THE EXTRAP'lRAiMIDAL MOTOR SYSTEM 



875 



of a functional interrelation between the cerebral 

 cortex and the striatum. There is a low-voltage 

 spontaneous electrical activity both in the caudate 

 nucleus and in the putamen. Howe\er, a high-voltage 

 spontaneous activity develops as soon as all fiber 

 connections with the cortex are severed. Direct stimu- 

 lation of the caudate nucleus or of structures projecting 

 to it induce slow waves of 180 to 250 msec, duration. 

 During this time a relatively inactive phase appears 

 in the isocortex, the hippocampus and the unspecific 

 thalamic nuclei [Umbach (260)]. After this phase 

 spindle acti\ity develops both in the caudate nu- 

 cleus and in the other structures. Spindle activity 

 can also be evoked in the anterior thalamic nuclei and 

 in the centrum medianum by deli\ering single shocks 

 to the caudate nucleus. Following low frequency 

 stimulation of the caudate nucleus the responses of 

 the oral ventral thalamic nuclei and the centrum 

 medianum are synchronized with the stimulus fre- 

 quency. This is also true for certain areas of the 

 frontal cortex. Stimulation of the saine thalamic nuclei 

 at higher frequency can produce a generalized de- 

 synchronization of the entire cortex [Shimamoto & 

 Verzeano (233)]. 



The caudate nucleus has a high seizure threshold 

 and a short .seizure duration. Seizure activity in 

 other structures also can be inhibited by caudate 

 stimulation [Umbach (262)]. When the excitability of 

 the caudate nucleus suddenly increases during a 

 seizure in such a way that high \oltage potentials de- 

 velop, there is usually a simultaneous inhibition of the 

 tonic phase followed by the onset of the clonic phase 

 of the seizure. In animals with simultaneous lesions 

 in the cortex and the striatum epileptic seizures and 

 electrical seizure activity in the EEG are ijoth par- 

 ticularly serious and longer lasting than in those with 

 cortical lesions alone [Kennard & Nims (146)]. 



Consequently, the caudate nucleus seems to have 

 (even more than the putamen) restraining functions 

 controlling the level of excitability of the cerebral 

 cortex as a whole. The lack of inhibition acutely 

 following bilateral caudate destruction seems to be 

 the reason for the transitory disorientation of the 

 operated cats. This inhibitory function may play an 

 important role under normal conditions in selectively 

 inhibiting impulses from other sensory systems or 

 from areas of activity which do not belong to the 

 pattern of excitation most significant at the moment. 

 Thus it is likely that the striatal system not only con- 

 trols motor acti\ity but also the cerebral cortex since 

 it is a link in the unspecific projection system. 



striatum: studies in ma.n. Atrophy of the striatum 

 (putamen and caudate nucleus) was the first definite 

 anatomical change observed in an extrapyramidal 

 motor disease with a well-defined symptomatology, 

 namely Huntington's chorea (Alzheimer, Vogt & 

 Vogt). It has since been repeatedly confirmed that 

 destruction of the small ner\-e cells of the striatum is 

 the major lesion in this disease. This motor disorder 

 is characterized by rapid in\'oluntary aimless move- 

 ments with irregular distribution which is enhanced 

 by voluntary movement. Voluntary motility is severely 

 impaired by hyperkinetic in\oluntary manifestations 

 and also by a general muscular weakness and hy- 

 potonia but not by pyramidal pareses which do not 

 belong to the picture. 



However, the lesions in Huntington's chorea are 

 not restricted to the striatal system but also occur 

 in the grey matter of the cerebral cortex, in parts of 

 the superior olives, in the tuberal nuclei of the hypo- 

 thalamus (Wahren) and in other nuclei. There are 

 cases with very severe chorea in spite of a very slight 

 involvement of the cerebral cortex. Other processes, 

 such as senile or encephalitic damage, may also cause 

 choreiform motor disorders, as in Sydenham's chorea. 



Necrosis of the putamen is characteristically ac- 

 companied by severe hyperkinetic disorders which 

 may be choreiform or, as in Wilson's disease, inay be 

 athetotic or torsion-dystonic in character. 



When perivascular foci {etat precrible) perforate 

 the striatum, the only clinical sign resulting is a 

 simple postural tremor when the patient is at rest 

 without hypotonia, rigor or akinesis [Hassler (80)]. 



According to the observations in man by 

 Narabayashi & Okuma and Cooper, the injection of 

 procaine in tlie putamen may cause a transitory 

 tremor at rest. Larger cystic foci in the base of the 

 putamen do not produce clinical symptoms, as far 

 as we know. More or less extensive hemorrhages in- 

 volving the corpus striatum often cannot be diag- 

 nosed by their clinical manifestations. Unilateral 

 removal of the head of the caudate nuclei had neithei 

 disadvantageous clinical effects nor therapeutic 

 efTects on parkinsonian symptoms, as the operations 

 of Meyers (187, 188) and Browder & Kaplan (16) 

 showed. 



It may therefore be concluded that single circum- 

 scribed striatal foci of small or medium size usually 

 do not cause clinical disorders. Di.sseminated damage 

 in larger areas or large single foci cause both static 

 tremor and tremor at rest. Severe diffuse destruction 

 — with predilection for the small striatal celLs — causes 

 a choreiform hyperkinesia, it being assumed that 



