Obsessive-Compulsive Disorder

Pregnancy-related mental health conditions are the most common complication of pregnancy, yet half of all women suffering will not be treated.

I wanted to address the stigma associated with these conditions as well as the rampant misinformation online. So, I reached out to Jen Schwartz, patient advocate and founder of Motherhood Understand, an online community for moms impacted by maternal mental health conditions. Together, we conceived the idea for the #MomsNeedToKnow maternal mental health awareness campaign, which will run from Oct. 14 to 25. This is an evidence-based campaign, complete with references and citations, that speaks to patients where they are at, i.e., social media.

With my clinical expertise and Jen’s reach, we felt like it was a natural partnership, as well as an innovative approach to empowering women to take control of their mental health during the perinatal period. We teamed up with Jamina Bone, an illustrator, and developed 2 weeks of Instagram posts, focused on the themes of lesser-known diagnoses, maternal mental health myths, and treatment options. This campaign is designed to help women understand risk factors for perinatal mood and anxiety disorders, as well as the signs of these conditions. It will cover lesser-known diagnoses like postpartum obsessive-compulsive disorder and posttraumatic stress disorder, and will address topics such as the impact of infertility on mental health and clarify the roles of different clinicians who can help.

Moreover, the campaign aims to address stigma and myths around psychiatric treatment during pregnancy – and also provides resources.

Dr. Lakshmin, a perinatal psychiatrist, is clinical assistant professor of psychiatry at George Washington University in Washington.

This article was updated 10/12/19.

Pregnancy-related mental health conditions are the most common complication of pregnancy, yet half of all women suffering will not be treated.

I wanted to address the stigma associated with these conditions as well as the rampant misinformation online. So, I reached out to Jen Schwartz, patient advocate and founder of Motherhood Understand, an online community for moms impacted by maternal mental health conditions. Together, we conceived the idea for the #MomsNeedToKnow maternal mental health awareness campaign, which will run from Oct. 14 to 25. This is an evidence-based campaign, complete with references and citations, that speaks to patients where they are at, i.e., social media.

With my clinical expertise and Jen’s reach, we felt like it was a natural partnership, as well as an innovative approach to empowering women to take control of their mental health during the perinatal period. We teamed up with Jamina Bone, an illustrator, and developed 2 weeks of Instagram posts, focused on the themes of lesser-known diagnoses, maternal mental health myths, and treatment options. This campaign is designed to help women understand risk factors for perinatal mood and anxiety disorders, as well as the signs of these conditions. It will cover lesser-known diagnoses like postpartum obsessive-compulsive disorder and posttraumatic stress disorder, and will address topics such as the impact of infertility on mental health and clarify the roles of different clinicians who can help.

Moreover, the campaign aims to address stigma and myths around psychiatric treatment during pregnancy – and also provides resources.

Dr. Lakshmin, a perinatal psychiatrist, is clinical assistant professor of psychiatry at George Washington University in Washington.

This article was updated 10/12/19.

Pregnancy-related mental health conditions are the most common complication of pregnancy, yet half of all women suffering will not be treated.

I wanted to address the stigma associated with these conditions as well as the rampant misinformation online. So, I reached out to Jen Schwartz, patient advocate and founder of Motherhood Understand, an online community for moms impacted by maternal mental health conditions. Together, we conceived the idea for the #MomsNeedToKnow maternal mental health awareness campaign, which will run from Oct. 14 to 25. This is an evidence-based campaign, complete with references and citations, that speaks to patients where they are at, i.e., social media.

With my clinical expertise and Jen’s reach, we felt like it was a natural partnership, as well as an innovative approach to empowering women to take control of their mental health during the perinatal period. We teamed up with Jamina Bone, an illustrator, and developed 2 weeks of Instagram posts, focused on the themes of lesser-known diagnoses, maternal mental health myths, and treatment options. This campaign is designed to help women understand risk factors for perinatal mood and anxiety disorders, as well as the signs of these conditions. It will cover lesser-known diagnoses like postpartum obsessive-compulsive disorder and posttraumatic stress disorder, and will address topics such as the impact of infertility on mental health and clarify the roles of different clinicians who can help.

Moreover, the campaign aims to address stigma and myths around psychiatric treatment during pregnancy – and also provides resources.

Dr. Lakshmin, a perinatal psychiatrist, is clinical assistant professor of psychiatry at George Washington University in Washington.

This article was updated 10/12/19.

The evidence is robust and disheartening: As if the personal suffering and societal stigma of mental illness are not bad enough, psychiatric patients also have a shorter life­span.¹ In the past, most studies have focused on early mortality and loss of potential life-years in schizophrenia,² but many subsequent reports indicate that premature death occurs in all major psychiatric disorders.

Here is a summary of the sobering facts:

• Schizophrenia. In a study of 30,210 patients with schizophrenia, compared with >5 million individuals in the general population in Denmark (where they have an excellent registry), mortality was 16-fold higher among patients with schizophrenia if they had a single somatic illness.³ The illnesses were mostly respiratory, gastrointestinal, or cardiovascular).³ The loss of potential years of life was staggeringly high: 18.7 years for men, 16.3 years for women.⁴ A study conducted in 8 US states reported a loss of 2 to 3 decades of life across each of these states.⁵ The causes of death in patients with schizophrenia were mainly heart disease, cancer, stroke, and pulmonary diseases. A national database in Sweden found that unmedicated patients with schizophrenia had a significantly higher death rate than those receiving antipsychotics.^6,7 Similar findings were reported by researchers in Finland.⁸ The Swedish study by Tiihonen et al⁶ also found that mortality was highest in patients receiving benzodiazepines along with antipsychotics, but there was no increased mortality among patients with schizophrenia receiving antidepressants.
• Bipolar disorder. A shorter life expectancy has also been reported in bipolar disorder,⁹ with a loss of 13.6 years for men and 12.1 years for women. Early death was caused by physical illness (even when suicide deaths were excluded), especially cardio­vascular disease.¹⁰
• Major depressive disorder (MDD). A reduction of life expectancy in persons with MDD (unipolar depression) has been reported, with a loss of 14 years in men and 10 years in women.¹¹ Although suicide contributed to the shorter lifespan, death due to accidents was 500% higher among persons with unipolar depression; the largest causes of death were physical illnesses. Further, Zubenko et al¹² reported alarming findings about excess mortality among first- and second-degree relatives of persons with early-onset depression (some of whom were bipolar). The relatives died an average of 8 years earlier than the local population, and 40% died before reaching age 65. Also, there was a 5-fold increase in infant mortality (in the first year of life) among the relatives. The most common causes of death in adult relatives were heart disease, cancer, and stroke. It is obvious that MDD has a significant negative impact on health and longevity in both patients and their relatives.
• Attention-deficit/hyperactivity disorder (ADHD). A 220% increase in mortality was reported in persons with ADHD at all ages.¹³ Accidents were the most common cause of death. The mortality rate ratio (MRR) was 1.86 for ADHD before age 6, 1.58 for ADHD between age 6 to 17, and 4.25 for those age ≥18. The rate of early mortality was higher in girls and women (MRR = 2.85) than boys and men (MRR = 1.27).
• Obsessive-compulsive disorder (OCD). A study from Denmark of 10,155 persons with OCD followed for 10 years reported a significantly higher risk of death from both natural (MRR = 1.68) and unnatural causes (MRR = 2.61), compared with the general population.¹⁴ Patients with OCD and comorbid depression, anxiety, or substance use had a further increase in mortality risk, but the mortality risk of individuals with OCD without psychiatric comorbidity was still 200% higher than that of the general population.
• Anxiety disorders. One study found no increase in mortality among patients who have generalized anxiety, unless it was associated with depression.¹⁵ Another study reported that the presence of anxiety reduced the risk of cardiovascular mortality in persons with depression.¹⁶ The absence of increased mortality in anxiety disorders was also confirmed in a meta-analysis of 36 studies.¹⁷ However, a study of postmenopausal women with panic attacks found a 3-fold increase in coronary artery disease and stroke in that cohort,¹⁸ which confirmed the findings of an older study¹⁹ that demonstrated a 2-fold increase of mortality among 155 men with panic disorder after a 12-year follow-up. Also, a 25-year follow-up study found that suicide accounted for 20% of deaths in the anxiety group compared with 16.2% in the depression group,²⁰ showing a significant risk of suicide in panic disorder, even exceeding that of depression.
• Oppositional defiant disorder (ODD) and conduct disorder (CD). In a 12-year follow-up study of 9,495 individuals with “disruptive behavioral disorders,” which included ODD and CD, the mortality rate was >400% higher in these patients compared with 1.92 million individuals in the general population (9.66 vs 2.22 per 10,000 person­-years).²¹ Comorbid substance use disorder and ADHD further increased the mortality rate in this cohort.
• Posttraumatic stress disorder (PTSD). Studies show that there is a significantly increased risk of early cardiovascular mortality in PTSD,²² and that the death rate may be associated with accelerated “DNA methylation age” that leads to a 13% increased risk for all-cause mortality.²³
• Borderline personality disorder (BPD). A recent longitudinal study (24 years of follow-up with evaluation every 2 years) reported a significantly higher mortality in patients with BPD compared with those with other personality disorders. The age range when the study started was 18 to 35. The rate of suicide death was Palatino LT Std>400% higher in BPD (5.9% vs 1.4%). Also, non-suicidal death was 250% higher in BPD (14% vs 5.5%). The causes of non-suicidal death included cardiovascular disease, substance-related complications, cancer, and accidents.²⁴
• Other personality disorders. Certain personality traits have been associated with shorter leukocyte telomeres, which signal early death. These traits include neuroticism, conscientiousness, harm avoidance, and reward dependence.²⁵ Another study found shorter telomeres in persons with high neuroticism and low agreeableness²⁶ regardless of age or sex. Short telomeres, which reflect accelerated cellular senescence and aging, have also been reported in several major psychiatric disorders (schizophrenia, bipolar disorder, MDD, and anxiety).^27-29 The cumulative evidence is unassailable; psychiatric brain disorders are not only associated with premature death due to high suicide rates, but also with multiple medical diseases that lead to early mortality and a shorter lifespan. The shortened telomeres reflect high oxidative stress and inflammation, and both those toxic processes are known to be associated with major psychiatric disorders. Compounding the dismal facts about early mortality due to mental illness are the additional grave medical consequences of alcohol and substance use, which are highly comorbid with most psychiatric disorders, further exacerbating the premature death rates among psychiatric patients.

Continue to: There is an important take-home message...

There is an important take-home message in all of this: Our patients are at high risk for potentially fatal medical conditions that require early detection, and intensive ongoing treatment by a primary care clinician (not “provider”; I abhor the widespread use of that term for physicians or nurse practitioners) is an indispensable component of psychiatric care. Thus, collaborative care is vital to protect our psychiatric patients from early mortality and a shortened lifespan. Psychiatrists and psychiatric nurse practitioners must not only win the battle against mental illness, but also diligently avoid losing the war of life and death.

The evidence is robust and disheartening: As if the personal suffering and societal stigma of mental illness are not bad enough, psychiatric patients also have a shorter life­span.¹ In the past, most studies have focused on early mortality and loss of potential life-years in schizophrenia,² but many subsequent reports indicate that premature death occurs in all major psychiatric disorders.

Here is a summary of the sobering facts:

• Schizophrenia. In a study of 30,210 patients with schizophrenia, compared with >5 million individuals in the general population in Denmark (where they have an excellent registry), mortality was 16-fold higher among patients with schizophrenia if they had a single somatic illness.³ The illnesses were mostly respiratory, gastrointestinal, or cardiovascular).³ The loss of potential years of life was staggeringly high: 18.7 years for men, 16.3 years for women.⁴ A study conducted in 8 US states reported a loss of 2 to 3 decades of life across each of these states.⁵ The causes of death in patients with schizophrenia were mainly heart disease, cancer, stroke, and pulmonary diseases. A national database in Sweden found that unmedicated patients with schizophrenia had a significantly higher death rate than those receiving antipsychotics.^6,7 Similar findings were reported by researchers in Finland.⁸ The Swedish study by Tiihonen et al⁶ also found that mortality was highest in patients receiving benzodiazepines along with antipsychotics, but there was no increased mortality among patients with schizophrenia receiving antidepressants.
• Bipolar disorder. A shorter life expectancy has also been reported in bipolar disorder,⁹ with a loss of 13.6 years for men and 12.1 years for women. Early death was caused by physical illness (even when suicide deaths were excluded), especially cardio­vascular disease.¹⁰
• Major depressive disorder (MDD). A reduction of life expectancy in persons with MDD (unipolar depression) has been reported, with a loss of 14 years in men and 10 years in women.¹¹ Although suicide contributed to the shorter lifespan, death due to accidents was 500% higher among persons with unipolar depression; the largest causes of death were physical illnesses. Further, Zubenko et al¹² reported alarming findings about excess mortality among first- and second-degree relatives of persons with early-onset depression (some of whom were bipolar). The relatives died an average of 8 years earlier than the local population, and 40% died before reaching age 65. Also, there was a 5-fold increase in infant mortality (in the first year of life) among the relatives. The most common causes of death in adult relatives were heart disease, cancer, and stroke. It is obvious that MDD has a significant negative impact on health and longevity in both patients and their relatives.
• Attention-deficit/hyperactivity disorder (ADHD). A 220% increase in mortality was reported in persons with ADHD at all ages.¹³ Accidents were the most common cause of death. The mortality rate ratio (MRR) was 1.86 for ADHD before age 6, 1.58 for ADHD between age 6 to 17, and 4.25 for those age ≥18. The rate of early mortality was higher in girls and women (MRR = 2.85) than boys and men (MRR = 1.27).
• Obsessive-compulsive disorder (OCD). A study from Denmark of 10,155 persons with OCD followed for 10 years reported a significantly higher risk of death from both natural (MRR = 1.68) and unnatural causes (MRR = 2.61), compared with the general population.¹⁴ Patients with OCD and comorbid depression, anxiety, or substance use had a further increase in mortality risk, but the mortality risk of individuals with OCD without psychiatric comorbidity was still 200% higher than that of the general population.
• Anxiety disorders. One study found no increase in mortality among patients who have generalized anxiety, unless it was associated with depression.¹⁵ Another study reported that the presence of anxiety reduced the risk of cardiovascular mortality in persons with depression.¹⁶ The absence of increased mortality in anxiety disorders was also confirmed in a meta-analysis of 36 studies.¹⁷ However, a study of postmenopausal women with panic attacks found a 3-fold increase in coronary artery disease and stroke in that cohort,¹⁸ which confirmed the findings of an older study¹⁹ that demonstrated a 2-fold increase of mortality among 155 men with panic disorder after a 12-year follow-up. Also, a 25-year follow-up study found that suicide accounted for 20% of deaths in the anxiety group compared with 16.2% in the depression group,²⁰ showing a significant risk of suicide in panic disorder, even exceeding that of depression.
• Oppositional defiant disorder (ODD) and conduct disorder (CD). In a 12-year follow-up study of 9,495 individuals with “disruptive behavioral disorders,” which included ODD and CD, the mortality rate was >400% higher in these patients compared with 1.92 million individuals in the general population (9.66 vs 2.22 per 10,000 person­-years).²¹ Comorbid substance use disorder and ADHD further increased the mortality rate in this cohort.
• Posttraumatic stress disorder (PTSD). Studies show that there is a significantly increased risk of early cardiovascular mortality in PTSD,²² and that the death rate may be associated with accelerated “DNA methylation age” that leads to a 13% increased risk for all-cause mortality.²³
• Borderline personality disorder (BPD). A recent longitudinal study (24 years of follow-up with evaluation every 2 years) reported a significantly higher mortality in patients with BPD compared with those with other personality disorders. The age range when the study started was 18 to 35. The rate of suicide death was Palatino LT Std>400% higher in BPD (5.9% vs 1.4%). Also, non-suicidal death was 250% higher in BPD (14% vs 5.5%). The causes of non-suicidal death included cardiovascular disease, substance-related complications, cancer, and accidents.²⁴
• Other personality disorders. Certain personality traits have been associated with shorter leukocyte telomeres, which signal early death. These traits include neuroticism, conscientiousness, harm avoidance, and reward dependence.²⁵ Another study found shorter telomeres in persons with high neuroticism and low agreeableness²⁶ regardless of age or sex. Short telomeres, which reflect accelerated cellular senescence and aging, have also been reported in several major psychiatric disorders (schizophrenia, bipolar disorder, MDD, and anxiety).^27-29 The cumulative evidence is unassailable; psychiatric brain disorders are not only associated with premature death due to high suicide rates, but also with multiple medical diseases that lead to early mortality and a shorter lifespan. The shortened telomeres reflect high oxidative stress and inflammation, and both those toxic processes are known to be associated with major psychiatric disorders. Compounding the dismal facts about early mortality due to mental illness are the additional grave medical consequences of alcohol and substance use, which are highly comorbid with most psychiatric disorders, further exacerbating the premature death rates among psychiatric patients.

Continue to: There is an important take-home message...

There is an important take-home message in all of this: Our patients are at high risk for potentially fatal medical conditions that require early detection, and intensive ongoing treatment by a primary care clinician (not “provider”; I abhor the widespread use of that term for physicians or nurse practitioners) is an indispensable component of psychiatric care. Thus, collaborative care is vital to protect our psychiatric patients from early mortality and a shortened lifespan. Psychiatrists and psychiatric nurse practitioners must not only win the battle against mental illness, but also diligently avoid losing the war of life and death.

The evidence is robust and disheartening: As if the personal suffering and societal stigma of mental illness are not bad enough, psychiatric patients also have a shorter life­span.¹ In the past, most studies have focused on early mortality and loss of potential life-years in schizophrenia,² but many subsequent reports indicate that premature death occurs in all major psychiatric disorders.

Here is a summary of the sobering facts:

• Schizophrenia. In a study of 30,210 patients with schizophrenia, compared with >5 million individuals in the general population in Denmark (where they have an excellent registry), mortality was 16-fold higher among patients with schizophrenia if they had a single somatic illness.³ The illnesses were mostly respiratory, gastrointestinal, or cardiovascular).³ The loss of potential years of life was staggeringly high: 18.7 years for men, 16.3 years for women.⁴ A study conducted in 8 US states reported a loss of 2 to 3 decades of life across each of these states.⁵ The causes of death in patients with schizophrenia were mainly heart disease, cancer, stroke, and pulmonary diseases. A national database in Sweden found that unmedicated patients with schizophrenia had a significantly higher death rate than those receiving antipsychotics.^6,7 Similar findings were reported by researchers in Finland.⁸ The Swedish study by Tiihonen et al⁶ also found that mortality was highest in patients receiving benzodiazepines along with antipsychotics, but there was no increased mortality among patients with schizophrenia receiving antidepressants.
• Bipolar disorder. A shorter life expectancy has also been reported in bipolar disorder,⁹ with a loss of 13.6 years for men and 12.1 years for women. Early death was caused by physical illness (even when suicide deaths were excluded), especially cardio­vascular disease.¹⁰
• Major depressive disorder (MDD). A reduction of life expectancy in persons with MDD (unipolar depression) has been reported, with a loss of 14 years in men and 10 years in women.¹¹ Although suicide contributed to the shorter lifespan, death due to accidents was 500% higher among persons with unipolar depression; the largest causes of death were physical illnesses. Further, Zubenko et al¹² reported alarming findings about excess mortality among first- and second-degree relatives of persons with early-onset depression (some of whom were bipolar). The relatives died an average of 8 years earlier than the local population, and 40% died before reaching age 65. Also, there was a 5-fold increase in infant mortality (in the first year of life) among the relatives. The most common causes of death in adult relatives were heart disease, cancer, and stroke. It is obvious that MDD has a significant negative impact on health and longevity in both patients and their relatives.
• Attention-deficit/hyperactivity disorder (ADHD). A 220% increase in mortality was reported in persons with ADHD at all ages.¹³ Accidents were the most common cause of death. The mortality rate ratio (MRR) was 1.86 for ADHD before age 6, 1.58 for ADHD between age 6 to 17, and 4.25 for those age ≥18. The rate of early mortality was higher in girls and women (MRR = 2.85) than boys and men (MRR = 1.27).
• Obsessive-compulsive disorder (OCD). A study from Denmark of 10,155 persons with OCD followed for 10 years reported a significantly higher risk of death from both natural (MRR = 1.68) and unnatural causes (MRR = 2.61), compared with the general population.¹⁴ Patients with OCD and comorbid depression, anxiety, or substance use had a further increase in mortality risk, but the mortality risk of individuals with OCD without psychiatric comorbidity was still 200% higher than that of the general population.
• Anxiety disorders. One study found no increase in mortality among patients who have generalized anxiety, unless it was associated with depression.¹⁵ Another study reported that the presence of anxiety reduced the risk of cardiovascular mortality in persons with depression.¹⁶ The absence of increased mortality in anxiety disorders was also confirmed in a meta-analysis of 36 studies.¹⁷ However, a study of postmenopausal women with panic attacks found a 3-fold increase in coronary artery disease and stroke in that cohort,¹⁸ which confirmed the findings of an older study¹⁹ that demonstrated a 2-fold increase of mortality among 155 men with panic disorder after a 12-year follow-up. Also, a 25-year follow-up study found that suicide accounted for 20% of deaths in the anxiety group compared with 16.2% in the depression group,²⁰ showing a significant risk of suicide in panic disorder, even exceeding that of depression.
• Oppositional defiant disorder (ODD) and conduct disorder (CD). In a 12-year follow-up study of 9,495 individuals with “disruptive behavioral disorders,” which included ODD and CD, the mortality rate was >400% higher in these patients compared with 1.92 million individuals in the general population (9.66 vs 2.22 per 10,000 person­-years).²¹ Comorbid substance use disorder and ADHD further increased the mortality rate in this cohort.
• Posttraumatic stress disorder (PTSD). Studies show that there is a significantly increased risk of early cardiovascular mortality in PTSD,²² and that the death rate may be associated with accelerated “DNA methylation age” that leads to a 13% increased risk for all-cause mortality.²³
• Borderline personality disorder (BPD). A recent longitudinal study (24 years of follow-up with evaluation every 2 years) reported a significantly higher mortality in patients with BPD compared with those with other personality disorders. The age range when the study started was 18 to 35. The rate of suicide death was Palatino LT Std>400% higher in BPD (5.9% vs 1.4%). Also, non-suicidal death was 250% higher in BPD (14% vs 5.5%). The causes of non-suicidal death included cardiovascular disease, substance-related complications, cancer, and accidents.²⁴
• Other personality disorders. Certain personality traits have been associated with shorter leukocyte telomeres, which signal early death. These traits include neuroticism, conscientiousness, harm avoidance, and reward dependence.²⁵ Another study found shorter telomeres in persons with high neuroticism and low agreeableness²⁶ regardless of age or sex. Short telomeres, which reflect accelerated cellular senescence and aging, have also been reported in several major psychiatric disorders (schizophrenia, bipolar disorder, MDD, and anxiety).^27-29 The cumulative evidence is unassailable; psychiatric brain disorders are not only associated with premature death due to high suicide rates, but also with multiple medical diseases that lead to early mortality and a shorter lifespan. The shortened telomeres reflect high oxidative stress and inflammation, and both those toxic processes are known to be associated with major psychiatric disorders. Compounding the dismal facts about early mortality due to mental illness are the additional grave medical consequences of alcohol and substance use, which are highly comorbid with most psychiatric disorders, further exacerbating the premature death rates among psychiatric patients.

Continue to: There is an important take-home message...

There is an important take-home message in all of this: Our patients are at high risk for potentially fatal medical conditions that require early detection, and intensive ongoing treatment by a primary care clinician (not “provider”; I abhor the widespread use of that term for physicians or nurse practitioners) is an indispensable component of psychiatric care. Thus, collaborative care is vital to protect our psychiatric patients from early mortality and a shortened lifespan. Psychiatrists and psychiatric nurse practitioners must not only win the battle against mental illness, but also diligently avoid losing the war of life and death.

COPENHAGEN – High-frequency deep transcranial magnetic stimulation (dTMS) directed at the anterior cingulate cortex and medial prefrontal cortex proved to be a safe and effective nonpharmacologic treatment for symptoms of obsessive-compulsive disorder in an international, randomized, sham-controlled, double-blind clinical trial that earned the device clearance for that indication from the Food and Drug Administration.

Bruce Jancin/MDedge News

The operative word here is “deep,” lead investigator Lior Carmi, PhD, explained in presenting the pivotal trial results at the annual congress of the European College of Neuropsychopharmacology.

“Deep TMS is a relatively new form of TMS that allows direct stimulation of deeper neuronal pathways than standard TMS. It induces a direct effective field at a depth of 3-5 cm below the skull, compared to less than 1.5 cm for the standard TMS figure-eight coil,” said Dr. Carmi, of Chaim Sheba Medical Center in Ramat Gan, Israel.

The brain circuitry involved in obsessive-compulsive disorder (OCD) is very well known. Multiple potential targets for intervention are available. Dr. Carmi and coinvestigators focused on the anterior cingulate cortex and medial prefrontal cortex, because this is an area that’s very much involved in OCD – it’s the generator of increased error-related negativity on the Stroop task – and it can be stimulated by dTMS, whereas standard TMS can’t reach it.

This was not only the first major clinical trial to successfully target the anterior cingulate cortex and medial prefrontal cortex using any form of TMS, it also was the first study to employ individually tailored symptom provocation using photos or a written script immediately before each treatment session. At the first patient encounter, the investigators created a list of what distressed that particular individual – for example, touching a public bathroom door handle or experiencing doubt about whether the stove had been left on – and then prior to each treatment session they deliberately provoked each study participant using representations of those triggers. The treatment, real or sham, didn’t begin until a patient’s distress level measured 4-7 on a visual analog scale.

“The idea is to deliver the treatment when the brain circuitry is aroused and not while the patient is thinking about the shopping he needs to get done after the session is over,” Dr. Carmi explained.

He was first author of the recently published pivotal study (Am J Psychiatry. 2019 May 21. doi: 10.1176/appi.ajp.2019.18101180) in which 99 adults aged up to age 65 years with OCD refractory to at least one selective serotonin reuptake inhibitor underwent real or sham dTMS every weekday for 5 consecutive weeks, plus four sessions during week 6. That’s a total of 29 sessions, featuring 2,000 magnetic stimulations per session. The study was conducted at 11 centers in the United States, Canada, and Israel. Participants had to remain on an approved drug therapy for OCD or engaged in psychotherapy throughout the study.

The primary efficacy outcome was the change in scores on the Yale-Brown Obsessive Compulsive Scale (YBOCS) from baseline to 6 weeks. Patients who received dTMS averaged a 6.0-point reduction, significantly better than the 3.3-point reduction in the sham-treatment group. The treatment response rate, as defined by at least a 30% reduction from baseline in YBOCS score, was 38% with dTMS, compared with 11% in controls. One month after the final treatment session, the response rate was 45% in the active-treatment arm, compared with less than 18% in the sham-treatment group.

In addition, 55% of patients in the active-treatment group achieved a partial response of more than a 20% reduction in YBOCS score, a rate slightly more than twice that in the sham group.

To put those findings in perspective, Dr. Carmi highlighted treatment effect–size results from OCD drug trials involving fluoxetine, fluvoxamine, sertraline, and paroxetine, all FDA-approved for treatment of OCD. The placebo-subtracted mean change in YBOCS scores in the pharmacotherapy trials were similar to the sham treatment–subtracted result in the dTMS study, with one important distinction: “In terms of change in YBOCS, it took 10-12 weeks to get those results in the drug trials, while we have shown this in a 6-week period of time,” he noted.

The only adverse effect associated with dTMS was headaches. They occurred in about one-third of the dTMS group and in a similar proportion of controls early on in the study, but they became a nonissue later.

“I have to say, we recruited 99 patients for the multicenter study, but only 2 of them dropped out because of side effects,” Dr. Carmi noted.

He reported having no financial conflicts of interest regarding the study, sponsored by Brainsway, which markets the dTMS device for the FDA-cleared indications of treatment-resistant depression and OCD.

[email protected]

COPENHAGEN – High-frequency deep transcranial magnetic stimulation (dTMS) directed at the anterior cingulate cortex and medial prefrontal cortex proved to be a safe and effective nonpharmacologic treatment for symptoms of obsessive-compulsive disorder in an international, randomized, sham-controlled, double-blind clinical trial that earned the device clearance for that indication from the Food and Drug Administration.

Bruce Jancin/MDedge News

The operative word here is “deep,” lead investigator Lior Carmi, PhD, explained in presenting the pivotal trial results at the annual congress of the European College of Neuropsychopharmacology.

“Deep TMS is a relatively new form of TMS that allows direct stimulation of deeper neuronal pathways than standard TMS. It induces a direct effective field at a depth of 3-5 cm below the skull, compared to less than 1.5 cm for the standard TMS figure-eight coil,” said Dr. Carmi, of Chaim Sheba Medical Center in Ramat Gan, Israel.

The brain circuitry involved in obsessive-compulsive disorder (OCD) is very well known. Multiple potential targets for intervention are available. Dr. Carmi and coinvestigators focused on the anterior cingulate cortex and medial prefrontal cortex, because this is an area that’s very much involved in OCD – it’s the generator of increased error-related negativity on the Stroop task – and it can be stimulated by dTMS, whereas standard TMS can’t reach it.

This was not only the first major clinical trial to successfully target the anterior cingulate cortex and medial prefrontal cortex using any form of TMS, it also was the first study to employ individually tailored symptom provocation using photos or a written script immediately before each treatment session. At the first patient encounter, the investigators created a list of what distressed that particular individual – for example, touching a public bathroom door handle or experiencing doubt about whether the stove had been left on – and then prior to each treatment session they deliberately provoked each study participant using representations of those triggers. The treatment, real or sham, didn’t begin until a patient’s distress level measured 4-7 on a visual analog scale.

“The idea is to deliver the treatment when the brain circuitry is aroused and not while the patient is thinking about the shopping he needs to get done after the session is over,” Dr. Carmi explained.

He was first author of the recently published pivotal study (Am J Psychiatry. 2019 May 21. doi: 10.1176/appi.ajp.2019.18101180) in which 99 adults aged up to age 65 years with OCD refractory to at least one selective serotonin reuptake inhibitor underwent real or sham dTMS every weekday for 5 consecutive weeks, plus four sessions during week 6. That’s a total of 29 sessions, featuring 2,000 magnetic stimulations per session. The study was conducted at 11 centers in the United States, Canada, and Israel. Participants had to remain on an approved drug therapy for OCD or engaged in psychotherapy throughout the study.

The primary efficacy outcome was the change in scores on the Yale-Brown Obsessive Compulsive Scale (YBOCS) from baseline to 6 weeks. Patients who received dTMS averaged a 6.0-point reduction, significantly better than the 3.3-point reduction in the sham-treatment group. The treatment response rate, as defined by at least a 30% reduction from baseline in YBOCS score, was 38% with dTMS, compared with 11% in controls. One month after the final treatment session, the response rate was 45% in the active-treatment arm, compared with less than 18% in the sham-treatment group.

In addition, 55% of patients in the active-treatment group achieved a partial response of more than a 20% reduction in YBOCS score, a rate slightly more than twice that in the sham group.

To put those findings in perspective, Dr. Carmi highlighted treatment effect–size results from OCD drug trials involving fluoxetine, fluvoxamine, sertraline, and paroxetine, all FDA-approved for treatment of OCD. The placebo-subtracted mean change in YBOCS scores in the pharmacotherapy trials were similar to the sham treatment–subtracted result in the dTMS study, with one important distinction: “In terms of change in YBOCS, it took 10-12 weeks to get those results in the drug trials, while we have shown this in a 6-week period of time,” he noted.

The only adverse effect associated with dTMS was headaches. They occurred in about one-third of the dTMS group and in a similar proportion of controls early on in the study, but they became a nonissue later.

“I have to say, we recruited 99 patients for the multicenter study, but only 2 of them dropped out because of side effects,” Dr. Carmi noted.

He reported having no financial conflicts of interest regarding the study, sponsored by Brainsway, which markets the dTMS device for the FDA-cleared indications of treatment-resistant depression and OCD.

[email protected]

COPENHAGEN – High-frequency deep transcranial magnetic stimulation (dTMS) directed at the anterior cingulate cortex and medial prefrontal cortex proved to be a safe and effective nonpharmacologic treatment for symptoms of obsessive-compulsive disorder in an international, randomized, sham-controlled, double-blind clinical trial that earned the device clearance for that indication from the Food and Drug Administration.

Bruce Jancin/MDedge News

The operative word here is “deep,” lead investigator Lior Carmi, PhD, explained in presenting the pivotal trial results at the annual congress of the European College of Neuropsychopharmacology.

“Deep TMS is a relatively new form of TMS that allows direct stimulation of deeper neuronal pathways than standard TMS. It induces a direct effective field at a depth of 3-5 cm below the skull, compared to less than 1.5 cm for the standard TMS figure-eight coil,” said Dr. Carmi, of Chaim Sheba Medical Center in Ramat Gan, Israel.

The brain circuitry involved in obsessive-compulsive disorder (OCD) is very well known. Multiple potential targets for intervention are available. Dr. Carmi and coinvestigators focused on the anterior cingulate cortex and medial prefrontal cortex, because this is an area that’s very much involved in OCD – it’s the generator of increased error-related negativity on the Stroop task – and it can be stimulated by dTMS, whereas standard TMS can’t reach it.

This was not only the first major clinical trial to successfully target the anterior cingulate cortex and medial prefrontal cortex using any form of TMS, it also was the first study to employ individually tailored symptom provocation using photos or a written script immediately before each treatment session. At the first patient encounter, the investigators created a list of what distressed that particular individual – for example, touching a public bathroom door handle or experiencing doubt about whether the stove had been left on – and then prior to each treatment session they deliberately provoked each study participant using representations of those triggers. The treatment, real or sham, didn’t begin until a patient’s distress level measured 4-7 on a visual analog scale.

“The idea is to deliver the treatment when the brain circuitry is aroused and not while the patient is thinking about the shopping he needs to get done after the session is over,” Dr. Carmi explained.

He was first author of the recently published pivotal study (Am J Psychiatry. 2019 May 21. doi: 10.1176/appi.ajp.2019.18101180) in which 99 adults aged up to age 65 years with OCD refractory to at least one selective serotonin reuptake inhibitor underwent real or sham dTMS every weekday for 5 consecutive weeks, plus four sessions during week 6. That’s a total of 29 sessions, featuring 2,000 magnetic stimulations per session. The study was conducted at 11 centers in the United States, Canada, and Israel. Participants had to remain on an approved drug therapy for OCD or engaged in psychotherapy throughout the study.

The primary efficacy outcome was the change in scores on the Yale-Brown Obsessive Compulsive Scale (YBOCS) from baseline to 6 weeks. Patients who received dTMS averaged a 6.0-point reduction, significantly better than the 3.3-point reduction in the sham-treatment group. The treatment response rate, as defined by at least a 30% reduction from baseline in YBOCS score, was 38% with dTMS, compared with 11% in controls. One month after the final treatment session, the response rate was 45% in the active-treatment arm, compared with less than 18% in the sham-treatment group.

In addition, 55% of patients in the active-treatment group achieved a partial response of more than a 20% reduction in YBOCS score, a rate slightly more than twice that in the sham group.

To put those findings in perspective, Dr. Carmi highlighted treatment effect–size results from OCD drug trials involving fluoxetine, fluvoxamine, sertraline, and paroxetine, all FDA-approved for treatment of OCD. The placebo-subtracted mean change in YBOCS scores in the pharmacotherapy trials were similar to the sham treatment–subtracted result in the dTMS study, with one important distinction: “In terms of change in YBOCS, it took 10-12 weeks to get those results in the drug trials, while we have shown this in a 6-week period of time,” he noted.

The only adverse effect associated with dTMS was headaches. They occurred in about one-third of the dTMS group and in a similar proportion of controls early on in the study, but they became a nonissue later.

“I have to say, we recruited 99 patients for the multicenter study, but only 2 of them dropped out because of side effects,” Dr. Carmi noted.

He reported having no financial conflicts of interest regarding the study, sponsored by Brainsway, which markets the dTMS device for the FDA-cleared indications of treatment-resistant depression and OCD.

[email protected]

Patients with obsessive-compulsive disorder who participate in a motivational interviewing (MI) intervention before treatment with exposure and response prevention (ERP) get better short-term results, compared with those who participate in a relaxation intervention before ERP, a small study shows.

“These findings suggest that MI prior to ERP may confer a small but meaningful benefit for enhancing treatment outcome post ERP,” wrote Randi E. McCabe, PhD, of the department of psychiatry and behavioral neurosciences at McMaster University, Hamilton, Ont., and associates. The study was published in the Journal of Obsessive-Compulsive and Related Disorders.

Dr. McCabe and associates randomized 40 patients aged 18-65 years to the MI intervention and relaxation groups. All participants had a diagnosis of OCD as defined by the Structured Clinical Interview for DSM-IV. They also scored 16 or higher on the Yale-Brown Obsessive-Compulsive Scale (Y-BOCS) and said they were interested in the ERP treatment. After a few participants dropped out, 18 were left in the MI group and 17 were in the relaxation group.

The MI intervention consisted of three sessions that focused on raising awareness about the emotional and financial impact of the illness on patients’ lives, and addressing their concerns about ERP – which is a form of cognitive-behavioral therapy tailored to meet the needs of people with OCD. Meanwhile, the relaxation therapy was a three-session protocol consisting of progressive muscle relaxation.

Participants in both groups experienced reductions in symptoms in the short term, but the symptom reductions were more significant for participants in the MI group. For example, Y-BOCS scores were significantly lower among participants in the MI group posttreatment, compared with those in the relaxation intervention (13.72 vs. 16.20 at 3-month follow-up and 13.81 vs. 14.00 at 6-month follow-up). “Whereas Y-BOCS scores decreased from the severe range to the moderate range in the relaxation group, scores decreased from the severe to the mild range in the MI group,” the investigators wrote. Similar trends were found on other measures, including the DASS-21 depression scale and the DASS-21 anxiety stress scale. At the 12-month follow-up, however, “both groups looked similar,” Dr. McCabe and associates reported.

Several limitations were cited, including the small study size and the baseline differences in the participants’ self-reported OCD symptoms.

Nevertheless, the results suggest that intervening with MI before ERP might prove helpful for patients who need immediate relief from OCD symptoms, such as new parents and patients at risk of job loss, they wrote.

Dr. McCabe and her associates reported no disclosures.

[email protected]

SOURCE: McCabe RE et al. J Obsessive Compuls Relat Disord. 2019. doi: 10.1016/j.jocrd.2019.1004466.

Patients with obsessive-compulsive disorder who participate in a motivational interviewing (MI) intervention before treatment with exposure and response prevention (ERP) get better short-term results, compared with those who participate in a relaxation intervention before ERP, a small study shows.

“These findings suggest that MI prior to ERP may confer a small but meaningful benefit for enhancing treatment outcome post ERP,” wrote Randi E. McCabe, PhD, of the department of psychiatry and behavioral neurosciences at McMaster University, Hamilton, Ont., and associates. The study was published in the Journal of Obsessive-Compulsive and Related Disorders.

Dr. McCabe and associates randomized 40 patients aged 18-65 years to the MI intervention and relaxation groups. All participants had a diagnosis of OCD as defined by the Structured Clinical Interview for DSM-IV. They also scored 16 or higher on the Yale-Brown Obsessive-Compulsive Scale (Y-BOCS) and said they were interested in the ERP treatment. After a few participants dropped out, 18 were left in the MI group and 17 were in the relaxation group.

The MI intervention consisted of three sessions that focused on raising awareness about the emotional and financial impact of the illness on patients’ lives, and addressing their concerns about ERP – which is a form of cognitive-behavioral therapy tailored to meet the needs of people with OCD. Meanwhile, the relaxation therapy was a three-session protocol consisting of progressive muscle relaxation.

Participants in both groups experienced reductions in symptoms in the short term, but the symptom reductions were more significant for participants in the MI group. For example, Y-BOCS scores were significantly lower among participants in the MI group posttreatment, compared with those in the relaxation intervention (13.72 vs. 16.20 at 3-month follow-up and 13.81 vs. 14.00 at 6-month follow-up). “Whereas Y-BOCS scores decreased from the severe range to the moderate range in the relaxation group, scores decreased from the severe to the mild range in the MI group,” the investigators wrote. Similar trends were found on other measures, including the DASS-21 depression scale and the DASS-21 anxiety stress scale. At the 12-month follow-up, however, “both groups looked similar,” Dr. McCabe and associates reported.

Several limitations were cited, including the small study size and the baseline differences in the participants’ self-reported OCD symptoms.

Nevertheless, the results suggest that intervening with MI before ERP might prove helpful for patients who need immediate relief from OCD symptoms, such as new parents and patients at risk of job loss, they wrote.

Dr. McCabe and her associates reported no disclosures.

[email protected]

SOURCE: McCabe RE et al. J Obsessive Compuls Relat Disord. 2019. doi: 10.1016/j.jocrd.2019.1004466.

Patients with obsessive-compulsive disorder who participate in a motivational interviewing (MI) intervention before treatment with exposure and response prevention (ERP) get better short-term results, compared with those who participate in a relaxation intervention before ERP, a small study shows.

“These findings suggest that MI prior to ERP may confer a small but meaningful benefit for enhancing treatment outcome post ERP,” wrote Randi E. McCabe, PhD, of the department of psychiatry and behavioral neurosciences at McMaster University, Hamilton, Ont., and associates. The study was published in the Journal of Obsessive-Compulsive and Related Disorders.

Dr. McCabe and associates randomized 40 patients aged 18-65 years to the MI intervention and relaxation groups. All participants had a diagnosis of OCD as defined by the Structured Clinical Interview for DSM-IV. They also scored 16 or higher on the Yale-Brown Obsessive-Compulsive Scale (Y-BOCS) and said they were interested in the ERP treatment. After a few participants dropped out, 18 were left in the MI group and 17 were in the relaxation group.

The MI intervention consisted of three sessions that focused on raising awareness about the emotional and financial impact of the illness on patients’ lives, and addressing their concerns about ERP – which is a form of cognitive-behavioral therapy tailored to meet the needs of people with OCD. Meanwhile, the relaxation therapy was a three-session protocol consisting of progressive muscle relaxation.

Participants in both groups experienced reductions in symptoms in the short term, but the symptom reductions were more significant for participants in the MI group. For example, Y-BOCS scores were significantly lower among participants in the MI group posttreatment, compared with those in the relaxation intervention (13.72 vs. 16.20 at 3-month follow-up and 13.81 vs. 14.00 at 6-month follow-up). “Whereas Y-BOCS scores decreased from the severe range to the moderate range in the relaxation group, scores decreased from the severe to the mild range in the MI group,” the investigators wrote. Similar trends were found on other measures, including the DASS-21 depression scale and the DASS-21 anxiety stress scale. At the 12-month follow-up, however, “both groups looked similar,” Dr. McCabe and associates reported.

Several limitations were cited, including the small study size and the baseline differences in the participants’ self-reported OCD symptoms.

Nevertheless, the results suggest that intervening with MI before ERP might prove helpful for patients who need immediate relief from OCD symptoms, such as new parents and patients at risk of job loss, they wrote.

Dr. McCabe and her associates reported no disclosures.

[email protected]

SOURCE: McCabe RE et al. J Obsessive Compuls Relat Disord. 2019. doi: 10.1016/j.jocrd.2019.1004466.

SAN FRANCISCO – Obsessive-compulsive personality disorder (OCPD) is often confused with obsessive-compulsive disorder (OCD) because of overlapping traits, but there are key differences that psychiatrists should be familiar with. OCPD also presents some key challenges to interpersonal therapy, especially because psychiatrists themselves sometimes share these traits.

“There’s an overlap, and some people have both OCD and OCPD, but some people have just one or the other, and that’s important to tease out because it shifts treatment,” Holly D. Crisp-Han, MD, said in an interview. Dr. Crisp-Han is a clinical associate professor of psychiatry and behavioral sciences at Baylor College of Medicine, Houston. She and her colleague, Glen O. Gabbard, MD, clinical professor of psychiatry at Baylor, chaired a session on dynamic psychotherapy for the treatment of OCPD at the annual meeting of the American Psychiatric Association.

OCPD is the most common personality disorder, with some estimates putting its prevalence as high as nearly 8%. Whereas OCD is characterized by an ego-dystonic need for rituals and specific thoughts, OCPD is defined by ego-syntonic traits. In a study comparing patients with both disorders, researchers found that both groups had reduced psychosocial function and quality of life, but intrusive thoughts and feelings were absent in OCPD. Instead, these patients reported ritualized, methodical behaviors, such as list making, reorganizing personal effects, and repeatedly editing what they had written. OCD patients were also better at delaying rewards.

Dynamic psychotherapy has been shown to achieve better outcomes in OCPD than cognitive-behavioral therapy, though both have a place in the treatment of OCPD, according to Dr. Gabbard. However, it comes with significant challenges. The patient will often challenge the therapist’s interventions and feel threatened by any hint of losing control. Sessions can become ritualized.

OCPD patients are driven by an effort to avoid a tormenting superego rather than seeking pleasure, and they may project this superego onto the therapist. It’s important to identify and interpret patient distortion of the therapist’s attitude toward the patient. Ultimately, the goal of therapy is to modify the patient’s self-expectations.

Couples therapy can be a good idea in cases of extreme ego-syntonicity. The patient’s partner can provide a second perspective to complement the patient’s subjective view of the relationship.

A unique challenge with OCPD is that therapists may see reflections of themselves in the patient. “Many physicians, psychiatrists, and therapists themselves struggle with obsessive-compulsive types of problems. Those types of traits – perfectionism, hard work, overwork, diligence – are rewarded in a career in medicine, and in fact [are] necessary for a career in medicine. We all have to be alert to our own personality traits in order to be able to treat those traits in others,” Dr. Crisp-Han said.” If we don’t recognize those traits in ourselves, then we run the risk of falling into competitive patterns, or idealizations, or other kinds of problems with our patients.”

Therapists who are narcissistically vulnerable may get sucked into power struggles with patients, and can feel undervalued, Dr. Gabbard said. Because rituals can develop, the therapist may also become bored, and even come to feel controlled by the patient’s obsession with the therapeutic process.

But there are other challenges in sessions. The tendency toward ritualization can produce boredom in the therapist. “That’s one of the biggest problems you have, hanging in with somebody who’s repeating the same things over and over again in a dry tone. You start to feel controlled by everything the patient is doing with their agenda,” Dr. Gabbard said during the session. He suggested confronting the patient from time to time. “You can say, ‘Today you don’t sound like you’re that interested in what you’re saying to me; you sound very detached. What’s going on?’ You can feed back to the person how they’re coming across, which can be very valuable.”

Humor is another way to tackle therapy with OCPD patients, because an important therapeutic lesson is to take things a little less seriously, especially in the face of the perfectionism that often haunts OCPD patients. In fact, this can be one of the condition’s most devastating traits, always leading an OCPD patient to feel that he or she is failing, that no accomplishment is ever enough.

“You can work on perfectionism and interpersonal relationships, and the absence of fun and pleasure. This is one of the most fun things to work on in the transference, countertransference relationship. Have a little bit of fun with the patient, because that might be quite foreign,” Dr. Gabbard said. “It can be tricky, because you don’t want to act like you’re laughing at the patient, but you want to introduce some levity and lightness sometimes.”

He gave an example of a patient who was a Catholic priest, who felt intensely guilty over sex. The patient said, “In the Catholic Church, thinking about sex is exactly the same as having sex.” Dr. Gabbard thought for a moment and then replied, “Well, you know, in my experience, that’s not true.”

The patient chuckled along with him. “I tried to point out to him that not all Catholic theologians see it that way,” Dr. Gabbard said.

Dr. Crisp-Han and Dr. Gabbard have collaborated on a book focused on diagnosis and treatment challenges associated with narcissistic patients called “Narcissism and Its Discontents” (American Psychiatric Association Publishing, 2018). They reported no relevant financial disclosures.

SAN FRANCISCO – Obsessive-compulsive personality disorder (OCPD) is often confused with obsessive-compulsive disorder (OCD) because of overlapping traits, but there are key differences that psychiatrists should be familiar with. OCPD also presents some key challenges to interpersonal therapy, especially because psychiatrists themselves sometimes share these traits.

“There’s an overlap, and some people have both OCD and OCPD, but some people have just one or the other, and that’s important to tease out because it shifts treatment,” Holly D. Crisp-Han, MD, said in an interview. Dr. Crisp-Han is a clinical associate professor of psychiatry and behavioral sciences at Baylor College of Medicine, Houston. She and her colleague, Glen O. Gabbard, MD, clinical professor of psychiatry at Baylor, chaired a session on dynamic psychotherapy for the treatment of OCPD at the annual meeting of the American Psychiatric Association.

OCPD is the most common personality disorder, with some estimates putting its prevalence as high as nearly 8%. Whereas OCD is characterized by an ego-dystonic need for rituals and specific thoughts, OCPD is defined by ego-syntonic traits. In a study comparing patients with both disorders, researchers found that both groups had reduced psychosocial function and quality of life, but intrusive thoughts and feelings were absent in OCPD. Instead, these patients reported ritualized, methodical behaviors, such as list making, reorganizing personal effects, and repeatedly editing what they had written. OCD patients were also better at delaying rewards.

Dynamic psychotherapy has been shown to achieve better outcomes in OCPD than cognitive-behavioral therapy, though both have a place in the treatment of OCPD, according to Dr. Gabbard. However, it comes with significant challenges. The patient will often challenge the therapist’s interventions and feel threatened by any hint of losing control. Sessions can become ritualized.

OCPD patients are driven by an effort to avoid a tormenting superego rather than seeking pleasure, and they may project this superego onto the therapist. It’s important to identify and interpret patient distortion of the therapist’s attitude toward the patient. Ultimately, the goal of therapy is to modify the patient’s self-expectations.

Couples therapy can be a good idea in cases of extreme ego-syntonicity. The patient’s partner can provide a second perspective to complement the patient’s subjective view of the relationship.

A unique challenge with OCPD is that therapists may see reflections of themselves in the patient. “Many physicians, psychiatrists, and therapists themselves struggle with obsessive-compulsive types of problems. Those types of traits – perfectionism, hard work, overwork, diligence – are rewarded in a career in medicine, and in fact [are] necessary for a career in medicine. We all have to be alert to our own personality traits in order to be able to treat those traits in others,” Dr. Crisp-Han said.” If we don’t recognize those traits in ourselves, then we run the risk of falling into competitive patterns, or idealizations, or other kinds of problems with our patients.”

Therapists who are narcissistically vulnerable may get sucked into power struggles with patients, and can feel undervalued, Dr. Gabbard said. Because rituals can develop, the therapist may also become bored, and even come to feel controlled by the patient’s obsession with the therapeutic process.

But there are other challenges in sessions. The tendency toward ritualization can produce boredom in the therapist. “That’s one of the biggest problems you have, hanging in with somebody who’s repeating the same things over and over again in a dry tone. You start to feel controlled by everything the patient is doing with their agenda,” Dr. Gabbard said during the session. He suggested confronting the patient from time to time. “You can say, ‘Today you don’t sound like you’re that interested in what you’re saying to me; you sound very detached. What’s going on?’ You can feed back to the person how they’re coming across, which can be very valuable.”

Humor is another way to tackle therapy with OCPD patients, because an important therapeutic lesson is to take things a little less seriously, especially in the face of the perfectionism that often haunts OCPD patients. In fact, this can be one of the condition’s most devastating traits, always leading an OCPD patient to feel that he or she is failing, that no accomplishment is ever enough.

“You can work on perfectionism and interpersonal relationships, and the absence of fun and pleasure. This is one of the most fun things to work on in the transference, countertransference relationship. Have a little bit of fun with the patient, because that might be quite foreign,” Dr. Gabbard said. “It can be tricky, because you don’t want to act like you’re laughing at the patient, but you want to introduce some levity and lightness sometimes.”

He gave an example of a patient who was a Catholic priest, who felt intensely guilty over sex. The patient said, “In the Catholic Church, thinking about sex is exactly the same as having sex.” Dr. Gabbard thought for a moment and then replied, “Well, you know, in my experience, that’s not true.”

The patient chuckled along with him. “I tried to point out to him that not all Catholic theologians see it that way,” Dr. Gabbard said.

Dr. Crisp-Han and Dr. Gabbard have collaborated on a book focused on diagnosis and treatment challenges associated with narcissistic patients called “Narcissism and Its Discontents” (American Psychiatric Association Publishing, 2018). They reported no relevant financial disclosures.

SAN FRANCISCO – Obsessive-compulsive personality disorder (OCPD) is often confused with obsessive-compulsive disorder (OCD) because of overlapping traits, but there are key differences that psychiatrists should be familiar with. OCPD also presents some key challenges to interpersonal therapy, especially because psychiatrists themselves sometimes share these traits.

“There’s an overlap, and some people have both OCD and OCPD, but some people have just one or the other, and that’s important to tease out because it shifts treatment,” Holly D. Crisp-Han, MD, said in an interview. Dr. Crisp-Han is a clinical associate professor of psychiatry and behavioral sciences at Baylor College of Medicine, Houston. She and her colleague, Glen O. Gabbard, MD, clinical professor of psychiatry at Baylor, chaired a session on dynamic psychotherapy for the treatment of OCPD at the annual meeting of the American Psychiatric Association.

OCPD is the most common personality disorder, with some estimates putting its prevalence as high as nearly 8%. Whereas OCD is characterized by an ego-dystonic need for rituals and specific thoughts, OCPD is defined by ego-syntonic traits. In a study comparing patients with both disorders, researchers found that both groups had reduced psychosocial function and quality of life, but intrusive thoughts and feelings were absent in OCPD. Instead, these patients reported ritualized, methodical behaviors, such as list making, reorganizing personal effects, and repeatedly editing what they had written. OCD patients were also better at delaying rewards.

Dynamic psychotherapy has been shown to achieve better outcomes in OCPD than cognitive-behavioral therapy, though both have a place in the treatment of OCPD, according to Dr. Gabbard. However, it comes with significant challenges. The patient will often challenge the therapist’s interventions and feel threatened by any hint of losing control. Sessions can become ritualized.

OCPD patients are driven by an effort to avoid a tormenting superego rather than seeking pleasure, and they may project this superego onto the therapist. It’s important to identify and interpret patient distortion of the therapist’s attitude toward the patient. Ultimately, the goal of therapy is to modify the patient’s self-expectations.

Couples therapy can be a good idea in cases of extreme ego-syntonicity. The patient’s partner can provide a second perspective to complement the patient’s subjective view of the relationship.

A unique challenge with OCPD is that therapists may see reflections of themselves in the patient. “Many physicians, psychiatrists, and therapists themselves struggle with obsessive-compulsive types of problems. Those types of traits – perfectionism, hard work, overwork, diligence – are rewarded in a career in medicine, and in fact [are] necessary for a career in medicine. We all have to be alert to our own personality traits in order to be able to treat those traits in others,” Dr. Crisp-Han said.” If we don’t recognize those traits in ourselves, then we run the risk of falling into competitive patterns, or idealizations, or other kinds of problems with our patients.”

Therapists who are narcissistically vulnerable may get sucked into power struggles with patients, and can feel undervalued, Dr. Gabbard said. Because rituals can develop, the therapist may also become bored, and even come to feel controlled by the patient’s obsession with the therapeutic process.

But there are other challenges in sessions. The tendency toward ritualization can produce boredom in the therapist. “That’s one of the biggest problems you have, hanging in with somebody who’s repeating the same things over and over again in a dry tone. You start to feel controlled by everything the patient is doing with their agenda,” Dr. Gabbard said during the session. He suggested confronting the patient from time to time. “You can say, ‘Today you don’t sound like you’re that interested in what you’re saying to me; you sound very detached. What’s going on?’ You can feed back to the person how they’re coming across, which can be very valuable.”

Humor is another way to tackle therapy with OCPD patients, because an important therapeutic lesson is to take things a little less seriously, especially in the face of the perfectionism that often haunts OCPD patients. In fact, this can be one of the condition’s most devastating traits, always leading an OCPD patient to feel that he or she is failing, that no accomplishment is ever enough.

“You can work on perfectionism and interpersonal relationships, and the absence of fun and pleasure. This is one of the most fun things to work on in the transference, countertransference relationship. Have a little bit of fun with the patient, because that might be quite foreign,” Dr. Gabbard said. “It can be tricky, because you don’t want to act like you’re laughing at the patient, but you want to introduce some levity and lightness sometimes.”

He gave an example of a patient who was a Catholic priest, who felt intensely guilty over sex. The patient said, “In the Catholic Church, thinking about sex is exactly the same as having sex.” Dr. Gabbard thought for a moment and then replied, “Well, you know, in my experience, that’s not true.”

The patient chuckled along with him. “I tried to point out to him that not all Catholic theologians see it that way,” Dr. Gabbard said.

Dr. Crisp-Han and Dr. Gabbard have collaborated on a book focused on diagnosis and treatment challenges associated with narcissistic patients called “Narcissism and Its Discontents” (American Psychiatric Association Publishing, 2018). They reported no relevant financial disclosures.

SAN FRANCISCO – An expert in obsessive-compulsive disease had some surprising advice at the American Psychiatric Association annual meeting for treatment of adults with refractory illness. He endorsed amphetamines, caffeine, and once-weekly opioids in carefully selected patients.

M. Alexander Otto/MDedge News

“These are not things that will be taught to you in your residency,” said Lorrin M. Koran, MD, professor emeritus of psychiatry and behavioral sciences at Stanford (Calif.) University, and past director of the university’s OCD clinic and research program. “These are pharmacological pearls that have come to my attention over many years. I hope at the end of this talk you’ll be more comfortable, especially [with] stimulants, because [they are] very simple and very quick.”

Opioids are a last resort but can prove effective for some patients. “I had a woman who wrote me just last week who said her son’s been on an opioid for 9 years once a week,” Dr. Koran said. “He does very well, and if he stops, he relapses within a few days. He has not become dependent or abusive. You have to screen who you give these to.

“You and I are dedicated to helping people not suffer, so we might want to take a little risk” for people who are struggling, he said.

Bolus caffeine, not a casual cup

Inspired by findings from the 1980s-90s, Dr. Koran and his colleagues randomized 12 treatment-resistant adults at Stanford’s OCD clinic to dextroamphetamine (Dexedrine) 30 mg/day and 12 others to caffeine (NoDoz pills) 300 mg/day, both in pink capsules so patients couldn’t tell them apart. “They were really sick” at baseline, Dr. Koran said, with a mean Yale Brown OCD Scale (YBOCS) score of 28 points (J Clin Psychiatry. 2009 Nov;70[11]:1530-5).

Subjects remained on their antidepressants during the study. Patients with histories of substance abuse, heart disease, schizophrenia, bipolar disorder, or panic attacks were among those excluded.

Caffeine was supposed to be the placebo. But a curious thing happened: About half of patients in both groups did remarkably well after 1 week, with a mean YBOCS drop of 41% among the six amphetamine responders and 45% among seven caffeine responders – with more improvement after 5 weeks.

“I was shocked. In clinical trials, anything 25% or more is considered a response. What patients said was, ‘Gee doc, I still get my obsessions, but I can shift my attention. I can get away from them, so I don’t have to do my compulsions, anymore,’ ” Dr. Koran said.

There were a few dose reductions for insomnia and anxiety. However, overall, YBOCS improvement did not correlate with depression and anxiety scores, so responses appeared to be independent. There were no differences between the groups in liking their treatment or how high people felt.

“I encourage you to try this” – amphetamine or caffeine bolus – “for people who have not responded to say two [treatment] trials. It’s simple. It’s safe. It’s quick. You know within 3 days, 5 days, and it lasts.” Meanwhile, “the data for methylphenidate are less convincing,” Dr. Koran said.

He’s wondered why caffeine helps. After all, no one has ever come into the OCD clinic and said they felt better after their morning coffee. The hypothesis is that 300 mg of caffeine all at once triggers a spike of methylxanthines in the brain, which, much like amphetamines, promotes dopamine and serotonin release. Casually sipping coffee does not have the same effect.

When all else fails

Dr. Koran and his colleagues also ran a small trial of once-weekly opiates.

Spurred again by case histories and small studies, they randomized 23 refractory adults to once-weekly morphine 30 mg (with 15-mg dose adjustment as needed at 2 weeks), lorazepam 1 mg (with 0.5-mg adjustment at 2 weeks), or placebo. Subjects had OCD for at least 3 years, and had failed at least two antidepressant trials (some had been on atypicals). Median baseline YBOCS was 29 points. Subjects remained on their baseline medications during the study (J Clin Psychiatry. 2005 Mar;66[3]:353-9).

Seven patients responded to morphine with a drop of at least 25% in their YBOCS; five had at least a 40% drop. Patients who were not taking a selective serotonin or norepinephrine reuptake inhibitor did not respond to morphine.

There were four lorazepam responders, but only one with a reduction of 40% or more. There were no placebo responders.

Opioids are the “the last thing to think of” in OCD, but when all else fails, “you could try morphine in a properly screened individual,” as long as there is no personal or family history of substance abuse.

Dr. Koran said he had no conflicts of interest.

[email protected]

SAN FRANCISCO – An expert in obsessive-compulsive disease had some surprising advice at the American Psychiatric Association annual meeting for treatment of adults with refractory illness. He endorsed amphetamines, caffeine, and once-weekly opioids in carefully selected patients.

M. Alexander Otto/MDedge News

“These are not things that will be taught to you in your residency,” said Lorrin M. Koran, MD, professor emeritus of psychiatry and behavioral sciences at Stanford (Calif.) University, and past director of the university’s OCD clinic and research program. “These are pharmacological pearls that have come to my attention over many years. I hope at the end of this talk you’ll be more comfortable, especially [with] stimulants, because [they are] very simple and very quick.”

Opioids are a last resort but can prove effective for some patients. “I had a woman who wrote me just last week who said her son’s been on an opioid for 9 years once a week,” Dr. Koran said. “He does very well, and if he stops, he relapses within a few days. He has not become dependent or abusive. You have to screen who you give these to.

“You and I are dedicated to helping people not suffer, so we might want to take a little risk” for people who are struggling, he said.

Bolus caffeine, not a casual cup

Inspired by findings from the 1980s-90s, Dr. Koran and his colleagues randomized 12 treatment-resistant adults at Stanford’s OCD clinic to dextroamphetamine (Dexedrine) 30 mg/day and 12 others to caffeine (NoDoz pills) 300 mg/day, both in pink capsules so patients couldn’t tell them apart. “They were really sick” at baseline, Dr. Koran said, with a mean Yale Brown OCD Scale (YBOCS) score of 28 points (J Clin Psychiatry. 2009 Nov;70[11]:1530-5).

Subjects remained on their antidepressants during the study. Patients with histories of substance abuse, heart disease, schizophrenia, bipolar disorder, or panic attacks were among those excluded.

Caffeine was supposed to be the placebo. But a curious thing happened: About half of patients in both groups did remarkably well after 1 week, with a mean YBOCS drop of 41% among the six amphetamine responders and 45% among seven caffeine responders – with more improvement after 5 weeks.

“I was shocked. In clinical trials, anything 25% or more is considered a response. What patients said was, ‘Gee doc, I still get my obsessions, but I can shift my attention. I can get away from them, so I don’t have to do my compulsions, anymore,’ ” Dr. Koran said.

There were a few dose reductions for insomnia and anxiety. However, overall, YBOCS improvement did not correlate with depression and anxiety scores, so responses appeared to be independent. There were no differences between the groups in liking their treatment or how high people felt.

“I encourage you to try this” – amphetamine or caffeine bolus – “for people who have not responded to say two [treatment] trials. It’s simple. It’s safe. It’s quick. You know within 3 days, 5 days, and it lasts.” Meanwhile, “the data for methylphenidate are less convincing,” Dr. Koran said.

He’s wondered why caffeine helps. After all, no one has ever come into the OCD clinic and said they felt better after their morning coffee. The hypothesis is that 300 mg of caffeine all at once triggers a spike of methylxanthines in the brain, which, much like amphetamines, promotes dopamine and serotonin release. Casually sipping coffee does not have the same effect.

When all else fails

Dr. Koran and his colleagues also ran a small trial of once-weekly opiates.

Spurred again by case histories and small studies, they randomized 23 refractory adults to once-weekly morphine 30 mg (with 15-mg dose adjustment as needed at 2 weeks), lorazepam 1 mg (with 0.5-mg adjustment at 2 weeks), or placebo. Subjects had OCD for at least 3 years, and had failed at least two antidepressant trials (some had been on atypicals). Median baseline YBOCS was 29 points. Subjects remained on their baseline medications during the study (J Clin Psychiatry. 2005 Mar;66[3]:353-9).

Seven patients responded to morphine with a drop of at least 25% in their YBOCS; five had at least a 40% drop. Patients who were not taking a selective serotonin or norepinephrine reuptake inhibitor did not respond to morphine.

There were four lorazepam responders, but only one with a reduction of 40% or more. There were no placebo responders.

Opioids are the “the last thing to think of” in OCD, but when all else fails, “you could try morphine in a properly screened individual,” as long as there is no personal or family history of substance abuse.

Dr. Koran said he had no conflicts of interest.

[email protected]

SAN FRANCISCO – An expert in obsessive-compulsive disease had some surprising advice at the American Psychiatric Association annual meeting for treatment of adults with refractory illness. He endorsed amphetamines, caffeine, and once-weekly opioids in carefully selected patients.

M. Alexander Otto/MDedge News

“These are not things that will be taught to you in your residency,” said Lorrin M. Koran, MD, professor emeritus of psychiatry and behavioral sciences at Stanford (Calif.) University, and past director of the university’s OCD clinic and research program. “These are pharmacological pearls that have come to my attention over many years. I hope at the end of this talk you’ll be more comfortable, especially [with] stimulants, because [they are] very simple and very quick.”

Opioids are a last resort but can prove effective for some patients. “I had a woman who wrote me just last week who said her son’s been on an opioid for 9 years once a week,” Dr. Koran said. “He does very well, and if he stops, he relapses within a few days. He has not become dependent or abusive. You have to screen who you give these to.

“You and I are dedicated to helping people not suffer, so we might want to take a little risk” for people who are struggling, he said.

Bolus caffeine, not a casual cup

Inspired by findings from the 1980s-90s, Dr. Koran and his colleagues randomized 12 treatment-resistant adults at Stanford’s OCD clinic to dextroamphetamine (Dexedrine) 30 mg/day and 12 others to caffeine (NoDoz pills) 300 mg/day, both in pink capsules so patients couldn’t tell them apart. “They were really sick” at baseline, Dr. Koran said, with a mean Yale Brown OCD Scale (YBOCS) score of 28 points (J Clin Psychiatry. 2009 Nov;70[11]:1530-5).

Subjects remained on their antidepressants during the study. Patients with histories of substance abuse, heart disease, schizophrenia, bipolar disorder, or panic attacks were among those excluded.

Caffeine was supposed to be the placebo. But a curious thing happened: About half of patients in both groups did remarkably well after 1 week, with a mean YBOCS drop of 41% among the six amphetamine responders and 45% among seven caffeine responders – with more improvement after 5 weeks.

“I was shocked. In clinical trials, anything 25% or more is considered a response. What patients said was, ‘Gee doc, I still get my obsessions, but I can shift my attention. I can get away from them, so I don’t have to do my compulsions, anymore,’ ” Dr. Koran said.

There were a few dose reductions for insomnia and anxiety. However, overall, YBOCS improvement did not correlate with depression and anxiety scores, so responses appeared to be independent. There were no differences between the groups in liking their treatment or how high people felt.

“I encourage you to try this” – amphetamine or caffeine bolus – “for people who have not responded to say two [treatment] trials. It’s simple. It’s safe. It’s quick. You know within 3 days, 5 days, and it lasts.” Meanwhile, “the data for methylphenidate are less convincing,” Dr. Koran said.

He’s wondered why caffeine helps. After all, no one has ever come into the OCD clinic and said they felt better after their morning coffee. The hypothesis is that 300 mg of caffeine all at once triggers a spike of methylxanthines in the brain, which, much like amphetamines, promotes dopamine and serotonin release. Casually sipping coffee does not have the same effect.

When all else fails

Dr. Koran and his colleagues also ran a small trial of once-weekly opiates.

Spurred again by case histories and small studies, they randomized 23 refractory adults to once-weekly morphine 30 mg (with 15-mg dose adjustment as needed at 2 weeks), lorazepam 1 mg (with 0.5-mg adjustment at 2 weeks), or placebo. Subjects had OCD for at least 3 years, and had failed at least two antidepressant trials (some had been on atypicals). Median baseline YBOCS was 29 points. Subjects remained on their baseline medications during the study (J Clin Psychiatry. 2005 Mar;66[3]:353-9).

Seven patients responded to morphine with a drop of at least 25% in their YBOCS; five had at least a 40% drop. Patients who were not taking a selective serotonin or norepinephrine reuptake inhibitor did not respond to morphine.

There were four lorazepam responders, but only one with a reduction of 40% or more. There were no placebo responders.

Opioids are the “the last thing to think of” in OCD, but when all else fails, “you could try morphine in a properly screened individual,” as long as there is no personal or family history of substance abuse.

Dr. Koran said he had no conflicts of interest.

[email protected]

SAN FRANCISCO – The recent Food and Drug Administration approval of intranasal esketamine for treatment-resistant depression has prompted interest in using this class of drugs in other conditions, including obsessive-compulsive disorder.

“OCD is severe, and one in seven people with OCD will attempt suicide in their lifetime,” said Carolyn Rodriguez, MD, PhD, associate professor of psychiatry and behavioral sciences at Stanford (Calif.) University.

Dr. Rodriguez presented some of her research on the mechanism of action of ketamine and its potential benefits for OCD during a session at the annual meeting of the American Psychiatric Association.

OCD patients experience a lengthy delay between treatment initiation and clinical benefit, sometimes 2 to 3 months, and most don’t achieve complete symptom remission, according to Dr. Rodriguez. “To help patients, I wanted to look at therapies that could be rapid acting, and given the converging lines of evidence that glutamate may play a role as an excitatory chemical messenger that helps neurons communicate, I looked at ketamine, which blocks the glutamate receptor,” she said.

A small study published in 2013 by her group was the first randomized, clinical trial of ketamine in OCD. It included 15 adults who experienced near-constant obsessions. A single dose given over 40 minutes led to a dramatic decrease in intrusive thoughts. One week after the infusion, four of eight patients who received ketamine met the criteria for a treatment response (35% or more reduction in Yale-Brown Obsessive Compulsive Scale scores), compared with none of the seven patients in the placebo group.

Dr. Rodriguez is now preparing to conduct a new trial comparing ketamine with midazolam as an active placebo, with the intent of looking at the drug’s effects on the circuits involved in OCD. “We need a large study to see if this is something that can be replicated, and we don’t know how long the effects persist. We’re just at the tip of the iceberg with OCD. In depression, there are these large studies that have been replicated, and in OCD, at least for randomized studies, it’s just this one study (from 2013) and the one that we have coming,” Dr. Rodriguez said.

Given the severity of OCD, ketamine and esketamine have generated some excitement, especially as a bridge to other therapies, such as cognitive-behavioral therapy or selective serotonin reuptake inhibitors.

The FDA’s approval of esketamine in March further boosted interest, but Dr. Rodriguez cautions that more research needs to be done. There is also at least one potential twist to use of an inhaled version of the drug. Contamination OCD patients may be unwilling to use a spray. In fact, Dr. Rodriguez’s team had to cancel a study looking at an inhaled form of racemic ketamine in OCD because they couldn’t recruit enough subjects. “There are variants [in OCD], and that’s why it’s important to study all populations and not assume that depression studies will cover the whole spectrum of our patients,” she said.

Dr. Rodriguez has consulted for Epiodyne, Allergan, BlackThorn, and Rugen.

SAN FRANCISCO – The recent Food and Drug Administration approval of intranasal esketamine for treatment-resistant depression has prompted interest in using this class of drugs in other conditions, including obsessive-compulsive disorder.

“OCD is severe, and one in seven people with OCD will attempt suicide in their lifetime,” said Carolyn Rodriguez, MD, PhD, associate professor of psychiatry and behavioral sciences at Stanford (Calif.) University.

Dr. Rodriguez presented some of her research on the mechanism of action of ketamine and its potential benefits for OCD during a session at the annual meeting of the American Psychiatric Association.

OCD patients experience a lengthy delay between treatment initiation and clinical benefit, sometimes 2 to 3 months, and most don’t achieve complete symptom remission, according to Dr. Rodriguez. “To help patients, I wanted to look at therapies that could be rapid acting, and given the converging lines of evidence that glutamate may play a role as an excitatory chemical messenger that helps neurons communicate, I looked at ketamine, which blocks the glutamate receptor,” she said.

A small study published in 2013 by her group was the first randomized, clinical trial of ketamine in OCD. It included 15 adults who experienced near-constant obsessions. A single dose given over 40 minutes led to a dramatic decrease in intrusive thoughts. One week after the infusion, four of eight patients who received ketamine met the criteria for a treatment response (35% or more reduction in Yale-Brown Obsessive Compulsive Scale scores), compared with none of the seven patients in the placebo group.

Dr. Rodriguez is now preparing to conduct a new trial comparing ketamine with midazolam as an active placebo, with the intent of looking at the drug’s effects on the circuits involved in OCD. “We need a large study to see if this is something that can be replicated, and we don’t know how long the effects persist. We’re just at the tip of the iceberg with OCD. In depression, there are these large studies that have been replicated, and in OCD, at least for randomized studies, it’s just this one study (from 2013) and the one that we have coming,” Dr. Rodriguez said.

Given the severity of OCD, ketamine and esketamine have generated some excitement, especially as a bridge to other therapies, such as cognitive-behavioral therapy or selective serotonin reuptake inhibitors.

The FDA’s approval of esketamine in March further boosted interest, but Dr. Rodriguez cautions that more research needs to be done. There is also at least one potential twist to use of an inhaled version of the drug. Contamination OCD patients may be unwilling to use a spray. In fact, Dr. Rodriguez’s team had to cancel a study looking at an inhaled form of racemic ketamine in OCD because they couldn’t recruit enough subjects. “There are variants [in OCD], and that’s why it’s important to study all populations and not assume that depression studies will cover the whole spectrum of our patients,” she said.

Dr. Rodriguez has consulted for Epiodyne, Allergan, BlackThorn, and Rugen.

SAN FRANCISCO – The recent Food and Drug Administration approval of intranasal esketamine for treatment-resistant depression has prompted interest in using this class of drugs in other conditions, including obsessive-compulsive disorder.

“OCD is severe, and one in seven people with OCD will attempt suicide in their lifetime,” said Carolyn Rodriguez, MD, PhD, associate professor of psychiatry and behavioral sciences at Stanford (Calif.) University.

Dr. Rodriguez presented some of her research on the mechanism of action of ketamine and its potential benefits for OCD during a session at the annual meeting of the American Psychiatric Association.

OCD patients experience a lengthy delay between treatment initiation and clinical benefit, sometimes 2 to 3 months, and most don’t achieve complete symptom remission, according to Dr. Rodriguez. “To help patients, I wanted to look at therapies that could be rapid acting, and given the converging lines of evidence that glutamate may play a role as an excitatory chemical messenger that helps neurons communicate, I looked at ketamine, which blocks the glutamate receptor,” she said.

A small study published in 2013 by her group was the first randomized, clinical trial of ketamine in OCD. It included 15 adults who experienced near-constant obsessions. A single dose given over 40 minutes led to a dramatic decrease in intrusive thoughts. One week after the infusion, four of eight patients who received ketamine met the criteria for a treatment response (35% or more reduction in Yale-Brown Obsessive Compulsive Scale scores), compared with none of the seven patients in the placebo group.

Dr. Rodriguez is now preparing to conduct a new trial comparing ketamine with midazolam as an active placebo, with the intent of looking at the drug’s effects on the circuits involved in OCD. “We need a large study to see if this is something that can be replicated, and we don’t know how long the effects persist. We’re just at the tip of the iceberg with OCD. In depression, there are these large studies that have been replicated, and in OCD, at least for randomized studies, it’s just this one study (from 2013) and the one that we have coming,” Dr. Rodriguez said.

Given the severity of OCD, ketamine and esketamine have generated some excitement, especially as a bridge to other therapies, such as cognitive-behavioral therapy or selective serotonin reuptake inhibitors.

The FDA’s approval of esketamine in March further boosted interest, but Dr. Rodriguez cautions that more research needs to be done. There is also at least one potential twist to use of an inhaled version of the drug. Contamination OCD patients may be unwilling to use a spray. In fact, Dr. Rodriguez’s team had to cancel a study looking at an inhaled form of racemic ketamine in OCD because they couldn’t recruit enough subjects. “There are variants [in OCD], and that’s why it’s important to study all populations and not assume that depression studies will cover the whole spectrum of our patients,” she said.

Dr. Rodriguez has consulted for Epiodyne, Allergan, BlackThorn, and Rugen.

SAN FRANCISCO – Ketamine and the more recently Food and Drug Administration–approved esketamine have generated a great deal of excitement in psychiatry over their potential to treat depression and other psychiatric disorders. However, the mechanism of action is not completely understood, and efforts are underway to better understand the drugs.

Much has been made of ketamine’s interaction with the N-methyl-D-aspartate (NMDA) receptors. One belief is that chronic stress leads to the accumulation of extracellular glutamate, which leads to a range of negative consequences. Ketamine blocks excess glutamate in the synapse and may thus reverse these downstream effects.

But it may not be so clear cut, according to Nolan Williams, MD. During a session on ketamine’s mechanism of action at the annual meeting of the American Psychiatric Association, Dr. Williams, assistant professor of psychiatry and behavioral sciences at Stanford (Calif.) University, noted that ketamine is “one of the most dirty drugs we know. It affects most neurotransmitter systems and has all sorts of downstream effects.”

Pain research has already shown that ketamine’s mechanisms can be complex. It affects the opioid system, both directly and indirectly, and an opioid receptor antagonist blocks ketamine’s pain-relieving effect.

Since opioids are also known to have antidepressant effects, it’s natural to wonder if ketamine’s mechanism also involves the opioid system. The opioid antagonist naltrexone provides a tool to study the problem. Dr. Williams reasoned that if ketamine relies in whole or in part on the opioid system for its antidepressive effect, then administering naltrexone ahead of ketamine should blunt or even eliminate its efficacy.

To examine the question, the team conducted a study of 11 patients with treatment-resistant depression. Right away, it was clear that the participants had some bias toward the treatment. “They all said the same thing to me: ‘My psychiatrist said that your study doesn’t make any sense because this is an NMDA antagonist. I’m going to get two free ketamine infusions.’ So they were preloaded with this idea that they were going to get very potent antidepressant effects (even with naltrexone),” said Dr. Williams.

The study had a crossover design and included two ketamine infusions. Participants were randomized to get either naltrexone or placebo 1 hour before the first ketamine infusion, and then were allowed to relapse back to within 20% of their baseline depression score before receiving the second ketamine infusion, when they received naltrexone or placebo, whichever hadn’t been given in the first treatment.

Of 12 who completed the study, seven responded to placebo plus ketamine treatment, and six remitted. But when they crossed over to the naltrexone arm, the result was very different: In three of four measures, there was no significant difference between the pretreatment and posttreatment results. “The same people who were almost exclusively in remission during the ketamine plus placebo condition got nothing out of ketamine plus naltrexone,” said Dr. Williams. Naltrexone had a similar negating effect on the positive response to ketamine on the suicide item of the 17-item Hamilton Rating Scale for Depression.

The researchers also looked at whether ketamine’s dissociative effect could be responsible for its activity through altering the participant’s mental state, but determined that it may be necessary for the antidepressant effect – but it is not sufficient.

“What we concluded pretty strongly was that the opioid properties of ketamine are necessary to have the antidepressive effect. We’re not saying it’s sufficient, but it appears to be quite necessary,” Dr. Williams said. He added that the results don’t mean that ketamine’s effect on NMDA is unimportant. In fact, “it’s probable that the ketamine is driving the mood in a direction, and these glutamine-related changes are probably what’s maintaining the mood in that direction,” he added.

As to the clinical impacts of his findings, Dr. Williams emphasized the need to understand the mechanisms behind the ketamine class. He pointed out that in pivotal trials of esketamine, there were six deaths, three by suicide, all of them in the esketamine group. Surprisingly, two of those who took their own lives had scored a 0 on the Columbia-Suicide Severity Scale, both at baseline and at the visit immediately preceding their deaths. The score wasn’t available for the third. “These weren’t people who were particularly dangerously suicidal. So understanding the mechanism is really important to understanding the safety of this drug, who we should give it to, and what sorts of things we should watch out for,” Dr. Williams said.

The study was funded by the National Institutes of Health, Spectrum, the Brain and Behavior Research Foundation, and Stanford Bio-X. Dr. Williams had no disclosures.
 

SAN FRANCISCO – Ketamine and the more recently Food and Drug Administration–approved esketamine have generated a great deal of excitement in psychiatry over their potential to treat depression and other psychiatric disorders. However, the mechanism of action is not completely understood, and efforts are underway to better understand the drugs.

Much has been made of ketamine’s interaction with the N-methyl-D-aspartate (NMDA) receptors. One belief is that chronic stress leads to the accumulation of extracellular glutamate, which leads to a range of negative consequences. Ketamine blocks excess glutamate in the synapse and may thus reverse these downstream effects.

But it may not be so clear cut, according to Nolan Williams, MD. During a session on ketamine’s mechanism of action at the annual meeting of the American Psychiatric Association, Dr. Williams, assistant professor of psychiatry and behavioral sciences at Stanford (Calif.) University, noted that ketamine is “one of the most dirty drugs we know. It affects most neurotransmitter systems and has all sorts of downstream effects.”

Pain research has already shown that ketamine’s mechanisms can be complex. It affects the opioid system, both directly and indirectly, and an opioid receptor antagonist blocks ketamine’s pain-relieving effect.

Since opioids are also known to have antidepressant effects, it’s natural to wonder if ketamine’s mechanism also involves the opioid system. The opioid antagonist naltrexone provides a tool to study the problem. Dr. Williams reasoned that if ketamine relies in whole or in part on the opioid system for its antidepressive effect, then administering naltrexone ahead of ketamine should blunt or even eliminate its efficacy.

To examine the question, the team conducted a study of 11 patients with treatment-resistant depression. Right away, it was clear that the participants had some bias toward the treatment. “They all said the same thing to me: ‘My psychiatrist said that your study doesn’t make any sense because this is an NMDA antagonist. I’m going to get two free ketamine infusions.’ So they were preloaded with this idea that they were going to get very potent antidepressant effects (even with naltrexone),” said Dr. Williams.

The study had a crossover design and included two ketamine infusions. Participants were randomized to get either naltrexone or placebo 1 hour before the first ketamine infusion, and then were allowed to relapse back to within 20% of their baseline depression score before receiving the second ketamine infusion, when they received naltrexone or placebo, whichever hadn’t been given in the first treatment.

Of 12 who completed the study, seven responded to placebo plus ketamine treatment, and six remitted. But when they crossed over to the naltrexone arm, the result was very different: In three of four measures, there was no significant difference between the pretreatment and posttreatment results. “The same people who were almost exclusively in remission during the ketamine plus placebo condition got nothing out of ketamine plus naltrexone,” said Dr. Williams. Naltrexone had a similar negating effect on the positive response to ketamine on the suicide item of the 17-item Hamilton Rating Scale for Depression.

The researchers also looked at whether ketamine’s dissociative effect could be responsible for its activity through altering the participant’s mental state, but determined that it may be necessary for the antidepressant effect – but it is not sufficient.

“What we concluded pretty strongly was that the opioid properties of ketamine are necessary to have the antidepressive effect. We’re not saying it’s sufficient, but it appears to be quite necessary,” Dr. Williams said. He added that the results don’t mean that ketamine’s effect on NMDA is unimportant. In fact, “it’s probable that the ketamine is driving the mood in a direction, and these glutamine-related changes are probably what’s maintaining the mood in that direction,” he added.

As to the clinical impacts of his findings, Dr. Williams emphasized the need to understand the mechanisms behind the ketamine class. He pointed out that in pivotal trials of esketamine, there were six deaths, three by suicide, all of them in the esketamine group. Surprisingly, two of those who took their own lives had scored a 0 on the Columbia-Suicide Severity Scale, both at baseline and at the visit immediately preceding their deaths. The score wasn’t available for the third. “These weren’t people who were particularly dangerously suicidal. So understanding the mechanism is really important to understanding the safety of this drug, who we should give it to, and what sorts of things we should watch out for,” Dr. Williams said.

The study was funded by the National Institutes of Health, Spectrum, the Brain and Behavior Research Foundation, and Stanford Bio-X. Dr. Williams had no disclosures.
 

SAN FRANCISCO – Ketamine and the more recently Food and Drug Administration–approved esketamine have generated a great deal of excitement in psychiatry over their potential to treat depression and other psychiatric disorders. However, the mechanism of action is not completely understood, and efforts are underway to better understand the drugs.

Much has been made of ketamine’s interaction with the N-methyl-D-aspartate (NMDA) receptors. One belief is that chronic stress leads to the accumulation of extracellular glutamate, which leads to a range of negative consequences. Ketamine blocks excess glutamate in the synapse and may thus reverse these downstream effects.

But it may not be so clear cut, according to Nolan Williams, MD. During a session on ketamine’s mechanism of action at the annual meeting of the American Psychiatric Association, Dr. Williams, assistant professor of psychiatry and behavioral sciences at Stanford (Calif.) University, noted that ketamine is “one of the most dirty drugs we know. It affects most neurotransmitter systems and has all sorts of downstream effects.”

Pain research has already shown that ketamine’s mechanisms can be complex. It affects the opioid system, both directly and indirectly, and an opioid receptor antagonist blocks ketamine’s pain-relieving effect.

Since opioids are also known to have antidepressant effects, it’s natural to wonder if ketamine’s mechanism also involves the opioid system. The opioid antagonist naltrexone provides a tool to study the problem. Dr. Williams reasoned that if ketamine relies in whole or in part on the opioid system for its antidepressive effect, then administering naltrexone ahead of ketamine should blunt or even eliminate its efficacy.

To examine the question, the team conducted a study of 11 patients with treatment-resistant depression. Right away, it was clear that the participants had some bias toward the treatment. “They all said the same thing to me: ‘My psychiatrist said that your study doesn’t make any sense because this is an NMDA antagonist. I’m going to get two free ketamine infusions.’ So they were preloaded with this idea that they were going to get very potent antidepressant effects (even with naltrexone),” said Dr. Williams.

The study had a crossover design and included two ketamine infusions. Participants were randomized to get either naltrexone or placebo 1 hour before the first ketamine infusion, and then were allowed to relapse back to within 20% of their baseline depression score before receiving the second ketamine infusion, when they received naltrexone or placebo, whichever hadn’t been given in the first treatment.

Of 12 who completed the study, seven responded to placebo plus ketamine treatment, and six remitted. But when they crossed over to the naltrexone arm, the result was very different: In three of four measures, there was no significant difference between the pretreatment and posttreatment results. “The same people who were almost exclusively in remission during the ketamine plus placebo condition got nothing out of ketamine plus naltrexone,” said Dr. Williams. Naltrexone had a similar negating effect on the positive response to ketamine on the suicide item of the 17-item Hamilton Rating Scale for Depression.

The researchers also looked at whether ketamine’s dissociative effect could be responsible for its activity through altering the participant’s mental state, but determined that it may be necessary for the antidepressant effect – but it is not sufficient.

“What we concluded pretty strongly was that the opioid properties of ketamine are necessary to have the antidepressive effect. We’re not saying it’s sufficient, but it appears to be quite necessary,” Dr. Williams said. He added that the results don’t mean that ketamine’s effect on NMDA is unimportant. In fact, “it’s probable that the ketamine is driving the mood in a direction, and these glutamine-related changes are probably what’s maintaining the mood in that direction,” he added.

As to the clinical impacts of his findings, Dr. Williams emphasized the need to understand the mechanisms behind the ketamine class. He pointed out that in pivotal trials of esketamine, there were six deaths, three by suicide, all of them in the esketamine group. Surprisingly, two of those who took their own lives had scored a 0 on the Columbia-Suicide Severity Scale, both at baseline and at the visit immediately preceding their deaths. The score wasn’t available for the third. “These weren’t people who were particularly dangerously suicidal. So understanding the mechanism is really important to understanding the safety of this drug, who we should give it to, and what sorts of things we should watch out for,” Dr. Williams said.

The study was funded by the National Institutes of Health, Spectrum, the Brain and Behavior Research Foundation, and Stanford Bio-X. Dr. Williams had no disclosures.
 

Childbirth is a trigger for first-onset or recurrence of various psychiatric disorders; however, research and clinical efforts have focused mainly on postpartum mood disorders. Unfortunately, there is little research on identifying and managing obsessive-compulsive disorder (OCD) in the postpartum period.

In one prospective study of 461 women who recently gave birth, researchers found the prevalence of OCD symptoms was 11% at 2 weeks postpartum.¹ Mothers with OCD may have time-consuming or functionally impairing obsessions and/or compulsions that can include:

• anticipatory anxiety of contamination (eg, germs, illness)
• thoughts of accidental or intentional harm to their infant
• compulsions comprised of cleaning and checking behaviors
• avoidance of situations
• thought suppression.

Because both clinicians and patients may not be aware of the effects of childbirth on women with OCD, postpartum OCD may go underdiagnosed or be misdiagnosed as major depressive disorder (MDD) or an anxiety disorder. Additionally, women with OCD who lack insight or have delusional beliefs might be misdiagnosed with postpartum psychosis.

Here I offer methods to help effectively identify OCD in postpartum women, and suggest how to implement an individualized treatment approach.

Keys to identification and diagnosis

Mothers who present with postpartum anxiety or depression may have obsessions and compulsions. It is important to specifically screen for these symptoms because some mothers may be reluctant to discuss the content of their thoughts or behaviors.

Screen women who present with postpartum anxiety or depression for obsessions and compulsions by using questions based on DSM-5 criteria,² such as:

• Do you have unpleasant thoughts, urges, or images that repeatedly enter your mind?
• Do you feel driven to perform certain behaviors or mental acts over and over again?

A validated scale, such as the Yale-Brown Obsessive Compulsive Scale (Y-BOCS),³ can also be used to screen for obsessive/compulsive symptoms in these patients.

Continue to: Evaluate women who endorse...

Evaluate women who endorse obsessions or compulsions for OCD. Women who meet diagnostic criteria for OCD should also be assessed for common psychiatric comorbidities, including MDD, anxiety disorders, or bipolar disorder. Obsessive-compulsive disorder with absent insight and delusional beliefs should be differentiated from postpartum psychosis, which is often a manifestation of bipolar disorder.

Treatment: What to consider

When selecting a treatment, consider factors such as symptom severity, psychiatric comorbidities, the patient’s insight into her OCD symptoms, patient preference, and breastfeeding status. Cognitive-behavioral therapy with exposure response prevention is indicated for patients with mild to moderate OCD. Pharmacotherapy should be reserved for individuals with severe OCD. Selective serotonin reuptake inhibitors (SSRIs) are the mainstay pharmacologic treatment of postpartum OCD; however, there are currently no randomized controlled trials of SSRIs for women with postpartum OCD. Augmentation with quetiapine should be considered for women who have an inadequate response to SSRIs.

Acknowledgment

The author thanks Christine Baczynski for her help with the preparation of this article.

Childbirth is a trigger for first-onset or recurrence of various psychiatric disorders; however, research and clinical efforts have focused mainly on postpartum mood disorders. Unfortunately, there is little research on identifying and managing obsessive-compulsive disorder (OCD) in the postpartum period.

In one prospective study of 461 women who recently gave birth, researchers found the prevalence of OCD symptoms was 11% at 2 weeks postpartum.¹ Mothers with OCD may have time-consuming or functionally impairing obsessions and/or compulsions that can include:

• anticipatory anxiety of contamination (eg, germs, illness)
• thoughts of accidental or intentional harm to their infant
• compulsions comprised of cleaning and checking behaviors
• avoidance of situations
• thought suppression.

Because both clinicians and patients may not be aware of the effects of childbirth on women with OCD, postpartum OCD may go underdiagnosed or be misdiagnosed as major depressive disorder (MDD) or an anxiety disorder. Additionally, women with OCD who lack insight or have delusional beliefs might be misdiagnosed with postpartum psychosis.

Here I offer methods to help effectively identify OCD in postpartum women, and suggest how to implement an individualized treatment approach.

Keys to identification and diagnosis

Mothers who present with postpartum anxiety or depression may have obsessions and compulsions. It is important to specifically screen for these symptoms because some mothers may be reluctant to discuss the content of their thoughts or behaviors.

Screen women who present with postpartum anxiety or depression for obsessions and compulsions by using questions based on DSM-5 criteria,² such as:

• Do you have unpleasant thoughts, urges, or images that repeatedly enter your mind?
• Do you feel driven to perform certain behaviors or mental acts over and over again?

A validated scale, such as the Yale-Brown Obsessive Compulsive Scale (Y-BOCS),³ can also be used to screen for obsessive/compulsive symptoms in these patients.

Continue to: Evaluate women who endorse...

Evaluate women who endorse obsessions or compulsions for OCD. Women who meet diagnostic criteria for OCD should also be assessed for common psychiatric comorbidities, including MDD, anxiety disorders, or bipolar disorder. Obsessive-compulsive disorder with absent insight and delusional beliefs should be differentiated from postpartum psychosis, which is often a manifestation of bipolar disorder.

Treatment: What to consider

When selecting a treatment, consider factors such as symptom severity, psychiatric comorbidities, the patient’s insight into her OCD symptoms, patient preference, and breastfeeding status. Cognitive-behavioral therapy with exposure response prevention is indicated for patients with mild to moderate OCD. Pharmacotherapy should be reserved for individuals with severe OCD. Selective serotonin reuptake inhibitors (SSRIs) are the mainstay pharmacologic treatment of postpartum OCD; however, there are currently no randomized controlled trials of SSRIs for women with postpartum OCD. Augmentation with quetiapine should be considered for women who have an inadequate response to SSRIs.

Acknowledgment

The author thanks Christine Baczynski for her help with the preparation of this article.

Childbirth is a trigger for first-onset or recurrence of various psychiatric disorders; however, research and clinical efforts have focused mainly on postpartum mood disorders. Unfortunately, there is little research on identifying and managing obsessive-compulsive disorder (OCD) in the postpartum period.

In one prospective study of 461 women who recently gave birth, researchers found the prevalence of OCD symptoms was 11% at 2 weeks postpartum.¹ Mothers with OCD may have time-consuming or functionally impairing obsessions and/or compulsions that can include:

• anticipatory anxiety of contamination (eg, germs, illness)
• thoughts of accidental or intentional harm to their infant
• compulsions comprised of cleaning and checking behaviors
• avoidance of situations
• thought suppression.

Because both clinicians and patients may not be aware of the effects of childbirth on women with OCD, postpartum OCD may go underdiagnosed or be misdiagnosed as major depressive disorder (MDD) or an anxiety disorder. Additionally, women with OCD who lack insight or have delusional beliefs might be misdiagnosed with postpartum psychosis.

Here I offer methods to help effectively identify OCD in postpartum women, and suggest how to implement an individualized treatment approach.

Keys to identification and diagnosis

Mothers who present with postpartum anxiety or depression may have obsessions and compulsions. It is important to specifically screen for these symptoms because some mothers may be reluctant to discuss the content of their thoughts or behaviors.

Screen women who present with postpartum anxiety or depression for obsessions and compulsions by using questions based on DSM-5 criteria,² such as:

• Do you have unpleasant thoughts, urges, or images that repeatedly enter your mind?
• Do you feel driven to perform certain behaviors or mental acts over and over again?

A validated scale, such as the Yale-Brown Obsessive Compulsive Scale (Y-BOCS),³ can also be used to screen for obsessive/compulsive symptoms in these patients.

Continue to: Evaluate women who endorse...

Evaluate women who endorse obsessions or compulsions for OCD. Women who meet diagnostic criteria for OCD should also be assessed for common psychiatric comorbidities, including MDD, anxiety disorders, or bipolar disorder. Obsessive-compulsive disorder with absent insight and delusional beliefs should be differentiated from postpartum psychosis, which is often a manifestation of bipolar disorder.

Treatment: What to consider

When selecting a treatment, consider factors such as symptom severity, psychiatric comorbidities, the patient’s insight into her OCD symptoms, patient preference, and breastfeeding status. Cognitive-behavioral therapy with exposure response prevention is indicated for patients with mild to moderate OCD. Pharmacotherapy should be reserved for individuals with severe OCD. Selective serotonin reuptake inhibitors (SSRIs) are the mainstay pharmacologic treatment of postpartum OCD; however, there are currently no randomized controlled trials of SSRIs for women with postpartum OCD. Augmentation with quetiapine should be considered for women who have an inadequate response to SSRIs.

Acknowledgment

The author thanks Christine Baczynski for her help with the preparation of this article.

A clue to the neuroanatomy of obsessive-compulsive personality disorder may lay in abnormal hippocampal or amygdalar structures, according to a new observational imaging study.

MRI showed that the right and left volumes of the hippocampus and amygdala are smaller in patients with obsessive-compulsive personality disorder than in healthy controls, researchers found.

These findings lend support to the likelihood that obsessive-compulsive personality disorder “seems to be a neurocognitive function disorder rather than a personality disorder,” Mehmet Gurkan Gurok, of Firat University, Elazig, Turkey, and his associates reported in the Journal of Clinical Neuroscience.

The authors previously had investigated volumes of hippocampus and amygdala in patients with obsessive-compulsive disorder and found these patients had “increased white matter volumes, greater left and right thalamus volumes and significantly reduced left and right orbitofrontal cortex volumes, compared with healthy controls.”

For this study, they similarly used MRI to assess hippocampal and amygdalar volumes in 16 patients with obsessive-compulsive personality disorder (inpatients and outpatients at Firat University) and in 18 healthy controls – matched for age, sex, education, and handedness – who were studying at the hospital.

The researchers used the DSM-IV and the Structured Clinical Interview for the Diagnostic Schedule for Mental Disorders-Fourth Edition for diagnoses but noted later in their limitations that “the validity of diagnosis should be questioned” for personality disorders.

Participants were excluded if they had a comorbid Axis I psychiatric diagnosis besides depression, any contraindications for MRI, history of alcohol or substance dependence within the previous 6 months, use of psychoactive medications within 4 weeks of the study, or any current severe medical conditions. In addition, neither controls nor their first-degree relatives had a history of psychiatric disorders.

The findings showed that those with obsessive-compulsive personality disorder had smaller volumes on both sides of the hippocampus, compared with healthy controls. Amygdalar volume on both the left and right sides were similarly smaller in patients with obsessive-compulsive personality disorder, compared with healthy controls (left, P = .001; right, P = .002). The authors also reported they “did not find any correlation between hippocampus and amygdala volumes and any clinical and demographic variables.”

The research was funded by Firat University. The authors reported having no conflicts of interest.

SOURCE: Gurok MG et al. J Clin Neurosci. 2019 Apr 5. doi: 10.1016/j.jocn.2019.03.060.

A clue to the neuroanatomy of obsessive-compulsive personality disorder may lay in abnormal hippocampal or amygdalar structures, according to a new observational imaging study.

MRI showed that the right and left volumes of the hippocampus and amygdala are smaller in patients with obsessive-compulsive personality disorder than in healthy controls, researchers found.

These findings lend support to the likelihood that obsessive-compulsive personality disorder “seems to be a neurocognitive function disorder rather than a personality disorder,” Mehmet Gurkan Gurok, of Firat University, Elazig, Turkey, and his associates reported in the Journal of Clinical Neuroscience.

The authors previously had investigated volumes of hippocampus and amygdala in patients with obsessive-compulsive disorder and found these patients had “increased white matter volumes, greater left and right thalamus volumes and significantly reduced left and right orbitofrontal cortex volumes, compared with healthy controls.”

For this study, they similarly used MRI to assess hippocampal and amygdalar volumes in 16 patients with obsessive-compulsive personality disorder (inpatients and outpatients at Firat University) and in 18 healthy controls – matched for age, sex, education, and handedness – who were studying at the hospital.

The researchers used the DSM-IV and the Structured Clinical Interview for the Diagnostic Schedule for Mental Disorders-Fourth Edition for diagnoses but noted later in their limitations that “the validity of diagnosis should be questioned” for personality disorders.

Participants were excluded if they had a comorbid Axis I psychiatric diagnosis besides depression, any contraindications for MRI, history of alcohol or substance dependence within the previous 6 months, use of psychoactive medications within 4 weeks of the study, or any current severe medical conditions. In addition, neither controls nor their first-degree relatives had a history of psychiatric disorders.

The findings showed that those with obsessive-compulsive personality disorder had smaller volumes on both sides of the hippocampus, compared with healthy controls. Amygdalar volume on both the left and right sides were similarly smaller in patients with obsessive-compulsive personality disorder, compared with healthy controls (left, P = .001; right, P = .002). The authors also reported they “did not find any correlation between hippocampus and amygdala volumes and any clinical and demographic variables.”

The research was funded by Firat University. The authors reported having no conflicts of interest.

SOURCE: Gurok MG et al. J Clin Neurosci. 2019 Apr 5. doi: 10.1016/j.jocn.2019.03.060.

A clue to the neuroanatomy of obsessive-compulsive personality disorder may lay in abnormal hippocampal or amygdalar structures, according to a new observational imaging study.

MRI showed that the right and left volumes of the hippocampus and amygdala are smaller in patients with obsessive-compulsive personality disorder than in healthy controls, researchers found.

These findings lend support to the likelihood that obsessive-compulsive personality disorder “seems to be a neurocognitive function disorder rather than a personality disorder,” Mehmet Gurkan Gurok, of Firat University, Elazig, Turkey, and his associates reported in the Journal of Clinical Neuroscience.

The authors previously had investigated volumes of hippocampus and amygdala in patients with obsessive-compulsive disorder and found these patients had “increased white matter volumes, greater left and right thalamus volumes and significantly reduced left and right orbitofrontal cortex volumes, compared with healthy controls.”

For this study, they similarly used MRI to assess hippocampal and amygdalar volumes in 16 patients with obsessive-compulsive personality disorder (inpatients and outpatients at Firat University) and in 18 healthy controls – matched for age, sex, education, and handedness – who were studying at the hospital.

The researchers used the DSM-IV and the Structured Clinical Interview for the Diagnostic Schedule for Mental Disorders-Fourth Edition for diagnoses but noted later in their limitations that “the validity of diagnosis should be questioned” for personality disorders.

Participants were excluded if they had a comorbid Axis I psychiatric diagnosis besides depression, any contraindications for MRI, history of alcohol or substance dependence within the previous 6 months, use of psychoactive medications within 4 weeks of the study, or any current severe medical conditions. In addition, neither controls nor their first-degree relatives had a history of psychiatric disorders.

The findings showed that those with obsessive-compulsive personality disorder had smaller volumes on both sides of the hippocampus, compared with healthy controls. Amygdalar volume on both the left and right sides were similarly smaller in patients with obsessive-compulsive personality disorder, compared with healthy controls (left, P = .001; right, P = .002). The authors also reported they “did not find any correlation between hippocampus and amygdala volumes and any clinical and demographic variables.”

The research was funded by Firat University. The authors reported having no conflicts of interest.

SOURCE: Gurok MG et al. J Clin Neurosci. 2019 Apr 5. doi: 10.1016/j.jocn.2019.03.060.