Obsessive-Compulsive Disorder

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Continuing Education Activity

Obsessive-Compulsive Disorder (OCD) is a prevalent psychiatric disorder affecting 1% to 3% of the global population, characterized by intrusive thoughts, known as obsessions, and repetitive actions, or compulsions. These symptoms affect patients not only by consuming a significant portion of their time but also by causing marked distress and functional impairment. The complex etiology of OCD involves cognitive, genetic, and neural factors, making the condition's diagnosis challenging and necessitating the exclusion of other psychiatric conditions that present similarly. Further complicating matters, OCD frequently coexists with other psychiatric disorders, requiring comprehensive identification and treatment for optimal clinical outcomes. While the combination of medication and psychotherapy is generally effective, emerging evidence supports using neuromodulation techniques (eg, deep brain stimulation and transcranial magnetic stimulation) for treatment-resistant cases.

This activity reviews the epidemiology, etiology, clinical presentation, and management of OCD, providing healthcare professionals with the knowledge and tools to improve patient care for this complex and prevalent condition. Emphasizing the importance of prompt recognition for timely diagnosis and intervention, the activity presents evaluation strategies and offers guidelines for differentiating OCD from similar psychiatric disorders. Varying etiologies, clinical presentations, and prognostic factors pertinent to OCD are also reviewed. By participating in this transformative activity, healthcare professionals will augment their clinical expertise and enhance their collaborative capacities, significantly improving patient care in OCD management.


  • Identify the criteria utilized to diagnose a patient with obsessive-compulsive disorder.

  • Implement evidence-based treatment plans for patients with obsessive-compulsive disorder.

  • Assess the diverse etiological factors contributing to obsessive-compulsive disorder.

  • Implement interprofessional team strategies for improving care coordination and communication to improve outcomes for patients with obsessive-compulsive disorder.


Obsessive-compulsive disorder (OCD) is a disabling condition estimated to affect 1% to 3% of individuals throughout their lifetime.[1][2] This psychiatric disorder is characterized by obsessions and compulsions, which consume a significant amount of time and lead to notable distress and impairment. Obsessions refer to intrusive and repetitive thoughts, urges, or mental images that are challenging to control. These thoughts often lack a clear purpose and are accompanied by distress.[3] Compulsions involve repetitive actions or mental events that individuals with OCD feel compelled to perform to alleviate the distress caused by the obsessions or to prevent a feared consequence from occurring.[3] Additionally, individuals with OCD may also engage in avoidance behaviors of obsession-triggering situations.[2]

OCD is a heterogeneous condition that arises from a complex interplay of genetic and environmental risk factors.[4] Most adults are distressed by the ego-dystonic nature of their obsessions and are aware that their compulsive behaviors are abnormally excessive. Children often have difficulty describing their obsessions. In OCD patients, common obsessions and their associated compulsive behaviors include fear of contamination leading to excessive cleaning, fear of harm linked to repetitive checking of security measures, intrusive, aggressive, or sexual thoughts paired with mental rituals, and a focus on symmetry accompanied by ordering or counting.[5][6] Though hoarding behaviors are usually specific to hoarding disorder, they can occur in OCD to prevent perceived harm. These behavior sets are consistently observed worldwide, suggesting a degree of commonality in OCD symptom dimensions. OCD can also present with rarer symptoms, including scrupulosity, obsessive jealousy, and musical obsessions.[7][8][3]

The understanding of OCD has evolved significantly over time. Historically framed in religious terms as a moral failing or demonic possession, OCD was first medically described by Esquirol. Freud subsequently characterized the condition using the term obsessive neurosis, positing that OCD originated with a regression in the anal phase of psychosexual development.[9] In the third edition of the Diagnostic and Statistical Manual (DSM-III), OCD was grouped with phobias under a single diagnosis. Later, the DSM-IV classified the condition as an anxiety disorder. The DSM-5 has reclassified OCD into the category "Obsessive-Compulsive and Related Disorders," alongside conditions like hoarding and body dysmorphia. This reclassification acknowledges shared characteristics, such as phenomenology, comorbidity, and underlying neurobiological factors.[10] WHO lists OCD as 1 of the 10 most disabling conditions caused by financial loss and decreased quality of life.[11] In The Diagnostic and Statistical Manual of Mental Disorders fifth edition Text Revision (DSM-5 TR), which was published by the American Psychiatric Association (APA) in 2022, OCD sits under the category of obsessive-compulsive and related disorders where the following subcategories were placed:[3]

  • OCD
  • Body dysmorphic disorder (BDD)
  • Hoarding disorder
  • Trichotillomania
  • Excoriation (ie, skin-picking) disorder
  • Substance or medication-induced obsessive-compulsive and related disorder
  • Obsessive-compulsive and related disorder as a result of another medical condition
  • Other specified obsessive-compulsive and related disorder
  • Unspecified obsessive-compulsive and related disorder

The diagnosis of OCD is based on clinical assessment determining whether the DSM-5 TR criteria are met, which specify that either obsessions or compulsions must be present, the behaviors must be time-consuming, taking ≥1 hour per day, and significantly disrupting daily life.[3] (Refer to the History and Physical Examination section for more information on the diagnostic criteria for OCD). 


The etiology of OCD is complex, encompassing diverse factors, including cognitive, genetic, molecular, environmental, and neural elements. Evidence from twin studies points to a significant genetic predisposition with an estimated heritability quotient of approximately 48%.[12][13] However, this estimate is reduced to 35% when maternal effects (eg, prenatal exposure to stress or infection) are considered.[14] However, despite significant efforts through candidate gene association studies, reproducible genetic markers for OCD remain elusive. Many of these studies have focused on neurotransmitter pathways involving serotonin, dopamine, and glutamate without definitive results.[12] Nevertheless, the gene SLC1A1, responsible for encoding the neuronal glutamate transporter EAAT3, has surfaced as a potentially significant candidate.[15][12]

Recent studies point towards OCD being fundamentally a network-based disorder.[16] The cortico-striato-thalamo-cortical (CSTC) loop has become a pivotal framework for understanding its pathophysiology.[16] The CSTC loop involves a series of interconnected circuits that allow the prefrontal cortex to communicate with subcortical structures (eg, the striatum and the thalamus). This loop has 2 distinct pathways: the direct and the indirect. The direct pathway facilitates behavior initiation, whereas the indirect pathway inhibits or modulates these behaviors.[17] In OCD, hyperactivity in the direct pathway relative to the indirect pathway has been observed. This creates an imbalance that may cause repetitive, intrusive thoughts and compulsive actions.[13][18] Recent neuroimaging studies indicate heightened connectivity and activation within the CSTC loop in OCD.[13] Furthermore, OCD may occur with other neurological conditions that impact the CSTC circuitry, including Parkinson disease, Sydenham chorea, traumatic brain injury, Tourette syndrome, Huntington disease, and epilepsy.[19][20] 

Early findings of the effectiveness of clomipramine, which has robust serotonin reuptake inhibition observed during treatment, emphasized the role of serotonin in the pathogenesis of OCD.[13] However, this serotonin-centric model has faced scrutiny because other serotonin-modulating agents like buspirone and ondansetron have not proven effective in OCD.[21][22] Emerging studies point towards the glutaminergic system in the onset and progression of OCD.[13] Pharmacological agents like riluzole and troriluzole, which affect glutaminergic neurotransmission, have shown preliminary benefits.[23][24] The efficacy of antipsychotic drugs when used for augmentation in OCD suggests dopamine's role in OCD pathology.[25][13] Imaging studies corroborate this by demonstrating increased dopamine concentrations in the basal ganglia of patients with OCD. Moreover, dopamine agonists can induce OCD-like behaviors in both animals and humans. Interestingly, enhancing cortical dopamine has also shown promise in alleviating OCD symptoms.[26] However, the findings are preliminary and lack direct evidence.

The autoimmune etiology provides another intriguing dimension to OCD, particularly in Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal Infections (PANDAS) and Pediatric Acute-onset Neuropsychiatric Syndrome (PANS).[27] PANDAS is regarded as a subset of PANS. Unlike OCD, the onset of PANDAS and PANS is often sudden and severe, accompanied by additional symptoms, including handwriting deterioration, emotional lability, and episodic disease courses. These conditions are mediated by autoimmune responses triggered by infection, inflammatory reactions, or other toxins and have parallels with other autoimmune neuropsychiatric disorders (eg, Sydenham chorea).[27] Preliminary research indicates that striatal cholinergic interneurons may be the cellular targets of these autoimmune responses.[28] 

Cognitive and learning-based models of OCD posit that maladaptive beliefs fuel obsessional anxiety, leading to compulsive behaviors aimed at mitigating such anxiety.[25] Several cognitive impairments have been identified as contributing to obsessional anxiety, including:

  • Heightened responsibility
  • Overemphasis on thoughts
  • Controlling thoughts
  • Threat overestimation
  • Perfectionism
  • Intolerance of uncertainty

Empirical evidence supports the effectiveness of these models; exposure to obsession-linked stimuli increases anxiety while engaging in compulsive rituals lowers it.[25] Additionally, the learning-based model argues that the underlying learning mechanisms are not inherently pathological. This aligns with the observation that nonclinical populations also experience obsessive-like thoughts without distress. These models have been instrumental in developing psychological therapies for OCD, substantiating their theoretical and practical utility.[29][25]


OCD is a leading cause of psychiatric morbidity worldwide, affecting 1% to 3% of the population. Frequently, OCD is associated with comorbid psychiatric conditions.[3][13][25][30] OCD often has onset early in life and generally has a chronic cause. The most common demographic range affected is from ages 18 to 29 years.[3] Interestingly, nearly a quarter of males display symptoms before age 10, whereas the disorder usually emerges during adolescence for females.[3] Additionally, the peripartum and postpartum phases are marked as periods of increased risk for women, with OCD incidence during these times exceeding that in nonpregnant females.[31] Women are also about 1.6 times as likely as men to be affected by the disorder.[32]

A striking 90% of individuals with OCD meet the criteria for at least one additional psychiatric disorder, with anxiety disorders, mood disorders, impulse-control disorders, and substance use disorders being the most prevalent comorbid conditions.[3] Despite the disorder's significant impact, OCD frequently remains both underdiagnosed and undertreated, with only a small fraction of patients receiving appropriate medical care.[3][33]


While OCD is generally considered to stem from a mix of several etiological factors, some instances can be linked explicitly to neurological causes involving the basal ganglia.[12] Detailed evidence supports this from case reports associated with conditions such as Sydenham's chorea and ischemic events. These conditions result in disruptions to basal ganglia regions like the globus pallidus and caudate, leading to obsessive-compulsive behaviors.[13] In research conducted by the Enhancing Neuro Imaging Genetics through Meta-Analysis (ENIGMA) consortium, no marked structural brain differences were discerned between patients with OCD and healthy controls unless factoring in medication status.[34] Postmortem studies, albeit limited, have revealed abnormalities in the orbitofrontal cortex of patients with OCD.[35] Specifically, one such study found evidence for lower excitatory synaptic gene expression in the orbitofrontal cortex of subjects (N=8) when compared with unaffected controls.[35] These studies, however, have limitations, including small sample sizes.

History and Physical

The diagnosis of OCD is based on clinical assessment determining whether the DSM-5 TR criteria are met, which specify that either obsessions or compulsions must be present, the behaviors must be time-consuming, taking ≥1 hour per day, and significantly disrupting daily life.[3]

Obsessive-Compulsive Disorder Diagnostic Criteria

In DSM-5 TR, the diagnosis of OCD was based on the following criteria.

  • The presence of obsessions, compulsions, or both which meet the following definitions:[3]
    • Obsessions
      • Recurrent and persistent thoughts, urges, or images that are experienced at some time during the disturbance are intrusive and unwanted and, in most individuals, cause marked anxiety or distress.
      • The individual attempts to suppress such thoughts, urges, or images with some other thought or action (ie, by replacing them with a compulsion).
    • Compulsions
      • Repetitive behaviors or mental acts that the person feels driven to perform in response to an obsession or according to rules that must be applied rigidly.
      • The behaviors or mental acts aim at reducing anxiety or distress or preventing some dreaded situation; however, these behaviors or mental actions do not connect realistically with what they are designed to or are excessive.
  • The obsessions are time-consuming or cause clinically significant distress or impairment in social, occupational, or other critical functional areas.
  • Obsessive-compulsive symptoms do not arise from the physiological effects of a substance (eg, a drug of abuse, a medication) or another medical condition.
  • The symptoms of another mental disorder do not better explain the disturbance. Differential diagnoses should be considered before an OCD diagnosis is made. (Refer to the Differential Diagnoses section for more information on conditions with clinical features similar to OCD.) These symptoms should not be attributable to other psychiatric or medical disorders. The belief that obsessions lead to compulsions is common; however, the relationship between the conditions is not always straightforward. Theoretically, obsessions and compulsions can occur independently of each other. Patients with OCD typically seek outpatient care and often possess insight into their condition, although exceptions exist in children or severe cases. These individuals usually experience distress due to the ego-dystonic nature of their symptoms.

Clinical Assessment

A thorough medical history and mental status examination are vital in diagnosing the condition, differentiating OCD from other disorders, gauging prognosis, and devising a treatment plan. During the assessment, determining whether the patient is grappling with obsessions, compulsions, or both is critical. Symptoms should also be categorized into the following specific dimensions.

  • Contamination: cleanliness obsessions and cleaning compulsions
  • Harmful thoughts: fears of causing harm and compulsive checking
  • Forbidden thoughts: aggressive, sexual, or religious obsessions with corresponding mental rituals; often suggest a worse prognosis.[3] 
  • Symmetry: compulsions (eg, repeating, ordering, and counting) [3][25] 

Safety assessments are also conducted to look for immediate risks to the patient or others. Screening for comorbid conditions, including depression, bipolar disorder, and other anxiety disorders, should be performed, and the patient's past psychiatric and general medical history should be reviewed. All medications, supplements, and known allergies or sensitivities should be obtained also. Furthermore, clinicians should gather pertinent information on the patient's psychosocial background, including familial relationships, stressors, and educational history. A family history focusing on OCD and other psychiatric conditions is also obtained to provide a holistic view of the patient's health.

Additionally, OCP may have specific nuances in its presentation, such as with postpartum OCD, with which clinicians should be familiar. For instance, some new mothers may experience distressing, obsessive thoughts about harming their baby and may be reluctant to disclose these for fear of judgment or consequences. In such sensitive cases, building rapport and ensuring a confidential and nonjudgmental setting for disclosure becomes paramount. However, the clinician must vigilantly assess the safety of the patient and the child. An individualized treatment plan for each patient should be created using a comprehensive approach.

Mental Status Examination

The mental status examination (MSE) for patients with OCD may differ depending upon the severity of symptoms, specific manifestations of the disorder, and any coexisting conditions. The following are some MSE findings that are common during the clinical assessment.

  • Appearance and behavior: Patients generally present as well-groomed but exhibit visible anxiety. Manifestations of OCD, such as frequent hand-washing, checking behaviors, or rearrangement of objects, are often observed during the interview and serve as a diagnostic indicator.
  • Psychomotor activity: Individuals are observed engaging in repetitive actions (eg, tapping, checking, or constantly washing their hands). These behaviors are compulsively performed, even when causing visible distress to the patient.
  • Speech: While articulation is generally coherent and goal-oriented, intrusive thoughts may periodically disrupt the flow of speech. Depending on the individual, these thoughts may or may not be vocalized during the examination.
  • Mood and affect: Patients usually report feelings of anxiety or distress, and their emotional expression (ie, affect) appears consistent with these reported experiences, often displaying heightened signs of stress.
  • Thought content: Obsessive thoughts differ among patients but commonly revolve around themes like contamination, harm to oneself or others, a quest for symmetry, or distressing sexual or religious beliefs. Compulsions to counteract these obsessions are frequently reported.
  • Thought process: Generally linear and coherent, intrusive, obsessive thoughts intermittently interrupt the thought process. Patients usually acknowledge these thoughts as irrational yet find themselves compelled to respond with corresponding compulsions.
  • Perceptual abnormalities: Unlike some other psychiatric disorders, hallucinations or illusions are seldom observed in OCD patients.
  • Cognition: Patients typically remain alert and oriented to time, place, and person. Overall cognitive function is usually preserved, although sometimes compromised by the pervasive nature of the obsessive thoughts.
  • Insight and judgment: A significant feature in most OCD cases is the preservation of insight. Patients often recognize the irrational nature of their obsessions and compulsions but report feeling powerless to control them. Judgment may specifically falter when resisting the urge to perform compulsive behaviors.


Screening for the correct symptoms of OCD is essential. A common tool is the short OCD screener. At 6 questions long and a sensitivity of 97%, this screening modality is a simple and effective way to identify patients with symptoms of OCD.[36] However, the most widely accepted tool to screen for OCD is the Yale-Brown Obsessive-Compulsive Scale (Y-BOCS).[37] The Y-BOCS rates on a scale from 0 to 40, with 40 indicating the most severe symptomatology.[38] This scale requires the patient to rank the following based on severity:[38] 

  • Time occupied by obsessive thoughts and compulsions
  • Interference of obsessive thoughts
  • Distress of obsessive thoughts
  • Resistance against obsessions
  • Degree of control over obsessive thoughts
  • Time occupied by compulsive behavior
  • Interference of compulsive behavior
  • Distress associated with compulsive behavior
  • Resistance against compulsive behavior
  • Degree of control over compulsive behaviors

Treatment / Management


Cognitive-behavioral therapy (CBT) is an evidence-based psychotherapeutic intervention for OCD.[39][40] Within the framework of CBT, exposure and response prevention (ERP) emerges as the most empirically substantiated behavioral technique. ERP entails subjecting patients to stimuli that provoke anxiety while guiding them to abstain from subsequent compulsive behaviors.[41] Various delivery modalities, including individual and group settings, as well as in-person and internet-based formats, have proven effective in treating OCD.[41]

A key determinant of therapeutic efficacy is the patient’s adherence to at-home assignments, most notably those involving home-based ERP exercises. CBT serves as a first-line treatment for OCD, especially when this technique aligns with the patient’s treatment preferences, access to qualified clinicians is available, and no compelling comorbid conditions necessitate pharmacotherapy. Although meta-analyses suggest that CBT often outperforms pharmacological interventions, such conclusions should be drawn cautiously, taking into account variables such as patient selection criteria and baseline severity of OCD symptoms.[3] Emerging research indicates that intensive CBT protocols, often condensed into a brief period and occasionally administered in an inpatient context, hold promise for both initial and advanced treatment of severe OCD cases.[42]


Selective serotonin reuptake inhibitors (SSRIs) are recommended as the first-line medications due to their proven efficacy, safety, and tolerability.[43] Higher dosages than those used for other anxiety disorders or major depressive disorder are typically prescribed, improving effectiveness but increasing the risk of adverse effects such as gastrointestinal and sexual complications.[44] Therefore, careful assessment of side effects is critical for individual dosage optimization. Uniform effect sizes of commonly used SSRIs have been observed in systematic reviews, yet each SSRI has its adverse effect profile.[45].

Selection criteria of SSRIs for OCD include prior treatment response, adverse event potential, drug interactions, coexisting medical conditions, and cost and availability of the drug.[3] Treatment guidelines recommend an 8- to 12-week SSRI trial to determine efficacy. However, recent meta-analyses show significant symptom improvement within the first 2 weeks of SSRI treatment.[46][47]. An open-label fluoxetine study indicated that early symptom reduction within 4 weeks predicted 12-week treatment success.[48] Maintenance treatment is generally advised for at least 12 to 24 months postremission, but longer durations may be needed due to relapse risk upon medication discontinuation.[49]

Clomipramine, a tricyclic antidepressant (TCA), was the first drug to show efficacy in treating OCD. Meta-analyses suggest its higher efficacy compared to SSRIs, but this finding requires caution as early clomipramine studies included fewer treatment-resistant patients. Direct comparisons indicate equivalent efficacy between clomipramine and SSRIs. SSRIs are preferred for long-term treatment due to their superior safety profiles and tolerability than other antidepressants.[3] 

Approximately half of patients with OCD fail to respond to first-line treatments.[50] Factors predicting poor response include higher symptom severity, marked functional impairments, specific obsession and compulsion subtypes (eg, sexual, religious, and hoarding), limited insight, high comorbidity rates, and lack of adherence to treatment protocols.[3] Combinatorial strategies involving CBT and SSRIs can be effective for those demonstrating poor response.[3] However, CBT is frequently constrained by availability or patient intolerance to exposure techniques.

Alternative approaches include switching SSRIs, using supratherapeutic doses, or switching to serotonin-noradrenaline reuptake inhibitors.[3] SSRIs may also be augmented with antipsychotics, tricyclic antidepressants (eg, clomipramine), or glutamatergic agents.[51][52][3] The combination of fluoxetine and clomipramine outperforms fluoxetine with an antipsychotic. However, the fluoxetine and clomipramine combination carries the risk of elevated blood levels of both drugs, leading to potentially severe adverse events (eg, seizures, cardiac arrhythmias, and serotonergic syndrome).[53] Augmentation with antipsychotics, especially risperidone and aripiprazole, shows some evidence of efficacy; however, only one-third of SSRI-resistant patients experience clinically meaningful improvements, warranting meticulous risk-benefit evaluations.[51] Glutamatergic system modulators (eg, memantine, N-acetylcysteine, lamotrigine, topiramate, riluzole, troriluzole, and ketamine) have been explored as augmentation therapies and have shown some promise.[3] Among these, N-acetylcysteine has the most substantial amount of evidence.[54]


In addition to the established treatment options such as Exposure and Response Prevention (ERP), Serotonin Reuptake Inhibitors (SRIs), and antipsychotic augmentation of SRIs, there exists a limited array of other evidence-based alternatives. Nonetheless, several treatment modalities have shown promise for cases refractory to standard interventions.

  • Transcranial magnetic stimulation: Studies employing repetitive transcranial magnetic stimulation (rTMS) targeted at various brain regions (eg, the dorsolateral prefrontal cortex [dlPFC], dorsomedial prefrontal cortex [dmPFC], and orbitofrontal cortex [OFC]) have yielded mixed outcomes. However, these studies generally support the idea of cortico-striatal hyperactivity as an underlying factor in OCD.[55] Deep transcranial magnetic stimulation (dTMS), which utilizes an H-shaped coil, can reach depths of 3 to 5 cm, targeting midline structures such as the medial prefrontal cortex (mPFC) and anterior cingulate cortex (ACC). These areas are believed to be hyperactive in OCD.[56] Significantly, dTMS has gained US Food and Drug Administration (FDA) approval for the treatment of OCD.[57]
  • Stereotactic ablation: The introduction of the stereotaxic frame during the last century significantly improved the accuracy of lesion-based treatments for persistent psychiatric disorders. Dorsal anterior cingulotomy and anterior capsulotomy are the most commonly employed ablation methods. The former disrupts the cingulum bundle to sever communication among essential limbic regions, while the latter isolates the anterior limb of the internal capsule to disconnect the OFC and dACC.[58]. Both interventions are designed to regulate hyperactive CSTC circuits, which are believed to underlie OCD.[59] Cingulotomy has shown 41%, whereas capsulotomy had a 54% effectiveness rate.[58] 
  • Deep brain stimulation: Deep brain stimulation (DBS) is a reversible, adjustable treatment for intractable OCD with response rates between 40% and 70%, involving the neurosurgical implantation of an electrode that can activate neighboring neural circuitry.[60][13] DBS targets the anterior limb of the internal capsule and the ventral striatum (VS). Regulatory endorsements exist, but adoption is limited by cost and required expertise.[13] Electrode placement remains under debate, focusing on deep gray matter structures (eg, VS or nucleus accumbens [NAc], anterior limb of the internal capsule, and subthalamic nucleus [STN]) or white matter pathways connecting the prefrontal cortex to the thalamus.[61] Emerging research challenges the notion of high-frequency DBS as “functional ablation,” pointing to complex therapeutic mechanisms.[13] DBS modulates activity in brain regions linked to OCD, and the degree of modulation correlates with symptom improvement. Different DBS targets may yield specific benefits; ventral capsule (VC) and VS targeting improve comorbid depression, while STN targeting improves cognitive flexibility.[62] Future DBS targeting may be individualized based on clinical or neurobiological measures.[13] 

Differential Diagnosis

OCD has symptoms similar to several other psychiatric conditions. Differentiating OCD from these conditions is essential for accurate diagnosis and effective treatment planning, as part of the criteria for OCD diagnosis involves ensuring that the symptoms of another mental disorder do not better explain the disturbance. However, OCD may also occur along with other psychiatric disorders, which can complicate clinical diagnosis. The following are some commonly considered differential diagnoses and the features that can separate from OCD:[3]

  • Generalized Anxiety Disorders: OCD involves irrational or odd obsessions, distinct from real-life worries found in generalized anxiety disorder. Compulsions are typically present in OCD but not in anxiety disorders.
  • Specific Phobia: Unlike OCD, fears in specific phobia are circumscribed to particular objects or situations and don't involve rituals or compulsions.
  • Social Anxiety Disorder: Fears with this condition are related to social interactions, and avoidant behaviors are aimed at reducing social fears rather than neutralizing obsessions.
  • Major Depressive Disorder: Ruminative thoughts in major depressive disorder (MDD) are mood-congruent and not linked to compulsive behaviors, unlike the intrusive obsessions in OCD.
  • Body Dysmorphic Disorder: This condition involves obsessions and compulsions related only to physical appearance.
  • Trichotillomania: Compulsive hair-pulling without the presence of obsessions differentiates trichotillomania from OCD.
  • Hoarding Disorder: Difficulty in discarding possessions characterizes hoarding disorder; if hoarding is driven by OCD-like obsessions, an OCD diagnosis is given instead.
  • Eating Disorders: Unlike OCD, the focus of obsessions and compulsions in disorders like anorexia nervosa is on weight and food. Ritualized eating behaviors are associated with eating disorders.
  • Tic Disorders: Tics and stereotyped movements are generally less complex than compulsions and are not aimed at neutralizing obsessions. A dual diagnosis may be warranted for overlapping symptoms.
  • Psychotic Disorders: Although some OCD patients may have poor insight or delusional beliefs, they do not exhibit other psychotic symptoms like hallucinations.
  • Obsessive-compulsive personality disorder: OCD is characterized by intrusive, distressing obsessions and compulsions aimed at alleviating this distress, with individuals often recognizing their symptoms as excessive. In contrast, obsessive-compulsive personality disorder (OCPD) involves a chronic pattern of perfectionism and rigid control, without the presence of obsessions or compulsions, and is often perceived by the individual as rational and desirable.


OCD is a chronic condition characterized by fluctuating periods of symptom exacerbation and remission. Due to this disorder, daily functioning is significantly impaired. Furthermore, OCD is associated with an elevated risk of mortality.[13][63] Despite the utilization of CBT and SSRIs, a substantial proportion of patients remain unresponsive. Specifically, between 25% and 40% of patients do not experience symptom alleviation when treated with either CBT or SSRIs.[39][13] Furthermore, only a minority achieve full remission, and approximately half of successfully treated patients continue to manifest residual symptoms.

OCD associated with hoarding symptoms generally results in a more unfavorable prognosis. Clinical data from DSM-IV field trials involving 431 patients revealed that the fear of harm was the most commonly reported obsessive symptom. A significant association between OCD and suicidal tendencies has been confirmed, with contributory factors including coexisting anxiety and depression, as well as a history of suicide attempts.[64] Additionally, the association between OCD and suicidal tendencies remains significant even when controlling for depressive symptoms or mood instability.[65]


OCD is included in the top 10 disabling disorders by the WHO. Patients with OCD tend to avoid situations that make them uncomfortable, which may lead to decreased social interactions and a poor quality of life. Most who struggle with OCD go undetected for years. If OCD goes untreated, the pattern is harder to break as structural changes to the brain take place.[66][67] Duration of untreated OCD is associated with worse clinical outcomes.[68] Early intervention is vital.


Utilizing cognitive behavioral therapy (CBT) with a focus on exposure and response prevention is the cornerstone of nonpharmacological treatment for OCD. Therefore, seeking consultation with a highly skilled and experienced therapist in administering this specialized form of therapy is crucial. Medical consultations may vary depending on the severity and specific nature of the compulsions exhibited. For instance, if a patient engages in excessive hand-washing, dermatological issues like dermatitis may arise, necessitating consultation with a dermatologist. Comprehensive treatment should address the patient holistically, encompassing psychological symptoms and any resulting medical conditions. Coordination of care with other healthcare clinicians (eg, pediatrics or family medicine) is also vital, especially for monitoring potential side effects of medications, including weight gain and tics.

Deterrence and Patient Education

In OCD, the patient's insight is not lacking. Only 2% to 4% lack insight into their OCD.[69] However, most people do not seek treatment until the disorder has become severely advanced. As most symptoms present during adolescence, clinicians should inform and educate appropriate individuals, including parents, fellow medical personnel, and those in the school systems, about this disorder.

Enhancing Healthcare Team Outcomes

Managing OCD requires an integrated, interprofessional healthcare team to offer patient-focused care, optimize treatment outcomes, ensure patient safety, and maximize team efficiency. The team comprises primary care physicians, psychiatrists, clinical psychologists, occupational therapists, pharmacists, and social workers, each with a distinct but collaborative role. Effective communication among team members is critical for optimal patient care.

Primary care physicians usually serve as the initial point of contact and are responsible for quickly identifying OCD symptoms and referring patients to specialized care. Psychiatrists oversee diagnosis and pharmacotherapy, while clinical psychologists conduct specialized psychometric tests to either confirm or rule out the OCD diagnosis, in addition to providing cognitive behavioral therapy. Clear, open communication among team members enables rapid intervention. Occupational therapists assess the patient's daily functioning, and social workers facilitate access to community resources. Pharmacists play a crucial role in managing medication interactions and ensuring medication adherence, particularly in instances of polypharmacy.

Ethical considerations like obtaining informed consent are paramount, as is aligning care with autonomy, beneficence, and nonmaleficence principles. Shared decision-making is emphasized, placing patient preferences at the center of all treatment decisions. Ongoing education and professional development keep the team updated on best practices in OCD treatment. This interprofessional approach to OCD management prioritizes comprehensive, safe, and high-quality patient care.



Hannah Brock


Abid Rizvi


Manassa Hany


2/17/2024 1:17:37 PM



Zai G, Barta C, Cath D, Eapen V, Geller D, Grünblatt E. New insights and perspectives on the genetics of obsessive-compulsive disorder. Psychiatric genetics. 2019 Oct:29(5):142-151. doi: 10.1097/YPG.0000000000000230. Epub     [PubMed PMID: 31464995]

Level 3 (low-level) evidence


Strom NI, Soda T, Mathews CA, Davis LK. A dimensional perspective on the genetics of obsessive-compulsive disorder. Translational psychiatry. 2021 Jul 21:11(1):401. doi: 10.1038/s41398-021-01519-z. Epub 2021 Jul 21     [PubMed PMID: 34290223]

Level 3 (low-level) evidence


Stein DJ, Costa DLC, Lochner C, Miguel EC, Reddy YCJ, Shavitt RG, van den Heuvel OA, Simpson HB. Obsessive-compulsive disorder. Nature reviews. Disease primers. 2019 Aug 1:5(1):52. doi: 10.1038/s41572-019-0102-3. Epub 2019 Aug 1     [PubMed PMID: 31371720]


Blanco-Vieira T, Radua J, Marcelino L, Bloch M, Mataix-Cols D, do Rosário MC. The genetic epidemiology of obsessive-compulsive disorder: a systematic review and meta-analysis. Translational psychiatry. 2023 Jun 28:13(1):230. doi: 10.1038/s41398-023-02433-2. Epub 2023 Jun 28     [PubMed PMID: 37380645]

Level 1 (high-level) evidence


Mataix-Cols D, Rosario-Campos MC, Leckman JF. A multidimensional model of obsessive-compulsive disorder. The American journal of psychiatry. 2005 Feb:162(2):228-38     [PubMed PMID: 15677583]


Bloch MH, Landeros-Weisenberger A, Rosario MC, Pittenger C, Leckman JF. Meta-analysis of the symptom structure of obsessive-compulsive disorder. The American journal of psychiatry. 2008 Dec:165(12):1532-42. doi: 10.1176/appi.ajp.2008.08020320. Epub 2008 Oct 15     [PubMed PMID: 18923068]

Level 1 (high-level) evidence


Taylor S, McKay D, Miguel EC, De Mathis MA, Andrade C, Ahuja N, Sookman D, Kwon JS, Huh MJ, Riemann BC, Cottraux J, O'Connor K, Hale LR, Abramowitz JS, Fontenelle LF, Storch EA. Musical obsessions: a comprehensive review of neglected clinical phenomena. Journal of anxiety disorders. 2014 Aug:28(6):580-9. doi: 10.1016/j.janxdis.2014.06.003. Epub 2014 Jun 16     [PubMed PMID: 24997394]


Greenberg D, Huppert JD. Scrupulosity: a unique subtype of obsessive-compulsive disorder. Current psychiatry reports. 2010 Aug:12(4):282-9. doi: 10.1007/s11920-010-0127-5. Epub     [PubMed PMID: 20544313]


Fornaro M, Gabrielli F, Albano C, Fornaro S, Rizzato S, Mattei C, Solano P, Vinciguerra V, Fornaro P. Obsessive-compulsive disorder and related disorders: a comprehensive survey. Annals of general psychiatry. 2009 May 18:8():13. doi: 10.1186/1744-859X-8-13. Epub 2009 May 18     [PubMed PMID: 19450269]

Level 3 (low-level) evidence


Hollander E, Braun A, Simeon D. Should OCD leave the anxiety disorders in DSM-V? The case for obsessive compulsive-related disorders. Depression and anxiety. 2008:25(4):317-29. doi: 10.1002/da.20500. Epub     [PubMed PMID: 18412058]

Level 3 (low-level) evidence


Veale D, Roberts A. Obsessive-compulsive disorder. BMJ (Clinical research ed.). 2014 Apr 7:348():g2183. doi: 10.1136/bmj.g2183. Epub 2014 Apr 7     [PubMed PMID: 24709802]


Fernandez TV, Leckman JF, Pittenger C. Genetic susceptibility in obsessive-compulsive disorder. Handbook of clinical neurology. 2018:148():767-781. doi: 10.1016/B978-0-444-64076-5.00049-1. Epub     [PubMed PMID: 29478613]


Goodman WK, Storch EA, Sheth SA. Harmonizing the Neurobiology and Treatment of Obsessive-Compulsive Disorder. The American journal of psychiatry. 2021 Jan 1:178(1):17-29. doi: 10.1176/appi.ajp.2020.20111601. Epub     [PubMed PMID: 33384007]


Mahjani B, Klei L, Hultman CM, Larsson H, Devlin B, Buxbaum JD, Sandin S, Grice DE. Maternal Effects as Causes of Risk for Obsessive-Compulsive Disorder. Biological psychiatry. 2020 Jun 15:87(12):1045-1051. doi: 10.1016/j.biopsych.2020.01.006. Epub 2020 Jan 22     [PubMed PMID: 32199606]


Escobar AP, Wendland JR, Chávez AE, Moya PR. The Neuronal Glutamate Transporter EAAT3 in Obsessive-Compulsive Disorder. Frontiers in pharmacology. 2019:10():1362. doi: 10.3389/fphar.2019.01362. Epub 2019 Nov 15     [PubMed PMID: 31803055]


Yuste R. From the neuron doctrine to neural networks. Nature reviews. Neuroscience. 2015 Aug:16(8):487-97. doi: 10.1038/nrn3962. Epub 2015 Jul 8     [PubMed PMID: 26152865]


Maraone A, Tarsitani L, Pinucci I, Pasquini M. Antiglutamatergic agents for obsessive-compulsive disorder: Where are we now and what are possible future prospects? World journal of psychiatry. 2021 Sep 19:11(9):568-580. doi: 10.5498/wjp.v11.i9.568. Epub 2021 Sep 19     [PubMed PMID: 34631461]


Shitova AD, Zharikova TS, Kovaleva ON, Luchina AM, Aktemirov AS, Olsufieva AV, Sinelnikov MY, Pontes-Silva A, Zharikov YO. Tourette syndrome and obsessive-compulsive disorder: A comprehensive review of structural alterations and neurological mechanisms. Behavioural brain research. 2023 Sep 13:453():114606. doi: 10.1016/j.bbr.2023.114606. Epub 2023 Jul 30     [PubMed PMID: 37524204]


Bird JS, Shah E, Shotbolt P. Epilepsy and concomitant obsessive-compulsive disorder. Epilepsy & behavior case reports. 2018:10():106-110. doi: 10.1016/j.ebcr.2018.07.001. Epub 2018 Jul 20     [PubMed PMID: 30271707]

Level 3 (low-level) evidence


Parmar A, Verma R. A Case of Obsessive-Compulsive Disorder Comorbid with Miyoshi Myopathy. Indian journal of psychological medicine. 2018 Jan-Feb:40(1):86-88. doi: 10.4103/IJPSYM.IJPSYM_1_17. Epub     [PubMed PMID: 29403136]

Level 3 (low-level) evidence


Simpson HB, Slifstein M, Bender J Jr, Xu X, Hackett E, Maher MJ, Abi-Dargham A. Serotonin 2A receptors in obsessive-compulsive disorder: a positron emission tomography study with [11C]MDL 100907. Biological psychiatry. 2011 Nov 1:70(9):897-904. doi: 10.1016/j.biopsych.2011.06.023. Epub     [PubMed PMID: 21855857]


Pallanti S, Bernardi S, Antonini S, Singh N, Hollander E. Ondansetron augmentation in patients with obsessive-compulsive disorder who are inadequate responders to serotonin reuptake inhibitors: improvement with treatment and worsening following discontinuation. European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology. 2014 Mar:24(3):375-80. doi: 10.1016/j.euroneuro.2013.12.003. Epub 2013 Dec 11     [PubMed PMID: 24406025]


Sakurai H, Dording C, Yeung A, Foster S, Jain F, Chang T, Trinh NH, Bernard R, Boyden S, Iqbal SZ, Wilkinson ST, Mathew SJ, Mischoulon D, Fava M, Cusin C. Longer-term open-label study of adjunctive riluzole in treatment-resistant depression. Journal of affective disorders. 2019 Nov 1:258():102-108. doi: 10.1016/j.jad.2019.06.065. Epub 2019 Jul 2     [PubMed PMID: 31400624]


Grassi G, Cecchelli C, Vignozzi L, Pacini S. Investigational and Experimental Drugs to Treat Obsessive-Compulsive Disorder. Journal of experimental pharmacology. 2020:12():695-706. doi: 10.2147/JEP.S255375. Epub 2021 Jan 5     [PubMed PMID: 33447096]


Jalal B, Chamberlain SR, Sahakian BJ. Obsessive-compulsive disorder: Etiology, neuropathology, and cognitive dysfunction. Brain and behavior. 2023 Jun:13(6):e3000. doi: 10.1002/brb3.3000. Epub 2023 May 3     [PubMed PMID: 37137502]


Grant JE, Hook R, Valle S, Chesivoir E, Chamberlain SR. Tolcapone in obsessive-compulsive disorder: a randomized double-blind placebo-controlled crossover trial. International clinical psychopharmacology. 2021 Sep 1:36(5):225-229. doi: 10.1097/YIC.0000000000000368. Epub     [PubMed PMID: 34310432]

Level 1 (high-level) evidence


Murphy TK, Patel PD, McGuire JF, Kennel A, Mutch PJ, Parker-Athill EC, Hanks CE, Lewin AB, Storch EA, Toufexis MD, Dadlani GH, Rodriguez CA. Characterization of the pediatric acute-onset neuropsychiatric syndrome phenotype. Journal of child and adolescent psychopharmacology. 2015 Feb:25(1):14-25. doi: 10.1089/cap.2014.0062. Epub 2014 Oct 14     [PubMed PMID: 25314221]


Xu J, Liu RJ, Fahey S, Frick L, Leckman J, Vaccarino F, Duman RS, Williams K, Swedo S, Pittenger C. Antibodies From Children With PANDAS Bind Specifically to Striatal Cholinergic Interneurons and Alter Their Activity. The American journal of psychiatry. 2021 Jan 1:178(1):48-64. doi: 10.1176/appi.ajp.2020.19070698. Epub 2020 Jun 16     [PubMed PMID: 32539528]


Abramowitz JS. The psychological treatment of obsessive-compulsive disorder. Canadian journal of psychiatry. Revue canadienne de psychiatrie. 2006 Jun:51(7):407-16     [PubMed PMID: 16838822]


Baxter AJ, Vos T, Scott KM, Ferrari AJ, Whiteford HA. The global burden of anxiety disorders in 2010. Psychological medicine. 2014 Aug:44(11):2363-74. doi: 10.1017/S0033291713003243. Epub 2014 Jan 22     [PubMed PMID: 24451993]


Fairbrother N, Collardeau F, Albert AYK, Challacombe FL, Thordarson DS, Woody SR, Janssen PA. High Prevalence and Incidence of Obsessive-Compulsive Disorder Among Women Across Pregnancy and the Postpartum. The Journal of clinical psychiatry. 2021 Mar 23:82(2):. pii: 20m13398. doi: 10.4088/JCP.20m13398. Epub 2021 Mar 23     [PubMed PMID: 34033273]


Fawcett EJ, Power H, Fawcett JM. Women Are at Greater Risk of OCD Than Men: A Meta-Analytic Review of OCD Prevalence Worldwide. The Journal of clinical psychiatry. 2020 Jun 23:81(4):. pii: 19r13085. doi: 10.4088/JCP.19r13085. Epub 2020 Jun 23     [PubMed PMID: 32603559]


Senter MS, Patel SR, Dixon LB, Myers RW, Simpson HB. Defining and Addressing Gaps in Care for Obsessive-Compulsive Disorder in the United States. Psychiatric services (Washington, D.C.). 2021 Jul 1:72(7):784-793. doi: 10.1176/appi.ps.202000296. Epub 2021 May 7     [PubMed PMID: 33957763]


Bruin WB, Taylor L, Thomas RM, Shock JP, Zhutovsky P, Abe Y, Alonso P, Ameis SH, Anticevic A, Arnold PD, Assogna F, Benedetti F, Beucke JC, Boedhoe PSW, Bollettini I, Bose A, Brem S, Brennan BP, Buitelaar JK, Calvo R, Cheng Y, Cho KIK, Dallaspezia S, Denys D, Ely BA, Feusner JD, Fitzgerald KD, Fouche JP, Fridgeirsson EA, Gruner P, Gürsel DA, Hauser TU, Hirano Y, Hoexter MQ, Hu H, Huyser C, Ivanov I, James A, Jaspers-Fayer F, Kathmann N, Kaufmann C, Koch K, Kuno M, Kvale G, Kwon JS, Liu Y, Lochner C, Lázaro L, Marques P, Marsh R, Martínez-Zalacaín I, Mataix-Cols D, Menchón JM, Minuzzi L, Moreira PS, Morer A, Morgado P, Nakagawa A, Nakamae T, Nakao T, Narayanaswamy JC, Nurmi EL, O'Neill J, Pariente JC, Perriello C, Piacentini J, Piras F, Piras F, Reddy YCJ, Rus-Oswald OG, Sakai Y, Sato JR, Schmaal L, Shimizu E, Simpson HB, Soreni N, Soriano-Mas C, Spalletta G, Stern ER, Stevens MC, Stewart SE, Szeszko PR, Tolin DF, Venkatasubramanian G, Wang Z, Yun JY, van Rooij D, ENIGMA-OCD Working Group, Thompson PM, van den Heuvel OA, Stein DJ, van Wingen GA. Structural neuroimaging biomarkers for obsessive-compulsive disorder in the ENIGMA-OCD consortium: medication matters. Translational psychiatry. 2020 Oct 8:10(1):342. doi: 10.1038/s41398-020-01013-y. Epub 2020 Oct 8     [PubMed PMID: 33033241]


de Oliveira KC, Grinberg LT, Hoexter MQ, Brentani H, Suemoto CK, Nery FG, Lima LC, Alho ATDL, Farfel JM, Ferretti-Rebustini REL, Leite REP, Moretto AC, da Silva AV, Lafer B, Miguel EC, Nitrini R, Jacob-Filho W, Heinsen H, Pasqualucci CA. Layer-specific reduced neuronal density in the orbitofrontal cortex of older adults with obsessive-compulsive disorder. Brain structure & function. 2019 Jan:224(1):191-203. doi: 10.1007/s00429-018-1752-8. Epub 2018 Oct 8     [PubMed PMID: 30298291]


Krebs G, Heyman I. Obsessive-compulsive disorder in children and adolescents. Archives of disease in childhood. 2015 May:100(5):495-9. doi: 10.1136/archdischild-2014-306934. Epub 2014 Nov 14     [PubMed PMID: 25398447]


Heyman I, Mataix-Cols D, Fineberg NA. Obsessive-compulsive disorder. BMJ (Clinical research ed.). 2006 Aug 26:333(7565):424-9     [PubMed PMID: 16931840]


Schruers K, Baldi S, van den Heuvel T, Goossens L, Luyten L, Leentjens AFG, Ackermans L, Temel Y, Viechtbauer W. The effects of deep-brain non-stimulation in severe obsessive-compulsive disorder: an individual patient data meta-analysis. Translational psychiatry. 2019 Aug 5:9(1):183. doi: 10.1038/s41398-019-0522-6. Epub 2019 Aug 5     [PubMed PMID: 31383848]

Level 1 (high-level) evidence


Öst LG, Havnen A, Hansen B, Kvale G. Cognitive behavioral treatments of obsessive-compulsive disorder. A systematic review and meta-analysis of studies published 1993-2014. Clinical psychology review. 2015 Aug:40():156-69. doi: 10.1016/j.cpr.2015.06.003. Epub 2015 Jun 14     [PubMed PMID: 26117062]

Level 1 (high-level) evidence


Öst LG, Riise EN, Wergeland GJ, Hansen B, Kvale G. Cognitive behavioral and pharmacological treatments of OCD in children: A systematic review and meta-analysis. Journal of anxiety disorders. 2016 Oct:43():58-69. doi: 10.1016/j.janxdis.2016.08.003. Epub 2016 Aug 13     [PubMed PMID: 27632568]

Level 1 (high-level) evidence


Hirschtritt ME, Bloch MH, Mathews CA. Obsessive-Compulsive Disorder: Advances in Diagnosis and Treatment. JAMA. 2017 Apr 4:317(13):1358-1367. doi: 10.1001/jama.2017.2200. Epub     [PubMed PMID: 28384832]

Level 3 (low-level) evidence


Kvale G, Hansen B, Björgvinsson T, Børtveit T, Hagen K, Haseth S, Kristensen UB, Launes G, Ressler KJ, Solem S, Strand A, van den Heuvel OA, Öst LG. Successfully treating 90 patients with obsessive compulsive disorder in eight days: the Bergen 4-day treatment. BMC psychiatry. 2018 Oct 4:18(1):323. doi: 10.1186/s12888-018-1887-4. Epub 2018 Oct 4     [PubMed PMID: 30286745]


Soomro GM, Altman D, Rajagopal S, Oakley-Browne M. Selective serotonin re-uptake inhibitors (SSRIs) versus placebo for obsessive compulsive disorder (OCD). The Cochrane database of systematic reviews. 2008 Jan 23:2008(1):CD001765. doi: 10.1002/14651858.CD001765.pub3. Epub 2008 Jan 23     [PubMed PMID: 18253995]

Level 1 (high-level) evidence


Bloch MH, McGuire J, Landeros-Weisenberger A, Leckman JF, Pittenger C. Meta-analysis of the dose-response relationship of SSRI in obsessive-compulsive disorder. Molecular psychiatry. 2010 Aug:15(8):850-5. doi: 10.1038/mp.2009.50. Epub 2009 May 26     [PubMed PMID: 19468281]

Level 1 (high-level) evidence


Stein DJ, Andersen EW, Tonnoir B, Fineberg N. Escitalopram in obsessive-compulsive disorder: a randomized, placebo-controlled, paroxetine-referenced, fixed-dose, 24-week study. Current medical research and opinion. 2007 Apr:23(4):701-11     [PubMed PMID: 17407626]

Level 1 (high-level) evidence


Issari Y, Jakubovski E, Bartley CA, Pittenger C, Bloch MH. Early onset of response with selective serotonin reuptake inhibitors in obsessive-compulsive disorder: a meta-analysis. The Journal of clinical psychiatry. 2016 May:77(5):e605-11. doi: 10.4088/JCP.14r09758. Epub     [PubMed PMID: 27249090]

Level 1 (high-level) evidence


Varigonda AL, Jakubovski E, Bloch MH. Systematic Review and Meta-Analysis: Early Treatment Responses of Selective Serotonin Reuptake Inhibitors and Clomipramine in Pediatric Obsessive-Compulsive Disorder. Journal of the American Academy of Child and Adolescent Psychiatry. 2016 Oct:55(10):851-859.e2. doi: 10.1016/j.jaac.2016.07.768. Epub 2016 Aug 4     [PubMed PMID: 27663940]

Level 1 (high-level) evidence


da Conceição Costa DL, Shavitt RG, Castro Cesar RC, Joaquim MA, Borcato S, Valério C, Miguel EC, Diniz JB. Can early improvement be an indicator of treatment response in obsessive-compulsive disorder? Implications for early-treatment decision-making. Journal of psychiatric research. 2013 Nov:47(11):1700-7. doi: 10.1016/j.jpsychires.2013.07.006. Epub 2013 Aug 13     [PubMed PMID: 23948637]


Batelaan NM, Bosman RC, Muntingh A, Scholten WD, Huijbregts KM, van Balkom AJLM. Risk of relapse after antidepressant discontinuation in anxiety disorders, obsessive-compulsive disorder, and post-traumatic stress disorder: systematic review and meta-analysis of relapse prevention trials. BMJ (Clinical research ed.). 2017 Sep 13:358():j3927. doi: 10.1136/bmj.j3927. Epub 2017 Sep 13     [PubMed PMID: 28903922]

Level 1 (high-level) evidence


Erzegovesi S, Cavallini MC, Cavedini P, Diaferia G, Locatelli M, Bellodi L. Clinical predictors of drug response in obsessive-compulsive disorder. Journal of clinical psychopharmacology. 2001 Oct:21(5):488-92     [PubMed PMID: 11593074]


Albert U, Carmassi C, Cosci F, De Cori D, Di Nicola M, Ferrari S, Poloni N, Tarricone I, Fiorillo A. Role and clinical implications of atypical antipsychotics in anxiety disorders, obsessive-compulsive disorder, trauma-related, and somatic symptom disorders: a systematized review. International clinical psychopharmacology. 2016 Sep:31(5):249-58. doi: 10.1097/YIC.0000000000000127. Epub     [PubMed PMID: 26974213]


Dold M, Aigner M, Lanzenberger R, Kasper S. Antipsychotic Augmentation of Serotonin Reuptake Inhibitors in Treatment-Resistant Obsessive-Compulsive Disorder: An Update Meta-Analysis of Double-Blind, Randomized, Placebo-Controlled Trials. The international journal of neuropsychopharmacology. 2015 May 4:18(9):. pii: pyv047. doi: 10.1093/ijnp/pyv047. Epub 2015 May 4     [PubMed PMID: 25939614]

Level 1 (high-level) evidence


Diniz JB, Shavitt RG, Fossaluza V, Koran L, Pereira CA, Miguel EC. A double-blind, randomized, controlled trial of fluoxetine plus quetiapine or clomipramine versus fluoxetine plus placebo for obsessive-compulsive disorder. Journal of clinical psychopharmacology. 2011 Dec:31(6):763-8. doi: 10.1097/JCP.0b013e3182367aee. Epub     [PubMed PMID: 22020357]

Level 1 (high-level) evidence


Costa DLC, Diniz JB, Requena G, Joaquim MA, Pittenger C, Bloch MH, Miguel EC, Shavitt RG. Randomized, Double-Blind, Placebo-Controlled Trial of N-Acetylcysteine Augmentation for Treatment-Resistant Obsessive-Compulsive Disorder. The Journal of clinical psychiatry. 2017 Jul:78(7):e766-e773. doi: 10.4088/JCP.16m11101. Epub     [PubMed PMID: 28617566]

Level 1 (high-level) evidence


Dunlop K, Woodside B, Olmsted M, Colton P, Giacobbe P, Downar J. Reductions in Cortico-Striatal Hyperconnectivity Accompany Successful Treatment of Obsessive-Compulsive Disorder with Dorsomedial Prefrontal rTMS. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology. 2016 Apr:41(5):1395-403. doi: 10.1038/npp.2015.292. Epub 2015 Oct 6     [PubMed PMID: 26440813]


Carmi L, Tendler A, Bystritsky A, Hollander E, Blumberger DM, Daskalakis J, Ward H, Lapidus K, Goodman W, Casuto L, Feifel D, Barnea-Ygael N, Roth Y, Zangen A, Zohar J. Efficacy and Safety of Deep Transcranial Magnetic Stimulation for Obsessive-Compulsive Disorder: A Prospective Multicenter Randomized Double-Blind Placebo-Controlled Trial. The American journal of psychiatry. 2019 Nov 1:176(11):931-938. doi: 10.1176/appi.ajp.2019.18101180. Epub 2019 May 21     [PubMed PMID: 31109199]

Level 1 (high-level) evidence


McCathern AG, Mathai DS, Cho RY, Goodman WK, Storch EA. Deep transcranial magnetic stimulation for obsessive compulsive disorder. Expert review of neurotherapeutics. 2020 Oct:20(10):1029-1036. doi: 10.1080/14737175.2020.1798232. Epub 2020 Aug 1     [PubMed PMID: 32684005]


Brown LT,Mikell CB,Youngerman BE,Zhang Y,McKhann GM 2nd,Sheth SA, Dorsal anterior cingulotomy and anterior capsulotomy for severe, refractory obsessive-compulsive disorder: a systematic review of observational studies. Journal of neurosurgery. 2016 Jan     [PubMed PMID: 26252455]

Level 1 (high-level) evidence


Miguel EC, Lopes AC, McLaughlin NCR, Norén G, Gentil AF, Hamani C, Shavitt RG, Batistuzzo MC, Vattimo EFQ, Canteras M, De Salles A, Gorgulho A, Salvajoli JV, Fonoff ET, Paddick I, Hoexter MQ, Lindquist C, Haber SN, Greenberg BD, Sheth SA. Evolution of gamma knife capsulotomy for intractable obsessive-compulsive disorder. Molecular psychiatry. 2019 Feb:24(2):218-240. doi: 10.1038/s41380-018-0054-0. Epub 2018 May 9     [PubMed PMID: 29743581]


Denys D, Graat I, Mocking R, de Koning P, Vulink N, Figee M, Ooms P, Mantione M, van den Munckhof P, Schuurman R. Efficacy of Deep Brain Stimulation of the Ventral Anterior Limb of the Internal Capsule for Refractory Obsessive-Compulsive Disorder: A Clinical Cohort of 70 Patients. The American journal of psychiatry. 2020 Mar 1:177(3):265-271. doi: 10.1176/appi.ajp.2019.19060656. Epub 2020 Jan 7     [PubMed PMID: 31906709]


Li N, Baldermann JC, Kibleur A, Treu S, Akram H, Elias GJB, Boutet A, Lozano AM, Al-Fatly B, Strange B, Barcia JA, Zrinzo L, Joyce E, Chabardes S, Visser-Vandewalle V, Polosan M, Kuhn J, Kühn AA, Horn A. A unified connectomic target for deep brain stimulation in obsessive-compulsive disorder. Nature communications. 2020 Jul 3:11(1):3364. doi: 10.1038/s41467-020-16734-3. Epub 2020 Jul 3     [PubMed PMID: 32620886]


Tyagi H, Apergis-Schoute AM, Akram H, Foltynie T, Limousin P, Drummond LM, Fineberg NA, Matthews K, Jahanshahi M, Robbins TW, Sahakian BJ, Zrinzo L, Hariz M, Joyce EM. A Randomized Trial Directly Comparing Ventral Capsule and Anteromedial Subthalamic Nucleus Stimulation in Obsessive-Compulsive Disorder: Clinical and Imaging Evidence for Dissociable Effects. Biological psychiatry. 2019 May 1:85(9):726-734. doi: 10.1016/j.biopsych.2019.01.017. Epub 2019 Jan 30     [PubMed PMID: 30853111]

Level 1 (high-level) evidence


Meier SM, Mattheisen M, Mors O, Schendel DE, Mortensen PB, Plessen KJ. Mortality Among Persons With Obsessive-Compulsive Disorder in Denmark. JAMA psychiatry. 2016 Mar:73(3):268-274. doi: 10.1001/jamapsychiatry.2015.3105. Epub     [PubMed PMID: 26818216]


Torres AR, Prince MJ, Bebbington PE, Bhugra D, Brugha TS, Farrell M, Jenkins R, Lewis G, Meltzer H, Singleton N. Obsessive-compulsive disorder: prevalence, comorbidity, impact, and help-seeking in the British National Psychiatric Morbidity Survey of 2000. The American journal of psychiatry. 2006 Nov:163(11):1978-85     [PubMed PMID: 17074950]

Level 3 (low-level) evidence


Bowen R, Rahman H, Dong LY, Khalaj S, Baetz M, Peters E, Balbuena L. Suicidality in People With Obsessive-Compulsive Symptoms or Personality Traits. Frontiers in psychiatry. 2018:9():747. doi: 10.3389/fpsyt.2018.00747. Epub 2019 Jan 14     [PubMed PMID: 30692943]


Nakao T, Okada K, Kanba S. Neurobiological model of obsessive-compulsive disorder: evidence from recent neuropsychological and neuroimaging findings. Psychiatry and clinical neurosciences. 2014 Aug:68(8):587-605. doi: 10.1111/pcn.12195. Epub 2014 Jun 18     [PubMed PMID: 24762196]


Fineberg NA, Apergis-Schoute AM, Vaghi MM, Banca P, Gillan CM, Voon V, Chamberlain SR, Cinosi E, Reid J, Shahper S, Bullmore ET, Sahakian BJ, Robbins TW. Mapping Compulsivity in the DSM-5 Obsessive Compulsive and Related Disorders: Cognitive Domains, Neural Circuitry, and Treatment. The international journal of neuropsychopharmacology. 2018 Jan 1:21(1):42-58. doi: 10.1093/ijnp/pyx088. Epub     [PubMed PMID: 29036632]


Perris F, Cipolla S, Catapano P, Sampogna G, Luciano M, Giallonardo V, Del Vecchio V, Fabrazzo M, Fiorillo A, Catapano F. Duration of Untreated Illness in Patients with Obsessive-Compulsive Disorder and Its Impact on Long-Term Outcome: A Systematic Review. Journal of personalized medicine. 2023 Sep 29:13(10):. doi: 10.3390/jpm13101453. Epub 2023 Sep 29     [PubMed PMID: 37888064]

Level 1 (high-level) evidence


Van Ameringen M, Patterson B, Simpson W. DSM-5 obsessive-compulsive and related disorders: clinical implications of new criteria. Depression and anxiety. 2014 Jun:31(6):487-93. doi: 10.1002/da.22259. Epub 2014 Mar 10     [PubMed PMID: 24616177]