Obsessive-Compulsive and Other Behavioural Changes With Bilateral Basal Ganglia Lesions

Abstract

Eight patients are reported who shared the combination of bilateral basal ganglia lesions and a frontal lobe-like syndrome. The main features were inertia and loss of drive, with preservation of intellectual function. Some patients showed stereotyped activities with compulsive and obsessive behaviour which were sometimes highly elaborate in pattern. Extrapyramidal clinical signs were absent or mild. Brain damage, related to anoxic or toxic encephalopathy, was demonstrated by CT scans and MRI. The lesions appeared to be confined to the lentiform nuclei, particularly affecting the pallidum, although there was generalized brain atrophy in 2 cases. Positron emission tomography (PET) in 7 patients revealed hypometabolism of the prefrontal cortex relative to other parts of the brain. The PET studies suggest dysfunction of the prefrontal cortex as a result of damage to the lentiform nuclei. These clinical, anatomical and functional observations emphasize the role of the circuits linking the prefrontal associative cortex and some specific areas of the neostriatum, including the pallidum. The existence of distinct nonoverlapping circuits in the motor field or in the associative field can explain the fact that basal ganglia lesions may give rise to a clinical picture that is either purely motor, purely behavioural (as in some of our patients), or both. Similarities existed between some symptoms found in our patients and certain features of major psychiatric illnesses such as severe depression, catatonic schizophrenia, and obsessive-compulsive disorder. This raises the hypothesis that some aspects of these psychiatric disorders could be related to structural and physiological disturbances in the systems linking the frontal associative cortex and the basal ganglia.

Association of QEEG Findings with Clinical Characteristics of OCD: Evidence of Left Frontotemporal Dysfunction

“…We are cautious about interpreting this finding in terms of sex, because our sample had fewer male OCD patients. One may speculate that the frontal hypermetabolism (4,31,32) or hypometabolism (5,33) found in PET studies, associated with sensitivity to hypoxia or hypercapnia, may be related to increased slow-wave activity predominantly in left frontotemporal regions after HV (28).…”

A Psychological and Neuroanatomical Model of Obsessive-Compulsive Disorder

“…Damage to the basal ganglia (especially the caudate), the OFC, and the ACC16–22 are associated with the acquisition of OCD symptoms following brain injury 15. Dysfunction of the basal ganglia secondary to a streptococcal infection23 or encephalitis lethargica24 has also been associated with the development of OCD symptoms.…”

Basal Ganglia Output and Cognition: Evidence from Anatomical, Behavioral, and Clinical Studies

“…Several reviews have been published on this subject (e.g., Heindel et al, 1989;Laplane et al, 1989;Levin et al, 1989;Saint-Cyr et al, 1988;Taylor et al, 1990;Owen et al, 1992Owen et al, , 1993Cummings, 1993;Farina et al, 1994;Partiot et al, 1996;Dubois & Pillon, 1997). Instead we would like to emphasize how the arrangement of output channels in the basal ganglia may provide an anatomical framework for understanding the consequences of basal ganglia pathology.…”

“…Patients with lesions largely localized to the globus pallidus display cognitive deficits, compulsive behaviors, and ''psychic akinesia,'' in addition to varying degrees of skeletomotor symptoms (Laplane et al, 1989;Strub, 1989;Bhatia & Marsden, 1994). It is generally accepted that alterations in pallidal output to motor areas of cortex account for the disturbances in motor function in these patients.…”