THE EXTRAPYRAMIDAL MOTOR SYSTEM 



887 



also be explained by this deficiency of the central 

 mechanism triggering the so-called 'external loop.' 

 This rapid gamma innervation of the muscle spindles 

 l)elongs essentially to the control circuit regulating 

 the length of the muscle in so far as it provides the 

 possibility of adjusting the sensitivity of the annulo- 

 spiral receptors. If this rapid central gamma innerva- 

 tion is missing, a phasic proprioceptive reflex may 

 still result from a sudden change in the length of the 

 muscle, whereas the continuous control and main- 

 tenance of the muscle length and its adaptation to 

 modified initial length becomes impo.ssible. Hence, 

 muscle length is not kept constant in muscular 

 rigidity — in contrast to spasticity — but changes in 

 accordance with external forces. On the contrary, 

 in parkinsonism muscle tension is maintained constant 

 against all external influences by the intact regulators 

 of muscle tension. 



In spite of the loss of central gamma innervation, 

 the peripheral gamma neurons remain morphologi- 

 cally intact for a long time. As the investigation of 

 Byrnes (29) showed, morphological changes are 

 seen in muscle spindles and their innervation only in 

 cases of rigidity of more than 10 years duration. To a 

 large extent the increase in muscle tone in rigor is 

 due to an enhancement of the myotatic reflexes, 

 that is of the tonic component of the stretch reflexes, 

 whereas there is no enhancement of the phasic 

 (monosynaptic) stretch reflexes. 



The reflex character of the so-called plastic muscle 

 tone, which is a component of rigidity, has been 

 demonstrated by its suppression following dorsal 

 root section [Foerster (57), Pollock & Davis (211)] 

 or elimination of muscle receptors by means of 

 novocaine injections in the muscles [Walshe (289)]. 

 Simultaneously, there is no impairment of muscular 

 strength. After suppression of all muscular afferents, 

 the previously rigid limb no longer adapts to changes 

 in length by maintaining a constant muscular tension 

 and also is unable to regain it. This plastic muscle 

 tone is only one component of rigidity. In Pollock & 

 Davis' case of parkinsonism, contractures developed 

 in the biceps, the flexor carpi ulnaris and the palmaris 

 longus 1 1 days after complete deafferentation of the 

 arm by means of rhizotomy which included C 4 to 

 T 4. This so-called resting rigidity following complete 

 suppression of the component sustained by reflex 

 mechanisms is caused by descending central in- 

 fluences originating in the brain stem and impinging 

 upon the alpha cells; this type of rigidity is inde- 

 pendent of the 'external loop.' It also could not be 

 diminished by novocaine injections in the muscle; 



it did, however, disappear during sleep. When the 

 head of the patient, spontaneou.sly turned toward the 

 side opposite to the deafferentation, was turned 

 back to the side of the deafferentiated arm, the tonic 

 contraction was diminished in the flexor muscles of 

 this arm [Pollock & Davis {211)]. 



Both plastic muscle tone and resting rigidity are 

 slightly decreased following interruption of the 

 pyramidal tract, as by Putnam's pyramidotomy. 

 Destruction of the caudate nucleus has no effect on 

 the contralateral muscular resistance [Meyers (186, 

 187), Browder (17)]. However, contralateral rigidity 

 decreases if the anterior limb of the internal capsule 

 and anterior parts of its posterior limb are simul- 

 taneously severed [Meyers (187, 188)]. Destruction 

 of the ansa lenticularis, either by direct exposure or by 

 stereotaxic methods, caused an improvement in 

 rigidity which was more pronounced than following 

 other types of operations (Meyers, Fenelon, Spiegel 

 and Wycis). Destruction of the pallidum either by 

 electrolytic lesions [Spiegel & Wycis (240-242)], 

 by procaine-oil injections [Narabayashi & Okuma 

 (199, 2ooj] or thermocoagulation (Leksell, Talairach, 

 Guiot, Hassler and Riechert) removes contralateral 

 rigidity. The same effect can be obtained by co- 

 agulating the nucleus ventro-oralis anterior (V.o.a.) 

 of the thalamus [Hassler & Riechert (86, 92)] where 

 the fibers form the internal pallidum terminate. 

 Thus, a lesion of the pallidum, or destruction of the 

 pallidocortical systems suppresses the rigor produced 

 by nucleus niger lesions. This is not consistent with 

 the earlier but now unacceptable pallidal theory of 

 parkinsonism which assumed that lesions in the 

 pallidum are responsible for rigidity and akinesia. 



The interruption of the pallidal system, where it 

 may occur, obviously produces — at least in part via 

 efferent corticospinal fibers from area 6aa — a loss 

 of the synchronizing and facilitatory influences upon 

 the interneuronal-anterior horn mechanisms. This 

 not only suppresses the enhancement of the myotatic 

 reflexes but also the descending impulses generating 

 resting rigidity. If the predominance of the peripheral 

 mechanisms controlling muscle tone is thereby sup- 

 pressed, plastic rigidity with stretch and shortening 

 reactions also disappears. If the ansa lenticularis 

 and the external pallidum are simultaneously de- 

 stroyed, the therapeutic effect may in part be due to 

 the suppression of the direct descending pallido- 

 reticulospinal influences upon the anterior horn 

 system. However, this explains parts of the effects 

 only. It does not explain the effect of localized lesions 

 restricted to the internal pallidum and in particular 



