THE CEREBELLUM 



I27I 



destroyed, extensor tonus appeared ipsilaterally and 

 flexed posture contralaterally. 



This situation has been subjected to a more com- 

 plete analysis in the decerebrate cat. Removal of the 

 anterior lobe cortex was followed by increased rigidity 

 ipsilaterally and flexion contralaterally (66, 316). If 

 the subadjacent tastigius was then destroyed, the 

 rigidity disappeared ipsilaterally and reappeared 

 contralaterally. On the basis of these results. Cham- 

 bers & Sprague (66, 316) considered that part of the 

 fastigial nucleus was activated by extracerebellar 

 afTerents independently of the cerebellar cortex. 

 Moruzzi & Pompeiano (244, 247) have confirmed 

 these results but, utilizing selective destruction of the 

 various portions of the nucleus, have come to a dif- 

 ferent conclusion. They described ipsilateral fastigial 

 atonia with contralateral increase in tonus which was 

 produced by destruction of the rostral part of the 

 nucleus alone. They also described contralateral 

 fastigial atonia and ipsilateral increase in tonus which 

 was produced by destruction of the caudal part of the 

 nucleus alone. They concluded that the increased 

 extensor tonus is dependent upon facilitatory activity 

 conveyed from the caudal part of the fastigius over 

 crossed fastigiobulbar fibers. When contralateral ex- 

 tensor tonus is deprived of this facilitation by caudal 

 fastigial lesions, inhibition from proprioceptors in the 

 rigid limb and from vestibular sources overbalances 

 other sources of extensor facilitation and the rigidity 

 disappears from the contralateral limb. When both 

 nuclei are destroyed, the extreme spasticity dis- 

 appears, the contralateral leg is relieved from some 

 of the inhibitory barrage and becomes rigid once 

 more. In another group of experiments, Batini & 

 Pompeiano (15, 18) have destroyed the origins of the 

 crossed fastigioiiulbar fibers bilaterally and decere- 

 brated their animals several days later. Destruction 

 of the medial and lateral portions of the anterior 

 end of the nucleus then gave rise, respectively, to 

 decrease and increase of rigidity ipsilaterally, thus con- 

 firming the dichotomy of the inhibitory and facilita- 

 tory pathways from the anterior lobe revealed by 

 stimulation studies (243, 245, 246 j. 



Spasticity and other signs of release from inhibition 

 ha\e not been oljser\ed following section of the indi- 

 vidual cerebellar peduncles. 



It is apparent from these studies that the disturb- 

 ances of postural tonus in the animal subjected to 

 cerebellar lesions are not produced in any simple 

 fasliion. The discharge of motor neurons in tonic ac- 

 ti\ity is determined by a balance of influences, among 

 which have been identified cerebellar inhibition, cere- 



bellar facilitation and postural reflex activities or- 

 ganized at the spinal cord level interrelating the limbs 

 on the two sides of the body. Consequently, a single 

 alteration of input to the spinal cord system terminat- 

 ing in the motor neuron may set into action .such a 

 number of interrelated events that it ijecomes impos- 

 sible to identify in any single phrase tlie nature of the 

 primary event. 



POSTERIOR LOBE OF CORPUS CEREBELLi. It will be re- 

 called that, among the signs of cerebellar deficiency, 

 atonia and asthenia were ascribed to loss of facilita- 

 tion. It will also be recalled that facilitatory influences 

 from the anterior lobe have been demonstrated by 

 stimulation experiments and have been abolished by 

 anterior lobe destruction. The anterior lobe, however, 

 is not the only portion of the cerebellum which might 

 be involved in facilitatory influences to the motor 

 neuron, for it will be remembered that the cerebellar 

 hemispheres have been shown to exert an efTect upon 

 the activity of the motor cortex. Thus, with the infor- 

 mation from the stimulation aftd electrophysiological 

 experiments at our disposal, it might be predicted that 

 atonia and asthenia would form part of the picture 

 of deficiencies produced by destruction of the pos- 

 terior lobe. 



Ablations involving most of posterior lobe. It will be 

 recalled that exaggerated postural tonus, hypotonia 

 and disturbances of phasic movement are all signs 

 reported to follow lesions of the anterior and posterior 

 vermis and its efferent paths. Bremer (36) was the 

 first to emphasize the importance of avoiding damage 

 to the vermis in order to reveal the deficits produced 

 by posterior lobe lesions uncomplicated by signs of in- 

 hibitory release. Opisthotonus and extensor rigidity 

 were entirely lacking from these animals, thus con- 

 firming, in a negative sense, the vermal origin of these 

 elements of the syndrome of cerebellar deficiency. 

 During the deficiency period Bremer's animals ex- 

 hibited hypotonia, dysmetria, tremor and weakness 

 of cortically-mediated reflexes, all on the ipsilateral 

 side. These signs were all of short duration, presum- 

 ably because of the rapidity and completeness of or- 

 ganic compensation. In the light of the repeated con- 

 firmations of Bremer's findings as a result of partial 

 lesions of the posterior lobe (see below), the com- 

 pletely negative results of Keller el al. (172) defy 

 understanding. 



The primate exhibits a similar group of signs follow- 

 ing posterior lobe lesions (31, 36, 62). In a summary of 

 experiments performed on different species of pri- 

 mates, Fulton & Dow (126J called attention to the in- 



