[The obsessive-compulsive syndrome: reflection of fronto-caudate dysregulation of the left hemisphere?]

Neuropsychological studies of the obsessional syndrome reveal bilateral frontal dysfunction. Early onset is characteristic of males, who have a more chronic course than females, and who are more often non-dextral. Hypermetabolic activity of the frontal and caudate, bilaterally, is found in most PET investigations, although one report is of relative hypofrontality and global cortical hypometabolism for absolute values. Given the frequency with which basal ganglia disease leads to obsessive-compulsive phenomena (Cf Sydenham's Chorea, Gilles de La Tourette) and frontal lobe inertia, a perturbation of frontal-caudate regulatory motor and ideational sub-systems in the obsessional syndrome appears probable. Bilateral caudate atrophy on CT scan has been reported. Further, EP investigations, both somatosensory and auditory, implicate the left hemisphere in obsessions; together with reduced P300 latencies and during imaginal flooding there is increased left (frontal) hemisphere flow (rCBF). Single case studies document the relationship of obsessions to left frontal-left caudate unilateral pathology. It is suggested that lateralized dysregulation of the left fronto-caudate network is the major cerebral determinant of obsessive-compulsive states.