THE RETICULAR FORMATION 



1^95 



pattern has been described for the reticular formation. 

 That some such order may exist, however, is indicated 

 by the microelectrode studies of Scheibel el al. (241) 

 and Hernandez-Peon & Hagbarth (iii) who were 

 able to activate some specific units in the reticular 

 formation by cerebellar polarization, but not others. 

 This matter clearly requires additional attention. 

 (The reader may care to consult Chapter LI in this 

 Handbook which considers cerebellar function.) 



VESTiBt'LAR SYSTEM. Following early truncation ex- 

 periments it was suggested that vestibular function 

 was facilitatory in nature and tliat its powers were 

 exerted directly upon the spinal cord (168). Subse- 

 quently, it was demonstrated that, while decerebrate 

 rigidity is ameliorated by vestibular destruction (18, 

 156), facilitation of cortically- or reflexly-induced 

 movement could be elicited by brain-stem stimulation 

 after destroying vestibular nuclei or interrupting 

 their descending connections (18). It was concluded, 

 therefore, that both structures (reticular formation 

 and vestibular nuclei) acted upon segmental reflexes. 



It has been suggested that vestibular influence is 

 directed principally at control of tonic reflex activity 

 while the reticular formation is concerned chiefly, if 

 not exclusively, with phasic responses (18). Because of 

 the functional relationships between brain-stem 

 structures, however, it is doubtful that a clear dis- 

 tinction of this kind can be supported. Ample evidence 

 now indicates that vestibular influences upon somatic 

 motor mechanisms are inextricably associated with 

 those of the reticular formation (95, 96, 135, 167), and 

 such connections are now known to represent the 

 principle route through which vestibular influences 

 are exerted upon the spinal cord (96). Thus, while 

 the vestibular nuclei are capable of acting directly 

 upon spinal reflexes, much more potent vestibulo- 

 spinal influences are exerted by way of the reticular 

 formation. 



Vestibuloreticulospinal influences are bilateral, 

 and reciprocal effects upon flexor and extensor mus- 

 cles have been reported (96). In addition to being 

 reciprocal, however, responses appear also to be re- 

 versible as discharges from a single reticular cell 

 were augmented when the head was turned in one 

 direction (vestibular stimulation) and suppressed 

 when turned to the opposite side (95). Reticulospinal 

 excitation was found to be tonically energized by the 

 vestibular apparatus as bilateral eighth nerve section 

 caused the monosynaptic reflex to diminish and its 

 latency to lengthen (96). Vestibulospinal conduction 

 was very rapid; the direct response had a latency of 



4 to 5 msec, to the ventral root of L7 while vestibulo- 

 reticulospinal transport required 7 to 9 msec. (93). 



B.-^s.-^iL GANGLIA. It is Well knowu that the basal ganglia 

 form an integral part of the 'extrapyramidal" system, 

 yet no striopallidal effector pathway directly to the 

 spinal cord has been demonstrated. It has been pro- 

 posed that the principal influence of basal ganglia 

 upon spinal motor activity is exerted through thalamic 

 and cerebellothalamic reverberation to the cortex 

 and through pyramidal or parapyramidal transport 

 (47, 86). While such reverberation doubtless has 

 functional importance, it is also probable that activity 

 generated within the basal ganglia is expressed di- 

 rectly upon the spinal cord by way of the reticular 

 system (55, 170). The striatum is known to relate 

 anatomically with activating cortical zones (98) and 

 with the reticular system (65, 223). Striopallidal con- 

 tact with the cortex (68, 176) and with the thalamic 

 and brain-stem reticular system (247) has been es- 

 tablished by physiological testing. Pathways exist, 

 therefore, to mediate direct as well as cortical trans- 

 mitted influences from basal ganglia. 



It has been reported that stimulation of the striatum 

 does not elicit movement, hence that the basal ganglia 

 required a background of cortically induced move- 

 ment to operate (86) Supporting this concept are the 

 observations that movements or postures elicited by 

 cortical excitation are inhibited (86, 186) or are 

 transferred into a state of plastic tonus (185) by 

 pallidal stimulation. Contrastingly, Sweet el al. (264) 

 have demonstrated that excitation of pallidal out- 

 flow in preparations in which the cerebral peduncles 

 had been transected resulted in repetitive movements 

 of the extremities. Ward (284) was unable to elicit 

 inhibitory responses upon stimulating the caudate 

 nucleus of unanesthetized animals. 



That the basal ganglia exert an inhibitory in- 

 fluence upon motor mechanisms which is not con- 

 ducted via the pyramidal tract is suggested by the 

 fact that spasticity is elicited by cortical motor re- 

 section and that it is enhanced by subsequent striopal- 

 lidal destruction (160, 184, 243). Conflicting evidence 

 is supplied by clinical observations in which tremor 

 and spasticity are alleviated by surgical lesions made 

 in the basal ganglia (57, 188, 257) thereby, according 

 to Cooper (57), eliminating facilitatory contributions 

 to muscular tonus and movement. 



In view of conflicting evidence, therefore, it must 

 be supposed that the basal ganglia contribute to 

 motor mechanisms largely by virtue of their connec- 

 tions with the thalamic and brain-stem reticular sys- 



