hospital in Glostrup, Denmark, the treatment is usually meant as a temporary measure during acute episodes, but patients often become addicted.
Dr. Baandrup said in an interview at the biennial meeting of the 15th International Congress on Schizophrenia Research that because it is well established that patients with severe mental illness often suffer from a diminished ability to secrete endogenous melatonin, “we wanted to see if we could facilitate tapering patients off their benzos using a prolonged-release melatonin.”
Dr. Baandrup and her colleagues randomly assigned 86 adults with a diagnosis of schizophrenia, schizoaffective disorder, or bipolar disorder who had been on a daily regimen of an antipsychotic and at least one benzodiazepine derivative for at least 3 months, to receive either prolonged-release melatonin 2 mg daily or matching placebo. In the intention-to-treat analysis, each group was guided by a caregiver to gradually taper their respective daily benzodiazepine dosage.
Participants were examined at baseline and at 8, 16, and 24 weeks, and were monitored weekly by telephone. All participants, researchers, treating clinicians, and outcome assessors were blinded to group assignment.
No significant difference was found between the groups as to mean benzodiazepine dosage at 24 weeks, the study’s primary outcome, but the placebo arm had a greater reduction in benzodiazepine dosage (8.01 mg in the study arm vs. 5.72 mg in placebo; difference between means, –2.29; 95% confidence interval, –5.78-1.21; P = .20).
Nearly half of the placebo group achieved complete cessation of benzodiazepine use, compared with more than one-third of the study group (21 out of 44 vs. 16 out of 42; odds ratio, 0.64; 95% confidence interval, 0.26-1.56; P = .32).
Serious or nonserious adverse events were similar across the groups.
A separate analysis of the data not presented at the conference as to whether melatonin had any effect on subjective sleep measures showed that those in the melatonin group had improved sleep according to the Pittsburgh Sleep Quality Index. When compared with the control group, “the difference was about 2 points, so it was only on the border of clinical significance, but their sleep did not get worse,” Dr. Baandrup said.
The investigators also used the Pittsburgh Sleep Diary to measure whether there were any objective differences in sleep between the melatonin and placebo groups, and found that reducing benzodiazepine use did not result in insomnia. “It remained the same from baseline to follow-up," Dr. Baandrup said. “Many patients are afraid to taper off their benzos because they fear their sleep will worsen, but we didn’t find that.”
Dr. Baandrup did not have any relevant disclosures.
On Twitter @whitneymcknight
COLORADO SPRINGS – Patients with schizophrenia and bipolar disorder can reduce or even discontinue their reliance on benzodiazepines when kept to a gradually tapered titration, results of a Danish study have shown.
Benzodiazepines often are prescribed to patients with severe mental illnesses to help relieve comorbid anxiety and insomnia. According to Dr. Lone Baandrup, a researcher at the Center for Neuropsychiatric Schizophrenia Research at the Copenhagen University Hospital in Glostrup, Denmark, the treatment is usually meant as a temporary measure during acute episodes, but patients often become addicted.
Dr. Baandrup said in an interview at the biennial meeting of the 15th International Congress on Schizophrenia Research that because it is well established that patients with severe mental illness often suffer from a diminished ability to secrete endogenous melatonin, “we wanted to see if we could facilitate tapering patients off their benzos using a prolonged-release melatonin.”
Dr. Baandrup and her colleagues randomly assigned 86 adults with a diagnosis of schizophrenia, schizoaffective disorder, or bipolar disorder who had been on a daily regimen of an antipsychotic and at least one benzodiazepine derivative for at least 3 months, to receive either prolonged-release melatonin 2 mg daily or matching placebo. In the intention-to-treat analysis, each group was guided by a caregiver to gradually taper their respective daily benzodiazepine dosage.
Participants were examined at baseline and at 8, 16, and 24 weeks, and were monitored weekly by telephone. All participants, researchers, treating clinicians, and outcome assessors were blinded to group assignment.
No significant difference was found between the groups as to mean benzodiazepine dosage at 24 weeks, the study’s primary outcome, but the placebo arm had a greater reduction in benzodiazepine dosage (8.01 mg in the study arm vs. 5.72 mg in placebo; difference between means, –2.29; 95% confidence interval, –5.78-1.21; P = .20).
Nearly half of the placebo group achieved complete cessation of benzodiazepine use, compared with more than one-third of the study group (21 out of 44 vs. 16 out of 42; odds ratio, 0.64; 95% confidence interval, 0.26-1.56; P = .32).
Serious or nonserious adverse events were similar across the groups.
A separate analysis of the data not presented at the conference as to whether melatonin had any effect on subjective sleep measures showed that those in the melatonin group had improved sleep according to the Pittsburgh Sleep Quality Index. When compared with the control group, “the difference was about 2 points, so it was only on the border of clinical significance, but their sleep did not get worse,” Dr. Baandrup said.
The investigators also used the Pittsburgh Sleep Diary to measure whether there were any objective differences in sleep between the melatonin and placebo groups, and found that reducing benzodiazepine use did not result in insomnia. “It remained the same from baseline to follow-up," Dr. Baandrup said. “Many patients are afraid to taper off their benzos because they fear their sleep will worsen, but we didn’t find that.”
Dr. Baandrup did not have any relevant disclosures.
On Twitter @whitneymcknight
COLORADO SPRINGS – Patients with schizophrenia and bipolar disorder can reduce or even discontinue their reliance on benzodiazepines when kept to a gradually tapered titration, results of a Danish study have shown.
Benzodiazepines often are prescribed to patients with severe mental illnesses to help relieve comorbid anxiety and insomnia. According to Dr. Lone Baandrup, a researcher at the Center for Neuropsychiatric Schizophrenia Research at the Copenhagen University Hospital in Glostrup, Denmark, the treatment is usually meant as a temporary measure during acute episodes, but patients often become addicted.
Dr. Baandrup said in an interview at the biennial meeting of the 15th International Congress on Schizophrenia Research that because it is well established that patients with severe mental illness often suffer from a diminished ability to secrete endogenous melatonin, “we wanted to see if we could facilitate tapering patients off their benzos using a prolonged-release melatonin.”
Dr. Baandrup and her colleagues randomly assigned 86 adults with a diagnosis of schizophrenia, schizoaffective disorder, or bipolar disorder who had been on a daily regimen of an antipsychotic and at least one benzodiazepine derivative for at least 3 months, to receive either prolonged-release melatonin 2 mg daily or matching placebo. In the intention-to-treat analysis, each group was guided by a caregiver to gradually taper their respective daily benzodiazepine dosage.
Participants were examined at baseline and at 8, 16, and 24 weeks, and were monitored weekly by telephone. All participants, researchers, treating clinicians, and outcome assessors were blinded to group assignment.
No significant difference was found between the groups as to mean benzodiazepine dosage at 24 weeks, the study’s primary outcome, but the placebo arm had a greater reduction in benzodiazepine dosage (8.01 mg in the study arm vs. 5.72 mg in placebo; difference between means, –2.29; 95% confidence interval, –5.78-1.21; P = .20).
Nearly half of the placebo group achieved complete cessation of benzodiazepine use, compared with more than one-third of the study group (21 out of 44 vs. 16 out of 42; odds ratio, 0.64; 95% confidence interval, 0.26-1.56; P = .32).
Serious or nonserious adverse events were similar across the groups.
A separate analysis of the data not presented at the conference as to whether melatonin had any effect on subjective sleep measures showed that those in the melatonin group had improved sleep according to the Pittsburgh Sleep Quality Index. When compared with the control group, “the difference was about 2 points, so it was only on the border of clinical significance, but their sleep did not get worse,” Dr. Baandrup said.
The investigators also used the Pittsburgh Sleep Diary to measure whether there were any objective differences in sleep between the melatonin and placebo groups, and found that reducing benzodiazepine use did not result in insomnia. “It remained the same from baseline to follow-up," Dr. Baandrup said. “Many patients are afraid to taper off their benzos because they fear their sleep will worsen, but we didn’t find that.”
Dr. Baandrup did not have any relevant disclosures.
On Twitter @whitneymcknight
AT THE INTERNATIONAL CONGRESS ON SCHIZOPHRENIA RESEARCH
Key clinical point: Patients with schizophrenia or bipolar disorder can reduce, or even discontinue, reliance on benzodiazepines when tapered gradually but steadily.
Major finding: No significant difference was found in benzodiazepine reduction rates between patients with psychosis given prolonged-release melatonin and placebo.
Data source: Negative, single-center, blinded parallel study of 86 patients with schizophrenia or bipolar disorder randomly assigned to long-acting melatonin or placebo while reducing their benzodiazepine dosage over 6 months.
Disclosures: Dr. Baandrup did not have any relevant disclosures.
FDA calls study of unexplained olanzapine deaths ‘inconclusive’
The Food and Drug Administration’s review of a study that looked into the unexplained deaths of two patients days after receiving injections of the long-acting injectable formulation of the atypical antipsychotic olanzapine are “inconclusive,” and no labeling changes are currently recommended, the agency has announced.
“We are unable to exclude the possibility that the deaths were caused by rapid, but delayed, entry of the drug into the bloodstream following intramuscular injection,” according to the drug safety communication issued March 23 by the FDA.
Patients who receive olanzapine pamoate must be monitored for 3 hours after an injection because of the risk of post-injection delirium sedation (PDSS) associated with the injection. These patients, however, died 3 to 4 days after having received appropriate IM doses of olanzapine pamoate (Zyprexa Relprevv) and were found to have very high levels of the drug. The deaths and subsequent investigation were announced by the FDA in 2013.
The March 23 statement said an animal study, conducted by olanzapine manufacturer Eli Lilly at the FDA’s request to determine whether an IM injection could result in “postmortem redistribution” of olanzapine pamoate, “suggested that much of the drug level increase could have occurred after death, a finding that could explain the extremely high blood levels” in the two patients.
Based on its review, the FDA is not recommending any changes to the prescribing information of olanzapine pamoate. However, the agency is advising health care professionals to continue to follow the Risk Evaluation and Mitigation Strategy in place for this drug, which includes mandatory enrollment of patients, prescribers, health care facilities, and pharmacies in the Zyprexa Relprevv Patient Care program. Patients “should not stop receiving treatment without first talking to their health care professionals,” the statement adds.
The REMS requirements include continuous monitoring of patients for 3 hours after the injection, which must be administered at a REMS-certified health care facility that has quick access to emergency response services. A medication guide explaining these and other risks associated with the drug are provided to patients.
The increased risk for severe sedation, including coma, and/or delirium after each olanzapine pamoate injection, also is described in a boxed warning in the prescribing information.
Adverse events associated with Zyprexa Relprevv should be reported to the FDA’s MedWatch program at 800-332-1088 or https://www.accessdata.fda.gov/scripts/medwatch/
The Food and Drug Administration’s review of a study that looked into the unexplained deaths of two patients days after receiving injections of the long-acting injectable formulation of the atypical antipsychotic olanzapine are “inconclusive,” and no labeling changes are currently recommended, the agency has announced.
“We are unable to exclude the possibility that the deaths were caused by rapid, but delayed, entry of the drug into the bloodstream following intramuscular injection,” according to the drug safety communication issued March 23 by the FDA.
Patients who receive olanzapine pamoate must be monitored for 3 hours after an injection because of the risk of post-injection delirium sedation (PDSS) associated with the injection. These patients, however, died 3 to 4 days after having received appropriate IM doses of olanzapine pamoate (Zyprexa Relprevv) and were found to have very high levels of the drug. The deaths and subsequent investigation were announced by the FDA in 2013.
The March 23 statement said an animal study, conducted by olanzapine manufacturer Eli Lilly at the FDA’s request to determine whether an IM injection could result in “postmortem redistribution” of olanzapine pamoate, “suggested that much of the drug level increase could have occurred after death, a finding that could explain the extremely high blood levels” in the two patients.
Based on its review, the FDA is not recommending any changes to the prescribing information of olanzapine pamoate. However, the agency is advising health care professionals to continue to follow the Risk Evaluation and Mitigation Strategy in place for this drug, which includes mandatory enrollment of patients, prescribers, health care facilities, and pharmacies in the Zyprexa Relprevv Patient Care program. Patients “should not stop receiving treatment without first talking to their health care professionals,” the statement adds.
The REMS requirements include continuous monitoring of patients for 3 hours after the injection, which must be administered at a REMS-certified health care facility that has quick access to emergency response services. A medication guide explaining these and other risks associated with the drug are provided to patients.
The increased risk for severe sedation, including coma, and/or delirium after each olanzapine pamoate injection, also is described in a boxed warning in the prescribing information.
Adverse events associated with Zyprexa Relprevv should be reported to the FDA’s MedWatch program at 800-332-1088 or https://www.accessdata.fda.gov/scripts/medwatch/
The Food and Drug Administration’s review of a study that looked into the unexplained deaths of two patients days after receiving injections of the long-acting injectable formulation of the atypical antipsychotic olanzapine are “inconclusive,” and no labeling changes are currently recommended, the agency has announced.
“We are unable to exclude the possibility that the deaths were caused by rapid, but delayed, entry of the drug into the bloodstream following intramuscular injection,” according to the drug safety communication issued March 23 by the FDA.
Patients who receive olanzapine pamoate must be monitored for 3 hours after an injection because of the risk of post-injection delirium sedation (PDSS) associated with the injection. These patients, however, died 3 to 4 days after having received appropriate IM doses of olanzapine pamoate (Zyprexa Relprevv) and were found to have very high levels of the drug. The deaths and subsequent investigation were announced by the FDA in 2013.
The March 23 statement said an animal study, conducted by olanzapine manufacturer Eli Lilly at the FDA’s request to determine whether an IM injection could result in “postmortem redistribution” of olanzapine pamoate, “suggested that much of the drug level increase could have occurred after death, a finding that could explain the extremely high blood levels” in the two patients.
Based on its review, the FDA is not recommending any changes to the prescribing information of olanzapine pamoate. However, the agency is advising health care professionals to continue to follow the Risk Evaluation and Mitigation Strategy in place for this drug, which includes mandatory enrollment of patients, prescribers, health care facilities, and pharmacies in the Zyprexa Relprevv Patient Care program. Patients “should not stop receiving treatment without first talking to their health care professionals,” the statement adds.
The REMS requirements include continuous monitoring of patients for 3 hours after the injection, which must be administered at a REMS-certified health care facility that has quick access to emergency response services. A medication guide explaining these and other risks associated with the drug are provided to patients.
The increased risk for severe sedation, including coma, and/or delirium after each olanzapine pamoate injection, also is described in a boxed warning in the prescribing information.
Adverse events associated with Zyprexa Relprevv should be reported to the FDA’s MedWatch program at 800-332-1088 or https://www.accessdata.fda.gov/scripts/medwatch/
What to tell your bipolar disorder patient who wants to breast-feed
Ms. K, age 35, soon will deliver her second child. She has a 12-year history of bipolar disorder, which was well controlled with lithium, 1,200 mg/d. During her first pregnancy 3 years ago, Ms. K stopped taking lithium because she was concerned about the risk of Ebstein’s anomaly. She experienced a bipolar relapse after her healthy baby was born, and developed postpartum psychosis that was treated by restarting lithium, 1,200 mg/d, and adding olanzapine, 10 mg/d.
Ms. K has continued these medications throughout her current pregnancy. She wants to breast-feed her infant and is concerned about the effects that psychotropics might have on her newborn.
Breast-feeding and medications
The benefits of breast-feeding for mother and infant are well-known. Despite this, some women with bipolar disorder are advised not to breast-feed or, worse, to discontinue their medications in order to breast-feed. Decisions about breast-feeding while taking medications should be based on evidence of benefits and risks to the infant, along with a discussion of the risks of untreated illness, which is high postpartum. The prescribing information for many of the medications used to treat bipolar disorder advise against breast-feeding, although there is little evidence of harm.
Drug dosages and levels in breast milk can be reported a few different ways:
• percentage of maternal dosage measured in the breast milk
• percentage weight-adjusted maternal dosage
• percentage of maternal plasma level, and milk-to-plasma ratio (M:P).
Daily infant dosage can be calculated by multiplying the average concentration of the drug in breast milk (mg/mL) by the average volume of milk the baby ingests in 24 hours (usually 150 mL).1 The relative infant dosage can be calculated as the percentage maternal dosage, which is the daily infant dosage (mg/kg/d) ÷ maternal dosage (mg/kg/d) × 100.1
According to the American Academy of Pediatrics, ≤10% of the maternal dosage is compatible with breast-feeding.1 Most psychotropics studied fall below this threshold. Keep in mind that all published research is for breast-feeding a full-term infant; exercise caution with premature or low birth weight infants. Infants born to mothers taking a psychotropic should be monitored for withdrawal symptoms, which might be associated with antidepressants and benzodiazepines, but otherwise are rare.
Lithium
Breast-feeding during lithium treatment has been considered contraindicated based on early reports that lithium was highly excreted in breast milk.2 A 2003 study2 of 11 women found that lithium was excreted in breast milk in amounts between zero and 30% of maternal dosage (mean, 12.2% ± 8.5%; median, 11.2%; 95% CI, 6.3% to 18.0%). Researchers measured serum concentrations in 2 infants and found that 1 received 17% to 20% of the maternal dosage, and the other showed 50%. None of the infants experienced adverse events. In a study of 10 mother-infant pairs, breast milk lithium concentration averaged 0.35 mEq/L (standard deviation [SD] = 0.10, range 0.19 to 0.48 mEq/L), with paired infant serum concentrations of 0.16 mEq/L (SD = 0.06, range 0.09 to 0.25 mEq/L).3 Some transient abnormalities were found in infant serum concentrations of thyroid-stimulating hormone (TSH), blood urea nitrogen, and creatinine; there were no adverse effects on development. The authors recommend monitoring for TSH abnormalities in infants.
Olanzapine
Olanzapine prescribing information cites a study reporting that 1.8% of the maternal dosage is transferred to breast milk.4 Yet the olanzapine prescribing information states, “It is recommended that women receiving olanzapine should not breast-feed.” Olanzapine use during breast-feeding has been studied more than many medications, in part because of a database maintained by the manufacturer. In a study using the manufacturer’s database (N = 102) adverse reactions were reported in 15.6% of the infants, with the most common being somnolence (3.9%), irritability (2%), tremor (2%), and insomnia (2%).5
Other second-generation antipsychotics
Aripiprazole. The only case report of aripiprazole excretion in human breast milk found a concentration of approximately 20% of the maternal plasma level and an M:P ratio of 0.18:0.2.6
Asenapine. According to asenapine prescribing information7 and a literature search, it is not known whether asenapine is excreted in breast milk of humans, although it is found in the milk of lactating rats.
Lurasidone. According to the lurasidone prescribing information8 and a literature search, it is not known whether lurasidone is excreted in human breast milk, although it is found in the milk of lactating rats.
Quetiapine. An initial study reported that 0.09% to 0.43% of the maternal dosage of quetiapine was excreted in breast milk.9 Further studies found excretion to be 0.09% of maternal dosage, with infant plasma levels reaching 6% of the maternal dosage.10 A case series found that one-third of babies exposed to quetiapine during breast-feeding showed some neurodevelopmental delay, although these mothers also were taking other psychotropics.11
Risperidone. A 2000 study12 of risperidone in lactation reported that 0.84% weight-adjusted maternal risperidone dosage and 3.46% of its metabolite 9-hydroxyrisperidone is transferred to the infant. A later study showed 2.3% to 4.7% of the maternal dosage is transferred, with no adverse events reported in infants.13 A case study reported no adverse events and normal neurodevelopment in a the child of a mother taking risperidone.14
Ziprasidone. According to the ziprasidone prescribing information15 and a literature search, is not known whether ziprasidone is excreted in human breast milk.
See the Table4,6-10,12,13,15 for a summary of the evidence levels of second-generation antipsychotics that are excreted in breast milk.
Other mood stabilizers
Carbamazepine has been measured in breast milk at 3.8% to 5.9% of the maternal dosage.16
Lamotrigine. In a study of 30 lactating women, the breast milk contained an average of 9.2% of the maternal dosage of lamotrigine.17 Mild thrombocytosis was detected in 7 of 8 infants; no other adverse effects were reported. A case study describes a woman who breast-fed while taking lamotrigine, 850 mg/d, and who experienced dizziness and visual disturbances. The infant had apnea episodes followed by a cyanotic crisis, which required resuscitation. The infant’s plasma lamotrigine level was 4.87 μg/mL. Symptoms disappeared when the mother stopped breast-feeding.18 Lamotrigine is considered to be moderately safe in breast-feeding patients with proper monitoring. The drug also has a known safety profile because of its use in children with epilepsy.
Valproic acid. Because of its high plasma protein binding, valproic acid does not pass readily into the breast milk. Newborns receive approximately 1.4% to 1.7% of the maternal dosage.16 Caution is advised, however, because of some reported adverse events. One case reported thrombocytopenic purpura and anemia in an infant.19 Valproic acid is considered to be compatible with breast-feeding with proper monitoring.
Benzodiazepines
Benzodiazepines can be helpful adjunctive medications to aid sleep, which is essential for the mother’s and infant’s health. In a prospectively recruited, retrospectively assessed cohort study that evaluated 124 women taking benzodiazepines while breast-feeding, adverse effects, specifically sedation, were noted in 1.6% of infants.20
Future developments in prescribing information
Under a 2008 FDA recommendation, the “Nursing Mothers” section of prescribing information would be replaced with a section entitled “Lactation.” This new heading would include the sub-headings Risk Summary, Clinical Considerations, and Data.1 It is expected that this new format will be more practical and will help clinicians and patients make informed decisions. The prescribing changes will be in effect on June 30, 2015.21
Related Resources
• Massachusetts General Hospital Center for Women’s Mental Health. www.womensmentalhealth.org.
• LactMed. http://toxnet.nlm.nih.gov/newtoxnet/lactmed.htm.
• MOTHERISK. www.motherisk.org/women/ breastfeeding.jsp.
Drug Brand Names
Aripiprazole • Abilify Olanzapine • Zyprexa
Asenapine • Saphris Quetiapine • Seroquel
Carbamazepine • Tegretol Risperidone • Risperdal
Lamotrigine • Lamictal Valproic acid • Depakene
Lithium • Eskalith, Lithobid Ziprasidone • Geodon
Lurasidone • Latuda
Disclosure
The author reports no financial relationships with any company whose products are mentioned in this article or with manufacturers of competing products.
1. Sach HC; Committee on Drugs. The transfer of drugs and therapeutics into human breast milk: an update on selected topics. Pediatrics. 2013;132(3);e796-e809.
2. Moretti ME, Koren G, Verjee Z, et al. Monitoring lithium in breast milk: an individualized approach for breast-feeding mothers. Ther Drug Monit. 2003;25(3):364-366.
3. Viguera AC, Newport DJ, Ritchie J, et al. Lithium in breast milk and nursing infants: clinical implications. Am J Psychiatry. 2007;164(2):342-345.
4. Xyprexa [package insert]. Indianapolis, IN: Eli Lilly and Company; 2014.
5. Brunner E, Falk DM, Jones M, et al. Olanzapine in pregnancy and breastfeeding: a review of data from global safety surveillance. BMC Pharmacol Toxicol. 2013;14:38.
6. Schlotterbeck P, Leube D, Kircher T, et al. Aripiprazole in human milk. Int J Neuropsychopharmacol. 2007;10(3):433.
7. Saphris [package insert]. St. Louis, MO: Forest Pharmaceuticals; 2014.
8. Latuda [package insert]. Marlborough, MA: Sunovion Pharmaceuticals; 2013.
9. Lee A, Giesbrecht E, Dunn E, et al. Excretion of quetiapine in breast milk. Am J Psychiatry. 2004;161(9):1715-1716.
10. Rampono J, Kristensen JH, Ilett KF, et al. Quetiapine and breastfeeding. Ann Pharmacother. 2007;41(4):711-714.
11. Misri S, Corral M, Wardrop AA, et al. Quetiapine augmentation in lactation: a series of case reports. J Clin Psychopharmacol. 2006;26(5):508-511.
12. Hill RC, McIvor RJ, Wojnar-Horton RE, et al. Risperidone distribution and excretion into human milk: case report and estimated infant exposure during breast-feeding. J Clin Psychopharmacol. 2000;20(2):285-286.
13. Ilett KF, Hackett LP, Kristensen JH, et al. Transfer of risperidone and 9-hydroxyrisperidone into human milk. Ann Pharmacother. 2004;38(2):273-276.
14. Aichhorn W, Stuppaek C, Whitworth AB. Risperidone and breast-feeding. J Psychopharmacol. 2005;19(2):211-213.
15. Geodon [package insert]. New York, NY: Pfizer; 2014.
16. Davanzo R, Dal Bo S, Bua J, et al. Antiepileptic drugs and breastfeeding. Ital J Pediatr. 2013;39:50.
17. Newport DJ, Pennell PB, Calamaras MR, et al. Lamotrigine in breast milk and nursing infants: determination of exposure. Pediatrics. 2008;122(1):e223-e231.
18. Nordmo E, Aronsen L, Wasland K, et al. Severe apnea in an infant exposed to lamotrigine in breast milk. Ann Pharmacother. 2009;43(11):1893-1897.
19. Stahl MM, Neiderud J, Vinge E. Thrombocytopenic purpura and anemia in a breast-fed infant whose mother was treated with valproic acid. J Pediatr. 1997;130(6):1001-1003.
20. Kelly LE, Poon S, Madadi P, et al. Neonatal benzodiazepines exposure during breastfeeding. J Pediatr. 2012;161(3):448-451.
21. U.S. Food and Drug Administration. FDA issues final rule on changes to pregnancy and lactation labeling information for prescription drug and biological products. http://www. fda.gov/NewsEvents/Newsroom/PressAnnouncements/ ucm425317.htm. Published December 3. 2014. Accessed March 4, 2015.
Ms. K, age 35, soon will deliver her second child. She has a 12-year history of bipolar disorder, which was well controlled with lithium, 1,200 mg/d. During her first pregnancy 3 years ago, Ms. K stopped taking lithium because she was concerned about the risk of Ebstein’s anomaly. She experienced a bipolar relapse after her healthy baby was born, and developed postpartum psychosis that was treated by restarting lithium, 1,200 mg/d, and adding olanzapine, 10 mg/d.
Ms. K has continued these medications throughout her current pregnancy. She wants to breast-feed her infant and is concerned about the effects that psychotropics might have on her newborn.
Breast-feeding and medications
The benefits of breast-feeding for mother and infant are well-known. Despite this, some women with bipolar disorder are advised not to breast-feed or, worse, to discontinue their medications in order to breast-feed. Decisions about breast-feeding while taking medications should be based on evidence of benefits and risks to the infant, along with a discussion of the risks of untreated illness, which is high postpartum. The prescribing information for many of the medications used to treat bipolar disorder advise against breast-feeding, although there is little evidence of harm.
Drug dosages and levels in breast milk can be reported a few different ways:
• percentage of maternal dosage measured in the breast milk
• percentage weight-adjusted maternal dosage
• percentage of maternal plasma level, and milk-to-plasma ratio (M:P).
Daily infant dosage can be calculated by multiplying the average concentration of the drug in breast milk (mg/mL) by the average volume of milk the baby ingests in 24 hours (usually 150 mL).1 The relative infant dosage can be calculated as the percentage maternal dosage, which is the daily infant dosage (mg/kg/d) ÷ maternal dosage (mg/kg/d) × 100.1
According to the American Academy of Pediatrics, ≤10% of the maternal dosage is compatible with breast-feeding.1 Most psychotropics studied fall below this threshold. Keep in mind that all published research is for breast-feeding a full-term infant; exercise caution with premature or low birth weight infants. Infants born to mothers taking a psychotropic should be monitored for withdrawal symptoms, which might be associated with antidepressants and benzodiazepines, but otherwise are rare.
Lithium
Breast-feeding during lithium treatment has been considered contraindicated based on early reports that lithium was highly excreted in breast milk.2 A 2003 study2 of 11 women found that lithium was excreted in breast milk in amounts between zero and 30% of maternal dosage (mean, 12.2% ± 8.5%; median, 11.2%; 95% CI, 6.3% to 18.0%). Researchers measured serum concentrations in 2 infants and found that 1 received 17% to 20% of the maternal dosage, and the other showed 50%. None of the infants experienced adverse events. In a study of 10 mother-infant pairs, breast milk lithium concentration averaged 0.35 mEq/L (standard deviation [SD] = 0.10, range 0.19 to 0.48 mEq/L), with paired infant serum concentrations of 0.16 mEq/L (SD = 0.06, range 0.09 to 0.25 mEq/L).3 Some transient abnormalities were found in infant serum concentrations of thyroid-stimulating hormone (TSH), blood urea nitrogen, and creatinine; there were no adverse effects on development. The authors recommend monitoring for TSH abnormalities in infants.
Olanzapine
Olanzapine prescribing information cites a study reporting that 1.8% of the maternal dosage is transferred to breast milk.4 Yet the olanzapine prescribing information states, “It is recommended that women receiving olanzapine should not breast-feed.” Olanzapine use during breast-feeding has been studied more than many medications, in part because of a database maintained by the manufacturer. In a study using the manufacturer’s database (N = 102) adverse reactions were reported in 15.6% of the infants, with the most common being somnolence (3.9%), irritability (2%), tremor (2%), and insomnia (2%).5
Other second-generation antipsychotics
Aripiprazole. The only case report of aripiprazole excretion in human breast milk found a concentration of approximately 20% of the maternal plasma level and an M:P ratio of 0.18:0.2.6
Asenapine. According to asenapine prescribing information7 and a literature search, it is not known whether asenapine is excreted in breast milk of humans, although it is found in the milk of lactating rats.
Lurasidone. According to the lurasidone prescribing information8 and a literature search, it is not known whether lurasidone is excreted in human breast milk, although it is found in the milk of lactating rats.
Quetiapine. An initial study reported that 0.09% to 0.43% of the maternal dosage of quetiapine was excreted in breast milk.9 Further studies found excretion to be 0.09% of maternal dosage, with infant plasma levels reaching 6% of the maternal dosage.10 A case series found that one-third of babies exposed to quetiapine during breast-feeding showed some neurodevelopmental delay, although these mothers also were taking other psychotropics.11
Risperidone. A 2000 study12 of risperidone in lactation reported that 0.84% weight-adjusted maternal risperidone dosage and 3.46% of its metabolite 9-hydroxyrisperidone is transferred to the infant. A later study showed 2.3% to 4.7% of the maternal dosage is transferred, with no adverse events reported in infants.13 A case study reported no adverse events and normal neurodevelopment in a the child of a mother taking risperidone.14
Ziprasidone. According to the ziprasidone prescribing information15 and a literature search, is not known whether ziprasidone is excreted in human breast milk.
See the Table4,6-10,12,13,15 for a summary of the evidence levels of second-generation antipsychotics that are excreted in breast milk.
Other mood stabilizers
Carbamazepine has been measured in breast milk at 3.8% to 5.9% of the maternal dosage.16
Lamotrigine. In a study of 30 lactating women, the breast milk contained an average of 9.2% of the maternal dosage of lamotrigine.17 Mild thrombocytosis was detected in 7 of 8 infants; no other adverse effects were reported. A case study describes a woman who breast-fed while taking lamotrigine, 850 mg/d, and who experienced dizziness and visual disturbances. The infant had apnea episodes followed by a cyanotic crisis, which required resuscitation. The infant’s plasma lamotrigine level was 4.87 μg/mL. Symptoms disappeared when the mother stopped breast-feeding.18 Lamotrigine is considered to be moderately safe in breast-feeding patients with proper monitoring. The drug also has a known safety profile because of its use in children with epilepsy.
Valproic acid. Because of its high plasma protein binding, valproic acid does not pass readily into the breast milk. Newborns receive approximately 1.4% to 1.7% of the maternal dosage.16 Caution is advised, however, because of some reported adverse events. One case reported thrombocytopenic purpura and anemia in an infant.19 Valproic acid is considered to be compatible with breast-feeding with proper monitoring.
Benzodiazepines
Benzodiazepines can be helpful adjunctive medications to aid sleep, which is essential for the mother’s and infant’s health. In a prospectively recruited, retrospectively assessed cohort study that evaluated 124 women taking benzodiazepines while breast-feeding, adverse effects, specifically sedation, were noted in 1.6% of infants.20
Future developments in prescribing information
Under a 2008 FDA recommendation, the “Nursing Mothers” section of prescribing information would be replaced with a section entitled “Lactation.” This new heading would include the sub-headings Risk Summary, Clinical Considerations, and Data.1 It is expected that this new format will be more practical and will help clinicians and patients make informed decisions. The prescribing changes will be in effect on June 30, 2015.21
Related Resources
• Massachusetts General Hospital Center for Women’s Mental Health. www.womensmentalhealth.org.
• LactMed. http://toxnet.nlm.nih.gov/newtoxnet/lactmed.htm.
• MOTHERISK. www.motherisk.org/women/ breastfeeding.jsp.
Drug Brand Names
Aripiprazole • Abilify Olanzapine • Zyprexa
Asenapine • Saphris Quetiapine • Seroquel
Carbamazepine • Tegretol Risperidone • Risperdal
Lamotrigine • Lamictal Valproic acid • Depakene
Lithium • Eskalith, Lithobid Ziprasidone • Geodon
Lurasidone • Latuda
Disclosure
The author reports no financial relationships with any company whose products are mentioned in this article or with manufacturers of competing products.
Ms. K, age 35, soon will deliver her second child. She has a 12-year history of bipolar disorder, which was well controlled with lithium, 1,200 mg/d. During her first pregnancy 3 years ago, Ms. K stopped taking lithium because she was concerned about the risk of Ebstein’s anomaly. She experienced a bipolar relapse after her healthy baby was born, and developed postpartum psychosis that was treated by restarting lithium, 1,200 mg/d, and adding olanzapine, 10 mg/d.
Ms. K has continued these medications throughout her current pregnancy. She wants to breast-feed her infant and is concerned about the effects that psychotropics might have on her newborn.
Breast-feeding and medications
The benefits of breast-feeding for mother and infant are well-known. Despite this, some women with bipolar disorder are advised not to breast-feed or, worse, to discontinue their medications in order to breast-feed. Decisions about breast-feeding while taking medications should be based on evidence of benefits and risks to the infant, along with a discussion of the risks of untreated illness, which is high postpartum. The prescribing information for many of the medications used to treat bipolar disorder advise against breast-feeding, although there is little evidence of harm.
Drug dosages and levels in breast milk can be reported a few different ways:
• percentage of maternal dosage measured in the breast milk
• percentage weight-adjusted maternal dosage
• percentage of maternal plasma level, and milk-to-plasma ratio (M:P).
Daily infant dosage can be calculated by multiplying the average concentration of the drug in breast milk (mg/mL) by the average volume of milk the baby ingests in 24 hours (usually 150 mL).1 The relative infant dosage can be calculated as the percentage maternal dosage, which is the daily infant dosage (mg/kg/d) ÷ maternal dosage (mg/kg/d) × 100.1
According to the American Academy of Pediatrics, ≤10% of the maternal dosage is compatible with breast-feeding.1 Most psychotropics studied fall below this threshold. Keep in mind that all published research is for breast-feeding a full-term infant; exercise caution with premature or low birth weight infants. Infants born to mothers taking a psychotropic should be monitored for withdrawal symptoms, which might be associated with antidepressants and benzodiazepines, but otherwise are rare.
Lithium
Breast-feeding during lithium treatment has been considered contraindicated based on early reports that lithium was highly excreted in breast milk.2 A 2003 study2 of 11 women found that lithium was excreted in breast milk in amounts between zero and 30% of maternal dosage (mean, 12.2% ± 8.5%; median, 11.2%; 95% CI, 6.3% to 18.0%). Researchers measured serum concentrations in 2 infants and found that 1 received 17% to 20% of the maternal dosage, and the other showed 50%. None of the infants experienced adverse events. In a study of 10 mother-infant pairs, breast milk lithium concentration averaged 0.35 mEq/L (standard deviation [SD] = 0.10, range 0.19 to 0.48 mEq/L), with paired infant serum concentrations of 0.16 mEq/L (SD = 0.06, range 0.09 to 0.25 mEq/L).3 Some transient abnormalities were found in infant serum concentrations of thyroid-stimulating hormone (TSH), blood urea nitrogen, and creatinine; there were no adverse effects on development. The authors recommend monitoring for TSH abnormalities in infants.
Olanzapine
Olanzapine prescribing information cites a study reporting that 1.8% of the maternal dosage is transferred to breast milk.4 Yet the olanzapine prescribing information states, “It is recommended that women receiving olanzapine should not breast-feed.” Olanzapine use during breast-feeding has been studied more than many medications, in part because of a database maintained by the manufacturer. In a study using the manufacturer’s database (N = 102) adverse reactions were reported in 15.6% of the infants, with the most common being somnolence (3.9%), irritability (2%), tremor (2%), and insomnia (2%).5
Other second-generation antipsychotics
Aripiprazole. The only case report of aripiprazole excretion in human breast milk found a concentration of approximately 20% of the maternal plasma level and an M:P ratio of 0.18:0.2.6
Asenapine. According to asenapine prescribing information7 and a literature search, it is not known whether asenapine is excreted in breast milk of humans, although it is found in the milk of lactating rats.
Lurasidone. According to the lurasidone prescribing information8 and a literature search, it is not known whether lurasidone is excreted in human breast milk, although it is found in the milk of lactating rats.
Quetiapine. An initial study reported that 0.09% to 0.43% of the maternal dosage of quetiapine was excreted in breast milk.9 Further studies found excretion to be 0.09% of maternal dosage, with infant plasma levels reaching 6% of the maternal dosage.10 A case series found that one-third of babies exposed to quetiapine during breast-feeding showed some neurodevelopmental delay, although these mothers also were taking other psychotropics.11
Risperidone. A 2000 study12 of risperidone in lactation reported that 0.84% weight-adjusted maternal risperidone dosage and 3.46% of its metabolite 9-hydroxyrisperidone is transferred to the infant. A later study showed 2.3% to 4.7% of the maternal dosage is transferred, with no adverse events reported in infants.13 A case study reported no adverse events and normal neurodevelopment in a the child of a mother taking risperidone.14
Ziprasidone. According to the ziprasidone prescribing information15 and a literature search, is not known whether ziprasidone is excreted in human breast milk.
See the Table4,6-10,12,13,15 for a summary of the evidence levels of second-generation antipsychotics that are excreted in breast milk.
Other mood stabilizers
Carbamazepine has been measured in breast milk at 3.8% to 5.9% of the maternal dosage.16
Lamotrigine. In a study of 30 lactating women, the breast milk contained an average of 9.2% of the maternal dosage of lamotrigine.17 Mild thrombocytosis was detected in 7 of 8 infants; no other adverse effects were reported. A case study describes a woman who breast-fed while taking lamotrigine, 850 mg/d, and who experienced dizziness and visual disturbances. The infant had apnea episodes followed by a cyanotic crisis, which required resuscitation. The infant’s plasma lamotrigine level was 4.87 μg/mL. Symptoms disappeared when the mother stopped breast-feeding.18 Lamotrigine is considered to be moderately safe in breast-feeding patients with proper monitoring. The drug also has a known safety profile because of its use in children with epilepsy.
Valproic acid. Because of its high plasma protein binding, valproic acid does not pass readily into the breast milk. Newborns receive approximately 1.4% to 1.7% of the maternal dosage.16 Caution is advised, however, because of some reported adverse events. One case reported thrombocytopenic purpura and anemia in an infant.19 Valproic acid is considered to be compatible with breast-feeding with proper monitoring.
Benzodiazepines
Benzodiazepines can be helpful adjunctive medications to aid sleep, which is essential for the mother’s and infant’s health. In a prospectively recruited, retrospectively assessed cohort study that evaluated 124 women taking benzodiazepines while breast-feeding, adverse effects, specifically sedation, were noted in 1.6% of infants.20
Future developments in prescribing information
Under a 2008 FDA recommendation, the “Nursing Mothers” section of prescribing information would be replaced with a section entitled “Lactation.” This new heading would include the sub-headings Risk Summary, Clinical Considerations, and Data.1 It is expected that this new format will be more practical and will help clinicians and patients make informed decisions. The prescribing changes will be in effect on June 30, 2015.21
Related Resources
• Massachusetts General Hospital Center for Women’s Mental Health. www.womensmentalhealth.org.
• LactMed. http://toxnet.nlm.nih.gov/newtoxnet/lactmed.htm.
• MOTHERISK. www.motherisk.org/women/ breastfeeding.jsp.
Drug Brand Names
Aripiprazole • Abilify Olanzapine • Zyprexa
Asenapine • Saphris Quetiapine • Seroquel
Carbamazepine • Tegretol Risperidone • Risperdal
Lamotrigine • Lamictal Valproic acid • Depakene
Lithium • Eskalith, Lithobid Ziprasidone • Geodon
Lurasidone • Latuda
Disclosure
The author reports no financial relationships with any company whose products are mentioned in this article or with manufacturers of competing products.
1. Sach HC; Committee on Drugs. The transfer of drugs and therapeutics into human breast milk: an update on selected topics. Pediatrics. 2013;132(3);e796-e809.
2. Moretti ME, Koren G, Verjee Z, et al. Monitoring lithium in breast milk: an individualized approach for breast-feeding mothers. Ther Drug Monit. 2003;25(3):364-366.
3. Viguera AC, Newport DJ, Ritchie J, et al. Lithium in breast milk and nursing infants: clinical implications. Am J Psychiatry. 2007;164(2):342-345.
4. Xyprexa [package insert]. Indianapolis, IN: Eli Lilly and Company; 2014.
5. Brunner E, Falk DM, Jones M, et al. Olanzapine in pregnancy and breastfeeding: a review of data from global safety surveillance. BMC Pharmacol Toxicol. 2013;14:38.
6. Schlotterbeck P, Leube D, Kircher T, et al. Aripiprazole in human milk. Int J Neuropsychopharmacol. 2007;10(3):433.
7. Saphris [package insert]. St. Louis, MO: Forest Pharmaceuticals; 2014.
8. Latuda [package insert]. Marlborough, MA: Sunovion Pharmaceuticals; 2013.
9. Lee A, Giesbrecht E, Dunn E, et al. Excretion of quetiapine in breast milk. Am J Psychiatry. 2004;161(9):1715-1716.
10. Rampono J, Kristensen JH, Ilett KF, et al. Quetiapine and breastfeeding. Ann Pharmacother. 2007;41(4):711-714.
11. Misri S, Corral M, Wardrop AA, et al. Quetiapine augmentation in lactation: a series of case reports. J Clin Psychopharmacol. 2006;26(5):508-511.
12. Hill RC, McIvor RJ, Wojnar-Horton RE, et al. Risperidone distribution and excretion into human milk: case report and estimated infant exposure during breast-feeding. J Clin Psychopharmacol. 2000;20(2):285-286.
13. Ilett KF, Hackett LP, Kristensen JH, et al. Transfer of risperidone and 9-hydroxyrisperidone into human milk. Ann Pharmacother. 2004;38(2):273-276.
14. Aichhorn W, Stuppaek C, Whitworth AB. Risperidone and breast-feeding. J Psychopharmacol. 2005;19(2):211-213.
15. Geodon [package insert]. New York, NY: Pfizer; 2014.
16. Davanzo R, Dal Bo S, Bua J, et al. Antiepileptic drugs and breastfeeding. Ital J Pediatr. 2013;39:50.
17. Newport DJ, Pennell PB, Calamaras MR, et al. Lamotrigine in breast milk and nursing infants: determination of exposure. Pediatrics. 2008;122(1):e223-e231.
18. Nordmo E, Aronsen L, Wasland K, et al. Severe apnea in an infant exposed to lamotrigine in breast milk. Ann Pharmacother. 2009;43(11):1893-1897.
19. Stahl MM, Neiderud J, Vinge E. Thrombocytopenic purpura and anemia in a breast-fed infant whose mother was treated with valproic acid. J Pediatr. 1997;130(6):1001-1003.
20. Kelly LE, Poon S, Madadi P, et al. Neonatal benzodiazepines exposure during breastfeeding. J Pediatr. 2012;161(3):448-451.
21. U.S. Food and Drug Administration. FDA issues final rule on changes to pregnancy and lactation labeling information for prescription drug and biological products. http://www. fda.gov/NewsEvents/Newsroom/PressAnnouncements/ ucm425317.htm. Published December 3. 2014. Accessed March 4, 2015.
1. Sach HC; Committee on Drugs. The transfer of drugs and therapeutics into human breast milk: an update on selected topics. Pediatrics. 2013;132(3);e796-e809.
2. Moretti ME, Koren G, Verjee Z, et al. Monitoring lithium in breast milk: an individualized approach for breast-feeding mothers. Ther Drug Monit. 2003;25(3):364-366.
3. Viguera AC, Newport DJ, Ritchie J, et al. Lithium in breast milk and nursing infants: clinical implications. Am J Psychiatry. 2007;164(2):342-345.
4. Xyprexa [package insert]. Indianapolis, IN: Eli Lilly and Company; 2014.
5. Brunner E, Falk DM, Jones M, et al. Olanzapine in pregnancy and breastfeeding: a review of data from global safety surveillance. BMC Pharmacol Toxicol. 2013;14:38.
6. Schlotterbeck P, Leube D, Kircher T, et al. Aripiprazole in human milk. Int J Neuropsychopharmacol. 2007;10(3):433.
7. Saphris [package insert]. St. Louis, MO: Forest Pharmaceuticals; 2014.
8. Latuda [package insert]. Marlborough, MA: Sunovion Pharmaceuticals; 2013.
9. Lee A, Giesbrecht E, Dunn E, et al. Excretion of quetiapine in breast milk. Am J Psychiatry. 2004;161(9):1715-1716.
10. Rampono J, Kristensen JH, Ilett KF, et al. Quetiapine and breastfeeding. Ann Pharmacother. 2007;41(4):711-714.
11. Misri S, Corral M, Wardrop AA, et al. Quetiapine augmentation in lactation: a series of case reports. J Clin Psychopharmacol. 2006;26(5):508-511.
12. Hill RC, McIvor RJ, Wojnar-Horton RE, et al. Risperidone distribution and excretion into human milk: case report and estimated infant exposure during breast-feeding. J Clin Psychopharmacol. 2000;20(2):285-286.
13. Ilett KF, Hackett LP, Kristensen JH, et al. Transfer of risperidone and 9-hydroxyrisperidone into human milk. Ann Pharmacother. 2004;38(2):273-276.
14. Aichhorn W, Stuppaek C, Whitworth AB. Risperidone and breast-feeding. J Psychopharmacol. 2005;19(2):211-213.
15. Geodon [package insert]. New York, NY: Pfizer; 2014.
16. Davanzo R, Dal Bo S, Bua J, et al. Antiepileptic drugs and breastfeeding. Ital J Pediatr. 2013;39:50.
17. Newport DJ, Pennell PB, Calamaras MR, et al. Lamotrigine in breast milk and nursing infants: determination of exposure. Pediatrics. 2008;122(1):e223-e231.
18. Nordmo E, Aronsen L, Wasland K, et al. Severe apnea in an infant exposed to lamotrigine in breast milk. Ann Pharmacother. 2009;43(11):1893-1897.
19. Stahl MM, Neiderud J, Vinge E. Thrombocytopenic purpura and anemia in a breast-fed infant whose mother was treated with valproic acid. J Pediatr. 1997;130(6):1001-1003.
20. Kelly LE, Poon S, Madadi P, et al. Neonatal benzodiazepines exposure during breastfeeding. J Pediatr. 2012;161(3):448-451.
21. U.S. Food and Drug Administration. FDA issues final rule on changes to pregnancy and lactation labeling information for prescription drug and biological products. http://www. fda.gov/NewsEvents/Newsroom/PressAnnouncements/ ucm425317.htm. Published December 3. 2014. Accessed March 4, 2015.
FDA green lights sublingual antipsychotic to treat bipolar I in children
For the first time in 5 years, the Food and Drug Administration has approved an application to market an antipsychotic to clinicians for treating bipolar I disorder in children aged 10-17 years.
Actavis, the Dublin-based pharmaceutical manufacturer, announced March 13 that the FDA has approved the company’s supplemental new drug application for asenapine (Saphris), a second-generation atypical antipsychotic, as monotherapy for the acute treatment of manic or mixed episodes associated with bipolar I disorder in this pediatric population.
The FDA approved asenapine in 2009 for treating adults with manic or mixed episodes of bipolar I, either as monotherapy or adjunctive to either lithium or valproate. It also is indicated for the acute or maintenance treatment of schizophrenia in adults.
Asenapine is administered as a sublingual tablet, and the company announced in the statement that it would begin marketing black cherry–flavored sublingual asenapine tablets in 2.5 mg, 5 mg, and 10 mg doses beginning in the second quarter of this year.
According to the manufacturer, the agency’s approval was granted based on the results of a 3-week monotherapy trial in 403 pediatric patients, aged 10-17 years, 302 of whom were treated twice daily with either 2.5 mg, 5 mg, or 10 mg of asenapine. The drug maker also said asenapine demonstrated improvement in the Young Mania Rating Scale total score and the Clinical Global Impressions-Bipolar Scale overall score, compared with placebo.
When asked about the approval, Dr. David Fassler said it's helpful to have a range of medications to treat pediatric patients with bipolar disorder. "However, the current approval is based on results of a relatively short-term clinical trial," said Dr. Fassler, clinical professor of psychiatry at the University of Vermont, Burlington. "In the real world, many young people ultimately take atypical antipsychotics for an extended period of time. Physicians and parents need data on the safety and efficacy of these medications when used on a more long-term or ongoing basis in order to make fully informed decisions about treatment options."
The most common side effects the company said it recorded in the pediatric clinical trial were sleepiness, dizziness, strange sense of taste, numbing of the mouth, nausea, increased appetite, feeling tired, and weight gain.
On Twitter @whitneymcknight
For the first time in 5 years, the Food and Drug Administration has approved an application to market an antipsychotic to clinicians for treating bipolar I disorder in children aged 10-17 years.
Actavis, the Dublin-based pharmaceutical manufacturer, announced March 13 that the FDA has approved the company’s supplemental new drug application for asenapine (Saphris), a second-generation atypical antipsychotic, as monotherapy for the acute treatment of manic or mixed episodes associated with bipolar I disorder in this pediatric population.
The FDA approved asenapine in 2009 for treating adults with manic or mixed episodes of bipolar I, either as monotherapy or adjunctive to either lithium or valproate. It also is indicated for the acute or maintenance treatment of schizophrenia in adults.
Asenapine is administered as a sublingual tablet, and the company announced in the statement that it would begin marketing black cherry–flavored sublingual asenapine tablets in 2.5 mg, 5 mg, and 10 mg doses beginning in the second quarter of this year.
According to the manufacturer, the agency’s approval was granted based on the results of a 3-week monotherapy trial in 403 pediatric patients, aged 10-17 years, 302 of whom were treated twice daily with either 2.5 mg, 5 mg, or 10 mg of asenapine. The drug maker also said asenapine demonstrated improvement in the Young Mania Rating Scale total score and the Clinical Global Impressions-Bipolar Scale overall score, compared with placebo.
When asked about the approval, Dr. David Fassler said it's helpful to have a range of medications to treat pediatric patients with bipolar disorder. "However, the current approval is based on results of a relatively short-term clinical trial," said Dr. Fassler, clinical professor of psychiatry at the University of Vermont, Burlington. "In the real world, many young people ultimately take atypical antipsychotics for an extended period of time. Physicians and parents need data on the safety and efficacy of these medications when used on a more long-term or ongoing basis in order to make fully informed decisions about treatment options."
The most common side effects the company said it recorded in the pediatric clinical trial were sleepiness, dizziness, strange sense of taste, numbing of the mouth, nausea, increased appetite, feeling tired, and weight gain.
On Twitter @whitneymcknight
For the first time in 5 years, the Food and Drug Administration has approved an application to market an antipsychotic to clinicians for treating bipolar I disorder in children aged 10-17 years.
Actavis, the Dublin-based pharmaceutical manufacturer, announced March 13 that the FDA has approved the company’s supplemental new drug application for asenapine (Saphris), a second-generation atypical antipsychotic, as monotherapy for the acute treatment of manic or mixed episodes associated with bipolar I disorder in this pediatric population.
The FDA approved asenapine in 2009 for treating adults with manic or mixed episodes of bipolar I, either as monotherapy or adjunctive to either lithium or valproate. It also is indicated for the acute or maintenance treatment of schizophrenia in adults.
Asenapine is administered as a sublingual tablet, and the company announced in the statement that it would begin marketing black cherry–flavored sublingual asenapine tablets in 2.5 mg, 5 mg, and 10 mg doses beginning in the second quarter of this year.
According to the manufacturer, the agency’s approval was granted based on the results of a 3-week monotherapy trial in 403 pediatric patients, aged 10-17 years, 302 of whom were treated twice daily with either 2.5 mg, 5 mg, or 10 mg of asenapine. The drug maker also said asenapine demonstrated improvement in the Young Mania Rating Scale total score and the Clinical Global Impressions-Bipolar Scale overall score, compared with placebo.
When asked about the approval, Dr. David Fassler said it's helpful to have a range of medications to treat pediatric patients with bipolar disorder. "However, the current approval is based on results of a relatively short-term clinical trial," said Dr. Fassler, clinical professor of psychiatry at the University of Vermont, Burlington. "In the real world, many young people ultimately take atypical antipsychotics for an extended period of time. Physicians and parents need data on the safety and efficacy of these medications when used on a more long-term or ongoing basis in order to make fully informed decisions about treatment options."
The most common side effects the company said it recorded in the pediatric clinical trial were sleepiness, dizziness, strange sense of taste, numbing of the mouth, nausea, increased appetite, feeling tired, and weight gain.
On Twitter @whitneymcknight
Dimensional aspects of DSM-5 personality disorder criteria discussed
HUNTINGTON BEACH, CALIF. – In the opinion of Dr. John M. Oldham, clinicians who deem the alternative personality disorder model of the DSM-5 as too confusing are misguided.
“If you’re going to compare DSM-5 alternative personality disorder model with the DSM-IV model, you have to do a fair comparison,” Dr. Oldham told attendees at the annual meeting of the American College of Psychiatrists. ”In fact, we reduced the number of items that you have to measure by 43%.”
So when people describe the DSM-5’s personality disorders criteria as more complicated, he continued, “what they really mean is, ‘it’s more complicated than what I do,’ not that it’s more complicated than [the] DSM-IV.”
Along with Dr. Andrew E. Skodol, Dr. Oldham cochaired a work group of experts convened by the American Psychiatric Association to update diagnostic criteria related to personality and personality disorders for the DSM-5. “We took our work and our charge seriously,” recalled Dr. Oldham, senior vice president and chief of staff at the Menninger Clinic, Houston. “It was not easy. We had many challenges. A great deal of research has been done in the factor analytic research psychology world around things like the five-factor model of personality. Such terms are not always terribly familiar in clinical medicine, so there was a problem with the lack of familiarity. Then there were vested interests different groups had that were influential in some ways.”
Ultimately, the alternative personality disorder model was placed in section III of the DSM-5. The model enables clinicians “to individually portray the dimensions of the patient’s pathology in a thorough and broad way,” Dr. Oldham explained. “We emphasize impairment in functioning. That’s an important new requirement. So you have to determine, by using the level of functioning scale, whether the person does or doesn’t have moderate or greater impairment. If you have a patient with mild impairment, you can describe what you’re concerned about, but you’re not putting that patient into a diagnostic box of pathology. There is a dimensional scope that enables you to capture many types of patients.”
An empirical study of 337 clinicians demonstrated that in 14 of 18 comparisons, respondents deemed the DSM-5 pathological personality traits as more clinical useful, compared with the DSM-IV, with respect to ease of use, communication of clinical information to other professionals, communication of clinical information to patients, comprehensiveness in describing pathology, and treatment planning (J. Abnorm. Psychol. 2013;122:836-41). “In fact, this was a preference to the new model, which was unfamiliar, compared to the model that these clinicians had been using for 20 years,” Dr. Oldham said.
The study also found that the new DSM-5 personality disorder model was more strongly related to clinical decision making in areas of global functioning, risk assessment, recommended treatment type and intensity, and prognosis.
According to unpublished data from the DSM-5 field trials conducted in the United States and Canada, more than 80% of clinicians in academic and routine clinical practice fields found the new personality disorder criteria “moderately” to “extremely” useful, compared with the DSM-IV. In fact, the respondents rated the new criteria as more useful than other changes to the DSM-5, including those related to bipolar and related disorders, schizophrenia spectrum and other psychotic disorders, and other conditions.
In addition, a test-retest reliability study conducted at 11 academic medical centers found that the new model for borderline personality disorder had a good test-retest reliability (.054), in the same ballpark as that for bipolar I disorder (0.56) and schizophrenia (.50) (Am. J. Psychiatry 2013;170:43-58). “This surprised a lot of people,” Dr. Oldham said.
About 1 year after the DSM-5’s release, Medscape Psychiatry surveyed almost 3,000 clinicians about their impressions of the new guidelines. Of the 2,828 respondents, nearly one-third (28%) were psychiatrists, 22% were psychologists, 13% were family medicine clinicians, and the rest were from other medical fields. The researchers found that 39% of survey respondents were considering the dimensional approaches offered in the new personality disorder criteria of the DSM-5.
“That’s not bad,” Dr. Oldham said.
He reported having no relevant financial conflicts.
On Twitter @dougbrunk
HUNTINGTON BEACH, CALIF. – In the opinion of Dr. John M. Oldham, clinicians who deem the alternative personality disorder model of the DSM-5 as too confusing are misguided.
“If you’re going to compare DSM-5 alternative personality disorder model with the DSM-IV model, you have to do a fair comparison,” Dr. Oldham told attendees at the annual meeting of the American College of Psychiatrists. ”In fact, we reduced the number of items that you have to measure by 43%.”
So when people describe the DSM-5’s personality disorders criteria as more complicated, he continued, “what they really mean is, ‘it’s more complicated than what I do,’ not that it’s more complicated than [the] DSM-IV.”
Along with Dr. Andrew E. Skodol, Dr. Oldham cochaired a work group of experts convened by the American Psychiatric Association to update diagnostic criteria related to personality and personality disorders for the DSM-5. “We took our work and our charge seriously,” recalled Dr. Oldham, senior vice president and chief of staff at the Menninger Clinic, Houston. “It was not easy. We had many challenges. A great deal of research has been done in the factor analytic research psychology world around things like the five-factor model of personality. Such terms are not always terribly familiar in clinical medicine, so there was a problem with the lack of familiarity. Then there were vested interests different groups had that were influential in some ways.”
Ultimately, the alternative personality disorder model was placed in section III of the DSM-5. The model enables clinicians “to individually portray the dimensions of the patient’s pathology in a thorough and broad way,” Dr. Oldham explained. “We emphasize impairment in functioning. That’s an important new requirement. So you have to determine, by using the level of functioning scale, whether the person does or doesn’t have moderate or greater impairment. If you have a patient with mild impairment, you can describe what you’re concerned about, but you’re not putting that patient into a diagnostic box of pathology. There is a dimensional scope that enables you to capture many types of patients.”
An empirical study of 337 clinicians demonstrated that in 14 of 18 comparisons, respondents deemed the DSM-5 pathological personality traits as more clinical useful, compared with the DSM-IV, with respect to ease of use, communication of clinical information to other professionals, communication of clinical information to patients, comprehensiveness in describing pathology, and treatment planning (J. Abnorm. Psychol. 2013;122:836-41). “In fact, this was a preference to the new model, which was unfamiliar, compared to the model that these clinicians had been using for 20 years,” Dr. Oldham said.
The study also found that the new DSM-5 personality disorder model was more strongly related to clinical decision making in areas of global functioning, risk assessment, recommended treatment type and intensity, and prognosis.
According to unpublished data from the DSM-5 field trials conducted in the United States and Canada, more than 80% of clinicians in academic and routine clinical practice fields found the new personality disorder criteria “moderately” to “extremely” useful, compared with the DSM-IV. In fact, the respondents rated the new criteria as more useful than other changes to the DSM-5, including those related to bipolar and related disorders, schizophrenia spectrum and other psychotic disorders, and other conditions.
In addition, a test-retest reliability study conducted at 11 academic medical centers found that the new model for borderline personality disorder had a good test-retest reliability (.054), in the same ballpark as that for bipolar I disorder (0.56) and schizophrenia (.50) (Am. J. Psychiatry 2013;170:43-58). “This surprised a lot of people,” Dr. Oldham said.
About 1 year after the DSM-5’s release, Medscape Psychiatry surveyed almost 3,000 clinicians about their impressions of the new guidelines. Of the 2,828 respondents, nearly one-third (28%) were psychiatrists, 22% were psychologists, 13% were family medicine clinicians, and the rest were from other medical fields. The researchers found that 39% of survey respondents were considering the dimensional approaches offered in the new personality disorder criteria of the DSM-5.
“That’s not bad,” Dr. Oldham said.
He reported having no relevant financial conflicts.
On Twitter @dougbrunk
HUNTINGTON BEACH, CALIF. – In the opinion of Dr. John M. Oldham, clinicians who deem the alternative personality disorder model of the DSM-5 as too confusing are misguided.
“If you’re going to compare DSM-5 alternative personality disorder model with the DSM-IV model, you have to do a fair comparison,” Dr. Oldham told attendees at the annual meeting of the American College of Psychiatrists. ”In fact, we reduced the number of items that you have to measure by 43%.”
So when people describe the DSM-5’s personality disorders criteria as more complicated, he continued, “what they really mean is, ‘it’s more complicated than what I do,’ not that it’s more complicated than [the] DSM-IV.”
Along with Dr. Andrew E. Skodol, Dr. Oldham cochaired a work group of experts convened by the American Psychiatric Association to update diagnostic criteria related to personality and personality disorders for the DSM-5. “We took our work and our charge seriously,” recalled Dr. Oldham, senior vice president and chief of staff at the Menninger Clinic, Houston. “It was not easy. We had many challenges. A great deal of research has been done in the factor analytic research psychology world around things like the five-factor model of personality. Such terms are not always terribly familiar in clinical medicine, so there was a problem with the lack of familiarity. Then there were vested interests different groups had that were influential in some ways.”
Ultimately, the alternative personality disorder model was placed in section III of the DSM-5. The model enables clinicians “to individually portray the dimensions of the patient’s pathology in a thorough and broad way,” Dr. Oldham explained. “We emphasize impairment in functioning. That’s an important new requirement. So you have to determine, by using the level of functioning scale, whether the person does or doesn’t have moderate or greater impairment. If you have a patient with mild impairment, you can describe what you’re concerned about, but you’re not putting that patient into a diagnostic box of pathology. There is a dimensional scope that enables you to capture many types of patients.”
An empirical study of 337 clinicians demonstrated that in 14 of 18 comparisons, respondents deemed the DSM-5 pathological personality traits as more clinical useful, compared with the DSM-IV, with respect to ease of use, communication of clinical information to other professionals, communication of clinical information to patients, comprehensiveness in describing pathology, and treatment planning (J. Abnorm. Psychol. 2013;122:836-41). “In fact, this was a preference to the new model, which was unfamiliar, compared to the model that these clinicians had been using for 20 years,” Dr. Oldham said.
The study also found that the new DSM-5 personality disorder model was more strongly related to clinical decision making in areas of global functioning, risk assessment, recommended treatment type and intensity, and prognosis.
According to unpublished data from the DSM-5 field trials conducted in the United States and Canada, more than 80% of clinicians in academic and routine clinical practice fields found the new personality disorder criteria “moderately” to “extremely” useful, compared with the DSM-IV. In fact, the respondents rated the new criteria as more useful than other changes to the DSM-5, including those related to bipolar and related disorders, schizophrenia spectrum and other psychotic disorders, and other conditions.
In addition, a test-retest reliability study conducted at 11 academic medical centers found that the new model for borderline personality disorder had a good test-retest reliability (.054), in the same ballpark as that for bipolar I disorder (0.56) and schizophrenia (.50) (Am. J. Psychiatry 2013;170:43-58). “This surprised a lot of people,” Dr. Oldham said.
About 1 year after the DSM-5’s release, Medscape Psychiatry surveyed almost 3,000 clinicians about their impressions of the new guidelines. Of the 2,828 respondents, nearly one-third (28%) were psychiatrists, 22% were psychologists, 13% were family medicine clinicians, and the rest were from other medical fields. The researchers found that 39% of survey respondents were considering the dimensional approaches offered in the new personality disorder criteria of the DSM-5.
“That’s not bad,” Dr. Oldham said.
He reported having no relevant financial conflicts.
On Twitter @dougbrunk
EXPERT ANALYSIS FROM THE ANNUAL MEETING OF THE AMERICAN COLLEGE OF PSYCHIATRISTS
