Obsessive compulsive disorder and the right hemisphere: topographic analysis of lesions after anterior capsulotomy performed with thermocoagulation.

Considerable but uncontrolled evidence suggests that stereotactic capsulotomy by means of thermolesions may provide symptomatic relief for patients with otherwise therapy refractory "malignant" obsessive compulsive disorder (OCD). Unlike in other functional stereotactic interventions, target localization for capsulotomy is based upon anatomical definition only. Few systematic attempts have been made to correlate the site and size of the capsular lesions with postoperative clinical outcome. Between 1976 and 1989 bilateral thermo-capsulotomy (TC) was performed in 22 OCD patients. In 19 patients complete quantitative pre- and postoperative psychiatric rating of OCD symptoms and long-term postoperative MRI studies were available. Cohorts of patients fulfilling criteria for good or poor outcome were contrasted, cases with intermediate treatment effect being excluded. Median postoperative MRI follow-up was 8.4 years (2.4-20.3 y). 9/19 patients fulfilled criteria for good postoperative outcome. In these patients all lesion sites overlapped covering a small area within the right anterior limb of the internal capsule. Lesions within the group of patients with poor outcome (n = 5) were located elsewhere, mostly further anterior in the internal capsule. Differences of lesion overlap between the two outcome groups were significant for the right side (Fisher's Exact Test: p < 0.005). Common topographic features of lesion sites within the right internal capsule were identified in OCD patients responding favourably to capsulotomy.

[1]  J. Mazziotta,et al.  Cerebral glucose metabolic rates in nondepressed patients with obsessive-compulsive disorder. , 1988, The American journal of psychiatry.

[2]  N. Alpert,et al.  Regional cerebral blood flow measured during symptom provocation in obsessive-compulsive disorder using oxygen 15-labeled carbon dioxide and positron emission tomography. , 1994, Archives of general psychiatry.

[3]  K. Bergström,et al.  Magnetic resonance images related to clinical outcome after psychosurgical intervention in severe anxiety disorder. , 1987, Journal of neurology, neurosurgery, and psychiatry.

[4]  C D Frith,et al.  Functional Anatomy of Obsessive–Compulsive Phenomena , 1994, British Journal of Psychiatry.

[5]  S. Simpson,et al.  Neuropsychiatry and SPECT of an Acute Obsessive–Compulsive Syndrome Patient , 1995, British Journal of Psychiatry.

[6]  D. Murphy,et al.  Local cerebral glucose metabolic rates in obsessive-compulsive disorder. Patients treated with clomipramine. , 1990, Archives of general psychiatry.

[7]  P Pietrini,et al.  Cerebral glucose metabolism in childhood-onset obsessive-compulsive disorder. Revisualization during pharmacotherapy. , 1992, Archives of general psychiatry.

[8]  G C Curtis,et al.  Neurophysiologic dysfunction in basal ganglia/limbic striatal and thalamocortical circuits as a pathogenetic mechanism of obsessive-compulsive disorder. , 1989, The Journal of neuropsychiatry and clinical neurosciences.

[9]  J. Mazziotta,et al.  Caudate glucose metabolic rate changes with both drug and behavior therapy for obsessive-compulsive disorder. , 1992, Archives of general psychiatry.

[10]  S. Cumming,et al.  Treatment of obsessive‐compulsive disorder by psychosurgery , 1993, Acta psychiatrica Scandinavica.

[11]  J. Rapoport,et al.  Cerebral glucose metabolism in childhood-onset obsessive-compulsive disorder. , 1989, Archives of general psychiatry.

[12]  C Lindquist,et al.  Neurosurgical treatment for refractory obsessive-compulsive disorder: implications for understanding frontal lobe function. , 1994, The Journal of neuropsychiatry and clinical neurosciences.