THE EXTRAPYRAMIDAL MOTOR SYSTEM 



889 



as the investigations of Ingram et al. (128) showed, this 

 effect is not due to the excitation of rubral elements 

 l)ut is produced by stimulation of the reticular forma- 

 tion and of its fiber tracts in the whole area extending 

 from the caudal subthalamus to the caudal pons. 



The existence of a pathway extending from the 

 pons to the thalamus and responsible for the so-called 

 tegmental reaction is confirmed by Hess' extensive 

 stimulation and destruction experiments. In un- 

 anesthetized unrestrained cats it can be shown to 

 mediate ipsivcrsive bending. The responsible fiber 

 tract is the tractus vestibuloreticulothalamicus (89). 



Rotation of head and anterior body, occasionally 

 also considered as effects of ruber stimulation, are 

 not caused by stimulation of the ruber itself but of 

 the dorsomedially located and very excitable tractus 

 interstitiospinalis [Hassler & Hess (91)]. As Hess also 

 showed, very small stimulating electrodes in the 

 nucleus ruber may also produce contralateral move- 

 ments of the limbs and the facial muscles. These 

 movements are caused by stimulation of the fibers 

 of the brachium conjunctivum cro.ssing the nucleus 

 ruber. 



The purest effect of ruber stimulation is obtained 

 in rodents where it is possible to perform an almost 

 isolated stimulation of its efferent pathway, the 

 rubrospinal tract. In cats rubrospinal stimulation 

 causes raising of the head and the anterior body, as 

 Hess & Weisschedel (112) first demonstrated and 

 as one of us [Hassler (89)] could confirm by study 

 of the Hess material. This movement is not necessarily 

 the only effect produced by stimulation of the large 

 cell elements of the nucleus ruber; however, it is the 

 only clearly demonstrated effect. The distribution of 

 the ruber neurons within the nucleus is so sparse 

 that a stimulus intensity producing definite effects 

 by stimulation of fiber tracts in the neighborhood is 

 still too weak to stimulate enough ruber cells to yield 

 a visible motor effect. 



Destruction of the nucleus ruber in cats [von 

 Economo & Karplus (275), Rademaker (216), 

 Mussen (197), Ingrain & Ranson (126)], which 

 contains large cells, produces only a short transitory 

 unsteadiness in gait and ataxia with overstepping if 

 the destruction is extensive enough to cause a definite 

 degeneration of the rubrospinal tract. A contralateral 

 decrease of muscle tone and proprioceptive reflex 

 activity should also be seen after this type of lesion as 

 well as turning postures or turning movements. 

 The latter are due to a concomitant lesion of the 

 mesencephalic reticular formation and of the ipsi- 

 lateral vestibuloreticulothalamic pathway. As Ingram 



et al. (127) demonstrated, localized ruber lesions do 

 not produce impairment of labyrinthine and body 

 righting reflexes, as Rademaker thought, but only 

 impairment of placing and hopping responses in dogs. 



In cats changes of muscle tone following bilateral 

 lesions in the nucleus ruber are reported to be vari- 

 able; an extensor rigidity and increased resistance to 

 pa.ssive movement has frequently been described 

 [von Economo & Karplus (275), Rademaker (216)]. 

 The latter considered this extensor rigidity primarily 

 as a result of the interruption of Forel's tegmental 

 crossing of the rubrospinal tract. However, as Hess 

 has shown, circumscribed destruction of the rubro- 

 spinal decussation and of the higher parasagittal 

 mesencephalic areas produces in cats a loss of the 

 lifting movements with a permanent lowering of the 

 head. The extensor rigidity earlier described is 

 probably due to the fact that certain other mesen- 

 cephalic structures are simultaneously seriously 

 damaged, von Economo & Karplus, as well as Lafora, 

 had previously observed slow involuntary movements 

 comparable to athetotic-choreiform hyperkinesia 

 following unilateral or bilateral lesions of the nucleus 

 ruber. Recently Lafora {156) again emphasized the 

 presence of such hyperkinetic symptoms following 

 ruber lesions. 



In monkeys destruction of the nucleus ruber or 

 interruption of one rubrospinal tract causes asynergia 

 and a coarse tremor with unimpaired postural re- 

 flexes [Keller & Hare {142)]. This effect seems to be 

 due to the interruption within the red nucleus of 

 fibers coming from the brachium conjunctivum. 

 According to Mettler and Carpenter, interruption 

 in the macaque of the brachium conjunctivum fibers 

 leaving the red nucleus in a rostral direction toward 

 the thalamus does not have any significant effect. 

 Therefore, the very thin rubrospinal tract is considered 

 in monkeys as responsible for the tremor, ataxia 

 and asynergia following lesions of the brachium 

 conjunctivum. In the macaque unilateral or bilateral 

 lesions of the red nucleus produce, according to 

 Mettler, a transitory ataxia, asynergia and tremor 

 from which the animals completely recover. Only 

 after very extensive bilateral lesions of the nucleus 

 ruber does the animal show a specific additional 

 impairment, a hypokinesia, which, however, does 

 not impair motor dexterity. In monkeys Carpenter 

 did not obser\-e any hyperkinesia following localized 

 destruction of the nucleus ruber. 



In clinical neurology an upper and a lower ruber 

 syndrome are recognized. The upper syndrome 

 [Chiray et al. (36)] consists of hemiataxia and hemi- 



