Chapter 10: Obsessive-Compulsive Disorder

The neurobiological basis of obsessive-compulsive disorder involves dysfunction within cortico-striato-thalamic circuits, particularly imbalances in serotonergic neurotransmission and abnormalities in the basal ganglia and prefrontal cortex that disrupt the brain's ability to filter intrusive thoughts and regulate behavioral responses. Exposure and response prevention represents the gold-standard behavioral intervention, functioning by gradually confronting feared stimuli while resisting compulsive behaviors, thereby extinguishing anxiety responses and reducing symptom severity. Pharmacological treatment primarily relies on selective serotonin reuptake inhibitors and clomipramine, a tricyclic antidepressant with potent serotonergic properties, typically requiring higher doses than those used for mood disorders to achieve therapeutic benefit. The chapter then shifts to psychotic disorders, describing hallucinations, delusions, and disorganized thinking as cardinal features that fundamentally alter perception and cognition. Biological theories of psychosis emphasize dopamine dysregulation, particularly hyperactivity in mesolimbic pathways and hypoactivity in mesocortical systems, alongside glutamatergic dysfunction and documented structural brain abnormalities including ventricular enlargement and cortical thinning. Antipsychotic medications work primarily through dopamine receptor antagonism, with first-generation agents producing more pronounced extrapyramidal side effects and second-generation antipsychotics offering improved tolerability profiles while carrying metabolic risks, making medication selection and monitoring essential components of comprehensive treatment planning.