876 



HANDBOOK OF PHYSIOLOnY 



NEtROPHYSIOLGGY II 



there is no participation of the palHdum or nucleus 

 niger. The fact that it is not as yet possible to destroy 

 the small striatal cells selectively may account for the 

 difficulty of producing experimental chorea by means 

 of lesions in the corpus striatum. The hyperkinetic 

 choreic motor phenomena occasionally produced by 

 means of lesions in the nucleus lentiformis may be 

 due to an unintentional interruption of the strionigral 

 fascicle in the pallidum shortly before its entry into 

 the nucleus niger. In Huntington's chorea this fiber 

 tract is always degenerated and replaced by glial 

 proliferations [Vogt & Vogt (270)]. 



Concerning the functional significance of the corpus 

 striatum it is not possible to draw any final conclusions 

 because of the partial divergence between the clinical 

 and experimental results. However, on the basis of 

 all the data asailable, there is general agreement on 

 one point, that the striatum exerts an inhibitory con- 

 trol on cortical voluntary motor activity. The removal 

 of this inhibitory effect can no longer be compensated 

 when the striatal lesion has reached a certain size; 

 thus there appears a pathological excess of motor ac- 

 tivity either of rhythmic or of arrhythmic character. 

 Inhibition of cortical voluntary motor activity seems 

 to be an essential condition for the individual to be 

 able to concentrate temporarily on restricted sensory 

 perceptions or specific motor performances. 



p.allidum; -^ni.m.^l experiments. Tiie differentiation 

 between external and internal pallidum exists only 

 in the primates. In carnivores and rodents there is 

 only one pallidum; the internal pallidum is clearly 

 delimited and exists independently as the nucleus 

 entopeduncularis. This preliminary remark is neces- 

 sary iiecause of the difTering experimental results 

 obtained in primates and in nonprimates. 



Total bilateral destruction of either the pallidum 

 or the nucleus entopeduncularis has not yet been 

 successfully accomplished in subprimate mammals. 

 In cats and dogs no motor effects occur following 

 unilateral focal (but not total) destruction in the 

 pallidum, except an occasional diminished use of the 

 contralateral extremities. If combined with unilateral 

 lesions of the putamen, they produce a marked hyper- 

 tonus of the contralateral extremities with impairment 

 of postural reflexes. In the macaque small lesions 

 also have no lasting effect [Wilson (295)]. As Kennard 

 (145) observed, monkeys with bilateral isolated 

 stereotaxic lesions in the pallidum (without simul- 

 taneous lesions in the putamen) did not show any 

 abnormalities of behaxior. .Such symptoms appeared 



only after additional removal of area 8 which caused 

 an increase in spastic tonus and an action tremor. 

 However, in all cases where larger lesions in the 

 pallidum had been made, a definite action tremor with 

 hypertonia was observed probably as a result of inci- 

 dental damage to the internal capsule and other 

 structures. 



According to Mettler (182, 183) bilateral destruc- 

 tion of the pallidum without simultaneous cortical 

 or capsular lesions produces loss of associated move- 

 ments in monkeys; the animal becomes inactive and 

 cataleptic, and retains for some time even very un- 

 comfortable postures passively imposed upon it. 

 Similar effects following Ijilateral lesions of the hypo- 

 thalamus were called catalepsy by Ranson and 

 Magoun, as was the chronic somnolence with EEG 

 synchronization following destruction of the anterior 

 midbrain reticular formation in the macaque and in 

 cats [French & Magoun (63)]. They correspond to 

 the so-called adynamic state of Hess obtained in the 

 cat after bilateral lesions in the posterior hypo- 

 thalamus and anterior midbrain, that is after destruc- 

 tion of the so-called dynamogenic zone. Only in 

 monkeys [Brown (18)] and chimpanzees [Kennard 

 (144)] do combined lesions of the striatum and 

 pallidum produce slow worm-like nonintentional 

 movements of the extremities. 



It must be emphasized that these manifestations 

 following lesions of the pallidum cannot properly be 

 compared, as Lewy and others still do, with the 

 parkinsonian syndrome in man. 



Effects following experimental stimulation of the 

 pallidum in animals will now be discussed. Stimula- 

 tion of the so-called nucleus lentiformis (pallidum and 

 putamen) produces, according to von Bechterew 

 (273), tonic-clonic movements of the contralateral 

 extremities and the head, even after previous destruc- 

 tion of the motor cortex, von Bechterew considered 

 the pallidum as the origin of these convulsions. 

 Wilson (295) on the other hand declared the pallidum 

 to be electrically unexcitable. Phasic movements of 

 the extremities, elicited by stimulation of the motor 

 cortex, are converted into a 'state of plastic tonus' 

 [Mettler ct al. (184)]. The extremities are neither 

 rigid nor is there a tremor, but they retain passively 

 imposed postures for a long time and relax after a 

 considerable delay. 



Cortical motor responses and knee jerk reflexes can 

 be definitely enhanced by stimulation at a rate of 100 

 per sec. of the posterior pallidum [Peacock & Hodes 

 (206)]. In contrast, Hodes et al. (117) were able to 

 inhibit cortical motor responses and knee jerk reflexes 



