THE CEREBELLUM 



1267 



of the ablation. The estabHshment of the role of in- 

 hibitory withdrawal in the production of these signs 

 grew out of the observation that decerebrate rigidity 

 is remarkably augmented ijy removal of the cere- 

 bellum (22, 32). It remained only for Pollock & Davis 

 (262-265) through the reduction of cerebellar func- 

 tion by ischemia, and Camis (58, 59) through the 

 use of cold, to demonstrate that injury discharges 

 were not essential for the production of the signs of 

 overactivity. These latter investigators went a step 

 further with their demonstration of the importance of 

 the vestibular system in the production of these signs 

 through its excessive facilitatory influences on spinal 

 cord motor functions. Although at this stage of the 

 animal's recovery the major signs involve what might 

 be regarded as postural mechanisms, it was early 

 noticed that some reflex activities also share in the 

 efifects of inhibitory withdrawal. Tendon reflexes 

 (182, 183, 335) and many reflexes involved in the 

 maintenance of stance (277) become hyperactive 

 and remain so for months following the ablation. 



The immediate postoperative signs of inhibitory 

 withdrawal are remarkably mild in the monkey as 

 compared to the quadruped (9, 123, 188-190, 249, 

 290). This form shows no opisthotonus, the forelimbs 

 are not rigidly extended but held in the flexed posture, 

 and the signs of functional exhaltation disappear in 

 2 to 3 days. 



SIGNS OF FACILITATORY wiTHDRAW.AL. As the quad- 

 ruped begins to compensate for the overpowering 

 release from tonic inhibition, it begins to demonstrate 

 evidence of reduced motor neuron discharge giving 

 rise to signs which Luciani (188-190) called atonia 

 and asthenia. With the first attempts to right itself 

 and to assume the standing posture, the animal's hind 

 legs are completely devoid of weight-bearing func- 

 tion. Even the forelegs fail to sustain weight for long. 

 Later, the first attempts to walk are terminated by 

 the collapse of the hind limbs or by a fall precipitated 

 by forelimb collapse. The animal progresses through 

 a stage wherein he seeks the support of walls but 

 eventually emerges into the stage of stabilized de- 

 ficiency. The deficiency of postural tonus and the 

 weakness of muscular contraction are obvious only 

 during the early part of the deficiency period in the 

 animals with total ablation. They may be demon- 

 strated for longer periods of time in the hemidecere- 

 bellate animals in which there is opportunity to make 

 comparison with the normal side in the same animal. 

 The reality of the atonia and asthenia as a sign of 

 cerebellar deficiency was denied by Dusser de Barenne 



(113, 114). It is possible that this investigator missed 

 the relatively brief period during which it may be 

 demonstrated in the totally decerebellate animal. 

 Dusser de Barenne suggested that atonia and asthenia 

 as described by Luciani were the result of inadvertent 

 damage to the vestibular nuclei. However, intentional 

 damage to the vestibular system produces an entirely 

 different syndrome in the chronic animal. In examin- 

 ing his animals for signs of asthenia or weakness, it 

 is possible that he confused evidences of weakness and 

 fatigability. 



In the primate, the evidences of facilitatory with- 

 drawal are more profound and persistent than in the 

 quadruped (9, 123, 188-190, 249). Macaques were 

 unable to stand because of atonia and asthenia for a 

 protracted period after operation. As walking became 

 possible, it was accomplished only with lateral sway- 

 ing and with frequent pau.ses during hind limb col- 

 lapse. 



DISORDERS OF PHASIC CONTRACTIONS. As the quadruped 

 gradually compensated for its deficiencies, locomo- 

 tion improved and the animal developed competence 

 in caring for itself. Full return to normal never oc- 

 curred after complete removal of the cerebellum and 

 residual deficits remained which manifested them- 

 selves most clearly in lack of adequate control of 

 phasic contractions. This was evident for both forms 

 of phasic contraction, whether reflexly or voluntarily 

 induced. 



The phasic postural reactions, so carefully and com- 

 pletely examined and defined by Rademaker (277), 

 were found to be altered during the period of stabilized 

 deficiency. The reflex supporting reaction elicitable 

 from tactile and proprioceptive receptors in the feet 

 and toes was exaggerated. The changes of weight- 

 bearing strength which are produced by displacing 

 the body to one side revealed an exaggeration of con- 

 tralateral inhibition. The hopping reaction, which was 

 lacking early in the recovery period, was delayed and 

 poorly executed during this period. In addition to 

 these postural reflexes, tendon reflexes have been ob- 

 served to be hyperexcitable for months following com- 

 plete removal of the cerebellum (182, 183, 335). The 

 reflex status of the totally decerebellate primate has 

 never been reported as the subject of a detailed 

 study. 



Perhaps the most dramatic of the permanent de- 

 ficiencies following total ablation are the deficiencies 

 of control in time and strength of voluntarily-ev'oked 

 phasic reactions. The various signs which are now 

 called collectively cerebellar ataxia, were first de- 



