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Hyperactivity in this region reinforces obsessive thoughts and behaviors.
Acts as a relay station, filtering sensory information.
Dysfunction contributes to compulsive behaviors.
Plays a role in the initiation and control of movements and habits.
Includes structures like the striatum.
Dysregulation leads to heightened awareness of perceived "errors."
Associated with error detection and emotional regulation.
Overactivity in the OFC contributes to excessive worry and intrusive thoughts.
Involved in decision-making and evaluating rewards.
Cortico-striato-thalamo-cortical (CSTC)
Epigenetics:
Environmental stressors, infections (e.g., PANDAS syndrome), and trauma may modify gene expression and contribute to OCD development.
Neuroinflammation:
Elevated cytokines and inflammatory markers in OCD patients suggest a possible role of immune dysregulation.
PANDAS (Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal Infections):
Inflammatory processes may alter brain function in susceptible individuals.
In some cases, OCD is triggered by autoimmune responses following streptococcal infections.
Variants in genes regulating serotonin (e.g., SLC6A4), glutamate, and dopamine pathways have been implicated.
Family studies indicate a heritability rate of 45-65% in first-degree relatives.
Glutamate:
Emerging research implicates glutamate in OCD, suggesting excitatory-inhibitory imbalances in neural circuits.
Dopamine:
Hyperactivity in the striatum exacerbates compulsions.
Altered dopamine activity may influence compulsive behaviors and habit formation.
Serotonin (5-HT):
SSRIs (Selective Serotonin Reuptake Inhibitors) help restore serotonin balance.
Dysregulation affects mood, anxiety, and inhibitory control.
Reduced serotonin signaling is a significant factor in OCD.