THE RETICULAR FORMATION 



1^97 



appears following division below this region. It is 

 con\enient to consider in explanation that the succes- 

 sive transections eliminate inputs to the reticular 

 formation which are more inhibitory than facilitatory 

 thereby creating an imbalance in reticulospinal out- 

 put in the direction of facilitation. With each succes- 

 sive additional transection, less and less supraseg- 

 mental control over reciprocal function, tonic or 

 phasic, is retained. Finally, the last transection 

 eliminates most, if not all, that is facilitatory, leaving 

 only inhibitory centers or none at all. 



As in truncation experiments, alterations of the 

 tonic state can be achieved by surgically modifying the 

 cerebral loci which appear to be particularly con- 

 cerned with motor systems. In cats, transient spas- 

 ticity can be induced by local resections of the peri- 

 cruciate region (156, 184, 243), the cerebellar vermis 

 (32, 156, 158) and striatum (156, 184) and destruc- 

 tion of all three increases and prolongs the rigidity. 

 This effect is subject to marked phylogenetic varia- 

 tion, as in the frog, for example, fairly normal ap- 

 pearing postures are possible in animals with the 

 bulk of the l^rain removed (i). In contrast, primates 

 exhibit severe postural rigidity and phasic incapacity 

 from cortical motor resection alone. (Clinical spastic- 

 its is discussed also by Denny-Brown in Chapter 

 XXXII oi \hh Handbook.) 



p.AR.^PLEGi.'^. The data support in general the concept 

 of brain-stem facilitatory input to segmental reflex 

 structures rather than of spinal release in explanation 

 of decerebrate rigidity (156, 169, 172). The problem 

 of clinical spasticity, however, presents additional 

 considerations. Paraplegic transections below the 

 brain stem, principally in the lower cervical and upper 

 thoracic regions, initiate flaccid paralysis due, pre- 

 sumably, to elimination of suprasegmental influences 

 and to spinal shock. As time elapses, however, spas- 

 ticity develops and may progress to heroic proportions. 

 Botii hypertonus, commonly in flexion, and hyper- 

 reflexia are displayed. As suprasegmental inputs to 

 the spinal cord are impossible as an explanation of 

 these states, other causative agents must be sought. 



A contributing feature to the spasticity of chronic 

 paraplegia may be the 'artificial synapse." Granit 

 et a/. (103) ha\e demonstrated that impulses are 

 'short-circuited" in acutely injured or transected 

 peripheral nerve; the excitatory discharge normally 

 conducted in a single fiber "leaks" into others. In the 

 spinal cord it would appear that such diffusion of 

 excitation could lead to mass-discharge. Renshaw & 

 Thermal! (226) showed that a similar phenomenon 



can and does occur following incision within the 

 spinal cord and the observations of Scarff & Pool 

 (237) suggest that in human paraplegics short cir- 

 cuiting is a prominent feature at the proximal end of 

 the distal segment below a transection. 



Another factor in the production of the spasticity of 

 paraplegia may be related to ephaptic discharge. It 

 has been suggested repeatedly that, in contrast to 

 synaptic transmission, one cell in the nervous system 

 may be capable of influencing its neighbor extra- 

 synaptically (or ephapticalh') simply by virtue of 

 proximity (14, 35, 91). Transection, conceivably, 

 could enhance or initiate such discharges in the 

 spinal cord. 



Finally, influences characterized by the Schiff- 

 Sherrington phenomenon possibly participate in the 

 spastic state of paraplegia. It can be demonstrated 

 that an increase in decerebrate rigidity can be in- 

 duced in thoracic neuromuscular segments following 

 transection at the thoracolumbar level (94, 233). This 

 transection presumably eliminates tonic inhibitory 

 influences arising in the lumbosacral region from the 

 upper spinal cord. These observations imply that 

 inhibition and perhaps facilitation can arise in the 

 spinal cord itself. Transections inducing paraplegia 

 doubtless severely distort these influences. 



AKINETIC MUTISM. In 1941 Cairns et al. (48) described 

 a patient with a cyst of the third ventricle which 

 pressed intermittently upon the mesencephalic brain 

 stem, inducing a state of immobility and vocal silence 

 called akinetic mutism. Ingraham et al. (122), Bailey 

 & Davis (19) and others (Ross-Duggan, J. & K. Rich- 

 land, unpublished observations; Skultety, F. M., 

 personal communication) were able to produce a 

 somewhat similar syndrome in cats, and Peterson el 

 al. (211) and others (81) in monkeys by placing 

 lesions in the region of the caudal hypothalamus- 

 midbrain tegmentum and the periaqueductal gray 

 substance. 



In his analysis of the problem, Magoun (169) sug- 

 gested that lesions responsible for this condition of 

 hypokinesis interfered with reticular influences 

 directed cephalically as well as caudally. There 

 appears to be, in milder degrees of akinetic mutism, 

 an element of lack of 'will' or of conation similar to 

 that exhibited by certain patients with lesions of the 

 cingulate gyrus (203), suggesting that cerebrothalamic 

 processes may have been rendered deficient by the 

 lesion. This defect coupled with deficiencies induced in 

 brain-stem facilitatory mechanisms were thought to 

 be responsible for the described syndrome. 



