Obsessive-compulsive Disorder

This is extremely high-yield — OCD is almost never alone:

The orbitofrontal cortico-striato-thalamo-cortical (CSTC) circuit dysfunction is widely cited as the major abnormality underpinning OCD ^[1][3].

How does this loop normally work?

The CSTC loops are parallel circuits that connect cortical areas → striatum (basal ganglia) → thalamus → back to the same cortical area. They exist for motor, cognitive, limbic and other functions. The orbitofrontal CSTC loop specifically handles:

• Decision-making about whether an action is "complete" or requires repetition
• Habit learning vs. goal-directed behaviour — the OFC mediates the balance between compulsivity (tendency toward habitual/routine behaviour) and impulsivity (tendency toward reward-driven/goal-directed behaviour) ^[3]
• Error monitoring — "Have I done this correctly? Is there danger?"

What goes wrong in OCD?

OCD arises from a hyperactive orbitofrontal CSTC loop ^[3]:

1. The OFC fires excessively → generates a persistent feeling that "something is wrong" or "incomplete"
2. This hyperactivity propagates through the caudate → thalamus → back to the OFC
3. The result is a self-reinforcing loop: the brain keeps signalling danger/incompleteness, driving the person to check, wash, count, etc.
4. Performing the compulsion provides temporary relief (the loop briefly quiets), but this negatively reinforces the cycle

Structural imaging summary: ↑ grey matter volume in striatum, ↓ grey matter in OFC, dorsomedial and anterior cingulate cortex ^[3].

Functional imaging summary: ↑ activity in OFC, caudate, ACC, and thalamus — all key nodes of the CSTC loop ^[3].

In the ICD-11 (2019, adopted progressively), OCD has been removed from the anxiety disorders and placed in its own category: "Obsessive-Compulsive and Related Disorders (OCRDs)". This reflects the understanding that while anxiety is prominent in OCD, the core pathology (CSTC loop dysfunction, compulsivity) is distinct from primary anxiety disorders.

The OCRD category includes:

• Obsessive-Compulsive Disorder
• Body Dysmorphic Disorder (BDD)
• Hoarding Disorder
• Trichotillomania (hair-pulling disorder)
• Excoriation Disorder (skin-picking disorder)
• Olfactory Reference Disorder (new in ICD-11)
• Hypochondriasis (illness anxiety disorder — placed here in ICD-11 but under somatic symptom disorders in DSM-5)

Similarly in DSM-5 (2013), OCD was moved out of anxiety disorders into "Obsessive-Compulsive and Related Disorders".

This is a clinically useful way to categorize OCD presentations. The four major dimensions are:

^[1][2]

OCD is largely a disorder of subjective experience, so signs on examination are relatively few compared to symptoms. However, astute observation can reveal:

The lecture slides emphasize that OCD patients typically maintain insight and regard their symptoms as senseless ^[2]. This is a hallmark distinguishing OCD from psychotic disorders — the patient recognises "I know this is irrational, but I can't stop." Over time, however, insight may diminish.

The lecture slides specifically highlight resistance as a key clinical feature ^[2]. The patient actively tries to resist the obsessions and compulsions. This is characteristic of OCD — in contrast to, say, impulsive behaviours in personality disorders where there may be less resistance.

This is the single most commonly tested differential in exams. Here is how to think about it from first principles:

• GAD = the brain's threat-detection system is set too sensitively for real-world concerns. The worry is about things that could plausibly happen — "Will I lose my job? Will my child get sick? Can I pay the mortgage?" These worries are ego-syntonic — the patient thinks it is reasonable to worry about these things.
• OCD = the brain's error-detection/completion circuit (CSTC loop) fires excessively, generating a sense that "something is wrong" about irrational, bizarre, or magical themes. The patient knows the worry is senseless but cannot stop it — this is ego-dystonic.

OCD compulsions are typically ritualistic/rule-driven (must be done in a certain way, a certain number of times) and may be unrelated to the feared outcome they are intended to prevent and/or clearly excessive ^[7]. GAD checking behaviours are usually directly related to preventing the feared outcome and are not usually excessive or time-consuming ^[7].

Some obsessions may resemble delusions due to oddity of beliefs or compulsive behaviours and weak resistance ^[3]. The critical question is: "Do you recognise these thoughts as your own?"

• In OCD: "Yes, they're my thoughts, but they're horrible and I can't stop them" → ego-dystonic, own thoughts
• In schizophrenia with thought insertion: "No, someone is putting these thoughts in my head" → ego-alien, externally attributed

In OCD, recurrent intrusive thoughts are present, but they are unrelated to a traumatic event. In PTSD, anxiety symptoms (worries, avoidance, arousal) are specifically related to traumatic events ^[9]. Both have intrusive thoughts and avoidance, but:

• PTSD intrusions = re-experiencing the trauma (flashbacks, nightmares of the event)
• OCD intrusions = unrelated to any specific event (contamination fears, checking doubts, etc.)

Note: Traumatic events can precipitate OCD onset, but the OCD content is typically about contamination, symmetry, etc. — not a replay of the trauma itself.

The OC-related disorders listed in both DSM-5 and ICD-11 share the compulsive quality but are distinguished by their restricted content domain ^[1][3]:

OCD should be diagnosed when hoarding behaviour arises from obsessions typical of OCD (e.g., obsessions concerning incompleteness or harm — not discarding old newspapers because they may contain information that could prevent harm) ^[3]. If hoarding is ego-syntonic and not driven by typical OCD themes, diagnose Hoarding Disorder.

Both involve repetitive movements, but they differ fundamentally in purpose:

• Tics are typically less complex than compulsions and not aimed at neutralizing obsessions ^[3]
• Tics are preceded by premonitory sensory urges (a physical "itch" or tension in a body part)
• Compulsions are preceded by obsessions (a cognitive experience — an intrusive thought causing anxiety)
• Tic disorders may occur together with OCD ^[3] — up to 30% of OCD patients have tics, and this co-occurrence should be specified as tic-related OCD ^[1][5]

This is presented across three lecture slides ^[1][2] and is the primary framework you should know:

Obsessions are defined by both (1) and (2) ^[1][14]:

"(1) Recurrent and persistent thoughts, urges, or images that are experienced, at some time during the disturbance, as intrusive and unwanted, and that in most individuals cause marked anxiety or distress" ^[1][14]

"(2) The individual attempts to ignore or suppress such thoughts, urges, or images, or to neutralize them with some other thought or action (i.e. by performing a compulsion)" ^[1][14]

Why two sub-criteria? Criterion A1 establishes the nature of the obsessions (intrusive, unwanted, distressing). Criterion A2 establishes the response — the patient does not passively accept them but actively tries to suppress or neutralise them. This distinguishes obsessions from, say, pleasant daydreams or goal-directed planning.

Compulsions are defined by both (1) and (2) ^[1][15]:

"(1) Repetitive behaviours (e.g., hand washing, ordering, checking) or mental acts (e.g., praying, counting, repeating words silently) that the individual feels driven to perform in response to an obsession, or according to rules that must be applied rigidly" ^[1][15]

"(2) The behaviours or mental acts are aimed at preventing or reducing anxiety or distress, or preventing some dreaded event or situation; however, these behaviours or mental acts are not connected in a realistic way with what they are designed to neutralize or prevent, or are clearly excessive" ^[1][15]

Why two sub-criteria? Criterion B1 establishes the driven quality (compulsion = compelled to do). Criterion B2 is crucial — it captures the irrationality or excessiveness of the act. Washing your hands after using the toilet is rational; washing them 50 times until they bleed is "clearly excessive." Praying once before a meal is connected realistically to religious practice; praying 300 times to prevent your family from dying is "not connected in a realistic way."

Specifiers ^[1][17]:

The ICD-10 criteria are slightly different in emphasis ^[3]:

The ICD-11 (2019/2022) has updated the criteria. Key changes from ICD-10:

• OCD is moved from "Neurotic, stress-related and somatoform disorders" (F4) to a new category: "Obsessive-Compulsive and Related Disorders"
• The resistance requirement is relaxed (consistent with DSM-5)
• Insight specifiers are added (good/fair, poor, absent)
• Minimum duration requirement is retained but less rigid

These are not routine — they are indicated only when the clinical picture is atypical (e.g., acute onset, late onset after age 40, neurological signs, treatment resistance, presentation in a child post-infection):

Before initiating pharmacotherapy (particularly SSRIs or clomipramine), the following baseline investigations may be warranted:

These are mentioned in the notes for understanding pathophysiology, not for clinical diagnosis ^[3]:

SSRIs are first-line for OCD because they have the best side-effect profile ^[3][21].

How SSRIs work in OCD: SSRIs block the serotonin transporter (SERT) → ↑ synaptic 5-HT availability → over weeks, this leads to desensitisation of presynaptic 5-HT1A autoreceptors and postsynaptic 5-HT receptor changes → modulation of serotonergic tone in the CSTC loop → ↓ hyperactivity of the OFC-caudate-thalamic circuit → ↓ obsessions and compulsions.

Why higher doses are needed in OCD vs depression: The SERT occupancy required to modulate the CSTC loop in OCD appears to be higher than that needed for the mood circuits in depression. Studies suggest that OCD requires ~80% SERT occupancy (achieved at higher doses) vs ~60–70% for depression.

^[2][21]

Key prescribing principles for SSRIs in OCD:

• Duration: ≥ 1–2 years after achieving remission, then slowly tapered ^[3]
• Relapse is common in the first few weeks after stopping ^[3]
• Start low, go slow — but titrate to the maximum tolerated dose before declaring treatment failure
• Allow 8–12 weeks at adequate dose before assessing response (vs 4–6 weeks for depression)
• An adequate trial = maximum tolerated dose for ≥ 8–12 weeks
• Try at least 2 different SSRIs before moving to clomipramine

Common side effects of SSRIs (explained mechanistically):

Clomipramine is a tricyclic antidepressant (TCA) that is the most potent serotonin reuptake inhibitor among TCAs. Its name: "chloro" + "imipramine" — it is a chlorinated derivative of imipramine.

Clomipramine is used if SSRI fails ^[3][21].

Why clomipramine works for OCD: Clomipramine is an extremely potent SERT blocker (more potent than most SSRIs). Its active metabolite, desmethylclomipramine, also inhibits noradrenaline reuptake, but the parent compound's serotonergic action is what drives the anti-obsessional effect.

Why it's not first-line: The side-effect profile is significantly worse than SSRIs:

Prescribing: Start 25 mg/day, titrate to 100–250 mg/day. ECG mandatory before starting and at dose increases (check QTc). Contraindicated in recent MI, heart block, severe liver disease.

Venlafaxine is listed as an alternative to SSRIs ^[3]. It is an SNRI ("serotonin-noradrenaline reuptake inhibitor") — at lower doses it acts predominantly as an SRI, and at higher doses it recruits noradrenergic blockade. The anti-OCD effect is likely mediated primarily by the serotonergic component.

Evidence for venlafaxine in OCD is weaker than for SSRIs or clomipramine — it is used when SSRIs and clomipramine cannot be used or have failed.

Anxiolytics are used for short-term relief, but not more than 2–4 weeks at a time ^[3].

Why short-term only? Benzodiazepines (BZDs) enhance GABA-A receptor function → rapid anxiolysis. However:

• They do NOT treat the core OCD pathology (CSTC loop hyperactivity)
• Tolerance and dependence develop rapidly (within 2–4 weeks)
• Withdrawal can exacerbate anxiety
• They impair the learning that occurs during CBT/ERP (BZDs dampen the anxiety that is therapeutically necessary for habituation)

Role: Bridge therapy during the initial 2–4 weeks of SSRI treatment when anxiety may paradoxically worsen due to acute serotonergic stimulation.

Psychoeducation to improve patient's understanding and reassurance ^[3][22].

This is always the first step. Key points to communicate:

• OCD is a recognised medical condition, not a character flaw
• The intrusive thoughts do NOT mean the patient will act on them (crucial for those with aggressive/sexual obsessions)
• Treatment is effective in the majority of cases
• Both medication and psychological therapy work
• Recovery takes time — 8–12 weeks for medication, typically 12–16 sessions for CBT

Psychological support and reassurance ^[22] — but note that excessive reassurance-seeking from the therapist can itself become a compulsion. The therapist must balance being supportive while not feeding into the OCD cycle.

This is the gold-standard psychological treatment for OCD.

Name breakdown:

• Exposure = deliberate confrontation with the feared stimulus/obsessional trigger
• Response Prevention = deliberately NOT performing the compulsion

Exposure and response prevention (ERP) involves exposure to environmental cues that increase symptoms, but preventing the compulsive response (e.g., stopping the patient from washing their hands when they want to) ^[3].

Why ERP works — from first principles:

1. The obsession triggers anxiety → the compulsion provides temporary relief (negative reinforcement)
2. This relief prevents the natural process of habituation (the brain's ability to learn that the feared outcome does not occur)
3. By blocking the compulsion (response prevention) while maintaining exposure to the trigger:
   • Anxiety initially spikes (this is expected and patients must be warned)
   • Over time (typically 45–90 minutes), anxiety naturally decreases through habituation
   • With repeated sessions, the brain learns: "I touched the 'contaminated' surface, I didn't wash, and nothing bad happened"
4. This weakens the obsession-anxiety-compulsion cycle

Effect: ~2/3 with moderately severe rituals improve substantially, comparable to SSRIs ^[3].

Limitations: Less effective for obsessional thoughts that occur without rituals ^[3] — because pure obsessions have no overt compulsion to prevent. For these patients, the cognitive component is more important.

Typical protocol: 12–16 sessions, each 60–90 minutes, with between-session homework (self-directed ERP). A hierarchy of feared situations is constructed from least to most anxiety-provoking, and exposure progresses gradually.

Cognitive therapy as part of CBT ^[3]:

Involves: tackling underlying cognitive beliefs of obsessive thoughts ^[3]:

• Thought stopping and distraction for ruminations ^[3][22] — resistive thoughts only increase their occurrence ^[22]. This is a counterintuitive but crucial principle: the more you try to suppress a thought, the more it rebounds (Wegner's "white bear" experiment). Instead, patients learn to acknowledge the thought without engaging with it.

• Modification of responsibility beliefs: Try to suggest less threatening alternative explanations and discuss any other cognitive distortions ^[3]. For example:

  • "Having the thought 'I might harm my child' does NOT mean I am a dangerous person" (thought-action fusion)
  • "Just because I thought about contamination does NOT mean I am contaminated" (magical thinking)
  • "I am not personally responsible for preventing every possible harm" (inflated responsibility)

Effect: not as effective on its own but increases the effect of behavioural interventions when combined ^[3].

Why does OCD cause depression? From first principles:

1. Chronic distress: The patient endures hours daily of intrusive, ego-dystonic thoughts they cannot control → learned helplessness → demoralisation
2. Functional impairment: OCD progressively restricts the patient's life — they cannot work, socialise, or engage in pleasurable activities → behavioural withdrawal → depressive symptoms
3. Self-criticism and shame: Because the obsessions are ego-dystonic ("I know this is irrational but I can't stop"), patients often feel defective, weak, or "crazy" → ↓ self-esteem → depressive cognitions
4. Shared neurobiology: Both OCD and depression involve serotonergic dysfunction, and the CSTC loop connects to limbic circuits involved in mood regulation
5. Bidirectional relationship: Depression worsens OCD (depressive cognitions amplify the catastrophic appraisals underlying obsessions), and OCD worsens depression (more OC symptoms → more demoralisation)

Clinical significance: Comorbid depression is a worse prognostic factor ^[3] — it reduces engagement with CBT (apathy, hopelessness impair the effort required for ERP), increases suicide risk, and predicts poorer treatment response.

Why is suicide risk elevated?

1. Chronic suffering without relief: OCD rarely remits (~20% in 40 years) if untreated ^[3] — years of unrelenting distress erodes the will to continue
2. Comorbid depression: The single strongest predictor of suicidality in OCD
3. Hopelessness: Especially in treatment-refractory OCD, patients may feel there is "no way out"
4. Shame and secrecy: Many patients conceal their symptoms for years due to shame (especially those with taboo obsessions about sexuality, violence, or religion) → social isolation → suicide risk
5. Absent insight: Patients with delusional-level conviction may experience greater distress because they genuinely believe the catastrophic consequences of their obsessions

> 70% have a lifetime diagnosis of an anxiety disorder such as panic disorder, social anxiety disorder, GAD, and phobia ^[5].

Why the high comorbidity?

• Shared anxiety circuitry: The amygdala-prefrontal circuits involved in anxiety disorders overlap with the CSTC loop involved in OCD
• Shared genetic vulnerability: Common genetic variants (affecting serotonin, GABA, and glutamate systems) predispose to both OCD and other anxiety disorders
• Behavioural overlap: The avoidance behaviour in OCD can generalise to produce phobia-like presentations; the hypervigilance can resemble GAD

Specific patterns:

• Social anxiety disorder: Avoidance of public situations due to contamination fears or fear of performing rituals in public → mimics and may co-occur with SAD
• Panic disorder: Intense anxiety from obsessions can escalate to panic attacks → some OCD patients develop comorbid panic disorder
• Specific phobias: Obsessional phobias (e.g., avoiding kitchens due to knife-related obsessions) may evolve into specific phobia-like presentations

Up to 30% have a lifetime tic disorder ^[5].

This is not merely comorbidity — there is shared striatal pathology. Tic-related OCD has distinct features:

• Earlier age of onset
• Male predominance
• More symmetry/ordering obsessions
• More "just right" feelings (sensory rather than cognitive)
• Poorer response to SSRIs alone → often requires antipsychotic augmentation

Why? Patients use substances to self-medicate the chronic anxiety and distress of OCD. Alcohol and benzodiazepines are GABAergic → rapidly reduce anxiety → powerful negative reinforcement → dependence risk. This is particularly insidious because the substance provides temporary relief but worsens OCD in the long run (disrupts sleep architecture, impairs cognitive processing, interferes with CBT).

The shared compulsive quality links OCD and eating disorders. Both involve repetitive, rule-governed behaviours driven by anxiety. Anorexia nervosa in particular shares the rigidity and perfectionism associated with the OFC-striatal circuit.

Why? OCD consumes enormous time (the obsessions or compulsions take > 1 hour/day ^[1] — and in severe cases, 6–8+ hours/day). This directly reduces productive work time. Additionally:

• Checking rituals delay task completion
• Contamination avoidance restricts which workplaces/tasks are tolerable
• Concentration is impaired by constant intrusive thoughts
• Sick days accumulate due to depression and exhaustion

Studies show OCD patients have significantly higher rates of unemployment, underemployment, and occupational disability compared to matched controls. The economic burden is substantial.

Why? Avoidance behaviour may become pervasive and severely restrict functioning ^[3]:

• Contamination fears → avoidance of public spaces, social gatherings, physical contact → social isolation
• Shame about symptoms → concealment → emotional distance from friends and family
• Reassurance-seeking → strains relationships (partners/family become frustrated with constant demands for reassurance)
• Family accommodation → family members adapt their own behaviour to accommodate the patient's OCD (e.g., washing their own hands repeatedly, avoiding certain words/topics) → reinforces OCD and creates dysfunctional family dynamics

Particularly relevant given that 25% of OCD onset is before age 14 ^[3]. Children and adolescents with OCD may:

• Spend hours on homework due to checking/perfectionism → poor academic performance despite normal intelligence
• Avoid school due to contamination or social fears
• Be misidentified as having ADHD (poor concentration) or behavioural problems

• Marital/partner relationships: OCD is associated with higher rates of relationship dissatisfaction, separation, and divorce. Partners experience caregiver burden, frustration, and their own psychological distress
• Parent-child relationships: Parents with OCD may impose rituals on their children (e.g., excessive cleaning rules); children may learn maladaptive anxiety responses (modelling)
• Family accommodation: When family members participate in rituals or modify their behaviour to reduce the patient's distress, this paradoxically reinforces the OCD cycle

• Defined as failure to respond to ≥ 2 adequate SSRI trials + adequate CBT with ERP
• Affects ~30–40% of patients
• Leads to escalation to clomipramine, augmentation strategies, and ultimately consideration of neurosurgical interventions (DBS, psychosurgery)
• The longer OCD goes untreated, the more entrenched the CSTC loop hyperactivity becomes — akin to a "neuroplastic groove" that becomes harder to reverse

OCD rarely remits (~20% in 40 years) if untreated ^[3]. Even with treatment:

• ~40% remission at 15 years ^[3]
• Many patients have a waxing and waning course with partial remissions and relapses
• Relapse is common in the first few weeks after stopping medication ^[3]
• Long-term or lifelong treatment may be necessary, especially after multiple relapses

Over time, some patients' insight may deteriorate from good/fair → poor → absent/delusional. With absent insight, the patient is completely convinced the OCD beliefs are true ^[1]. This creates a clinical crisis:

• CBT becomes less effective (patient does not see the obsessions as irrational)
• The presentation begins to resemble a psychotic disorder → risk of misdiagnosis and inappropriate treatment
• Social functioning deteriorates further (patient acts on delusional beliefs)
• May require antipsychotic augmentation