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.