MOTOR FUNCTION IN A PATIENT WITH BILATERAL LESIONS OF THE GLOBUS-PALLIDUS

Citation
R. Haaxma et al., MOTOR FUNCTION IN A PATIENT WITH BILATERAL LESIONS OF THE GLOBUS-PALLIDUS, Movement disorders, 10(6), 1995, pp. 761-777
Citations number
84
Categorie Soggetti
Clinical Neurology
Journal title
ISSN journal
08853185
Volume
10
Issue
6
Year of publication
1995
Pages
761 - 777
Database
ISI
SICI code
0885-3185(1995)10:6<761:MFIAPW>2.0.ZU;2-Q
Abstract
This study describes the long-term motor deficits of a patient who, af ter a toxic encephalopathy, sustained extensive bilateral damage to bo th segments of the globus pallidus (GP) and the right substantia nigra (SN). There were no signs of lesions of the pyramidal tracts or of ot her motor structures. The most obvious deficits were an abnormal gait with an exaggerated knee extension and a tendency to fall slowly, espe cially when pushed backward. In contrast, Romberg's test on an unstabl e platform was normal, as were long-latency leg reflexes induced by pe rturbations. Inadequate anticipatory and compensatory postural respons es, in particular across the hip and knee joints, and slow movements s eemed responsible for the falls. Muscle tone was normal but reflex stu dies showed signs of abnormal facilitation and inhibition at various l evels of the neuraxis. We conclude that the GP and SN lesions caused d efective input to premotor cortical and brain stem target zones, Dysfu nctioning of these zones leads to improper control of the descending v entromedial motor system responsible for locomotion, postural control, and reflex status. The deficits in upper extremity motor performance included delayed and slow movements, inaccurate amplitudes of ballisti c responses, a lack of predictive control, and deficits in bimanual co ordination. Sensory feedback, proprioceptive more than visual, played a powerful compensating role in rapid aiming movements. Regional blood flow (studied using O-15(2)) was reduced in multiple frontal cortical regions, among which are the hand areas of the supplementary and prem otor cortex. We hypothesize that this reflected impaired functioning o f these areas, caused by defective bilateral output from GP and SN, an d resulting in the motor deficits of the arm and hand.