Obsessive-compulsive disorder

Clinical picture (children and adolescents)

• Common themes: contamination and cleaning, fear of harm and checking, symmetry and a "not just right" feeling, counting, forbidden or repugnant thoughts. Children cannot always describe their obsessions; compulsions often draw in the family as well (family accommodation, reassurance seeking). A
• Prevalence: about 2.3% lifetime and 1.2% in the past year (Ruscio et al., 2010). Onset is earlier in males. A
• Onset: in a substantial share of patients, symptoms begin in childhood or adolescence; tic disorders and ADHD co-occur more often in early-onset OCD. B
• Co-occurring conditions: anxiety disorders, depression, tic disorders and Tourette syndrome, ADHD. A

Circuits and networks

• Orbitofrontal Cortex: appraisal of error and danger signals; in OCD, the "something is wrong" signal is mistuned. One of the most consistently activated regions in symptom-provocation studies. B
• Anterior Cingulate Cortex: error monitoring; in OCD the error-related brain response (ERN) is enlarged, also shown in children. B
• Caudate Nucleus and Putamen: habit and action selection; compulsions becoming automatic. Right caudate metabolism decreases in those who respond to behavior therapy or medication (Baxter et al., 1992). B
• Thalamus: the return arm of the loop; in ENIGMA, thalamic volume was larger in unmedicated children and adolescents (Boedhoe et al., 2017). A
• Globus Pallidus and Hippocampus: in ENIGMA, adults had a larger pallidum and smaller hippocampus; pediatric and adult patterns differ (Boedhoe et al., 2017). A
• Inferior Parietal Lobule and Superior Parietal Lobule: in ENIGMA, the parietal cortex was thinner in both children and adults; effects are small (Boedhoe et al., 2018). A
• Dorsolateral Prefrontal Cortex: cognitive flexibility and inhibition; difficulty stopping compulsive behavior. B
• Networks: an imbalance between the Frontoparietal control network (cognitive control) and Salience network (salience, error) networks and the limbic network has been proposed. C

Neurotransmitter systems

• Serotonin (serotonin): the efficacy of SSRIs and clomipramine is the key evidence; OCD needs higher doses and longer treatment than depression. A
• Dopamine (dopamine): in SSRI non-responders, especially with co-occurring tics, adding a low-dose antipsychotic helps. A
• Glutamate: the main excitatory transmitter of the cortico-striatal loop; trials of glutamate-modulating drugs are ongoing, evidence is limited. C
• Heritability: about 47% in a Swedish twin study (Mataix-Cols et al., 2013). A

Imaging and neurobiological findings

• ENIGMA-OCD subcortical (1,830 patients, 1,759 controls): larger thalamus in unmedicated children (d = 0.38); larger pallidum and smaller hippocampus in adults (Boedhoe et al., 2017). A
• ENIGMA-OCD cortex (1,905 patients, 1,760 controls): thinner inferior and superior parietal cortex in children, thinner inferior parietal cortex in adults; small effect sizes (d = −0.10 to −0.33). Differences were more widespread in medicated patients (Boedhoe et al., 2018). A
• In an ENIGMA study comparing ADHD, autism and OCD, small differences in cortical surface area were shared by all three disorders; no OCD-specific structural difference was found (Boedhoe et al., 2020). A

Developmental course

• That brain findings differ between pediatric and adult OCD suggests the disorder affects the loops of the developing brain at different stages (Boedhoe et al., 2017). B
• A substantial share of childhood-onset OCD diminishes or remits by adulthood; in others it runs a chronic course. B

Treatment and the systems it targets

• First line: cognitive behavioral therapy (CBT) with exposure and response prevention. In children and adolescents (ages 7–17, 112 patients), remission rates at 12 weeks: CBT + sertraline 53.6%, CBT alone 39.3%, sertraline alone 21.4%, placebo 3.6% (POTS, 2004). A
• Medication: FDA-approved drugs for children are sertraline (age 6 and up), fluoxetine (7), fluvoxamine (8) and clomipramine (10); they inhibit serotonin reuptake. A
• For treatment-resistant adult OCD there are deep brain stimulation (targeting the ventral capsule and ventral striatum) and transcranial magnetic stimulation options; they are not used in children. B
• Family involvement: reducing family accommodation of compulsions is part of treatment. B

Link to the book (The Green Walnut on the Couch)

• In the book (translated from the Turkish original):
  • OFC and vmPFC, clinical: "OCD, borderline and narcissistic organization, decision making"; where it appears in the book: "mistuning in OCD (Chapters 2 and 12)".
  • ACC, clinical: "Social pain, grief, error monitoring in OCD"; where it appears in the book: "overactivity of the error-detection loop in OCD (Chapter 2)".
  • Basal ganglia, clinical: "OCD, tics, defenses that have become habits"; where it appears in the book: "Compulsions becoming automatic and the change in caudate metabolism with treatment (Chapter 2)".
  • Chapter 2 of the book: "Phase 1 — Foundation (0–6 months): Damasio, Freud; OCD and autism".
• Affective neuroscience interpretation (hypothesis): From Panksepp's perspective: a compulsion can be read as a loop, turned into habit in the basal ganglia, in which the urge of SEEKING to "do something" tries to switch off the anxiety triggered by the FEAR system; this reading fits the book's basal ganglia note ("why is a pattern so stubborn"), but it is not based on direct evidence. C

In the atlas

Regions

Core structures in bold.

Networks

Neurotransmitter pathways

Panksepp systems

References

1. Boedhoe PSW et al. (2020). Subcortical brain volume, regional cortical thickness, and cortical surface area across disorders: findings from the ENIGMA ADHD, ASD, and OCD Working Groups. American Journal of Psychiatry, 177(9), 834–843. DOI: 10.1176/appi.ajp.2020.19030331.
2. Baxter LR et al. (1992). Caudate glucose metabolic rate changes with both drug and behavior therapy for obsessive-compulsive disorder. Archives of General Psychiatry, 49(9), 681–689. Search PubMed
3. Boedhoe PSW et al. (2017). Distinct subcortical volume alterations in pediatric and adult OCD: a worldwide meta- and mega-analysis. American Journal of Psychiatry, 174(1), 60–69. Search PubMed
4. Boedhoe PSW et al. (2018). Cortical abnormalities associated with pediatric and adult obsessive-compulsive disorder: findings from the ENIGMA Obsessive-Compulsive Disorder Working Group. American Journal of Psychiatry, 175(5), 453–462. DOI: 10.1176/appi.ajp.2017.17050485.
5. Mataix-Cols D et al. (2013). Population-based, multigenerational family clustering study of obsessive-compulsive disorder. JAMA Psychiatry, 70(7), 709–717. Search PubMed
6. Pediatric OCD Treatment Study (POTS) Team (2004). Cognitive-behavior therapy, sertraline, and their combination for children and adolescents with obsessive-compulsive disorder. JAMA, 292(16), 1969–1976. Search PubMed
7. Ruscio AM et al. (2010). The epidemiology of obsessive-compulsive disorder in the National Comorbidity Survey Replication. Molecular Psychiatry, 15(1), 53–63. Search PubMed