THE PYRAMIDAL TRACT: ITS EXCITATION AND FUNCTIONS 



839 



equal to that supplying the subcervical segments and 

 therefore greater than that exclusively supplying the 

 leg segments, one would expect the arm to be more 

 impaired. The contrary superiority of arm over leg is 

 probably a measure of the effectiveness of the un- 

 crossed paths (39, 60, 89, 93) which supply chiefly the 

 cervical segments. 



Superficial reflexes such as the abdominal and 

 cremasteric, and local reactions to pin prick, are 

 severely attentuated or abolished. Deep reflexes are 

 elevated in threshold, slow and full, presumably be- 

 cause they are unchecked by antagonistic reciprocal 

 contraction. Tonic neck reflexes are absent and clonus 

 does not occur. Contact and visual placing reactions 

 and proprioceptive hopping and placing are weak. In 

 both the monkey and the chimpanzee, a forced grasp 

 reflex is prominent, i.e. stretch on the flexor tendons 

 of the digits induces strong digital flexion. This reflex 

 may be so severe that it interferes with climbing, the 

 animal often getting 'hung up' because it is unable to 

 release its grip on the cage bars. Occurrence of forced 

 grasping is surprising since previous cortical extirpa- 

 tion studies suggested that the grasp reflex is released 

 by interruption of 'extrapyramidal' rather than py- 

 ramidal fibers (37), and even more so because the 

 other signs of pyramidotomy suggest interruption of 

 an excitatory pathway rather than release of spinal 

 reflex centers from descending inhibitory impulses. 



In the monkey the plantar reflex is obtunded, but 

 the pattern is normal (ventroflexion). In the chim- 

 panzee, however, a Babinski sign with dorsiflexion 

 and fanning of the toes is a constant and enduring 

 finding after pyramidal section as it is following lesions 

 of area 4 (38). 



In both the monkey and the chimpanzee (but more 

 prominently in the monkey) decreased skin tempera- 

 tures are consistently found in the paretic extremities, 

 suggesting a tonic inhibitory effect of pyramidal fibers 

 on sympathetic preganglionic neurons (but see 53). 

 Finally, both monkeys and chimpanzees surviving 

 pyramidotomy for 2 months or more show decreased 

 muscle mass in the paretic extremity, and histological 

 examination of the muscle shows atrophy with shrink- 

 ing of fiber size. 



Particular interest attaches to the finding of hypo- 

 tonia following experimental pyramidotomy in pri- 

 mates because it conflicts with the persistent teaching 

 of clinical neurology that pyramidal tract interrup- 

 tion produces spasticity. This contention has no 

 scientific basis because lesions in man are invariably 

 mixed. There is no known instance of isolated py- 

 ramidal tract interruption in man, with the possible 



exception of the much quoted case described by 

 Hausman (43) in which the resulting paralysis was 

 flaccid or 'flail-like' rather than spastic. 



Nevertheless, it may be forcibly argued that bulbar 

 pyramidotomy is not equivalent to total destruction 

 of the cells contributing to the pyramidal system. The 

 proximal portions of the neuron reinain intact. The 

 cell bodies show retrograde chromatolysis and reduc- 

 tion in size but do not undergo irreversible degenera- 

 tion (50) ; presumably, they remain functional. This 

 type of reaction is characteristic of cells having axons 

 which give off numerous collaterals central to the 

 point of amputation, and there is abundant evidence 

 that pyramidal fibers spawn many collateral branches 

 during their course from the cortex to the decussa- 

 tion. Branches to the striatum, the substantia nigra 

 and the brain-stem reticular formation have been 

 described; but some of these may be 'extrapyramidal' 

 endings rather than pyramidal collaterals. Numerous 

 true collaterals are given oflf to the pontine nuclei 

 (88, p. 967). In the bulb, particularly at the level of 

 the facial nerve nucleus, many fine collaterals run to 

 the large cells of the medial reticular formation (88, 

 p. 957; Scheibel, A. & M. Scheibel, personal com- 

 munication).^ There are, therefore, numerous points 

 at which impulses generated in corticospinal neurons 

 may be fed into descending pathways other than the 

 pyramid, and the distinction between pyramidal and 

 extrapyramidal systems loses functional significance. 



All pathways innervated by suprabulbar collateral 

 branches are left intact after pyramidotomy, which 

 amputates only the direct pathway from cortex to 

 spinal cord, and it is quite possible that interruption 

 of the same axons at levels rostral to the collateral 

 branching might yield quite different results. Signifi- 

 cantly, Tower (102) found that lesions in the pons 

 (where pyramidal collaterals are profuse), interrupt- 

 ing partially or completely the pontine corticospinal 

 bundle, produced clear-cut spasticity with "exag- 

 gerated postural and tendon reflexes, excessive tone 

 of 'clasp-knife' quality, and readily excitable clonus" 

 in monkeys. 



It may develop that electrical recording techniques 

 will give further information about the pyramidal 

 collateral pathways which are so difficult to follow 

 with certainty by anatomical techniques. Surface 

 stimulation of the bulbar pyramid should antidromi- 



' Cryptically in another place (88, p. 890) Ramon y Cajal 

 states that the pyramidal fibers give off no collaterals through- 

 out their bulbar course. Nevertheless, collaterals are shown 

 clearly and labeled as such in several figures (e.g. 88, figs. 409, 

 43"). 



