John F. Fulton 207 



to climb, walk, and run, they have obvious difficulty in finer prehension move- 

 ments. Spontaneous movements, moreover, are considerably slowed. Resist- 

 ance to passive manipulation is increased and marked tremor develops, not 

 seen in unilateral preparations. The tremor is definitely augmented by voli- 

 tional effort and as such possibly differs from Parkinson's tremor. This I shall 

 return to in a moment. 



Further and highly impressive evidence of the intimate association between 

 the cerebral cortex and the basal ganglia has come from Kennard's studies" 

 of the effect of ablating the cortex and basal ganglia of infant monkeys. Lesions 

 of the motor and premotor areas, if made shortly after birth, cause no serious 

 impairment in motor movement. At birth, motor acts are integrated largely 

 at the subcortical level. Lesions of the basal ganglia, on the other hand, if 

 made in infancy cause grave impairment of the motor behavior patterns, 

 indicating that at this stage in the animal's development the cortex has not 

 yet assumed control of basal ganglia activity. With the development of iso- 

 lated movements, as Marion Hines" and others have emphasized, the cerebral 

 cortex assumes dominance in the regulation of motor patterns. As the animal 

 matures, the basal ganglia no doubt remain in the background, giving sup- 

 port for complex adjtistments; all available evidence indicates that they func- 

 tion more in the postural sphere than in that of phasic movement. Biu the two 

 spheres of activity are so closely related that adequate separation is difficult, 

 for, as Stanley Cobb once said: "Every phasic movement begins and ends in 

 a posture." 



Tremor and the Clinical Basal-Ganglia Sy7idromes.—M.?iny attempts have 

 been made in the past to reproduce the involuntary movements which form 

 such a conspicuous part of the so-called basal-ganglia syndrome in men, that 

 is, Parkinson tremor, chorea, and athetoid movements. Kennard^" has been 

 able to induce in monkeys a tremor which often continues during rest and is 

 greatly exaggerated by motion. This has been done by two different pro- 

 cedures: (i) bilateral ablation of the globus pallidus, unassociated with lesions 

 of the cerebral cortex, and (ii) bilateral lesions of caudate and putamen ac- 

 companied by subtotal removal of the precentral convolution (either area 4 or 

 area 6). Tremor established in this manner can be abolished if the remaining 

 portion of the precentral convolution is removed. Integrity, therefore, of the 

 motor projections, extrapyramidal or pyramidal, from the cortex is essential 

 to the production of tremor associated with lesions of either the neostriatum 

 or the paleostriatum. This observation has a bearing upon the neurosurgical 

 procedures recently proposed for the relief of Parkinson tremor, chorea, hemi- 

 ballismus, etc., and will be discussed below. 



Kennard has had less success in producing athetosis and chorea. Athetoid 

 movements have been seen in several infant monkeys following bilateral 

 lesions of the caudate and putamen. Such movements, although unmistakable 

 when present, are transient and difficult to reproduce from one animal to the 

 next. A characteristic jerking chorea was induced in one chimpanzee by a 



