THE CEREBELLUM 



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conjunctivum responsible for the ataxic signs and for 

 the tremor liave produced somewhat confusing re- 

 suhs (62, 206). 



Akhough section of the inferior cerebellar peduncle 

 has not been reported to give rise to any signs refer- 

 able to the fastigiobulbar fibers which it contains, 

 its interruption produces deficiencies which are ap- 

 parently due to its cereijellopetal fiber content. Ipsi- 

 lateral asthenia, hypotonia and dysmetria of transi- 

 tory nature are reported to occur in the dog and 

 monkey (25, 1 18-120). These signs get quantitatively 

 more pronounced without change of quality as the 

 lesion involves the corpus restiformis at higher and 

 higher levels. Turner & German (340) report that 

 disturbances of locomotion followed .section of the 

 middle cerebellar peduncle. 



Persj>ective 



It will be recalled that the experiments in\olving 

 electrical recording and the experiments involving 

 stimulation revealed a degree of somatotopic organi- 

 zation of the cerebellar cortex which was somewhat 

 diffuse, showing overlapping fields and indistinct 

 borders. The experiments involving ablation reveal 

 the .same sort of picture insofar as the vermis is con- 

 cerned, with only the paramedian lobule affording 

 good correlation with electrophysiological data. 



However vague the somatotopic picture may be as 

 revealed by all methods of study, there are certain 

 correlations which deserve attention. The major in- 

 fluence on postural tonus revealed by stimulation 

 concerns the anterior lobe and the fastigial outflow. 

 The major source of the inhibitory release responsible 

 for the dynamic signs of spasticity following ablation 

 is the anterior lobe and fastigial outflow. This is the 

 area in which are concentrated the terminations of the 

 spinocerebellar afferent systems. On the other hand, 

 the electrophysiological experiments revealed that 

 cerebrocerebellar afferents terminate in the anterior 

 as well as the posterior lobe, thus failing to reveal a 

 differentiation, on this basis, between the paleocere- 

 bellum and the neocerebellum. It is perhaps sig- 

 nificant that atonia and ataxia as signs of cerebellar 

 deficiency also fail to afford a distinction between the 

 paleocerebellum and neocerebellum since they are 

 associated with lesions in both portions of the organ. 



The reader is only too aware that the deficits which 

 follow cerebellar ablation are complex and difficult 

 to understand solely on the basis of the observation 

 and description of the deficits. Real understanding 

 will come only when the details of the mechanisms 



and the disturbed functions which underly these 

 deficits are better known. Such mechanisms can be 

 revealed only by more sophisticated testing of motor 

 neuron control systems carried out in the presence 

 and in the absence of cerebellar function. .Such ex- 

 periments may be directed toward the question of 

 how the cerebellum affects a gi\en control system. 

 Some experiments of this variety have been carried 

 out but only a start has been made. This sort of in- 

 formation will be briefl\' reviewed in the following 

 section of this chapter. 



MECH.-^NISMS OF CEREBELL.-\R FUNCTION 



Aiechani.sms of Influence upon Postural Tonus 



The tonic discharge of a spinal cord motor neuron 

 represents, at any moment, the integrated result of a 

 multitude of influences which serve to adjust the rate 

 of discharge in such a way as to fulfill the needs of 

 posture. One type of maladjustment of this function 

 may arise (a) as a result of an excessive barrage of 

 excitatory impulses driving the motor neurons at a 

 higher frequency, or b) as a result of a withdrawal of 

 tonic inhibition, leaving the motor neurons more re- 

 sponsive to excitatory impulses which are then 

 capable of increasing the rate of discharge. Either of 

 these changes would, until compensated, appear as 

 an exaggeration of tonic muscle contraction. Diminu- 

 tion of tonic muscle activity could, of course, also 

 arise in two ways by the reverse of the changes de- 

 scribed above. 



ORIGINS OF HYPERTONUS. The Origins of the hyper- 

 tonus or spasticity which follows immediately after 

 cerebellar ablation, more obviously in quadrupeds 

 than in primates, are numerous and not fully under- 

 stood. Even though vestibular reflexes still remain in- 

 tact (94, 194) after removal of the cerebellum, this 

 is not to say that the vestibular system is not altered 

 in its function. The facilitatory effect of the lateral 

 vestibular nucleus upon tonic activities of the spinal 

 motor neurons has been fully demonstrated (10). It 

 is quite probable that the release of these nuclei from 

 tonic cerebellar inhibition (97) is one of the important 

 sources for the dynamic increase in tonus (184, 266, 

 318). Further contribution to the overactivity of motor 

 neurons probably originates through a release from 

 inhibition of tonic proprioceptive reflexes originating 

 in neck musculature (12, 16). It is possible that such 

 release is not direct, but secondary to withdrawal of 



