836 THE SPINAL CORD. 



spinal nerve cells, examined by Nissl's and other histological methods, are found 

 scalloped in contour, shrunken, and with diffusely staining nucleus. Fixed 

 twelve hours after the compression, all the cells are found altered ; and fixed 

 twenty-four hours after the compression, the outlines of all the cells are hardly 

 discernible, and only their diffusely stained nuclei indicate their position. 

 Not in every experiment is the whole grey matter of the region subjected to 

 the stasis destroyed. The ventral horn of the grey matter suffers especially 

 severely. The dorsal horn may remain comparatively unharmed. Clarke's 

 column of cells seems, like the spinal ganglion cells, little harmed. When the 

 cord is fixed seven to nine days after the compression, secondary degeneration 

 is found to have occurred in a large region of distribution. Close round the 

 ventral horns in the lumbar region is a dense ring of degenerated fibres, which 

 are traceable headwards, and come to lie at the periphery of the whole ventro- 

 lateral column, except in its dorsal fifth and in the depth of the ventral fissure. 

 Some of these ascending fibres have a contralateral origin, and pass through 

 the ventral commissure. Fibres in the dorsal columns also degenerate. These 

 are the " endogenous fibres " of the dorsal columns. 1 As studied in the rabbit, 

 they seem to be axons from cells of the dorsal grey horn, which enter the 

 dorsal white column all along the limiting layer against the grey matter, and 

 gradually pass into the dorsal mesial column, lying along the lip of the 

 dorsal median fissure (septum). They can be traced forward to enter GolPs 

 nucleus. The dorsal division of the cerebellar tract is little injured, but that 

 is in part due to the fact that the cells (Clarke's column) of that tract for the 

 most part lie headward of the region of stasis. The afferent roots are hardly 

 at all degenerated. 



Compression of the aorta of the dog close below the renal arteries does not 

 usually produce spinal symptoms, 2 although it does so in some cases. 3 

 Fredericq 4 and Colson 5 produced paraplegia in the dog by blocking the 

 thoracic aorta through one carotid. That motor paralysis should result from 

 the stasis is only in accord with anticipation, seeing that degeneration of the 

 motor root cells ensues ; but the total anaesthesia that has been observed might 

 not have been expected, in view of the intact condition of the afferent root cells. 

 Only a very few fibres in the afferent roots 6 degenerate after the compression, 

 the spinal ganglion cells seeming more resistant than the intraspinal ; and the 

 dorsal columns seem, except for the endogenous fibres, intact. Cutaneous 

 sensation seems therefore to employ a path which early in its intraspinal 

 course involves the grey matter. Miinzer and Wiener ~ observed that in 

 three of their twenty- one experiments one of the dorsal horns of grey matter 

 was not necrotic. In each of these experiments the hind-limb of the same 

 side as the sound dorsal grey horn was noted not to be anaesthetic ; from its 

 skin could still be provoked cutaneous pain. 



Anaemia and asphyxia cause transient exaltation of the reflex reactions of the 

 spinal cord. The spinal effect of excitation of the peripheral end of the vagus 

 is explicable in this way. The same causes can produce spinal convulsions. 

 When the spinal cord of the cat has been severed in the thoracic region, if 

 the circulation be arrested in the isolated portion of the cord, contractions of 

 the muscles of the hind-limbs and tail ensue. 8 The actual sequence of the 

 excitation of the musculature is not constant, but one posture is so frequently 

 assumed as to be characteristic, namely, strong flexion of hip, combined with 

 strong extension at knee and ankle; toward the end of the seizure, lifting 

 of the tail and swaying of it laterally often occurs. These convulsions occur 



1 Singer and Miinzer, loc. cit.; Miinzer and Wiener, loc. cit.; Sarbo, Neurol. Centralbl., 

 Leipzig, 1895, Bd. xiv. S. 664. 



a Miinzer and Wiener, loc. cit. 3 Stenson, Sehiff. 



4 Trav. du lab., Liege, 1890, tome iii. p. 5. 5 Ibid., p. 111. 



ti Singer and Miinzer, loc. cit.; Miinzer and Wiener, loc. cit. 



7 Arck.f. exper. Path. u. Pharmakol., Leipzig, 1895, Bd. xxxv. S. 114. 



8 Schift', Arch./, d. gcs. Physiol., Bonn, 1883, Bd. xxx. S. 202. 



