Current Psychiatry

Sleep disturbance is not associated with age and IQ in young children with autism spectrum disorder (ASD) and disruptive behaviors, according to Cynthia R. Johnson, PhD, and her associates.

They assessed 177 children aged 3-7 who were participating in the Research Units on Behavioral Intervention study, a 24-week trial. All of the children had a diagnosis of autism spectrum disorder, based on DSM-IV criteria. The diagnoses were corroborated by the Autism Diagnostic Observation Schedule and the Autism Diagnostic Interview–Revised.

The children were randomized into a parent training group or a parent education group. After getting parents to complete several forms, including the Children’s Sleep Habits Questionnaire, Dr. Johnson and her associates found no age differences between children who fell into the category of “good sleepers” (n = 52), and those characterized as “poor sleepers” (n = 46) (P = .57). In both sleep groups, more than 70% of the children had an IQ of 70 or above, and no significant difference was found in good sleepers, compared with poor sleepers, in IQ variable (P = .87) (Sleep Med. 2018. 44:61-6).

In addition, the researchers found that poor sleepers had significantly higher scores on the Aberrant Behavior Checklist subscales of irritability, hyperactivity, stereotypic behavior, and social withdrawal/lethargy, compared with good sleepers. All subscales of the parenting stress index and the PSI total score also were significantly higher in the poor sleepers group, compared with children in the good sleepers group, reported Dr. Johnson of the University of Florida, Gainesville, and her associates.

Additional studies are needed within a “comprehensive biopsychosocial model” to advance the understanding of why some children with autism experience disrupted sleep patterns and others do not. “Our findings support the value of screening for sleep disturbances in all children with ASD, regardless of age and cognitive level,” Dr. Johnson and her associates concluded. “With improved sleep, better outcomes for children with ASD could be expected.”

Read the full study in Sleep Medicine

[email protected]

Sleep disturbance is not associated with age and IQ in young children with autism spectrum disorder (ASD) and disruptive behaviors, according to Cynthia R. Johnson, PhD, and her associates.

They assessed 177 children aged 3-7 who were participating in the Research Units on Behavioral Intervention study, a 24-week trial. All of the children had a diagnosis of autism spectrum disorder, based on DSM-IV criteria. The diagnoses were corroborated by the Autism Diagnostic Observation Schedule and the Autism Diagnostic Interview–Revised.

The children were randomized into a parent training group or a parent education group. After getting parents to complete several forms, including the Children’s Sleep Habits Questionnaire, Dr. Johnson and her associates found no age differences between children who fell into the category of “good sleepers” (n = 52), and those characterized as “poor sleepers” (n = 46) (P = .57). In both sleep groups, more than 70% of the children had an IQ of 70 or above, and no significant difference was found in good sleepers, compared with poor sleepers, in IQ variable (P = .87) (Sleep Med. 2018. 44:61-6).

In addition, the researchers found that poor sleepers had significantly higher scores on the Aberrant Behavior Checklist subscales of irritability, hyperactivity, stereotypic behavior, and social withdrawal/lethargy, compared with good sleepers. All subscales of the parenting stress index and the PSI total score also were significantly higher in the poor sleepers group, compared with children in the good sleepers group, reported Dr. Johnson of the University of Florida, Gainesville, and her associates.

Additional studies are needed within a “comprehensive biopsychosocial model” to advance the understanding of why some children with autism experience disrupted sleep patterns and others do not. “Our findings support the value of screening for sleep disturbances in all children with ASD, regardless of age and cognitive level,” Dr. Johnson and her associates concluded. “With improved sleep, better outcomes for children with ASD could be expected.”

Read the full study in Sleep Medicine

[email protected]

Sleep disturbance is not associated with age and IQ in young children with autism spectrum disorder (ASD) and disruptive behaviors, according to Cynthia R. Johnson, PhD, and her associates.

They assessed 177 children aged 3-7 who were participating in the Research Units on Behavioral Intervention study, a 24-week trial. All of the children had a diagnosis of autism spectrum disorder, based on DSM-IV criteria. The diagnoses were corroborated by the Autism Diagnostic Observation Schedule and the Autism Diagnostic Interview–Revised.

The children were randomized into a parent training group or a parent education group. After getting parents to complete several forms, including the Children’s Sleep Habits Questionnaire, Dr. Johnson and her associates found no age differences between children who fell into the category of “good sleepers” (n = 52), and those characterized as “poor sleepers” (n = 46) (P = .57). In both sleep groups, more than 70% of the children had an IQ of 70 or above, and no significant difference was found in good sleepers, compared with poor sleepers, in IQ variable (P = .87) (Sleep Med. 2018. 44:61-6).

In addition, the researchers found that poor sleepers had significantly higher scores on the Aberrant Behavior Checklist subscales of irritability, hyperactivity, stereotypic behavior, and social withdrawal/lethargy, compared with good sleepers. All subscales of the parenting stress index and the PSI total score also were significantly higher in the poor sleepers group, compared with children in the good sleepers group, reported Dr. Johnson of the University of Florida, Gainesville, and her associates.

Additional studies are needed within a “comprehensive biopsychosocial model” to advance the understanding of why some children with autism experience disrupted sleep patterns and others do not. “Our findings support the value of screening for sleep disturbances in all children with ASD, regardless of age and cognitive level,” Dr. Johnson and her associates concluded. “With improved sleep, better outcomes for children with ASD could be expected.”

Read the full study in Sleep Medicine

[email protected]

Suicidal behaviors are associated with poor sleep in college students, even after controlling for depression, a cross-sectional analysis shows. Specifically, students were 6.54 times as likely to be classified with suicide risk if they were depressed and 2.70 times as likely if they had poor quality of sleep.

“Our findings add to a growing body of literature pointing to sleep as an important component to include in screening and intervention efforts to prevent suicidal ideation and attempts on college campuses,” wrote Stephen P. Becker, PhD, a pediatric psychologist affiliated with Cincinnati Children’s Hospital Medical Center, and his colleagues.

Wavebreak Media/Thinkstockphotos

Suicidal behaviors are associated with poor sleep in college students, even after controlling for depression, a cross-sectional analysis shows. Specifically, students were 6.54 times as likely to be classified with suicide risk if they were depressed and 2.70 times as likely if they had poor quality of sleep.

“Our findings add to a growing body of literature pointing to sleep as an important component to include in screening and intervention efforts to prevent suicidal ideation and attempts on college campuses,” wrote Stephen P. Becker, PhD, a pediatric psychologist affiliated with Cincinnati Children’s Hospital Medical Center, and his colleagues.

Wavebreak Media/Thinkstockphotos

Suicidal behaviors are associated with poor sleep in college students, even after controlling for depression, a cross-sectional analysis shows. Specifically, students were 6.54 times as likely to be classified with suicide risk if they were depressed and 2.70 times as likely if they had poor quality of sleep.

“Our findings add to a growing body of literature pointing to sleep as an important component to include in screening and intervention efforts to prevent suicidal ideation and attempts on college campuses,” wrote Stephen P. Becker, PhD, a pediatric psychologist affiliated with Cincinnati Children’s Hospital Medical Center, and his colleagues.

Wavebreak Media/Thinkstockphotos

The longer that patients with schizophrenia go without treatment for a psychotic episode, the more their hippocampus atrophies, suggests a study published Feb. 21 in JAMA Psychiatry.

To conduct the study, researchers studied 71 patients between March 5, 2013, and Oct. 8, 2014, who were experiencing their first psychotic episode and were antipsychotic naive. The research team matched those patients with 73 healthy controls, treated the patients with antipsychotics, and performed MRIs on members of both groups at baseline and 8 weeks later. The primary outcome measure was change in left and right hippocampal volume integrity, which is inversely associated with hippocampal atrophy.

Results showed that many patients with psychosis had lower median hippocampal volume integrity. Furthermore, those patients’ left hippocampal volume integrity decreased at a median annualized rate of 4.1%, and their right hippocampal volume integrity decreased at a rate of 3.3%. The duration of untreated psychosis was correlated with both decreases, but this association was only significant with left hippocampal volume integrity.

This relationship is “consistent with a persistent, possibly deleterious, effect of untreated psychosis on brain structure,” wrote Donald C. Goff, MD, of the psychiatry department at New York University, and his associates. “Larger longitudinal studies of longer duration are needed to examine the association between [duration of untreated psychosis], hippocampal volume, and clinical outcomes.”

Dr. Goff reported receiving research support from the National Institute of Mental Health, the Stanley Medical Research Institute, and Avanir Pharmaceuticals. Another author reported receiving support from numerous entities and honoraria for serving on an advisory board for Allergan. No other disclosures were reported.

Read more at JAMA Psychiatry.


 

The longer that patients with schizophrenia go without treatment for a psychotic episode, the more their hippocampus atrophies, suggests a study published Feb. 21 in JAMA Psychiatry.

To conduct the study, researchers studied 71 patients between March 5, 2013, and Oct. 8, 2014, who were experiencing their first psychotic episode and were antipsychotic naive. The research team matched those patients with 73 healthy controls, treated the patients with antipsychotics, and performed MRIs on members of both groups at baseline and 8 weeks later. The primary outcome measure was change in left and right hippocampal volume integrity, which is inversely associated with hippocampal atrophy.

Results showed that many patients with psychosis had lower median hippocampal volume integrity. Furthermore, those patients’ left hippocampal volume integrity decreased at a median annualized rate of 4.1%, and their right hippocampal volume integrity decreased at a rate of 3.3%. The duration of untreated psychosis was correlated with both decreases, but this association was only significant with left hippocampal volume integrity.

This relationship is “consistent with a persistent, possibly deleterious, effect of untreated psychosis on brain structure,” wrote Donald C. Goff, MD, of the psychiatry department at New York University, and his associates. “Larger longitudinal studies of longer duration are needed to examine the association between [duration of untreated psychosis], hippocampal volume, and clinical outcomes.”

Dr. Goff reported receiving research support from the National Institute of Mental Health, the Stanley Medical Research Institute, and Avanir Pharmaceuticals. Another author reported receiving support from numerous entities and honoraria for serving on an advisory board for Allergan. No other disclosures were reported.

Read more at JAMA Psychiatry.


 

The longer that patients with schizophrenia go without treatment for a psychotic episode, the more their hippocampus atrophies, suggests a study published Feb. 21 in JAMA Psychiatry.

To conduct the study, researchers studied 71 patients between March 5, 2013, and Oct. 8, 2014, who were experiencing their first psychotic episode and were antipsychotic naive. The research team matched those patients with 73 healthy controls, treated the patients with antipsychotics, and performed MRIs on members of both groups at baseline and 8 weeks later. The primary outcome measure was change in left and right hippocampal volume integrity, which is inversely associated with hippocampal atrophy.

Results showed that many patients with psychosis had lower median hippocampal volume integrity. Furthermore, those patients’ left hippocampal volume integrity decreased at a median annualized rate of 4.1%, and their right hippocampal volume integrity decreased at a rate of 3.3%. The duration of untreated psychosis was correlated with both decreases, but this association was only significant with left hippocampal volume integrity.

This relationship is “consistent with a persistent, possibly deleterious, effect of untreated psychosis on brain structure,” wrote Donald C. Goff, MD, of the psychiatry department at New York University, and his associates. “Larger longitudinal studies of longer duration are needed to examine the association between [duration of untreated psychosis], hippocampal volume, and clinical outcomes.”

Dr. Goff reported receiving research support from the National Institute of Mental Health, the Stanley Medical Research Institute, and Avanir Pharmaceuticals. Another author reported receiving support from numerous entities and honoraria for serving on an advisory board for Allergan. No other disclosures were reported.

Read more at JAMA Psychiatry.


 

Virtual reality–based cognitive-behavioral therapy could help reduce momentary paranoia and anxiety, and improve social cognition in individuals with psychotic disorders.

Researchers reported the results of a randomized controlled trial of personalized virtual reality-based cognitive-behavioral therapy in 116 patients with a DSM IV–diagnosed psychotic disorder and paranoid ideation in an article published online Feb. 8 in Lancet Psychiatry.

SOURCE: Lancet Psychiatry. 2018 Feb 8. doi: 10.1016/S2215-0366(18)30053-1.

Virtual reality–based cognitive-behavioral therapy could help reduce momentary paranoia and anxiety, and improve social cognition in individuals with psychotic disorders.

Researchers reported the results of a randomized controlled trial of personalized virtual reality-based cognitive-behavioral therapy in 116 patients with a DSM IV–diagnosed psychotic disorder and paranoid ideation in an article published online Feb. 8 in Lancet Psychiatry.

SOURCE: Lancet Psychiatry. 2018 Feb 8. doi: 10.1016/S2215-0366(18)30053-1.

Virtual reality–based cognitive-behavioral therapy could help reduce momentary paranoia and anxiety, and improve social cognition in individuals with psychotic disorders.

Researchers reported the results of a randomized controlled trial of personalized virtual reality-based cognitive-behavioral therapy in 116 patients with a DSM IV–diagnosed psychotic disorder and paranoid ideation in an article published online Feb. 8 in Lancet Psychiatry.

SOURCE: Lancet Psychiatry. 2018 Feb 8. doi: 10.1016/S2215-0366(18)30053-1.

SAN DIEGO – A new study finds that physicians at two multiple sclerosis centers in the Southeast often failed to annually screen patients for depression and cognitive decline. Physicians who did perform screening hardly ever used validated tools and often didn’t refer appropriate patients for higher-level care.

In addition, researchers interviewed 13 leading MS specialists from coast to coast and “found that about half reported not using formal screening tools to assess cognitive impairment and depression,” said study coauthor Tamar Sapir, PhD, chief scientific officer with Prime Education, a firm based in Fort Lauderdale, Fla., that provides a variety of health-related services such as training and research.

SOURCE: Buckle GJ et al. ACTRIMS Forum 2018, abstract No. P161.

SAN DIEGO – A new study finds that physicians at two multiple sclerosis centers in the Southeast often failed to annually screen patients for depression and cognitive decline. Physicians who did perform screening hardly ever used validated tools and often didn’t refer appropriate patients for higher-level care.

In addition, researchers interviewed 13 leading MS specialists from coast to coast and “found that about half reported not using formal screening tools to assess cognitive impairment and depression,” said study coauthor Tamar Sapir, PhD, chief scientific officer with Prime Education, a firm based in Fort Lauderdale, Fla., that provides a variety of health-related services such as training and research.

SOURCE: Buckle GJ et al. ACTRIMS Forum 2018, abstract No. P161.

SAN DIEGO – A new study finds that physicians at two multiple sclerosis centers in the Southeast often failed to annually screen patients for depression and cognitive decline. Physicians who did perform screening hardly ever used validated tools and often didn’t refer appropriate patients for higher-level care.

In addition, researchers interviewed 13 leading MS specialists from coast to coast and “found that about half reported not using formal screening tools to assess cognitive impairment and depression,” said study coauthor Tamar Sapir, PhD, chief scientific officer with Prime Education, a firm based in Fort Lauderdale, Fla., that provides a variety of health-related services such as training and research.

SOURCE: Buckle GJ et al. ACTRIMS Forum 2018, abstract No. P161.

The alpha-1 adrenergic receptor prazosin failed to improve recurring nightmares or sleep quality compared with placebo in veterans with PTSD in a 26-week randomized trial of 304 adult veterans.

In several previous randomized trials lasting fewer than 15 weeks, veterans with PTSD and recurring nightmares who received prazosin showed benefits, including improved sleep quality and PTSD symptoms, compared with placebo patients, wrote Murray A. Raskind, MD, of the Department of Veterans Affairs Puget Sound Health Care System, Seattle, and his colleagues.

In a study published in the New England Journal of Medicine, the researchers randomized 152 veterans with sleep problems and PTSD to prazosin and 152 to a placebo. The participants were recruited from 12 VA medical centers. The average age of the participants was 52 years, more than 96% were male, and about two-thirds were white. Demographics were similar between the two groups.

After 10 weeks and after 26 weeks, there were no significant differences between the two groups in changes from baseline measures of recurring nightmares, using the mean change from baseline in Clinician-Administered PTSD Score item B2 (recurrent distressing dreams). Similarly, no significant differences appeared between the two groups based on Pittsburgh Sleep Quality Index scores.

“A possible explanation for these negative results is selection bias resulting from recruitment of patients who were mainly in clinically stable condition, since symptoms in such patients were less likely to be ameliorated with antiadrenergic treatment,” reported Dr. Raskind and his colleagues.

The average maintenance dose of prazosin was 14.8 mg, compared with 16.4 mg in the placebo group; 187 male study participants reached the maximum dose of 20 mg/day (54% of the prazosin group and 70% of the placebo group).

After 10 weeks, no significant differences were found between the two groups in changes from baseline measures of “recurring distressing dreams,” using the mean change from baseline in Clinician-Administered PTSD Score item B2 (recurrent distressing dreams). The between group difference was 0.2. In addition, no significant differences were found at 10 weeks in the average change from baseline Pittsburgh Sleep Quality Index scores.

Similarly, no significant differences appeared between the two groups at 26 weeks. “A possible explanation for these negative results is selection bias resulting from recruitment of patients who were mainly in clinically stable condition, since symptoms in such patients were less likely to be ameliorated with antiadrenergic treatment,” the researchers said.

On average, patients in the prazosin group had significantly greater decreases in blood pressure, compared with the placebo group. In addition, they had fewer reports of new or worsening suicidal ideation, compared with the placebo group (8% vs.15%).

“Given the concern about suicide among veterans, it is noteworthy that the specifically solicited adverse event of new or worsening suicidal ideation was less common in the prazosin group than in the placebo group, but the absolute number of events was small; this issue warrants further study,” the researchers said.

The study was limited by several factors, including the absence of screening for sleep apnea or sleep-disordered breathing, Dr. Raskind and his colleagues noted. However, the results suggest that “further studies with more refined characterization of autonomic nervous system activity and nocturnal behaviors are needed to determine whether there might be subgroups of veterans with PTSD who can benefit from prazosin.”

Dr. Raskind had no financial conflicts to disclose. The study was supported by the Department of Veterans Affairs Cooperative Studies Program.

[email protected]

SOURCE: Raskind MA et al. N Engl J Med. 2018 Feb 8;378:507-17. doi: 10.1056/NEJMoa1507598.

The alpha-1 adrenergic receptor prazosin failed to improve recurring nightmares or sleep quality compared with placebo in veterans with PTSD in a 26-week randomized trial of 304 adult veterans.

In several previous randomized trials lasting fewer than 15 weeks, veterans with PTSD and recurring nightmares who received prazosin showed benefits, including improved sleep quality and PTSD symptoms, compared with placebo patients, wrote Murray A. Raskind, MD, of the Department of Veterans Affairs Puget Sound Health Care System, Seattle, and his colleagues.

In a study published in the New England Journal of Medicine, the researchers randomized 152 veterans with sleep problems and PTSD to prazosin and 152 to a placebo. The participants were recruited from 12 VA medical centers. The average age of the participants was 52 years, more than 96% were male, and about two-thirds were white. Demographics were similar between the two groups.

After 10 weeks and after 26 weeks, there were no significant differences between the two groups in changes from baseline measures of recurring nightmares, using the mean change from baseline in Clinician-Administered PTSD Score item B2 (recurrent distressing dreams). Similarly, no significant differences appeared between the two groups based on Pittsburgh Sleep Quality Index scores.

“A possible explanation for these negative results is selection bias resulting from recruitment of patients who were mainly in clinically stable condition, since symptoms in such patients were less likely to be ameliorated with antiadrenergic treatment,” reported Dr. Raskind and his colleagues.

The average maintenance dose of prazosin was 14.8 mg, compared with 16.4 mg in the placebo group; 187 male study participants reached the maximum dose of 20 mg/day (54% of the prazosin group and 70% of the placebo group).

After 10 weeks, no significant differences were found between the two groups in changes from baseline measures of “recurring distressing dreams,” using the mean change from baseline in Clinician-Administered PTSD Score item B2 (recurrent distressing dreams). The between group difference was 0.2. In addition, no significant differences were found at 10 weeks in the average change from baseline Pittsburgh Sleep Quality Index scores.

Similarly, no significant differences appeared between the two groups at 26 weeks. “A possible explanation for these negative results is selection bias resulting from recruitment of patients who were mainly in clinically stable condition, since symptoms in such patients were less likely to be ameliorated with antiadrenergic treatment,” the researchers said.

On average, patients in the prazosin group had significantly greater decreases in blood pressure, compared with the placebo group. In addition, they had fewer reports of new or worsening suicidal ideation, compared with the placebo group (8% vs.15%).

“Given the concern about suicide among veterans, it is noteworthy that the specifically solicited adverse event of new or worsening suicidal ideation was less common in the prazosin group than in the placebo group, but the absolute number of events was small; this issue warrants further study,” the researchers said.

The study was limited by several factors, including the absence of screening for sleep apnea or sleep-disordered breathing, Dr. Raskind and his colleagues noted. However, the results suggest that “further studies with more refined characterization of autonomic nervous system activity and nocturnal behaviors are needed to determine whether there might be subgroups of veterans with PTSD who can benefit from prazosin.”

Dr. Raskind had no financial conflicts to disclose. The study was supported by the Department of Veterans Affairs Cooperative Studies Program.

[email protected]

SOURCE: Raskind MA et al. N Engl J Med. 2018 Feb 8;378:507-17. doi: 10.1056/NEJMoa1507598.

The alpha-1 adrenergic receptor prazosin failed to improve recurring nightmares or sleep quality compared with placebo in veterans with PTSD in a 26-week randomized trial of 304 adult veterans.

In several previous randomized trials lasting fewer than 15 weeks, veterans with PTSD and recurring nightmares who received prazosin showed benefits, including improved sleep quality and PTSD symptoms, compared with placebo patients, wrote Murray A. Raskind, MD, of the Department of Veterans Affairs Puget Sound Health Care System, Seattle, and his colleagues.

In a study published in the New England Journal of Medicine, the researchers randomized 152 veterans with sleep problems and PTSD to prazosin and 152 to a placebo. The participants were recruited from 12 VA medical centers. The average age of the participants was 52 years, more than 96% were male, and about two-thirds were white. Demographics were similar between the two groups.

After 10 weeks and after 26 weeks, there were no significant differences between the two groups in changes from baseline measures of recurring nightmares, using the mean change from baseline in Clinician-Administered PTSD Score item B2 (recurrent distressing dreams). Similarly, no significant differences appeared between the two groups based on Pittsburgh Sleep Quality Index scores.

“A possible explanation for these negative results is selection bias resulting from recruitment of patients who were mainly in clinically stable condition, since symptoms in such patients were less likely to be ameliorated with antiadrenergic treatment,” reported Dr. Raskind and his colleagues.

The average maintenance dose of prazosin was 14.8 mg, compared with 16.4 mg in the placebo group; 187 male study participants reached the maximum dose of 20 mg/day (54% of the prazosin group and 70% of the placebo group).

After 10 weeks, no significant differences were found between the two groups in changes from baseline measures of “recurring distressing dreams,” using the mean change from baseline in Clinician-Administered PTSD Score item B2 (recurrent distressing dreams). The between group difference was 0.2. In addition, no significant differences were found at 10 weeks in the average change from baseline Pittsburgh Sleep Quality Index scores.

Similarly, no significant differences appeared between the two groups at 26 weeks. “A possible explanation for these negative results is selection bias resulting from recruitment of patients who were mainly in clinically stable condition, since symptoms in such patients were less likely to be ameliorated with antiadrenergic treatment,” the researchers said.

On average, patients in the prazosin group had significantly greater decreases in blood pressure, compared with the placebo group. In addition, they had fewer reports of new or worsening suicidal ideation, compared with the placebo group (8% vs.15%).

“Given the concern about suicide among veterans, it is noteworthy that the specifically solicited adverse event of new or worsening suicidal ideation was less common in the prazosin group than in the placebo group, but the absolute number of events was small; this issue warrants further study,” the researchers said.

The study was limited by several factors, including the absence of screening for sleep apnea or sleep-disordered breathing, Dr. Raskind and his colleagues noted. However, the results suggest that “further studies with more refined characterization of autonomic nervous system activity and nocturnal behaviors are needed to determine whether there might be subgroups of veterans with PTSD who can benefit from prazosin.”

Dr. Raskind had no financial conflicts to disclose. The study was supported by the Department of Veterans Affairs Cooperative Studies Program.

[email protected]

SOURCE: Raskind MA et al. N Engl J Med. 2018 Feb 8;378:507-17. doi: 10.1056/NEJMoa1507598.

Neurosteroids may be tied to the gender differences found in the susceptibility to schizophrenia, a cross-sectional, case control study showed.

“These findings suggest that neurosteroids are involved in the pathophysiology of schizophrenia in male patients but not so much in female patients,” reported Yu-Chi Huang, MD, of the department of psychiatry at Kaohsiung Chang Gung Memorial Hospital, Kaohsiung City, Taiwan, and associates.

To conduct the study, the researchers recruited 65 patients with schizophrenia from an outpatient department and psychiatry ward of the hospital. Eligible patients were aged 18-65 years, diagnosed with schizophrenia as defined by the DSM-IV-TR, and taking a stable dose of antipsychotics for at least 1 month before the start of the study. In addition, the participants could have no history of major physical illnesses and had to be of ethnic Han Chinese origin. Thirty-six of the patients were men.

The control group was made up of 103 healthy hospital staff and community members who were within the same age range as the patients. The controls could have no history of illicit drug use, physical illnesses, or psychiatric disorders and had to be ethnic Han Chinese. Forty-seven members of the control group were males (Psychoneuroendocrinology. 2017 Oct;84:87-93).

Participants fasted and blood samples were obtained. Dehydroepiandrosterone (DHEA) levels were measured using the DHEA ELISA [enyme-linked immunosorbent assay] – ADKI-900-093, dehydroepiandrosterone sulfate (DHEAS) levels were measured with the Architect DHEA-S reagent kit, and pregnenolone levels were measured using the pregnenolone ELISA kit. Psychiatric diagnoses were assessed for both groups using a psychiatric interview based on the Mini-International Neuropsychiatric Interview, the Positive and Negative Syndrome Scale (PANSS), and the 17-item Hamilton Depression Rating Scale. Several factors tied to schizophrenia were evaluated, including the age of onset, illness duration, and use of antipsychotics. The numbers were placed into a database and analyzed.

After controlling for age and body mass index, the researchers found that in male patients with schizophrenia, DHEA and DHEAS serum levels were positively associated with the age of onset of schizophrenia (P less than .05) and negatively associated with the duration of illness (P less than .05). In addition, they found that pregnenolone levels were associated positively with general symptoms of the PANSS in the male schizophrenia patients (P less than .05 ). Furthermore, the levels of DHEA, DHEAS, and pregnenolone were lower among the male schizophrenia patients, compared with the serum levels of the healthy male controls. No differences were found in serum levels among the female patients with schizophrenia and the healthy controls.

The findings suggest that DHEA, DHEAS, and pregnenolone could be markers of the duration of illness and the severity of general symptoms among male patients with schizophrenia. To read the entire study, click here.

[email protected]

Neurosteroids may be tied to the gender differences found in the susceptibility to schizophrenia, a cross-sectional, case control study showed.

“These findings suggest that neurosteroids are involved in the pathophysiology of schizophrenia in male patients but not so much in female patients,” reported Yu-Chi Huang, MD, of the department of psychiatry at Kaohsiung Chang Gung Memorial Hospital, Kaohsiung City, Taiwan, and associates.

To conduct the study, the researchers recruited 65 patients with schizophrenia from an outpatient department and psychiatry ward of the hospital. Eligible patients were aged 18-65 years, diagnosed with schizophrenia as defined by the DSM-IV-TR, and taking a stable dose of antipsychotics for at least 1 month before the start of the study. In addition, the participants could have no history of major physical illnesses and had to be of ethnic Han Chinese origin. Thirty-six of the patients were men.

The control group was made up of 103 healthy hospital staff and community members who were within the same age range as the patients. The controls could have no history of illicit drug use, physical illnesses, or psychiatric disorders and had to be ethnic Han Chinese. Forty-seven members of the control group were males (Psychoneuroendocrinology. 2017 Oct;84:87-93).

Participants fasted and blood samples were obtained. Dehydroepiandrosterone (DHEA) levels were measured using the DHEA ELISA [enyme-linked immunosorbent assay] – ADKI-900-093, dehydroepiandrosterone sulfate (DHEAS) levels were measured with the Architect DHEA-S reagent kit, and pregnenolone levels were measured using the pregnenolone ELISA kit. Psychiatric diagnoses were assessed for both groups using a psychiatric interview based on the Mini-International Neuropsychiatric Interview, the Positive and Negative Syndrome Scale (PANSS), and the 17-item Hamilton Depression Rating Scale. Several factors tied to schizophrenia were evaluated, including the age of onset, illness duration, and use of antipsychotics. The numbers were placed into a database and analyzed.

After controlling for age and body mass index, the researchers found that in male patients with schizophrenia, DHEA and DHEAS serum levels were positively associated with the age of onset of schizophrenia (P less than .05) and negatively associated with the duration of illness (P less than .05). In addition, they found that pregnenolone levels were associated positively with general symptoms of the PANSS in the male schizophrenia patients (P less than .05 ). Furthermore, the levels of DHEA, DHEAS, and pregnenolone were lower among the male schizophrenia patients, compared with the serum levels of the healthy male controls. No differences were found in serum levels among the female patients with schizophrenia and the healthy controls.

The findings suggest that DHEA, DHEAS, and pregnenolone could be markers of the duration of illness and the severity of general symptoms among male patients with schizophrenia. To read the entire study, click here.

[email protected]

Neurosteroids may be tied to the gender differences found in the susceptibility to schizophrenia, a cross-sectional, case control study showed.

“These findings suggest that neurosteroids are involved in the pathophysiology of schizophrenia in male patients but not so much in female patients,” reported Yu-Chi Huang, MD, of the department of psychiatry at Kaohsiung Chang Gung Memorial Hospital, Kaohsiung City, Taiwan, and associates.

To conduct the study, the researchers recruited 65 patients with schizophrenia from an outpatient department and psychiatry ward of the hospital. Eligible patients were aged 18-65 years, diagnosed with schizophrenia as defined by the DSM-IV-TR, and taking a stable dose of antipsychotics for at least 1 month before the start of the study. In addition, the participants could have no history of major physical illnesses and had to be of ethnic Han Chinese origin. Thirty-six of the patients were men.

The control group was made up of 103 healthy hospital staff and community members who were within the same age range as the patients. The controls could have no history of illicit drug use, physical illnesses, or psychiatric disorders and had to be ethnic Han Chinese. Forty-seven members of the control group were males (Psychoneuroendocrinology. 2017 Oct;84:87-93).

Participants fasted and blood samples were obtained. Dehydroepiandrosterone (DHEA) levels were measured using the DHEA ELISA [enyme-linked immunosorbent assay] – ADKI-900-093, dehydroepiandrosterone sulfate (DHEAS) levels were measured with the Architect DHEA-S reagent kit, and pregnenolone levels were measured using the pregnenolone ELISA kit. Psychiatric diagnoses were assessed for both groups using a psychiatric interview based on the Mini-International Neuropsychiatric Interview, the Positive and Negative Syndrome Scale (PANSS), and the 17-item Hamilton Depression Rating Scale. Several factors tied to schizophrenia were evaluated, including the age of onset, illness duration, and use of antipsychotics. The numbers were placed into a database and analyzed.

After controlling for age and body mass index, the researchers found that in male patients with schizophrenia, DHEA and DHEAS serum levels were positively associated with the age of onset of schizophrenia (P less than .05) and negatively associated with the duration of illness (P less than .05). In addition, they found that pregnenolone levels were associated positively with general symptoms of the PANSS in the male schizophrenia patients (P less than .05 ). Furthermore, the levels of DHEA, DHEAS, and pregnenolone were lower among the male schizophrenia patients, compared with the serum levels of the healthy male controls. No differences were found in serum levels among the female patients with schizophrenia and the healthy controls.

The findings suggest that DHEA, DHEAS, and pregnenolone could be markers of the duration of illness and the severity of general symptoms among male patients with schizophrenia. To read the entire study, click here.

[email protected]

As a group, anxiety disorders are the most common mental illness in the Unites States, affecting 40 million adults. There is a nearly 30% lifetime prevalence of anxiety disorders in the general population.¹ DSM-5 anxiety disorders include generalized anxiety disorder, social anxiety disorder (social phobia), panic disorder, specific phobia, and separation anxiety disorder. Although DSM-IV-TR also classified obsessive-compulsive disorder (OCD) and posttraumatic stress disorder (PTSD) as anxiety disorders, these diagnoses were reclassified in DSM-5. Anxiety also is a frequent symptom of many other psychiatric disorders, especially major depressive disorder.

Although benzodiazepines have many potential uses, they also carry risks that prescribers should recognize. This article reviews some of the risks of benzodiazepine use, identifies patients with higher risks of adverse effects, and presents a practical approach to prescribing these medications.

A wide range of risks

Abuse and addiction. Perhaps the most commonly recognized risk associated with benzodiazepine use is the potential for abuse and addiction.⁴ Prolonged benzodiazepine use typically results in physiologic tolerance, requiring higher dosing to achieve the same initial effect.⁵ American Psychiatric Association practice guidelines recognize the potential for benzodiazepine use to result in symptoms of dependence, including cravings and withdrawal, stating that “with ongoing use, all benzodiazepines will produce physiological dependence in most patients.”⁶ High-potency, short-acting compounds such as alprazolam have a higher risk for dependence, toxicity, and abuse.⁷ However, long-acting benzodiazepines (such as clonazepam) also can be habit-forming.⁸ Because of these properties, it is generally advisable to avoid prescribing benzo­diazepines (and short-acting compounds in particular) when treating patients with current or past substance use disorders, except when treating withdrawal.⁹

Limited efficacy for other disorders. Although benzodiazepines can help reduce anxiety in patients with anxiety disorders, they have shown less promise in treating other disorders in which anxiety is a common symptom. Treating PTSD with benzodiazepines does not appear to offer any advantage over placebo, and may even result in increased symptoms over time.^10,11 There is limited evidence supporting the use of benzodiazepines to treat OCD.^12,13 Patients with borderline personality disorder who are treated with benzodiazepines may experience an increase in behavioral dysregulation.¹⁴

Physical ailments. Benzodiazepines can affect comorbid physical ailments. One study found that long-term benzodiazepine use among patients with comorbid pain disorders was correlated with high utilization of medical services and high disability levels.¹⁵ Benzodiazepine use also has been associated with an increased risk of exacerbating respiratory conditions, such as chronic obstructive pulmonary disease,¹⁶ and increased risk of pneumonia.^17,18

Pregnancy and breastfeeding. Benzo­diazepines carry risks for women who are pregnant or breastfeeding. Benzodiazepine use during pregnancy may increase the relative risk of major malformations and oral clefts. It also may result in neonatal lethargy, sedation, and weight loss. Benzodiazepine withdrawal symptoms can occur in the neonate.¹⁹ Benzodiazepines are secreted in breast milk and can result in sedation among breastfed infants.²⁰

Geriatric patients. Older adults may be particularly vulnerable to the adverse effects of benzodiazepines. The Beers Criteria for Potentially Inappropriate Medication Use in Older Adults recommends against prescribing benzodiazepines to geriatric patients.²¹ Benzodiazepine use has been associated with an increased risk for falls among older adults,^22,23 with an increased risk of fractures²⁴ that can be fatal.²⁵ Benzodiazepines also have been associated with an increased risk of cognitive dysfunction and dementia.^26,27 Despite the documented risks of using benzodiazepines in geriatric patients, benzodiazepines continue to be frequently prescribed to this age group.^28,29 One study found that the rate of prescribing benzo­diazepines by primary care physicians increased from 2003 to 2012, primarily among older adults with no diagnosis of pain or a psychiatric disorder.³⁰

Mortality. Benzodiazepine use also carries an increased risk of mortality. Benzo­diazepine users are at increased risk of motor vehicle accidents because of difficulty maintaining road position.³¹ Some research has shown that patients with schizophrenia treated with benzodiazepines have an increased risk of death compared with those who are prescribed antipsychotics or antidepressants.³² Another study showed that patients with schizophrenia who were prescribed benzodiazepines had a greater risk of death by suicide and accidental poisoning.³³ Benzodiazepine use has been associated with suicidal ideation and an increased risk of suicide.³⁴ Prescription opioids and benzodiazepines are the top 2 causes of overdose-related deaths (benzo­diazepines are involved in approximately 31% of fatal overdoses³⁵), and from 2002 to 2015 there was a 4.3-fold increase in deaths from benzodiazepine overdose in the United States.³⁶ CDC guidelines recommend against co-prescribing opioids and benzodiazepines because of the risk of death by respiratory depression.³⁷ As of August 2016, the FDA required black-box warnings for opioids and benzodiazepines regarding the risk of respiratory depression and death when these agents are used in combination, noting that “If these medicines are prescribed together, limit the dosages and duration of each drug to the minimum possible while achieving the desired clinical effect.”^38,39

A sensible approach to prescribing

Given the risks posed by benzodiazepines, what would constitute a sensible approach to their use? Clearly, there are some patients for whom benzodiazepine use should be minimized or avoided (Table 3). In a patient who is deemed a good candidate for benzo­diazepines, a long-acting agent may be preferable because of the increased risk of dependence associated with short-acting compounds. Start with a low dose, and use the lowest dose that adequately treats the patient’s symptoms.⁴⁰ Using scheduled rather than “as-needed” dosing may help reduce behavioral escape patterns that reinforce anxiety and dependence in the long term.

Before starting a patient on a benzo­diazepine, discuss with him (her) the risks of use and an exit plan to discontinue the medication. For example, a benzodiazepine may be prescribed at the same time as a selective serotonin reuptake inhibitor (SSRI), with the goal of weaning off the benzodiazepine once the SSRI has achieved efficacy.⁶ Inform the patient that prescribing or treatment may be terminated if it is discovered that the patient is abusing or diverting the medication (regularly reviewing the state prescription monitoring program database can help determine if this has occurred). Strongly consider using non-benzodiazepine treatments for anxiety with (or eventually in place of) benzodiazepines (Table 4⁴¹).

As a group, anxiety disorders are the most common mental illness in the Unites States, affecting 40 million adults. There is a nearly 30% lifetime prevalence of anxiety disorders in the general population.¹ DSM-5 anxiety disorders include generalized anxiety disorder, social anxiety disorder (social phobia), panic disorder, specific phobia, and separation anxiety disorder. Although DSM-IV-TR also classified obsessive-compulsive disorder (OCD) and posttraumatic stress disorder (PTSD) as anxiety disorders, these diagnoses were reclassified in DSM-5. Anxiety also is a frequent symptom of many other psychiatric disorders, especially major depressive disorder.

Although benzodiazepines have many potential uses, they also carry risks that prescribers should recognize. This article reviews some of the risks of benzodiazepine use, identifies patients with higher risks of adverse effects, and presents a practical approach to prescribing these medications.

A wide range of risks

Abuse and addiction. Perhaps the most commonly recognized risk associated with benzodiazepine use is the potential for abuse and addiction.⁴ Prolonged benzodiazepine use typically results in physiologic tolerance, requiring higher dosing to achieve the same initial effect.⁵ American Psychiatric Association practice guidelines recognize the potential for benzodiazepine use to result in symptoms of dependence, including cravings and withdrawal, stating that “with ongoing use, all benzodiazepines will produce physiological dependence in most patients.”⁶ High-potency, short-acting compounds such as alprazolam have a higher risk for dependence, toxicity, and abuse.⁷ However, long-acting benzodiazepines (such as clonazepam) also can be habit-forming.⁸ Because of these properties, it is generally advisable to avoid prescribing benzo­diazepines (and short-acting compounds in particular) when treating patients with current or past substance use disorders, except when treating withdrawal.⁹

Limited efficacy for other disorders. Although benzodiazepines can help reduce anxiety in patients with anxiety disorders, they have shown less promise in treating other disorders in which anxiety is a common symptom. Treating PTSD with benzodiazepines does not appear to offer any advantage over placebo, and may even result in increased symptoms over time.^10,11 There is limited evidence supporting the use of benzodiazepines to treat OCD.^12,13 Patients with borderline personality disorder who are treated with benzodiazepines may experience an increase in behavioral dysregulation.¹⁴

Physical ailments. Benzodiazepines can affect comorbid physical ailments. One study found that long-term benzodiazepine use among patients with comorbid pain disorders was correlated with high utilization of medical services and high disability levels.¹⁵ Benzodiazepine use also has been associated with an increased risk of exacerbating respiratory conditions, such as chronic obstructive pulmonary disease,¹⁶ and increased risk of pneumonia.^17,18

Pregnancy and breastfeeding. Benzo­diazepines carry risks for women who are pregnant or breastfeeding. Benzodiazepine use during pregnancy may increase the relative risk of major malformations and oral clefts. It also may result in neonatal lethargy, sedation, and weight loss. Benzodiazepine withdrawal symptoms can occur in the neonate.¹⁹ Benzodiazepines are secreted in breast milk and can result in sedation among breastfed infants.²⁰

Geriatric patients. Older adults may be particularly vulnerable to the adverse effects of benzodiazepines. The Beers Criteria for Potentially Inappropriate Medication Use in Older Adults recommends against prescribing benzodiazepines to geriatric patients.²¹ Benzodiazepine use has been associated with an increased risk for falls among older adults,^22,23 with an increased risk of fractures²⁴ that can be fatal.²⁵ Benzodiazepines also have been associated with an increased risk of cognitive dysfunction and dementia.^26,27 Despite the documented risks of using benzodiazepines in geriatric patients, benzodiazepines continue to be frequently prescribed to this age group.^28,29 One study found that the rate of prescribing benzo­diazepines by primary care physicians increased from 2003 to 2012, primarily among older adults with no diagnosis of pain or a psychiatric disorder.³⁰

Mortality. Benzodiazepine use also carries an increased risk of mortality. Benzo­diazepine users are at increased risk of motor vehicle accidents because of difficulty maintaining road position.³¹ Some research has shown that patients with schizophrenia treated with benzodiazepines have an increased risk of death compared with those who are prescribed antipsychotics or antidepressants.³² Another study showed that patients with schizophrenia who were prescribed benzodiazepines had a greater risk of death by suicide and accidental poisoning.³³ Benzodiazepine use has been associated with suicidal ideation and an increased risk of suicide.³⁴ Prescription opioids and benzodiazepines are the top 2 causes of overdose-related deaths (benzo­diazepines are involved in approximately 31% of fatal overdoses³⁵), and from 2002 to 2015 there was a 4.3-fold increase in deaths from benzodiazepine overdose in the United States.³⁶ CDC guidelines recommend against co-prescribing opioids and benzodiazepines because of the risk of death by respiratory depression.³⁷ As of August 2016, the FDA required black-box warnings for opioids and benzodiazepines regarding the risk of respiratory depression and death when these agents are used in combination, noting that “If these medicines are prescribed together, limit the dosages and duration of each drug to the minimum possible while achieving the desired clinical effect.”^38,39

A sensible approach to prescribing

Given the risks posed by benzodiazepines, what would constitute a sensible approach to their use? Clearly, there are some patients for whom benzodiazepine use should be minimized or avoided (Table 3). In a patient who is deemed a good candidate for benzo­diazepines, a long-acting agent may be preferable because of the increased risk of dependence associated with short-acting compounds. Start with a low dose, and use the lowest dose that adequately treats the patient’s symptoms.⁴⁰ Using scheduled rather than “as-needed” dosing may help reduce behavioral escape patterns that reinforce anxiety and dependence in the long term.

Before starting a patient on a benzo­diazepine, discuss with him (her) the risks of use and an exit plan to discontinue the medication. For example, a benzodiazepine may be prescribed at the same time as a selective serotonin reuptake inhibitor (SSRI), with the goal of weaning off the benzodiazepine once the SSRI has achieved efficacy.⁶ Inform the patient that prescribing or treatment may be terminated if it is discovered that the patient is abusing or diverting the medication (regularly reviewing the state prescription monitoring program database can help determine if this has occurred). Strongly consider using non-benzodiazepine treatments for anxiety with (or eventually in place of) benzodiazepines (Table 4⁴¹).

As a group, anxiety disorders are the most common mental illness in the Unites States, affecting 40 million adults. There is a nearly 30% lifetime prevalence of anxiety disorders in the general population.¹ DSM-5 anxiety disorders include generalized anxiety disorder, social anxiety disorder (social phobia), panic disorder, specific phobia, and separation anxiety disorder. Although DSM-IV-TR also classified obsessive-compulsive disorder (OCD) and posttraumatic stress disorder (PTSD) as anxiety disorders, these diagnoses were reclassified in DSM-5. Anxiety also is a frequent symptom of many other psychiatric disorders, especially major depressive disorder.

Although benzodiazepines have many potential uses, they also carry risks that prescribers should recognize. This article reviews some of the risks of benzodiazepine use, identifies patients with higher risks of adverse effects, and presents a practical approach to prescribing these medications.

A wide range of risks

Abuse and addiction. Perhaps the most commonly recognized risk associated with benzodiazepine use is the potential for abuse and addiction.⁴ Prolonged benzodiazepine use typically results in physiologic tolerance, requiring higher dosing to achieve the same initial effect.⁵ American Psychiatric Association practice guidelines recognize the potential for benzodiazepine use to result in symptoms of dependence, including cravings and withdrawal, stating that “with ongoing use, all benzodiazepines will produce physiological dependence in most patients.”⁶ High-potency, short-acting compounds such as alprazolam have a higher risk for dependence, toxicity, and abuse.⁷ However, long-acting benzodiazepines (such as clonazepam) also can be habit-forming.⁸ Because of these properties, it is generally advisable to avoid prescribing benzo­diazepines (and short-acting compounds in particular) when treating patients with current or past substance use disorders, except when treating withdrawal.⁹

Limited efficacy for other disorders. Although benzodiazepines can help reduce anxiety in patients with anxiety disorders, they have shown less promise in treating other disorders in which anxiety is a common symptom. Treating PTSD with benzodiazepines does not appear to offer any advantage over placebo, and may even result in increased symptoms over time.^10,11 There is limited evidence supporting the use of benzodiazepines to treat OCD.^12,13 Patients with borderline personality disorder who are treated with benzodiazepines may experience an increase in behavioral dysregulation.¹⁴

Physical ailments. Benzodiazepines can affect comorbid physical ailments. One study found that long-term benzodiazepine use among patients with comorbid pain disorders was correlated with high utilization of medical services and high disability levels.¹⁵ Benzodiazepine use also has been associated with an increased risk of exacerbating respiratory conditions, such as chronic obstructive pulmonary disease,¹⁶ and increased risk of pneumonia.^17,18

Pregnancy and breastfeeding. Benzo­diazepines carry risks for women who are pregnant or breastfeeding. Benzodiazepine use during pregnancy may increase the relative risk of major malformations and oral clefts. It also may result in neonatal lethargy, sedation, and weight loss. Benzodiazepine withdrawal symptoms can occur in the neonate.¹⁹ Benzodiazepines are secreted in breast milk and can result in sedation among breastfed infants.²⁰

Geriatric patients. Older adults may be particularly vulnerable to the adverse effects of benzodiazepines. The Beers Criteria for Potentially Inappropriate Medication Use in Older Adults recommends against prescribing benzodiazepines to geriatric patients.²¹ Benzodiazepine use has been associated with an increased risk for falls among older adults,^22,23 with an increased risk of fractures²⁴ that can be fatal.²⁵ Benzodiazepines also have been associated with an increased risk of cognitive dysfunction and dementia.^26,27 Despite the documented risks of using benzodiazepines in geriatric patients, benzodiazepines continue to be frequently prescribed to this age group.^28,29 One study found that the rate of prescribing benzo­diazepines by primary care physicians increased from 2003 to 2012, primarily among older adults with no diagnosis of pain or a psychiatric disorder.³⁰

Mortality. Benzodiazepine use also carries an increased risk of mortality. Benzo­diazepine users are at increased risk of motor vehicle accidents because of difficulty maintaining road position.³¹ Some research has shown that patients with schizophrenia treated with benzodiazepines have an increased risk of death compared with those who are prescribed antipsychotics or antidepressants.³² Another study showed that patients with schizophrenia who were prescribed benzodiazepines had a greater risk of death by suicide and accidental poisoning.³³ Benzodiazepine use has been associated with suicidal ideation and an increased risk of suicide.³⁴ Prescription opioids and benzodiazepines are the top 2 causes of overdose-related deaths (benzo­diazepines are involved in approximately 31% of fatal overdoses³⁵), and from 2002 to 2015 there was a 4.3-fold increase in deaths from benzodiazepine overdose in the United States.³⁶ CDC guidelines recommend against co-prescribing opioids and benzodiazepines because of the risk of death by respiratory depression.³⁷ As of August 2016, the FDA required black-box warnings for opioids and benzodiazepines regarding the risk of respiratory depression and death when these agents are used in combination, noting that “If these medicines are prescribed together, limit the dosages and duration of each drug to the minimum possible while achieving the desired clinical effect.”^38,39

A sensible approach to prescribing

Given the risks posed by benzodiazepines, what would constitute a sensible approach to their use? Clearly, there are some patients for whom benzodiazepine use should be minimized or avoided (Table 3). In a patient who is deemed a good candidate for benzo­diazepines, a long-acting agent may be preferable because of the increased risk of dependence associated with short-acting compounds. Start with a low dose, and use the lowest dose that adequately treats the patient’s symptoms.⁴⁰ Using scheduled rather than “as-needed” dosing may help reduce behavioral escape patterns that reinforce anxiety and dependence in the long term.

Before starting a patient on a benzo­diazepine, discuss with him (her) the risks of use and an exit plan to discontinue the medication. For example, a benzodiazepine may be prescribed at the same time as a selective serotonin reuptake inhibitor (SSRI), with the goal of weaning off the benzodiazepine once the SSRI has achieved efficacy.⁶ Inform the patient that prescribing or treatment may be terminated if it is discovered that the patient is abusing or diverting the medication (regularly reviewing the state prescription monitoring program database can help determine if this has occurred). Strongly consider using non-benzodiazepine treatments for anxiety with (or eventually in place of) benzodiazepines (Table 4⁴¹).

Compulsive sexual behavior (CSB), also referred to as sexual addiction or hypersexuality, is characterized by repetitive and intense preoccupations with sexual fantasies, urges, and behaviors that are distressing to the individual and/or result in psychosocial impairment. Individuals with CSB often perceive their sexual behavior to be excessive but are unable to control it. CSB can involve fantasies and urges in addition to or in place of the behavior but must cause clinically significant distress and interference in daily life to qualify as a disorder.

Because of the lack of large-scale, population-based epidemiological studies assessing CSB, its true prevalence among adults is unknown. A study of 204 psychiatric inpatients found a current prevalence of 4.4%,¹ while a university-based survey estimated the prevalence of CSB at approximately 2%.² Others have estimated that the prevalence is between 3% to 6% of adults in the United States,^3,4 with males comprising the majority (≥80%) of affected individuals.⁵

CSB usually develops during late adolescence/early adulthood, and most who present for treatment are male.⁵ Mood states, including depression, happiness, and loneliness, may trigger CSB.⁶ Many individuals report feelings of dissociation while engaging in CSB-related behaviors, whereas others report feeling important, powerful, excited, or gratified.

Why CSB is difficult to diagnose

Although CSB may be common, it usually goes undiagnosed. This potentially problematic behavior often is not diagnosed because of:

• Shame and secrecy. Embarrassment and shame, which are fundamental to CSB, appear to explain, in part, why few patients volunteer information regarding this behavior unless specifically asked.¹
• Patient lack of knowledge. Patients often do not know that their behavior can be successfully treated.
• Clinician lack of knowledge. Few health care professionals have education or training in CSB. A lack of recognition of CSB also may be due to our limited understanding regarding the limits of sexual normality. In addition, the classification of CSB is unclear and not agreed upon (Box^7-9), and moral judgments often are involved in understanding sexual behaviors.¹⁰

Box
Classifying compulsive sexual behavior

No consensus on diagnostic criteria

Accurately diagnosing CSB is difficult because of a lack of consensus about the diagnostic criteria for the disorder. Christenson et al¹¹ developed an early set of criteria for CSB as part of a larger survey of impulse control disorders. They used the following 2 criteria to diagnose CSB: (1) excessive or uncontrolled sexual behavior(s) or sexual thoughts/urges to engage in behavior, and (2) these behaviors or thoughts/urges lead to significant distress, social or occupational impairment, or legal and financial consequences.^11,12

During the DSM-5 revision process, a second approach to the diagnostic criteria was proposed for hypersexuality disorder. Under the proposed criteria for hypersexuality, a person would meet the diagnosis if ≥3 of the following were endorsed over a 6-month period: (a) time consumed by sexual fantasies, urges, or behaviors repetitively interferes with other important (non-sexual) goals, activities, and obligations; (b) repetitively engaging in sexual fantasies, urges, or behaviors in response to dysphoric mood states; (c) repetitively engaging in sexual fantasies, urges, or behaviors in response to stressful life events; (d) repetitive but unsuccessful efforts to control or significantly reduce these sexual fantasies, urges, or behaviors; and (e) repetitively engaging in sexual behaviors while disregarding the risk for physical or emotional harm to self or others.⁹

These 2 proposed approaches to diagnosis are somewhat similar. Both suggest that the core underlying issues involve sexual urges or behaviors that are difficult to control and that lead to psychosocial dysfunction. Differences in the criteria, however, could result in different rates of CSB diagnosis; therefore, further research will need to determine which diagnostic approach reflects the neurobiology underlying CSB.

Avoid misdiagnosis

Before making a diagnosis of CSB, it is important for clinicians to consider whether they are stigmatizing “negative consequences,” distress, or social impairment based on unconscious bias toward certain sexual behaviors. In addition, we need to ensure that we are not holding sex to different standards than other behaviors (for example, there are many things in life we do that result in negative consequences and yet do not classify as a mental disorder, such as indulging in less healthy food choices). Furthermore, excessive sexual behaviors might be associated with the normal coming out process for LGBTQ individuals, partner relationship problems, or sexual/gender identity. Therefore, the behavior needs to be assessed in the context of these psychosocial environmental factors.

Differential diagnosis

Various psychiatric disorders also may include excessive sexual behavior as part of their clinical presentation, and it is important to differentiate that behavior from CSB.

Bipolar disorder. Excessive sexual behavior can occur as part of a manic episode in bipolar disorder. If the problematic sexual behavior also occurs when the person’s mood is stable, the individual may have CSB and bipolar disorder. This distinction is important because the treatment for bipolar disorder is often different for CSB, because anticonvulsants have only case reports attesting to their use in CSB.

Substance abuse. Excessive sexual behavior can occur when a person is abusing substances, particularly stimulants such as cocaine and amphetamines.¹³ If the sexual behavior does not occur when the person is not using drugs, then the appropriate diagnosis would not likely be CSB.

Obsessive-compulsive disorder (OCD). Individuals with OCD often are preoccupied with sexual themes and feel that they think about sex excessively.¹⁴ Although patients with OCD may be preoccupied with thoughts of sex, the key difference is that persons with CSB report feeling excited by these thoughts and derive pleasure from the behavior, whereas the sexual thoughts of OCD are perceived as unpleasant.

Other disorders that may give rise to hypersexual behavior include neurocognitive disorders, attention-deficit/hyperactivity disorder, autism spectrum disorders, and depressive disorders.

Adverse effects of medication. It is important to ask the patient whether he (she)developed CSB after starting a medication. Certain medications (eg, medications for Parkinson’s disease or restless leg syndrome, or aripiprazole to treat depression or psychosis) may cause patients to engage in problematic sexual behavior.^15,16 If the sexual behavior decreases or stops when the medication dosage is reduced or the medication is stopped, a diagnosis of CSB would not be appropriate.

Comorbidity is common

Research suggests that approximately one-half of adults with CSB meet criteria for at least 1 other psychiatric disorder, such as mood, anxiety, substance use, impulse control, or personality disorders. A study of men with CSB (N = 103) found that 71% met criteria for a mood disorder, 40% for an anxiety disorder, 41% for a substance use disorder, and 24% for an impulse control disorder such as gambling disorder.¹⁷ Therefore, to successfully treat CSB, clinicians also may need to focus on how and to what extent these co-occurring disorders drive the sexual behavior.

Co-occurring medical conditions also are common among individuals with CSB. Medical concerns may include unwanted pregnancy, sexually transmitted infections, and HIV/AIDS. Thus, treating psychiatric comorbidities and providing education about sexual health, with referrals to primary care specialists, often are part of CSB treatment.

Neuroimaging and cognition

One imaging study that compared participants with and without CSB found that participants with CSB had higher activity in the ventral striatum, anterior cingulate cortex, and amygdala relative to controls during a cue-reactivity functional MRI task.¹⁸ These findings show notable similarities to the patterns of activation seen in patients addicted to drugs when assessed using drug-craving paradigms. An additional neuroimaging study assessing patients with hypersexuality using diffusion tensor imaging noted that diffusivity in a prefrontal white matter tract within a superior frontal region was greater in patients with CSB.¹⁸ This study also indicated that there was a negative correlation between observed diffusion in the noted location and overall severity score for CSB symptoms such as frequency of urges or behaviors.

In terms of cognition, a preliminary assessment of young adults with CSB compared with healthy controls did not find any differences between groups across several tasks, although the previously mentioned diffusion tensor imaging study reported elevated impulsivity in CSB.¹⁸

Approaches to treatment

Most people with CSB are reluctant to mention it to their health care providers, and most physicians are generally uncomfortable talking about sex with their patients, in part, because of a lack of training.¹⁹ Patients are more likely to bring up the topic when they are receiving treatment for anxiety, depression, or substance abuse. Therefore, clinicians must consider that sexual behavior might be associated with a coping mechanism, distressing outcome, or comorbid condition in these patients.

Pharmacologic treatment

Evidence for the pharmacologic treatment of CSB consists primarily of small, open-label studies, case series, or retrospective analyses, except for 1 double-blind, placebo-controlled study. Based on this evidence, there may be several pharma­cologic treatment options for patients with CSB; however, there are no FDA-approved medications for CSB.

Antidepressants. One of the most thoroughly documented categories of pharmacologic treatment for CSB is selective serotonin reuptake inhibitors (SSRIs). Several retrospective analyses and case series have reported on the general efficacy of SSRIs in reducing symptoms of CSB.^20-23 Citalopram, the only treatment for CSB that has been assessed using a double-blind, placebo-controlled methodology, was associated with significant decreases in CSB symptoms, including sexual desire/drive, frequency of masturbation, and pornography use.²⁴

In addition to SSRIs, several additional case reports have suggested that other classes of antidepressants, such as serotonin-norepinephrine reuptake inhibitors and tricyclic antidepressants, or stimulants may be beneficial when treating CSB.²⁵ Several case reports have indicated significant improvement of CSB symptoms using clomipramine.²² A retrospective study of nefazodone also has suggested that it may be an option for treating CSB. Patients reported notable reductions in the frequency of sexual obsessions/compulsions while taking nefazodone and reported no notable sexual adverse effects.²⁶ One branded version of nefazodone, Serzone, was associated with rare but severe liver problems and was withdrawn from the U.S. market in 2004.

Although some initial evidence regarding antidepressant use, particularly SSRIs, to treat CSB has suggested that these medications may be potentially beneficial, the findings are far from conclusive, with only 1 controlled trial and only single-subject case reports for many of the medications studied.

Naltrexone, an opioid antagonist, has received support from available cases, open-label studies, and retrospective analyses.^17,27 Although evidence for the use of naltrexone in CSB is limited to case reports and retrospective analyses, results have been positive. Naltrexone has shown notable decreases in CSB symptom severity when used as monotherapy and when used in combination with other treatments.

Anticonvulsants. Several case reports have suggested that certain anticonvulsants may be beneficial for treating CSB. Topiramate may be a particularly useful option.²⁸ Other anticonvulsants showing benefit for CSB in case reports include valproic acid, lamotrigine, and levetiracetam.¹⁸

Psychotherapy

Evidence supporting specific types of psychotherapy for CSB is limited and largely drawn from uncontrolled studies and case reports.

Cognitive-behavioral therapy (CBT) is one of the more common psychotherapeutic options used for CSB. Several uncontrolled studies and case reports have found that CBT is beneficial for CSB, although methodologies have varied.

Several cases found that combining CBT with motivational interviewing was associated with significant reductions in sexual behaviors, such as frequency of sexual partners and amount of time spent online during work hours.^29,30 Group CBT also has been shown to be effective for CSB.³¹

Acceptance and commitment therapy (ACT) has received some initial support, with 1 uncontrolled study and 1 controlled study.^32,33 The controlled study used 12 sessions of individual ACT compared with a wait-list condition.³² Improvements in CSB symptoms were maintained for 3 months. The overall reduction in problematic Internet pornography use was reported as 92% immediately after the study ended, and 86% after 3 months.

Marital/relationship therapy has been used successfully in several case series and case reports, although no studies have assessed its efficacy in treating CSB using a randomized protocol. In 1 case report, the researcher found that participation in marital sex therapy elicited notable improvements over the course of 1 year and 20 sessions.³⁴

Compulsive sexual behavior (CSB), also referred to as sexual addiction or hypersexuality, is characterized by repetitive and intense preoccupations with sexual fantasies, urges, and behaviors that are distressing to the individual and/or result in psychosocial impairment. Individuals with CSB often perceive their sexual behavior to be excessive but are unable to control it. CSB can involve fantasies and urges in addition to or in place of the behavior but must cause clinically significant distress and interference in daily life to qualify as a disorder.

Because of the lack of large-scale, population-based epidemiological studies assessing CSB, its true prevalence among adults is unknown. A study of 204 psychiatric inpatients found a current prevalence of 4.4%,¹ while a university-based survey estimated the prevalence of CSB at approximately 2%.² Others have estimated that the prevalence is between 3% to 6% of adults in the United States,^3,4 with males comprising the majority (≥80%) of affected individuals.⁵

CSB usually develops during late adolescence/early adulthood, and most who present for treatment are male.⁵ Mood states, including depression, happiness, and loneliness, may trigger CSB.⁶ Many individuals report feelings of dissociation while engaging in CSB-related behaviors, whereas others report feeling important, powerful, excited, or gratified.

Why CSB is difficult to diagnose

Although CSB may be common, it usually goes undiagnosed. This potentially problematic behavior often is not diagnosed because of:

• Shame and secrecy. Embarrassment and shame, which are fundamental to CSB, appear to explain, in part, why few patients volunteer information regarding this behavior unless specifically asked.¹
• Patient lack of knowledge. Patients often do not know that their behavior can be successfully treated.
• Clinician lack of knowledge. Few health care professionals have education or training in CSB. A lack of recognition of CSB also may be due to our limited understanding regarding the limits of sexual normality. In addition, the classification of CSB is unclear and not agreed upon (Box^7-9), and moral judgments often are involved in understanding sexual behaviors.¹⁰

Box
Classifying compulsive sexual behavior

No consensus on diagnostic criteria

Accurately diagnosing CSB is difficult because of a lack of consensus about the diagnostic criteria for the disorder. Christenson et al¹¹ developed an early set of criteria for CSB as part of a larger survey of impulse control disorders. They used the following 2 criteria to diagnose CSB: (1) excessive or uncontrolled sexual behavior(s) or sexual thoughts/urges to engage in behavior, and (2) these behaviors or thoughts/urges lead to significant distress, social or occupational impairment, or legal and financial consequences.^11,12

During the DSM-5 revision process, a second approach to the diagnostic criteria was proposed for hypersexuality disorder. Under the proposed criteria for hypersexuality, a person would meet the diagnosis if ≥3 of the following were endorsed over a 6-month period: (a) time consumed by sexual fantasies, urges, or behaviors repetitively interferes with other important (non-sexual) goals, activities, and obligations; (b) repetitively engaging in sexual fantasies, urges, or behaviors in response to dysphoric mood states; (c) repetitively engaging in sexual fantasies, urges, or behaviors in response to stressful life events; (d) repetitive but unsuccessful efforts to control or significantly reduce these sexual fantasies, urges, or behaviors; and (e) repetitively engaging in sexual behaviors while disregarding the risk for physical or emotional harm to self or others.⁹

These 2 proposed approaches to diagnosis are somewhat similar. Both suggest that the core underlying issues involve sexual urges or behaviors that are difficult to control and that lead to psychosocial dysfunction. Differences in the criteria, however, could result in different rates of CSB diagnosis; therefore, further research will need to determine which diagnostic approach reflects the neurobiology underlying CSB.

Avoid misdiagnosis

Before making a diagnosis of CSB, it is important for clinicians to consider whether they are stigmatizing “negative consequences,” distress, or social impairment based on unconscious bias toward certain sexual behaviors. In addition, we need to ensure that we are not holding sex to different standards than other behaviors (for example, there are many things in life we do that result in negative consequences and yet do not classify as a mental disorder, such as indulging in less healthy food choices). Furthermore, excessive sexual behaviors might be associated with the normal coming out process for LGBTQ individuals, partner relationship problems, or sexual/gender identity. Therefore, the behavior needs to be assessed in the context of these psychosocial environmental factors.

Differential diagnosis

Various psychiatric disorders also may include excessive sexual behavior as part of their clinical presentation, and it is important to differentiate that behavior from CSB.

Bipolar disorder. Excessive sexual behavior can occur as part of a manic episode in bipolar disorder. If the problematic sexual behavior also occurs when the person’s mood is stable, the individual may have CSB and bipolar disorder. This distinction is important because the treatment for bipolar disorder is often different for CSB, because anticonvulsants have only case reports attesting to their use in CSB.

Substance abuse. Excessive sexual behavior can occur when a person is abusing substances, particularly stimulants such as cocaine and amphetamines.¹³ If the sexual behavior does not occur when the person is not using drugs, then the appropriate diagnosis would not likely be CSB.

Obsessive-compulsive disorder (OCD). Individuals with OCD often are preoccupied with sexual themes and feel that they think about sex excessively.¹⁴ Although patients with OCD may be preoccupied with thoughts of sex, the key difference is that persons with CSB report feeling excited by these thoughts and derive pleasure from the behavior, whereas the sexual thoughts of OCD are perceived as unpleasant.

Other disorders that may give rise to hypersexual behavior include neurocognitive disorders, attention-deficit/hyperactivity disorder, autism spectrum disorders, and depressive disorders.

Adverse effects of medication. It is important to ask the patient whether he (she)developed CSB after starting a medication. Certain medications (eg, medications for Parkinson’s disease or restless leg syndrome, or aripiprazole to treat depression or psychosis) may cause patients to engage in problematic sexual behavior.^15,16 If the sexual behavior decreases or stops when the medication dosage is reduced or the medication is stopped, a diagnosis of CSB would not be appropriate.

Comorbidity is common

Research suggests that approximately one-half of adults with CSB meet criteria for at least 1 other psychiatric disorder, such as mood, anxiety, substance use, impulse control, or personality disorders. A study of men with CSB (N = 103) found that 71% met criteria for a mood disorder, 40% for an anxiety disorder, 41% for a substance use disorder, and 24% for an impulse control disorder such as gambling disorder.¹⁷ Therefore, to successfully treat CSB, clinicians also may need to focus on how and to what extent these co-occurring disorders drive the sexual behavior.

Co-occurring medical conditions also are common among individuals with CSB. Medical concerns may include unwanted pregnancy, sexually transmitted infections, and HIV/AIDS. Thus, treating psychiatric comorbidities and providing education about sexual health, with referrals to primary care specialists, often are part of CSB treatment.

Neuroimaging and cognition

One imaging study that compared participants with and without CSB found that participants with CSB had higher activity in the ventral striatum, anterior cingulate cortex, and amygdala relative to controls during a cue-reactivity functional MRI task.¹⁸ These findings show notable similarities to the patterns of activation seen in patients addicted to drugs when assessed using drug-craving paradigms. An additional neuroimaging study assessing patients with hypersexuality using diffusion tensor imaging noted that diffusivity in a prefrontal white matter tract within a superior frontal region was greater in patients with CSB.¹⁸ This study also indicated that there was a negative correlation between observed diffusion in the noted location and overall severity score for CSB symptoms such as frequency of urges or behaviors.

In terms of cognition, a preliminary assessment of young adults with CSB compared with healthy controls did not find any differences between groups across several tasks, although the previously mentioned diffusion tensor imaging study reported elevated impulsivity in CSB.¹⁸

Approaches to treatment

Most people with CSB are reluctant to mention it to their health care providers, and most physicians are generally uncomfortable talking about sex with their patients, in part, because of a lack of training.¹⁹ Patients are more likely to bring up the topic when they are receiving treatment for anxiety, depression, or substance abuse. Therefore, clinicians must consider that sexual behavior might be associated with a coping mechanism, distressing outcome, or comorbid condition in these patients.

Pharmacologic treatment

Evidence for the pharmacologic treatment of CSB consists primarily of small, open-label studies, case series, or retrospective analyses, except for 1 double-blind, placebo-controlled study. Based on this evidence, there may be several pharma­cologic treatment options for patients with CSB; however, there are no FDA-approved medications for CSB.

Antidepressants. One of the most thoroughly documented categories of pharmacologic treatment for CSB is selective serotonin reuptake inhibitors (SSRIs). Several retrospective analyses and case series have reported on the general efficacy of SSRIs in reducing symptoms of CSB.^20-23 Citalopram, the only treatment for CSB that has been assessed using a double-blind, placebo-controlled methodology, was associated with significant decreases in CSB symptoms, including sexual desire/drive, frequency of masturbation, and pornography use.²⁴

In addition to SSRIs, several additional case reports have suggested that other classes of antidepressants, such as serotonin-norepinephrine reuptake inhibitors and tricyclic antidepressants, or stimulants may be beneficial when treating CSB.²⁵ Several case reports have indicated significant improvement of CSB symptoms using clomipramine.²² A retrospective study of nefazodone also has suggested that it may be an option for treating CSB. Patients reported notable reductions in the frequency of sexual obsessions/compulsions while taking nefazodone and reported no notable sexual adverse effects.²⁶ One branded version of nefazodone, Serzone, was associated with rare but severe liver problems and was withdrawn from the U.S. market in 2004.

Although some initial evidence regarding antidepressant use, particularly SSRIs, to treat CSB has suggested that these medications may be potentially beneficial, the findings are far from conclusive, with only 1 controlled trial and only single-subject case reports for many of the medications studied.

Naltrexone, an opioid antagonist, has received support from available cases, open-label studies, and retrospective analyses.^17,27 Although evidence for the use of naltrexone in CSB is limited to case reports and retrospective analyses, results have been positive. Naltrexone has shown notable decreases in CSB symptom severity when used as monotherapy and when used in combination with other treatments.

Anticonvulsants. Several case reports have suggested that certain anticonvulsants may be beneficial for treating CSB. Topiramate may be a particularly useful option.²⁸ Other anticonvulsants showing benefit for CSB in case reports include valproic acid, lamotrigine, and levetiracetam.¹⁸

Psychotherapy

Evidence supporting specific types of psychotherapy for CSB is limited and largely drawn from uncontrolled studies and case reports.

Cognitive-behavioral therapy (CBT) is one of the more common psychotherapeutic options used for CSB. Several uncontrolled studies and case reports have found that CBT is beneficial for CSB, although methodologies have varied.

Several cases found that combining CBT with motivational interviewing was associated with significant reductions in sexual behaviors, such as frequency of sexual partners and amount of time spent online during work hours.^29,30 Group CBT also has been shown to be effective for CSB.³¹

Acceptance and commitment therapy (ACT) has received some initial support, with 1 uncontrolled study and 1 controlled study.^32,33 The controlled study used 12 sessions of individual ACT compared with a wait-list condition.³² Improvements in CSB symptoms were maintained for 3 months. The overall reduction in problematic Internet pornography use was reported as 92% immediately after the study ended, and 86% after 3 months.

Marital/relationship therapy has been used successfully in several case series and case reports, although no studies have assessed its efficacy in treating CSB using a randomized protocol. In 1 case report, the researcher found that participation in marital sex therapy elicited notable improvements over the course of 1 year and 20 sessions.³⁴

Compulsive sexual behavior (CSB), also referred to as sexual addiction or hypersexuality, is characterized by repetitive and intense preoccupations with sexual fantasies, urges, and behaviors that are distressing to the individual and/or result in psychosocial impairment. Individuals with CSB often perceive their sexual behavior to be excessive but are unable to control it. CSB can involve fantasies and urges in addition to or in place of the behavior but must cause clinically significant distress and interference in daily life to qualify as a disorder.

Because of the lack of large-scale, population-based epidemiological studies assessing CSB, its true prevalence among adults is unknown. A study of 204 psychiatric inpatients found a current prevalence of 4.4%,¹ while a university-based survey estimated the prevalence of CSB at approximately 2%.² Others have estimated that the prevalence is between 3% to 6% of adults in the United States,^3,4 with males comprising the majority (≥80%) of affected individuals.⁵

CSB usually develops during late adolescence/early adulthood, and most who present for treatment are male.⁵ Mood states, including depression, happiness, and loneliness, may trigger CSB.⁶ Many individuals report feelings of dissociation while engaging in CSB-related behaviors, whereas others report feeling important, powerful, excited, or gratified.

Why CSB is difficult to diagnose

Although CSB may be common, it usually goes undiagnosed. This potentially problematic behavior often is not diagnosed because of:

• Shame and secrecy. Embarrassment and shame, which are fundamental to CSB, appear to explain, in part, why few patients volunteer information regarding this behavior unless specifically asked.¹
• Patient lack of knowledge. Patients often do not know that their behavior can be successfully treated.
• Clinician lack of knowledge. Few health care professionals have education or training in CSB. A lack of recognition of CSB also may be due to our limited understanding regarding the limits of sexual normality. In addition, the classification of CSB is unclear and not agreed upon (Box^7-9), and moral judgments often are involved in understanding sexual behaviors.¹⁰

Box
Classifying compulsive sexual behavior

No consensus on diagnostic criteria

Accurately diagnosing CSB is difficult because of a lack of consensus about the diagnostic criteria for the disorder. Christenson et al¹¹ developed an early set of criteria for CSB as part of a larger survey of impulse control disorders. They used the following 2 criteria to diagnose CSB: (1) excessive or uncontrolled sexual behavior(s) or sexual thoughts/urges to engage in behavior, and (2) these behaviors or thoughts/urges lead to significant distress, social or occupational impairment, or legal and financial consequences.^11,12

During the DSM-5 revision process, a second approach to the diagnostic criteria was proposed for hypersexuality disorder. Under the proposed criteria for hypersexuality, a person would meet the diagnosis if ≥3 of the following were endorsed over a 6-month period: (a) time consumed by sexual fantasies, urges, or behaviors repetitively interferes with other important (non-sexual) goals, activities, and obligations; (b) repetitively engaging in sexual fantasies, urges, or behaviors in response to dysphoric mood states; (c) repetitively engaging in sexual fantasies, urges, or behaviors in response to stressful life events; (d) repetitive but unsuccessful efforts to control or significantly reduce these sexual fantasies, urges, or behaviors; and (e) repetitively engaging in sexual behaviors while disregarding the risk for physical or emotional harm to self or others.⁹

These 2 proposed approaches to diagnosis are somewhat similar. Both suggest that the core underlying issues involve sexual urges or behaviors that are difficult to control and that lead to psychosocial dysfunction. Differences in the criteria, however, could result in different rates of CSB diagnosis; therefore, further research will need to determine which diagnostic approach reflects the neurobiology underlying CSB.

Avoid misdiagnosis

Before making a diagnosis of CSB, it is important for clinicians to consider whether they are stigmatizing “negative consequences,” distress, or social impairment based on unconscious bias toward certain sexual behaviors. In addition, we need to ensure that we are not holding sex to different standards than other behaviors (for example, there are many things in life we do that result in negative consequences and yet do not classify as a mental disorder, such as indulging in less healthy food choices). Furthermore, excessive sexual behaviors might be associated with the normal coming out process for LGBTQ individuals, partner relationship problems, or sexual/gender identity. Therefore, the behavior needs to be assessed in the context of these psychosocial environmental factors.

Differential diagnosis

Various psychiatric disorders also may include excessive sexual behavior as part of their clinical presentation, and it is important to differentiate that behavior from CSB.

Bipolar disorder. Excessive sexual behavior can occur as part of a manic episode in bipolar disorder. If the problematic sexual behavior also occurs when the person’s mood is stable, the individual may have CSB and bipolar disorder. This distinction is important because the treatment for bipolar disorder is often different for CSB, because anticonvulsants have only case reports attesting to their use in CSB.

Substance abuse. Excessive sexual behavior can occur when a person is abusing substances, particularly stimulants such as cocaine and amphetamines.¹³ If the sexual behavior does not occur when the person is not using drugs, then the appropriate diagnosis would not likely be CSB.

Obsessive-compulsive disorder (OCD). Individuals with OCD often are preoccupied with sexual themes and feel that they think about sex excessively.¹⁴ Although patients with OCD may be preoccupied with thoughts of sex, the key difference is that persons with CSB report feeling excited by these thoughts and derive pleasure from the behavior, whereas the sexual thoughts of OCD are perceived as unpleasant.

Other disorders that may give rise to hypersexual behavior include neurocognitive disorders, attention-deficit/hyperactivity disorder, autism spectrum disorders, and depressive disorders.

Adverse effects of medication. It is important to ask the patient whether he (she)developed CSB after starting a medication. Certain medications (eg, medications for Parkinson’s disease or restless leg syndrome, or aripiprazole to treat depression or psychosis) may cause patients to engage in problematic sexual behavior.^15,16 If the sexual behavior decreases or stops when the medication dosage is reduced or the medication is stopped, a diagnosis of CSB would not be appropriate.

Comorbidity is common

Research suggests that approximately one-half of adults with CSB meet criteria for at least 1 other psychiatric disorder, such as mood, anxiety, substance use, impulse control, or personality disorders. A study of men with CSB (N = 103) found that 71% met criteria for a mood disorder, 40% for an anxiety disorder, 41% for a substance use disorder, and 24% for an impulse control disorder such as gambling disorder.¹⁷ Therefore, to successfully treat CSB, clinicians also may need to focus on how and to what extent these co-occurring disorders drive the sexual behavior.

Co-occurring medical conditions also are common among individuals with CSB. Medical concerns may include unwanted pregnancy, sexually transmitted infections, and HIV/AIDS. Thus, treating psychiatric comorbidities and providing education about sexual health, with referrals to primary care specialists, often are part of CSB treatment.

Neuroimaging and cognition

One imaging study that compared participants with and without CSB found that participants with CSB had higher activity in the ventral striatum, anterior cingulate cortex, and amygdala relative to controls during a cue-reactivity functional MRI task.¹⁸ These findings show notable similarities to the patterns of activation seen in patients addicted to drugs when assessed using drug-craving paradigms. An additional neuroimaging study assessing patients with hypersexuality using diffusion tensor imaging noted that diffusivity in a prefrontal white matter tract within a superior frontal region was greater in patients with CSB.¹⁸ This study also indicated that there was a negative correlation between observed diffusion in the noted location and overall severity score for CSB symptoms such as frequency of urges or behaviors.

In terms of cognition, a preliminary assessment of young adults with CSB compared with healthy controls did not find any differences between groups across several tasks, although the previously mentioned diffusion tensor imaging study reported elevated impulsivity in CSB.¹⁸

Approaches to treatment

Most people with CSB are reluctant to mention it to their health care providers, and most physicians are generally uncomfortable talking about sex with their patients, in part, because of a lack of training.¹⁹ Patients are more likely to bring up the topic when they are receiving treatment for anxiety, depression, or substance abuse. Therefore, clinicians must consider that sexual behavior might be associated with a coping mechanism, distressing outcome, or comorbid condition in these patients.

Pharmacologic treatment

Evidence for the pharmacologic treatment of CSB consists primarily of small, open-label studies, case series, or retrospective analyses, except for 1 double-blind, placebo-controlled study. Based on this evidence, there may be several pharma­cologic treatment options for patients with CSB; however, there are no FDA-approved medications for CSB.

Antidepressants. One of the most thoroughly documented categories of pharmacologic treatment for CSB is selective serotonin reuptake inhibitors (SSRIs). Several retrospective analyses and case series have reported on the general efficacy of SSRIs in reducing symptoms of CSB.^20-23 Citalopram, the only treatment for CSB that has been assessed using a double-blind, placebo-controlled methodology, was associated with significant decreases in CSB symptoms, including sexual desire/drive, frequency of masturbation, and pornography use.²⁴

In addition to SSRIs, several additional case reports have suggested that other classes of antidepressants, such as serotonin-norepinephrine reuptake inhibitors and tricyclic antidepressants, or stimulants may be beneficial when treating CSB.²⁵ Several case reports have indicated significant improvement of CSB symptoms using clomipramine.²² A retrospective study of nefazodone also has suggested that it may be an option for treating CSB. Patients reported notable reductions in the frequency of sexual obsessions/compulsions while taking nefazodone and reported no notable sexual adverse effects.²⁶ One branded version of nefazodone, Serzone, was associated with rare but severe liver problems and was withdrawn from the U.S. market in 2004.

Although some initial evidence regarding antidepressant use, particularly SSRIs, to treat CSB has suggested that these medications may be potentially beneficial, the findings are far from conclusive, with only 1 controlled trial and only single-subject case reports for many of the medications studied.

Naltrexone, an opioid antagonist, has received support from available cases, open-label studies, and retrospective analyses.^17,27 Although evidence for the use of naltrexone in CSB is limited to case reports and retrospective analyses, results have been positive. Naltrexone has shown notable decreases in CSB symptom severity when used as monotherapy and when used in combination with other treatments.

Anticonvulsants. Several case reports have suggested that certain anticonvulsants may be beneficial for treating CSB. Topiramate may be a particularly useful option.²⁸ Other anticonvulsants showing benefit for CSB in case reports include valproic acid, lamotrigine, and levetiracetam.¹⁸

Psychotherapy

Evidence supporting specific types of psychotherapy for CSB is limited and largely drawn from uncontrolled studies and case reports.

Cognitive-behavioral therapy (CBT) is one of the more common psychotherapeutic options used for CSB. Several uncontrolled studies and case reports have found that CBT is beneficial for CSB, although methodologies have varied.

Several cases found that combining CBT with motivational interviewing was associated with significant reductions in sexual behaviors, such as frequency of sexual partners and amount of time spent online during work hours.^29,30 Group CBT also has been shown to be effective for CSB.³¹

Acceptance and commitment therapy (ACT) has received some initial support, with 1 uncontrolled study and 1 controlled study.^32,33 The controlled study used 12 sessions of individual ACT compared with a wait-list condition.³² Improvements in CSB symptoms were maintained for 3 months. The overall reduction in problematic Internet pornography use was reported as 92% immediately after the study ended, and 86% after 3 months.

Marital/relationship therapy has been used successfully in several case series and case reports, although no studies have assessed its efficacy in treating CSB using a randomized protocol. In 1 case report, the researcher found that participation in marital sex therapy elicited notable improvements over the course of 1 year and 20 sessions.³⁴