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Obsessive-compulsive disorder (OCD) is characterized by repetitive thoughts, urges, and images (obsessions) and/or repetitive behaviors or mental acts aimed at reducing anxiety or distress (compulsions). OCD is thought to have a lifetime prevalence of between 1% to 3% and is a significant cause of disability worldwide.

 with other psychiatric disorders, which warrants consideration particularly in difficult to treat cases. First-line treatment options for OCD may include psychotherapeutic or pharmacological strategies. Specifically, selective serotonin reuptake inhibitors (SSRIs) and 

 (CBT), particularly exposure response therapy (ERP), have been shown to be effective in the treatment of OCD.

 However, many patients do not achieve a full response, often defined as a more than 35% reduction on the Yale-Brown Obsessive Compulsive Scale (Y-BOCS), with these treatment options.

It is important to take consideration of clinical features, access, and tolerability when choosing between these options. Monotherapy with CBT with ERP may be recommended in patients with mild or moderate OCD. While monotherapy with an SSRI is often recommended in patients with more severe OCD, or in history of treatment response to SSRIs or 

“Melissa” is a 40-year-old female in an outpatient clinic with a history of OCD. When she first presented to clinic, she was prescribed sertraline, to which the OCD did not respond. She was switched to fluvoxamine, which was titrated to the maximum tolerated dose of 300 mg a day with partial response. She was also encouraged to begin CBT with ERP and has been consistent with treatment.

Melissa continues to endorse OCD symptoms, recounting how she spends several hours “checking the locks on my doors,” which frequently makes her late to work and appointments. She did not tolerate clomipramine or augmenting trials of risperidone or aripiprazole and is reluctant to trial any additional medications or surgery. 

 (TMS), which was recently approved by the Food and Drug Administration (FDA) as an adjunct to OCD, may be considered in Melissa’s case.

An inadequate treatment response with monotherapy of SSRIs or 

 may warrant combining these modalities if available and tolerable.

 An important note about SSRI trials, is that prolonged trials (8 to 12 weeks) may be needed for optimal efficacy. A meta-analysis of dose-response also suggested that higher doses are associated with greater efficacy compared to low or moderate doses although this can also be associated with greater adverse side effects.

 Clinical guidelines suggest that certain cases may warrant consideration of greater than FDA max doses of medications. Interestingly, data suggest that a lower demethylation rate of clomipramine may be associated with greater clinical outcomes, which may warrant consideration and potential augmenting with an enzyme inhibitor if a patient fails to respond to clomipramine.

With a partial treatment response, augmenting with an antipsychotic is a common and evidence supported strategy, although only about a third of patients will respond.

 and aripiprazole have shown the greatest efficacy, and low doses (up to 3 mg a day of risperidone and up to 15 mg a day of 

 have also been used as augmenting agents, although evidence is limited and mixed.

 Haloperidol also has limited supportive evidence in OCD, although it is associated with poor tolerability.

Our understanding of the biological underpinnings of 

 continues to evolve, and molecular changes in glutamatergic signaling, immunological factors, as well as circuit-level dysfunction in the cortico-striato-thalamic-cortical (CSTC) tracts have been implicated in OCD. As a result, several novel options for treatment-resistant OCD are under investigation.

Glutamatergic dysfunction has been gaining evidence as playing a role in OCD, and numerous agents that modulate glutamatergic signaling are under investigation.

 One such agent is N-acetylcysteine (NAC), which effects the cystine-glutamate antiporter and can modulate glutamatergic neurotransmission. A recent systematic review and meta-analysis of 5 randomized controlled trials (RCTs) suggested that NAC administered in doses of 600 to 3000 mg a day is safe, although there are still questions regarding efficacy.

, which inhibits synaptic glutamate release and promotes uptake of glutamate by astrocytes has been investigated, with supportive results in early open-label studies and mixed results in subsequent controlled studies.

 Troriluzole, a precursor of riluzole, is now under investigation in treatment-resistant OCD. Augmenting with memantine (an N-methyl-D-aspartate receptor (NMDA-R) antagonist) has shown a benefit in open-label studies as well as subsequent RCTs.

—that has shown promise in the setting of treatment-resistant depression, has also been studied in OCD, with mixed results.

 Interestingly, there is some suggestion that CBT may enhance the effects of IV ketamine/intranasal esketamine.

 Lamotrigine and topiramate, both compounds capable of modulating glutamatergic signaling, have also been trialed as augmentation agents in OCD, although evidence is mixed.

Co-agonists of the NMDA receptor and related compounds have also been investigated. Glycine, an NMDA-R co-agonist, was shown to have a modest effect on OCD symptoms, although this did not reach statistical significance and glycine was poorly tolerated.

 Compounds related to glycine have also been investigated. Rapastinel, a partial agonist at the glycine site of the NMDA-R, showed an acute positive effect on OCD symptoms in an open label trial, although these dissipated 1 week postinfusion.

 Sarcosine, a glycine transporter antagonist, showed a benefit in some OCD patients in an open-label study.

 D-cycloserine, a partial agonist at the glycine site of the NMDA-R, has mixed data, but may play an augmenting role in ERP therapy for OCD.

Aberrant functioning of the immune system is thought to play a role in OCD. Specifically, autoimmune disorders have been associated with OCD in children and adults, and inflammatory markers have been found to be elevated in the brains of individuals with OCD compared to healthy controls.

 Given these observations, anti-inflammatory and immune modulating agents have been investigated as a possible treatment option in OCD with limited, but promising results. Celecoxib, a nonsteroidal anti-inflammatory drug, with a mechanism of cyclooxygenase-2 enzyme inhibition, has been trialed as an SSRI augmenting agent in 2 trials and demonstrated superiority to placebo.

 Minocycline, an antibiotic with anti-inflammatory and anti-glutamatergic properties, was shown to have a positive treatment effect when combined with 

 in a double-blind place-controlled study.

 Rituximab, an intravenously administered monoclonal antibody, is being tested in a study of treatment-resistant patients.

Interestingly, gut microbiota, which regulate and are involved in maintaining immune homeostasis, have also been found to be altered in adult OCD patients.

 This has led to investigation of probiotics, which may help normalize the gut microbiota as a possible treatment modality. Animal studies have shown that probiotics may confer a benefit in obsessive-compulsive-like behavior, while clinical trials in humans are still ongoing.

In recent years, there has been a focus on circuit-level brain changes in psychiatric disorders, and therapeutic modulation of these brain circuits. OCD has been associated with dysregulation in the CSTC loop, and noninvasive methods of stimulation, which can potentially alter these circuits, have been investigated as treatment options.

Repetitive transcranial magnetic stimulation

 (rTMS), which uses magnetic pulses to modulate neurocircuitry, has been investigated in OCD. A recent meta-analysis reported that active TMS of the dorsolateral prefrontal cortex as well as the supplementary motor area (SMA) was more effective than sham stimulation for OCD.

A specific method of TMS developed by BrainsWay known as 

, which uses an H-shaped coil capable of stimulating deeper brain structures than traditional rTMS, has also been studied targeting the anterior cingulate cortex and medial prefrontal cortex, and found to be superior to sham stimulation.

 This modality was the first TMS device to be FDA approved as an adjunct for the treatment of OCD. Since then, MagVenture has also demonstrated safety and efficacy of its coil in treating OCD when directed toward the bilateral dorsomedial prefrontal cortex, and has received FDA approval for its device as an adjunctive treatment for OCD.

New developments in TMS technology including theta burst stimulation (TBS), which may shorten the treatment time required for TMS, have also been trialed in OCD, although a randomized trial of continuous TBS for 2 weeks did not observe a significant improvement in symptoms with active stimulation versus sham.

 Another method of neurostimulation being investigated is transcranial direct current stimulation (tDCS), which involves placement of 2 electrodes on the scalp with application of weak electric current. tDCS in OCD has typically focused on targeting the SMA and orbitofrontal cortex, although results are mixed.

 (ECT), which induces a generalized seizure and has remarkable efficacy in depression, has had some response in a limited number of case studies of OCD, although there are no RCTs that support this finding.

 Magnetic seizure therapy, which uses magnetic pulses to induce generalized seizures and is thought to be associated with less cognitive impairment than ECT, has also been investigated in an open-label pilot study of subjects with treatment-resistant OCD, although it was not found to be effective.

For highly refractory patients, ablative neurosurgery and deep brain stimulation (DBS) can be considered, often in addition to ongoing pharmacological treatment and 

. Common ablative procedures and sites include anterior capsulotomy (anterior limb of internal capsule) and anterior cingulotomy (anterior cingulate gyrus and cingulum bundle).

 A systematic review of 10 studies reported a mean reduction in Y-BOCS of 57% for anterior capsulotomy and 37% for anterior cingulotomy, with adverse effects of 21.4% for capsulotomy and 5.2% for cingulotomy.

 DBS, which is a reversible alternative to ablative surgery, involves placement of implanted electrodes in the brain to directly stimulate target areas. DBS has been used in the setting of Parkinson’s disease, dystonia, and epilepsy, and received FDA approval for humanitarian use for refractory OCD in 2009.

In DBS trials for OCD, electrodes have often been implanted in the ventral capsule/ventral striatum, although other targets have included the subthalamic nucleus (STN) as well as the inferior thalamic peduncle.

 A recent systematic review of DBS for OCD reported approximately 60.6% of patients with a response of less than 35% reduction in Y-BOCS, at short-term (1.5 year) follow-up.

 Interestingly, the proportion of responders increased on longer-term (>5 year) follow-up to 70.7%. Adverse events are typically transient, although hemorrhage and infection are a small risk. While there have been no direct comparison trials of DBS versus ablative neurosurgery, a retrospective review of 20 studies found that patients undergoing capsulotomy had a greater reduction in Y-BOCS (51%) versus DBS of the VC/VS (40%) and were 9% more likely to go into remission (Y-BOCS <8).

The review also noted similar complication rates between procedures. There is yet insufficient evidence to determine which procedure (DBS versus ablative neurosurgery) to use on an individual basis.

 Beyond these procedures, novel developments such as focused ultrasound are under investigation and may provide safer surgical options in the future.

Beyond the aforementioned treatment options, novel medications with unique mechanisms of action are currently under investigation for OCD, including 

, nabilone, nitrous oxide, tolcapone, ondansetron, and pregabalin.

, exercise, and acupuncture are also being investigated.

 Further data on these novel treatment options are needed.

While definitions of treatment-resistance vary, lack of response to SSRIs and CBT warrant next steps. With nonresponse, a switch to another serotonergic agent may be indicated. With a partial response, there is strong evidence to support the use of 

 as augmenting agents in OCD. Beyond this, the understanding of the pathophysiology and novel treatment options for OCD are in development.

Numerous glutamatergic agents are under investigation, data here is mixed warranting of further investigation. Medications that modulate the immune system and inflammatory response are also being studied and show promising preliminary results. Neurostimulation modalities are also being developed, initial research is supportive of TMS, and recent FDA approval of TMS as an adjunct for OCD will likely lead to an increase of use in clinical practice. Invasive surgical options including DBS and ablative procedures remain an option for treatment refractory cases who have failed numerous treatment options. Finally, medications with novel mechanisms of action and complementary treatment modalities are under investigation in OCD.

is a psychiatrist affiliated with the Department of Psychiatry at the University of California San Diego.

is a professor and chair of the Department of Psychiatry at the University of California San Diego.

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OCD is highly comorbid and warrants consideration in difficult to treat cases. Learn more here. 

Treatment-Resistant OCD: Strategies and Novel Treatment Options 

Jade Wu, PhD, of Duke University School of Medicine, presented on the impact of sleep-wake disorders on mental health at the 2021 Neuroscience Education Institute Congress.

In “Counting Sheep: Improving the Recognition and Management of Insomnia,” she discussed the neurobiology of sleep and its importance; evidence-based strategies for improving the diagnosis of 

 such as insomnia; and how these strategies can be applied to help promote healthy sleep.

 for insomnia focused on encouraging behavioral changes (eg, controlling stimuli, maintaining a consistent sleep-wake schedule); cognitive changes (eg, challenging unhelpful thoughts, correcting misconceptions about sleep); and other practices such as self-monitoring and mindfulness. She also recommended common US FDA-approved pharmacological agents that are indicated specifically for insomnia, including estazolam, quazepam, eszopiclone, and zaleplon.

Improving recognition and management of insomnia is important because the problem is so widespread. According to Wu, about 5% to 15% of adults meet the diagnostic criteria for insomnia, but between 35% and 50% of adults have significant insomnia symptoms. In addition, individuals with insomnia are at increased risk of suicide, drug use, posttraumatic stress disorder, depression, anxiety, and other psychiatric disorders, and physical symptoms like pain may also be exacerbated in individuals with insomnia.

“When we improve insomnia symptoms, we’re also improving depression and anxiety,” Wu said during her presentation. “We’re reducing inflammation, and just across the board, we’re improving a lot of other psychiatric medical and quality-of-life outcomes like chronic pain, functioning, quality of life—you name it. So, in a way, treating insomnia is like raising the water for all boats.”

A board-certified behavioral sleep medication specialist and researcher at Duke University School of Medicine, Wu’s current research focus is the treatment of sleep disorders in individuals with chronic illness.

1. Wu JQ. Counting sheep: improving the recognition and management of insomnia. Presented at: 2021 Neuroscience Education Institute Congress; November 4, 2021; Colorado Springs, CO.

How can cognitive behavioral therapy improve outcomes for individuals with insomnia?

Counting Sheep

Judith S. Beck, PhD, is president of the Beck Institute for Cognitive Behavior Therapy (CBT) 

, a nonprofit organization that provides state-of-the-art training and CBT certification to individuals and organizations, offers online courses on a variety of CBT topics, conducts research, and serves as a leading global resource for CBT. She is also Clinical Professor of Psychology in Psychiatry at the University of Pennsylvania Perelman School of Medicine. Dr Beck has written over 100 articles and chapters as well as books, workbooks, and pamphlets for professionals and nonprofessionals, including 

Cognitive Behavior Therapy, Third Edition: Basics and Beyond

Cognitive Therapy for Challenging Problems: What to Do When the Basics Don’t Work

. She has made hundreds of presentations nationally and internationally on various applications of CBT and is the primary developer of the Beck Institute’s online CBT training courses, which have been taken by health and mental health professionals in over 130 countries. Dr Beck maintains a clinical caseload at the Beck Institute’s in-house clinic in suburban Philadelphia, helping clients who are experiencing a range of challenges.

: CBT has had its fair share of criticisms over the years, and I have heard that Aaron T. Beck, MD, frequently engaged with (and at times even collaborated with) his critics. Is it accurate to say that your father’s ideas were not initially accepted by the mental health field? Do you think there are meaningful ways in which the field of CBT has benefitted from this engagement with the critics?

 as it was initially called) was not accepted by the psychoanalytic community, though my father’s ideas were favorably viewed among some psychologists, especially behavior therapists. He had originally trained as a psychoanalyst and then recognized that the theoretical constructs of psychoanalysis needed to be validated by research if psychoanalysis was to be accepted by other scientific fields.

At the time, he fully expected that his research would support the basic psychoanalytic tenets of depression. But he found the opposite. Most psychoanalysts rejected this research and later his development of cognitive therapy. More than a decade later, he found he was unable to get his first randomized controlled trial comparing imipramine with cognitive therapy for the treatment of depression published in journals. Initially he was also criticized by some behavior therapists but praised by others who integrated cognitive techniques into treatment. Throughout the years, my father has used valid criticism to refine his theories and treatment. For example, he has added a focus on processes as key agents of change. Depending on the cognitive formulation of the problem or disorder, and the individualized conceptualization of the disorder, he has supported including techniques from other evidence-based treatments. CBT has benefitted from legitimate criticism, and treatment has become more effective because of it.

: There appears to be considerable debate regarding manualized therapy in real-world clinical practice outside of research. Manuals have an understandable role to play in research settings, but to what extent should manuals constrain clinical practice? I might add here that during my own psychiatry residency training, I was taught CBT by a wonderful psychologist who emphasized basic principles of CBT and stressed the importance of developing an individualized CBT formulation to guide treatment, and I sometimes wonder how different that experience would have been if he had relied on manuals instead.

: There are various forms of CBT and to be clear, what I am talking about is the type of CBT developed by my father in the 1960s and 1970s (and refined ever since). At the Beck Institute, we do not use manuals in treatment, and we do not usually endorse the use of manuals outside of research settings. As you mentioned, manuals have a place in clinical trials to ensure that protocol therapists are delivering the same treatment to research subjects. Without manuals, the strong evidence base for CBT would not exist. But in real world settings, patients are complex. For example: they frequently have comorbidities and differ in individual characteristics such as culture, education, developmental level, socioeconomic status, and so on. Good CBT therapists tailor treatment to each individual patient, guided by their cognitive conceptualization, the patient’s presenting problems, strengths, aspirations, and goals for treatment. The treatment plan is developed, and the therapeutic interventions are selected in collaboration with the patient.

: Should CBT in clinical practice be restricted at the outset to a certain number of sessions (say 10-20 sessions) the way it is done in research settings? Or is CBT in clinical practice intended to be more open-ended and goal-dependent? My clinical observation is that when duration of CBT is not individualized and when the number of sessions is capped beforehand (often due to insurance restrictions or administrative reasons), a substantial number of patients are forced to end therapy without having experienced meaningful improvement.

: CBT in clinical practice should not be limited to a certain number of sessions. Many patients with straightforward cases of depression or anxiety can experience significant improvement within 6 to 12 sessions. However, patients with personality disorders, medical conditions, trauma histories, environmental stressors, and other complex conditions usually need a longer course of treatment. Of course, in practice, not all patients are able to complete a longer course of therapy due to monetary or practical constraints.

It is important that therapists understand and make every effort to work within these constraints, by being transparent with patients about their progress and making therapy as efficient as possible. We tell all our patients that it is not enough to come to therapy and talk for 50 minutes a week. The way they get better is to make small changes in their thinking and behavior every day. When therapists and patients finish discussing a problem or goal, therapists ask patients what they want to remember and what they want to do in the coming week. Then therapists motivate them to complete these Action Plans (formerly termed 

) between sessions to maximize the benefits of CBT and prevent relapse without prolonging treatment. Booster sessions, appropriately spaced in the weeks and months following the conclusion of treatment, are an effective way to ensure patient progress is maintained and that patients continue to practice their skills, and cope with new challenges that arise.

: Since the initial development of CBT for depression, we have seen the development of CBTs for a multitude of indications and special populations. Where has CBT been successfully applied over the decades?

: This question has been answered by research. Hofmann and colleagues did a review of meta-analyses a few years ago.

 They found that CBT has been most successfully applied to anxiety disorders, somatoform disorders, bulimia, anger control problems, and general stress. They also noted the efficacy of CBT in the treatment of depression, substance abuse, psychotic disorders, bipolar disorder, insomnia, personality disorders, criminal behaviors, and distress related to medical conditions. While most studies focus on adults, other studies show similar results for children and older adults. In addition, research has established the efficacy of appropriately tailored CBT in a multitude of settings: schools, residential programs, inpatient units, long-term psychiatric hospitals, forensic settings, community-based settings, and primary care and specialty medical clinics, to name a few.

: CBT for psychosis (CBTp) has emerged as a standard recommended treatment for schizophrenia in clinical practice guidelines such as by the National Institute for Health and Care Excellence in the United Kingdom and the American Psychiatric Association in the United States. Despite these recommendations, the availability of and access to CBTp remains limited. What are some of the difficulties that specialized interventions such as CBTp face with regards to dissemination, and what can be done about it?

: One challenge with the dissemination of specialized treatment, perhaps especially one like CBTp, is the lack of availability of individual therapy within different treatment services. While those who are especially help-seeking or those who have the support of family or other loved ones may be able to access a private practice provider, there are many individuals who cannot. In state hospitals, on community teams, in the forensic system, in residences—this is where you see many individuals who are given serious mental health diagnoses. These services often do not have the resources to offer individual therapy. Even if they did, a portion of the individuals are not help-seeking or not interested in a treatment focused on symptoms they do not see as obvious problems.

My understanding is, that as currently practiced, CBTp is primarily conducted by licensed clinicians, the vast majority of whom are psychologists. In the community and hospital settings where most care is delivered, there are many staff from other disciplines where CBTp training is not offered (social workers, licensed counselors, recreational and art therapists, occupational therapists), not to mention nonlicensed and paraprofessional staff such as direct care and peer specialists whose scope of practice does not include CBTp.

How can cognitive behavioral therapy be adapted to different cultures and address larger social issues?

Cognitive Behavioral Therapy

Treatment-Resistant OCD: Strategies and Novel Treatment Options

Counting Sheep

The Past, Present, and Future of Cognitive Behavioral Therapy: Q&A with Judith S. Beck, PhD

DTx and Cognitive Behavioral Therapy: Opportunities, Benefits, and Challenges of an Evolving Landscape

The Trauma-Focused CBT and Family Acceptance Project: An Integrated Framework for Children and Youth

Applying CBT to Psychiatry

Research Sheds Light on Two Types of Treatment for ADHD

Reducing Suicide Risk: The Role of Psychotherapy

The Quiz: Cognitive-Behavioral Therapy and Chronic Pain

Psychotherapeutic Interventions for Depression: Which Work Best?