Obsessive-compulsive disorder

• Obsessive-compulsive disorder (OCD) is a chronic condition in which intrusive, unwanted thoughts (obsessions) and repetitive rituals or mental acts (compulsions) occupy hours of a person's day, cause distress, and interfere with work, relationships and family life.
• It is common enough to matter in everyday practice: about 1% to 3% of people experience it during life, and it usually begins in late childhood or the twenties.
• The condition responds best to a combination of exposure and response prevention therapy and a serotonergic antidepressant, often continued at a high dose for at least 12 months.
• Many people only receive treatment after years of secrecy and severe disability; asking direct questions about intrusive thoughts and rituals is therefore part of the assessment of any anxious patient.
• It is one of a family of obsessive-compulsive and related disorders, and distinguishing it from anxiety disorders, obsessive-compulsive personality traits and psychotic illness is part of good care.

By the end of this page you should be able to:

1. Define obsessions and compulsions and explain why they are maintained.
2. Name the related disorders in the obsessive-compulsive spectrum and how they differ from OCD.
3. Assess a person, screen for risk and other causes, and distinguish OCD from its main alternatives.
4. Choose and monitor first-line psychological and pharmacological treatments, with realistic target doses and durations.
5. Plan treatment when first measures fail, including when clomipramine or expert multidisciplinary care is justified.
6. Describe the indications, procedures, likely benefit and limits of neurosurgical options for severe refractory illness.
7. Manage OCD across age groups and in low-resource settings without losing the essentials of care.

A useful working definition is that OCD is a psychiatric disorder in which a person has recurrent intrusive thoughts, images, urges or doubts that are unwanted and distressing (obsessions), and responds with repetitive mental or overt acts that are performed according to rigid rules in an attempt to reduce distress or prevent a feared event (compulsions), to the point that these symptoms take over significant time and disable ordinary life.^[7] The intrusive experiences are not simply worries about current problems: they are senseless or excessive to the person, and so is the action used to neutralise them.^[7]

Two points make the definition worth remembering. First, either obsessions or compulsions may be present, although most people have both. Second, the activities can be hidden. Mental rituals such as counting, repeating words, or checking a memory can be as disabling as washing or checking, and they are the most easily missed during a routine interview.^[1]

The insight a person has into the beliefs behind the symptoms varies widely, from good insight to completely fixed conviction, even in the same person at different times.^[7] Poor insight predicts poorer response to treatment and must be assessed rather than assumed.^[7]

Current psychiatric nosology has moved OCD out of the anxiety disorders and into a separate chapter of obsessive-compulsive and related disorders. The co-family includes body dysmorphic disorder (a preoccupation with perceived defects in appearance), hoarding disorder (difficulty discarding and accumulation of clutter), trichotillomania (recurrent hair pulling) and excoriation disorder (skin picking).^[7] A presentation does not count as OCD when the same experiences are better explained by an eating disorder, depressive disorder or another major condition.

The reason the family matters is practical. The serotonergic treatments that help OCD also help body dysmorphic disorder, but the psychological treatment of each differs in emphasis, and the other disorders in the spectrum need their own specific interventions.^[6]

OCD is common and usually starts early. Lifetime prevalence in the general population is 2 to 3%, and more than 1% of people are affected worldwide.^[2] In the United States the 12-month prevalence is about 1.2%, with an annual incidence of about 0.55 per 1,000 person-years.^[5]

The typical ages of onset form two peaks: late childhood or early adolescence, and early adulthood in the twenties.^[2] Adults as a whole are not divided by sex, but boys are more often affected in childhood and more often have familial, tic-related illness.^[2] The illness commonly runs a chronic, fluctuating course related to stress, and it causes more years of disability than multiple sclerosis and Parkinson disease combined.^[2] Under-recognition is severe: the mean time from onset to pharmacological treatment is nearly eight years, fewer than 40% of people coming to clinical attention receive OCD-specific therapy, and fewer than 10% receive evidence-based treatment.^[2]

Risk factors and associated conditions:

• Genetic contribution is strong in childhood-onset, tic-related and familial forms, and OCD and body dysmorphic disorder share overlapping genetic vulnerability.^[6]
• Neurological or developmental conditions such as tic disorders are common comorbidities, and obsessive-compulsive symptoms are found in a substantial minority of people with schizophrenia.^[7]
• Life events and triggers can initiate or worsen symptoms, and a minority of childhood cases follow streptococcal infection (see the PANDAS controversy below).^[7]
• Female sex when body dysmorphic disorder is present is associated with a somewhat different symptom focus.^[6]
• Body dysmorphic disorder itself carries a markedly elevated suicidal risk, higher than that in OCD alone.^[6]

Comorbidity is the rule rather than the exception. Over half of people with OCD have at least one other psychiatric disorder, most often an anxiety or depressive disorder, and comorbidity increases distress, affects adherence and worsens outcome.^[2][7] Other conditions to look for include substance use, eating disorders, attention-deficit disorders and obsessive-compulsive personality traits.^[7]

No single cause of OCD has been established. The condition is best understood as a disorder of circuits that link the prefrontal cortex to the basal ganglia and thalamus and back to the cortex: the cortico-striatal-thalamo-cortical system. The favoured model is an imbalance between the direct and indirect pathways through the basal ganglia, producing hyperactivation of these loops and difficulty stopping or inhibiting actions.^[2] A complementary model emphasises loss of top-down inhibition from the prefrontal cortex over the amygdala, which would explain the persistent anxiety and intrusion.^[2]

Serotonin dysfunction has been inferred from the effectiveness of drugs that block serotonin reuptake, even though none of these drugs was designed specifically for OCD. The clinical efficacy of SSRIs and clomipramine, a tricyclic antidepressant with potent serotonin reuptake inhibition, support a serotonergic role.^[2] Overlap between OCD and the related disorders, whose circuits rely on the same networks, makes biological sense of why they sit together in one nosological group.

Neuroimaging and neuropsychological studies add candidate mechanisms: excessive habit formation at the expense of goal-directed behaviour, and exaggerated performance monitoring (a brain electrical response to errors that is larger in OCD than in healthy controls). These are research constructs at present, but they explain why cognitive models of OCD have moved from "pure anxiety" toward compulsivity.^[7]

Some forms of OCD in children appear to be triggered or exacerbated by infection. The PANDAS hypothesis proposes cross-reactive antibodies against basal ganglia following group A streptococcal infection, although this remains controversial and the evidence base is weak.

People usually describe obsessions as unwanted mental intruders: thoughts of contamination, fear that they have harmed or will harm someone (for example by driving over someone), doubts about having switched off an appliance or locked a door, need for symmetry or exactness, forbidden or blasphemous sexual or religious ideas, and distress about "who I am without the rituals".^[1][2] The action taken to reduce distress or prevent catastrophe is the compulsion: washing or cleaning, checking taps and locks, counting, ordering, repeating phrases or prayers, reassurance seeking, or avoiding triggers. Some people have mostly mental rituals and no obvious behaviour; others have such perfect avoidance that they appear aloof rather than ill.

The presence of very vivid sexual, aggressive or death-related thoughts is a common theme of OCD, not a warning of violence. Such thoughts are frequently misread by non-specialists as risk.^[1] When the theme is uncertain, consultation with an OCD specialist is wise.^[1]

Some people have few or no overt symptoms and present through impairment or through family members rather than through self-reported distress. Obsessional themes can attach to religion, culture and family roles, and religious scrupulosity is a particularly difficult boundary to judge.^[1] Onset can follow pregnancy, and the postpartum period is a high-risk time for new obsessional thoughts, especially thoughts of harm to the infant; these are frightening to the parent and are not the same as psychotic illnesses, but they need careful, non-dismissive assessment.^[1]

A small group present with "pure" obsessions without overt compulsions. They should still be treated with cognitive-behavioural exposure to the obsessive thoughts and response prevention of mental rituals and neutralising strategies.^[1]

The mental state examination often shows an anxious, tense person who is only gradually revealing what has been hidden. Important points:

• Obsessions and compulsions: ask directly, then ask about mental neutralisation; use the screening questions in step 2 of NICE CG31 (do you wash or clean a lot; do you check things a lot; is there any thought that keeps bothering you that you would like to get rid of but cannot; do your daily activities take a long time to finish; are you concerned about putting things in a special order or very upset by mess; do these problems trouble you).^[1]
• Insight and overvalued ideas: record whether the belief that harm will occur if the ritual is not carried out is held with conviction, doubt or overvalued certainty. Poor insight is a predictor of resistance.^[7]
• Time course and function: estimate hours per day spent and impairment in work, home, relationships and care of dependants.
• Risk: suicidal ideation and self-harm risk, especially when depression is present; impact of compulsions on others, including dependent children; risk of reckless behaviour driven by doubt.^[1]
• Family accommodation: how much of the ritual is being carried out by a partner or parent; in children this is both a maintaining factor and the key to treatment.
• Body-focused repetitive behaviours: hair pulling, skin picking, nail biting or tics, because these change the differential diagnosis and treatment.
• General examination and basics: weight and nutrition in severe avoidance, skin condition in contamination, and signs of depression or anxiety disorders.

The person is usually not thought disordered, and cognitive testing is typically normal unless an acute depressive illness, substance use or a medical condition is present.

Many psychiatric presentations include doubt, repetition and checking. The task is to decide whether the symptoms are obsessions and compulsions in the specific sense, and if so whether OCD is the right diagnosis.

OCD is a clinical diagnosis. There is no blood test or imaging study that establishes it. A good diagnostic assessment includes the patient's meaning of the symptoms, the presence of comorbidity, and a structured interview based on DSM-5 or ICD-11 criteria, together with standardised rating of severity.

In addition, the diagnosis requires exclusion or clarification of medical conditions, substance use, prescribed drugs and the other disorders in its differential list, rather than a biological test. A careful medication and substance history is particularly important, because some drugs (for example clozapine, and other 5HT2A-blocking antipsychotics) can produce or worsen obsessive-compulsive symptoms.^[2]

Children are more likely than adults to be unable to describe obsessions and to present through parents. A child or adolescent with sudden onset of obsessive-compulsive symptoms, or symptoms associated with streptococcal infection, has a separate pathway described below.

OCD is treated in steps: recognise and assess, then psychosocial treatment with or without a serotonergic drug at an adequate dose for an adequate time, then escalate according to response, and only in a tiny minority pursue invasive options after exhaustive conventional care.

CBT that includes exposure and response prevention is an empirically supported first-line treatment for OCD in adults, children and young people. Compared with pharmacotherapy it has fewer adverse effects, and skills learned can be reused if symptoms recur. It is often underused, particularly in severe cases.^[5]

Key clinical principles that make ERP work, rather than simply "facing fears":

• A collaborative, therapist-guided hierarchy of avoided situations or thoughts, with targets that patients choose and agree to.
• Prolonged contact with the feared stimulus, in imagination or in vivo, until anxiety falls without performing the ritual.
• Prevention of both overt and covert rituals, including reassurance seeking, mental neutralisation and avoidance.
• Maintenance of homework and generalisation to real life, which is where the gains consolidate.
• Inclusion of family members as co-therapists when accommodation is present.^[1]
• Longer or home-based treatment for housebound people and those with contamination, hoarding or bedtime rituals that cannot be touched in an office.^[1]

For children and young people the family (and often school) must be involved, with developmentally adapted CBT as the first-line option and guided self-help reserved for mild impairment.^[1] If psychological treatment is declined or cannot be engaged, an SSRI may be considered with careful monitoring.^[1]

Several trials suggest that adding medication to CBT is superior to either alone in severe or resistant illness, and that professional disagreement about whether to start with CBT, an SSRI or both should be resolved by severity and patient preference rather than by habit.^[2]

The initial recommended SSRIs for adults with OCD are fluoxetine, fluvoxamine, paroxetine, sertraline and (off-label) citalopram.^[1] Clomipramine is a serotonergic tricyclic with long-established efficacy and may be used after an SSRI has failed or been poorly tolerated.^[1][2] SSRIs as monotherapy are first-line because they are effective and well tolerated, although clomipramine was the first drug shown to work and is probably slightly more effective than some SSRIs in head-to-head trials.^[2]

The doses used for OCD are higher than those usually needed for depression. Published target ranges, which are course-of-treatment goals rather than starting doses, are summarised below.^[2]

Practical notes that should be explicitly discussed with patients, from NICE CG31:

• An SSRI takes up to 12 weeks to show benefit for OCD (depressive symptoms usually improve more quickly), and there is commonly a delay before the onset of clinically meaningful change.^[1]
• SSRIs should be continued for at least 12 months when effective, and the need for continuation after 12 months of remission should be reviewed with the patient.^[1]
• SSRIs increase suicidal thoughts and self-harm risk in some younger people and in comorbid depression: younger adults, those younger than 30 years and those with comorbid depression need careful and frequent monitoring, especially in the first few weeks.^[1]
• High doses mean an SSRI dose increase should follow product guidance, with active monitoring for emerging akathisia, restlessness, agitation or suicidality; marked or prolonged akathisia on one SSRI should prompt a switch.^[1]
• Drastic reductions in dose, or stopping short of the usual 12 months, carry a real relapse risk. Taper gradually over several weeks when discontinuing.^[1]
• SSRIs for OCD have a dose-response: treatment works better at higher dose, and the drug should be maintained at the highest effective tolerated dose for at least 12 months.^[2]
• If there has been no response to a full SSRI course, check adherence, alcohol and substance use, and whether the dose has reached the recommended level before calling it treatment-resistant.^[1]

About 40 to 60% of patients do not respond adequately to first-line serotonergic treatment, and an estimated 10 to 20% remain refractory to all available pharmacological and psychological treatments.^[2][3] Before labelling a patient refractory, ensure that they have had an SSRI at adequate dose for at least 8 to 12 weeks, including at least 4 to 6 weeks at the maximum tolerable dose.^[2] The APA practice guideline for OCD, summarised in the psychopharmacology review cited above, gives exactly that figure.^[2]

The escalation sequence recommended by NICE CG31 is:

1. Give a full trial of one SSRI alone.
2. If response is inadequate, consider combined SSRI plus CBT (ERP), and after multidisciplinary review.
3. If that fails, offer a different SSRI or clomipramine; clomipramine is especially considered after an adequate trial of at least one SSRI has been ineffective or poorly tolerated.^[1]
4. For adults who remain refractory, consider additional CBT or cognitive therapy; adding an antipsychotic to an SSRI or clomipramine; or combining clomipramine with citalopram (off-label, with ECG monitoring).^[1]
5. Refer to a multidisciplinary team with specific OCD/BDD expertise after failure of a full trial of at least one SSRI alone, combined treatment, and clomipramine.^[1]

Augmentation evidence is mixed and patient-specific. A third or fewer treatment-resistant patients respond to an antipsychotic add-on; risperidone and aripiprazole have the most consistent evidence, haloperidol works in some with combined tics, quetiapine and olanzapine are less convincing. Antipsychotic augmentation is pharmacologically rational but not formally approved for OCD, and metabolic monitoring for weight, glucose and lipids must be planned.^[2] Combined clomipramine plus SSRI (clomipramine 25 to 75 mg/day added to fluoxetine, or clomipramine added to citalopram) outperforms some antipsychotic strategies in small studies, but ECG monitoring is needed because of the risk of serotonin syndrome.^[2]

Intensive options for severe illness include CBT at home, telephone CBT for the housebound and hoarding, inpatient treatment and specialised residential units. Residential treatment is so effective that it should be considered before invasive options.^[5]

For children and young people (8 years and older), CBT with family involvement is first-line for moderate to severe impairment; guided self-help may be considered if impairment is mild.^[1] Licensed SSRIs (sertraline or fluvoxamine) may be used for OCD in children; fluoxetine may be considered when there is significant comorbid depression or for body dysmorphic disorder.^[1] When psychological treatment is declined or cannot be engaged, an SSRI may be considered with careful monitoring.^{[1] [5]}

Medication should start at a low dose, with a quarter to a half of the normal starting dose for the first week, then increase gradually with close monitoring for adverse events; the maximum recommended dose for the child's age should not be exceeded.^[1] The SSRIs used in children should usually be combined with CBT/ERP; if CBT cannot be engaged, specific arrangements for close monitoring must be recorded.^[1] SSRIs should be continued for at least 6 months after remission in children, and withdrawn only if remission has been maintained for 6 months and that is the child's wish. Medication should be tapered gradually over several weeks, and CBT should continue throughout the withdrawal period to reduce relapse risk. Weekly monitoring is appropriate at the start and at dose changes, particularly for the emergence of suicidal thoughts, hostility or self-harm.^[1]

Clomipramine in children requires an ECG to exclude conduction abnormality before starting, a clear warning of toxicity in overdose, and gradual dose escalation; it should not be started in primary care without specialist oversight. The licensed (UK) position at the time of the guideline is that only sertraline and fluvoxamine are licensed for OCD in children, although fluoxetine is used off-label in comorbid depression or in body dysmorphic disorder under the guideline.^[1]

Body dysmorphic disorder (BDD) is condition-specific and worth treating as its own case, even when this page cannot cover it fully. Its core feature is a distressing or impairing preoccupation with non-existent or slight defects in appearance, accompanied by repetitive checking, camouflaging or reassurance. Point prevalence is nearly 2 to 3%, onset is usually in childhood or early adolescence, and appearance preoccupations occupy 3 to 8 hours a day. Like OCD, first-line treatment is an SSRI and CBT adapted to BDD, often at doses 80 to 120 mg/day fluoxetine in severe cases; unlike OCD, BDD has more frequent depression, substance use, suicidal ideation, attempted suicide and markedly poorer insight, and cosmetic treatment (surgery or dermatology) is not recommended.^{[6] [2]}

Neurosurgery is not recommended for OCD as routine treatment, and it is not a substitute for expert psychiatric and psychological care.^[1] It may be considered only when a person has severe, chronic, treatment-refractory illness, has exhausted adequate trials of serotonin reuptake inhibitors (including clomipramine) and ERP, and requests surgical assessment after discussion of what it can and cannot do. Decision making should follow existing published criteria, with multidisciplinary teams with a high degree of expertise recently involved in care, standardised pre- and post-operative assessment, access to independent advice on adequacy of previous treatment and consent, and the expectation that each centre publishes and shares audit information.^[1]

The candidates are few. In a well-characterised clinical sample, only about 0.6% of treatment-seeking patients met conservative criteria for surgery, after severe symptoms were required to have persisted despite multiple medication and ERP trials.^[5] Late onset, high initial burden and low treatment utilisation mean that earlier and adequate ERP remains the better investment for almost everyone.

What is actually done today (all stereotactic, not old leucotomy):

• Gamma ventral capsulotomy: gamma knife lesions in the ventral anterior limb of the internal capsule, the most widely used ablative procedure for OCD. Mean response rates are about 54 to 62% in meta-analyses, with improvement appearing 6 to 12 months post-procedure.^[3]
• Anterior cingulotomy: thermocoagulation of the anterior cingulate cortex and cingulum bundle, a popular approach in North America.
• Subcaudate tractotomy: transection of cortico-striatal pathways ventral to the caudate head; evidence is smaller.
• Deep brain stimulation (DBS): implanted electrodes most commonly target the ventral capsule/ventral striatum, nucleus accumbens, bed nucleus of the stria terminalis or (with reported level-I evidence) the subthalamic nucleus. A meta-analysis reports an average total Y-BOCS reduction of about 45% and a response rate of about 60%.^[3]

DBS is staged (electrode placement, generator implantation, then months of outpatient programming) and, unlike ablation, is potentially reversible. Ablation is cheaper and needs no maintenance but is irreversible. Either way the patient must understand that surgery is not a cure: pharmacotherapy and, later, ERP continue, and improvement is measured in months rather than days.^[3]

Pre-surgical requirements emphasised by specialist teams include: adequate trials of at least three different serotonin reuptake inhibitors including clomipramine, adequate ERP (at least 20 sessions with an experienced therapist), exclusion of psychosis, bipolar disorder, unstably remitted substances and current body dysmorphic disorder, generally a Y-BOCS of 28 or more and a GAF of 45 or less, and independent multidisciplinary review.^[5][3]

Adverse events deserve discussion before anyone consents:

• DBS: intracerebral haemorrhage during lead implantation (0.2 to 5%), infection (0 to 15%), immediate post-procedure seizures (about 4%), lead or extension fracture (about 2%), and stimulation-related effects such as dyskinesia, dysarthria, mood changes and behavioural disinhibition, which are usually reversible with reprogramming.^[3]
• Capsulotomy: headache, seizures, delirium, urinary incontinence, cerebral oedema, weight gain of more than 10% of body weight in 29%, and a 5% risk of delayed radiation-induced cyst formation up to 5 years later. Cognitive function is not worsened; nomenclature sub-types with symmetry/ordering or hoarding symptoms predict poorer surgical response.^[3]

A subset of children are described as having sudden onset of OCD symptoms, sometimes with tics and neuropsychiatric changes, following group A streptococcal infection (pediatric autoimmune neuropsychiatric disorder associated with streptococcal infection, PANDAS) or following other infections (paediatric acute-onset neuropsychiatric syndrome, PANS). The hypothesis is that immune cross-reactivity affects the basal ganglia. A natural history of infection-triggered onset, dramatic course, possible choreiform movement and antibodies is described, but the biological mechanism has not been definitively demonstrated and the condition is not universally accepted as a distinct disease.^[4][7]

The pragmatic approach supported by the reviews is:

• Treat the OCD itself with CBT/ERP and, if indicated, conventional serotonergic therapy first.
• Look for and treat an acute streptococcal infection when present.
• Antibiotics or immune modulation (intravenous immunoglobulin, plasma exchange, steroids, NSAIDs, adenotonsillectomy) have been studied in small, heterogeneous, often uncontrolled studies; pooled results for OCD outcomes have not reached statistical significance, and the literature lacks standardised protocols. These treatments must not delay the provision of evidence-based OCD care.^[4]
• The same caution applies to any claim that a child can be cured by treating infection rather than OCD: the evidence does not support it.

• Functional disability is severe: lost years of life expectancy to disability, relationships and education disrupted, and delayed treatment by years.^[2]
• Psychiatric comorbidity, especially depression and anxiety disorders, increases risk.^[2][7]
• Suicidality risk is elevated, particularly when depression or comorbid body dysmorphic disorder is present; risk assessment is standard care.^[1][6]
• Family impact and accommodation can make the disorder resistant to treatment; families may unwittingly participate in rituals.
• Iatrogenic effects of treatment: SSRI discontinuation or withdrawal symptoms; akathisia; anticholinergic and cardiotoxicity of clomipramine; serotonin syndrome when combining serotonergic agents; clozapine-induced obsessive-compulsive symptoms in psychotic illness; and surgical complications listed above.
• Psychosis spectrum overlap: about 30% of people with schizophrenia may have obsessive-compulsive symptomatology, and about 14% have OCD; this complicates both diagnosis and medication choice.^[7]

Untreated OCD usually runs a chronic, fluctuating course. With appropriate treatment most patients improve substantially, although complete remission may not occur, and between 40 and 60% do not respond fully to first-line serotonergic therapy alone.^[2] Ongoing treatment, maintenance of medication at an adequate dose, and consolidation of coping skills are usually needed. Relapse rates are lower when medication is continued for at least 12 months after remission, and when CBT skills are maintained.^[1] With neurosurgery in the small subgroup that receives it, improvement is expected 6 to 12 months after the procedure.^[3]

There is no primary prevention. Secondary prevention depends on early recognition:

• Provide accessible information to patients, families and carers about the involuntary nature of the symptoms; this improves engagement.^[1]
• Screen high-risk groups (depression, anxiety, alcohol and substance misuse, eating disorders, body dysmorphic disorder, skin and cosmetic clinic populations) by asking the direct NICE questions.^[1]
• Every mental health service should have access to a specialist OCD/BDD multidisciplinary team that trains professionals and provides evidence-based treatment.^[1]
• Collaboration with dermatology and cosmetic surgery professionals is important because many people with body dysmorphic disorder present to those services first.^[1]

Children: see the treatment section above. Use family-based CBT first, start SSRIs cautiously, and avoid monotherapy antipsychotics outside expert care.

Pregnancy and the postpartum: these sources do not provide pregnancy-specific medication protocols. In practice, perinatal mental health, obstetric and psychological services share decisions; ERP is a non-pharmacological mainstay; any psychotropic drug is chosen by risk-benefit rather than routine. New obsessions about harm to the infant after delivery should be assessed respectfully and promptly, because they are common, distressing and not equivalent to psychosis.

Older adults: OCD in later life is often long-standing and masked by depression, medical illness or cognitive change. Medications should be chosen for low anticholinergic burden and interactions (tricyclics and antipsychotics in particular carry risks in older adults), and psychotherapy should take account of mobility, sensory impairment and social isolation. The doses and durations cited are adult targets and should be titrated to tolerability.

• Transthoracic echocardiography is not relevant here, but the main diagnostic tool is the clinical interview: scrupulous time spent asking direct questions is both free and decisive. Records from local forms (screening, mental-state items) can be used.
• Family involvement and ERP can be delivered by trained health workers with supervision when specialist therapists are unavailable.
• A single serotonergic drug with careful titration is the realistic first pharmacological option; clomipramine is inexpensive but requires ECG monitoring and carries overdose toxicity.
• Reserve expert and surgical escalation for centres with multidisciplinary review, and refer severe, suicidal or complicated cases early.
• Public awareness reduces the years of silent illness and family burden, which is often the greatest cost.

• OCD is common (about 1 to 3% lifetime), usually starts young, and is disabling (more disability-years than MS plus Parkinson disease), yet it is treatable.^[2]
• Obsessions and compulsions are intrusive, unwanted and often hidden as mental rituals; insight is variable and poor insight predicts resistance.
• Screening is done with short, direct questions; high-risk groups include depression, anxiety, substance misuse, eating disorders and presentation to dermatology or cosmetic services.^[1]
• DSM-5-TR places OCD in the obsessive-compulsive and related disorders chapter; related conditions include body dysmorphic disorder, hoarding disorder, trichotillomania and excoriation disorder. Careful differential diagnosis is part of the assessment.^[7]
• Body dysmorphic disorder has higher suicidal risk, poorer insight and similar but BDD-specific CBT; cosmetic procedures are not recommended.^[6]
• CBT with exposure and response prevention is first-line psychological treatment for adults, children and young people; combine with SSRI for severe impairment.^[1]
• SSRIs are first-line pharmacotherapy at higher than antidepressant doses, continued for at least 12 months; citalopram is used off-label.^[1]
• High-dose strategy: fluoxetine 40 to 60, fluvoxamine 100 to 300, paroxetine 20 to 60, sertraline 50 to 200 (refractory 250 to 400), citalopram up to 60, escitalopram 20 mg/day target or 30 to 50 high-dose, clomipramine up to 250 mg/day.^[2]
• Treatment resistance is managed by adherence review, combined CBT plus SSRI, switching SSRI or clomipramine, antipsychotic augmentation, and expert referral. The APA (2007) minimum expectations are 8 to 12 weeks of SSRI treatment, with 4 to 6 weeks at maximum tolerable dose, before switching.^[2]
• Severe, chronic refractory cases may be considered for neurosurgery (capsulotomy or DBS) after independent multidisciplinary review; neurosurgery is not recommended as routine and is not standalone.^[1][3]
• In children, CBT with the family is first-line, and SSRIs start low and are continued at least 6 months post-remission, with close early monitoring.^[1]
• PANDAS/PANS remains controversial: treat the OCD and any active streptococcal infection with established treatments; the evidence for immune or surgical immune-modulation is not yet persuasive.^[4]
• Many people suffer for years before treatment; screening and specialist access are the practical prevention.^[1]

Obsessive-compulsive and related disorders, major depression, body dysmorphic disorder, hoarding disorder, trichotillomania, excoriation disorder, obsessive-compulsive personality disorder, tics and Tourette syndrome, anxiety disorders, psychotic and delusional disorders, depression in children and young people, perinatal mental health.