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HANDBOOK OF PHYSIOLOGY 



NEUROPHYSIOLOGY II 



interneuronal mechanisms of the anterior horns 

 producing tremor. Does the resting tremor depend 

 upon peripheral reflex mechanisms, especially af- 

 ferent impulses from muscle and tendon spindles? 

 Foerster (57) and Pollock & Davis (211) observed 

 that severing of the dorsal roots does not reduce the 

 resting tremor but makes it coarser and more ir- 

 regular. Suppression of the muscular afferents by 

 means of novocaine injection into the muscle also 

 does not decrease but rather enhances the tremor, 

 whereas the rigor disappears while muscular strength 

 is unimpaired [Walshe (289)]. Thus it seems that 

 resting tremor is mostly not dependent upon the 

 stretch reflexes of the muscles or their so-called 

 'external loops.' The circuit controlling muscle 

 length (with its receptor in the annulospiral endings) 

 sends inhibitory and regulating impulses through 

 muscle afferents to the interneuronal anterior horn 

 mechanisms which generate the tremor rhythm. 



Furthermore, the interneurons of the anterior 

 horn generating the tremor are controlled by syn- 

 chronizing and desynchronizing reticulospinal in- 

 fluences [Magoun & Rhines (174, 175), Niemer & 

 Magoun (201)]. The desynchronizing influence 

 which at the same time inhibits the slow myotatic 

 reflexes of the parkinsonian syndrome seems to 

 originate in the strionigral system and to use nigro- 

 reticulospinal pathways as efferents. Following 

 deficiency of this desynchronizing effect in the 

 parkinsonian syndrome, descending pallidoreticular 

 influences originating in the external pallidum 

 and exerting a synchronizing effect predominate and 

 enhance myotatic reflexes. Simultaneously enhanced 

 by facilitatory pyramidal impulses, these influences 

 induce the interneuronal system of the spinal cord 

 to produce the rhythmical tremor activity. Thus, 

 destruction of the niger cells upsets the balance 

 between one synchronizing and one desynchronizing 

 system and, accordingly, the tonic and synchronizing 

 influence of the pallidum predominates. Enhance- 

 ment of the tremor following stimulation of the 

 pallidum and its permanent improvement following 

 coagulation of the pallidum confirms this concept 

 of the origin of the resting tremor of parkinsonism. 

 (See also the discussion of tremor in the later section 

 of this chapter concerned with extrapyramidal in- 

 fluences on reflex activity.) 



A definite sign of a nucleus niger lesion in man is 

 the increase of muscle tone, the rigidity which is 

 characteristic of parkinsonism. The results of surgical 

 therapy of the rigidity are clearer than those for 

 resting tremor. Muscular resistance to passive move- 



ments in this state is different from that in spasticity. 

 It is not elastic but viscous, adapts by lengthening or 

 shortening to any new, passively imposed muscle 

 length and maintains constant the strength of its 

 resistance to passive movement. According to von 

 Hoist (280) the automatic muscle tension regulator 

 is in action alone in rigidity, adapting the muscle 

 length to every new limb position but maintaining 

 the muscle tension constant. The inhibitory Golgi 

 tendon organs and the facilitatory flower-spray 

 endings on the intrafusal muscle fibers of the muscle 

 spindles [Hassler (88)] are receptors for muscle ten- 

 sion. In parkinsonian rigidity a suppression of the 

 circuit controlling muscle length is suggested by the 

 maintenance of muscle tension and by the absence 

 of increased and irradiating tendon reflexes. 



According to Sommer (236) and Hoffmann (118) 

 a gamma innervation of the muscle spindles is re- 

 sponsible for the Jendrassik's sign and other reflex 

 enhancing mechanisms. Since in most parkinsonian 

 patients such refle.x enhancing mechanisms do not 

 afl"ect the rigid muscles (see fig. 21), there is probably 

 in them a deficient activity of central supranuclear 

 mechanisms for gamma innervation. However, in 

 parkinsonism the central excitability of the gamma 

 fibers is suppressed only for phasic proprioceptive 

 reflexes and not for myotatic reflexes [Schaltenbrand 

 & Hufschmidt (224)]. The responsiveness of gamma 

 cells to exteroceptive stimuli also remains unimpaired. 

 A central stimulation of the gamma cells still seems 

 to he possible during rigidity involving pathways 

 other than those active during reflex-enhancing 

 procedures. Granit & Holmgren (70) discovered two 

 different central pathways conveying impulses from 

 the mesencephalon to the gamma cells, a fast-conduct- 

 ing pathway in the lateral funiculus crossing to the 

 opposite side, and a slow pathway with so many 

 synapses that an almost total section of the spinal 

 cord is necessary to interrupt it completely. Only 

 the fast-conducting central pathway for gamma 

 innervation, which appears to be identical with 

 the nigroreticulospinal system, is deficient during 

 rigidity. 



During many movements gamma inner\ation 

 precedes the alpha innervation, the former having a 

 kind of 'starter function'; it is precisely this function, 

 however, which is missing in parkinsonism, in which 

 the greatest difficulty is in the starting of a movement. 

 This accounts for the loss of a considerable number 

 of involuntary movements, such as the spontaneous 

 synergic and associated movements. The impair- 

 ment of \oluntarv motor activity in general may 



