Obsessive-compulsive disorder and tic syndromes.
The phenomenology of OCD and TS seem to match perfectly with the existing conceptualization of the functional relationship between frontal cortical and subcortical circuits. Failed editing of thoughts and impulses, perseverative patterns, and inhibitory deficits are the most convenient descriptors of the symptoms, and some operationalized measures can capture evidence for such deficits in TS and OCD patients. Beyond these expectations borne from conceptual models and some broad patterns of distributed metabolic disturbances in neuroimaging studies, a specific causal pathology within CSPT circuitry needs to be identified in these disorders. This is not a criticism of the existing studies of TS and OCD; to the contrary, the scarcity of pathologic material, the limits of resolution of existing technologies, and the heterogeneity of the phenotypes make the accomplishments of these studies more impressive. As clinicians strive to integrate clinical and scientific findings into coherent models for the pathophysiology of OCD and TS, it is useful to identify practical and effective strategies for therapeutic interventions.
Swerdlow
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NR
Department of Psychiatry, University of California, San Diego, La Jolla, California, USA. nswerdlow@ucsd.edu
D001521:Behavior Therapy; D001689:Biological Psychiatry; D003131:Combined Modality Therapy; D003342:Corpus Striatum / Q000503:physiopathology*; D018492:Dopamine Antagonists / Q000627:therapeutic use; D006801:Humans; D009446:Neurobiology; D009448:Neurochemistry; D009771:Obsessive-Compulsive Disorder / Q000175:diagnosis / Q000453:epidemiology / Q000209:etiology / Q000503:physiopathology* / Q000628:therapy*; D015995:Prevalence; D017367:Selective Serotonin Reuptake Inhibitors / Q000627:therapeutic use; D013788:Thalamus / Q000503:physiopathology*; D013981:Tic Disorders / Q000175:diagnosis / Q000209:etiology / Q000503:physiopathology* / Q000628:therapy*
D018492:Dopamine Antagonists; D017367:Selective Serotonin Reuptake Inhibitors