The investigations of Van der Kolk especially, and his followers, certainly give the medulla an important place as the locus morbi of the malady; and it must be assumed, bearing in mind the existence of the vaso-motor centres of Dieters and the presentation of symptoms indicative of disturbance at the floor of the fourth ventricle, that the most important pathological changes must be looked for in this part of the brain.
Jackson's cortical explanation is, however, fully in consonance with the medullary theory. If we study the different stages of the attack, we shall find that there is probably a suspension of cortical inhibition—that a derangement of the cortical cells or discharge may cause a resulting disturbance in the bulb. On the other hand, a reflex irritation through the pneumogastric or from some distal part brings about the same disturbance of equilibrium. There is anæmia due to irritation of the vaso-motor centre, an inhibition of the great ganglion-cells, and a disturbance of function of the important cranial nerves. The primary anæmia and unconsciousness are accounted for by this primary irritation of sympathetic filaments and vascular constriction; the secondary hyperæmia is explained by the experiments of Kussmaul, which demonstrated the succeeding congestion; or by irritation of the spinal accessory and contraction of the muscles of the neck and compression of the large veins. The pupillary, ocular, respiratory, and other symptoms indicate the disturbance of the nerve-nuclei in the bulb. The respiratory difficulty and the interrupted decarbonization of the blood undoubtedly account for the secondary unconsciousness.
Van der Kolk34 in localizing the lesion in the medulla found capillary dilatations in the neighborhood of the hypoglossal nuclei in tongue-biters. In epileptic patients who were in the habit of biting their tongues during the fit the vessels were wider than in those who did not bite the tongue, on an average in the course of the hypoglossus by 0.096; in the corpus olivare, which certainly here plays an important part, by 0.098 mm.; and in the raphé by 0.055. In those who did not bite the tongue, on the contrary, the vessels in the path of the vagus were 0.111 wider than in those in the first, Table A.35
34 “On the Minute Structure and Functions of the Spinal Cord,” by J. L. C. Schroeder Van der Kolk, New Syd. Soc. Trans.
35 TABLE.
| Different Epileptics. | Hypoglossus. | Corpus olivare. | Raphé. | Vagus. |
| Table A—tongue biters | 0.306 | 0.315 | 0.315 | 0.237 |
| Table B—non biters | 0.210 | 0.217 | 0.217 | 0.348 |
| Difference | +0.096 A. | +0.098 A. | +0.055 A. | +0.111 B. |
Nothnagel36 is of the opinion that the anæmia of the brain is not the cause of the convulsions, but that the “excitation of the vaso-motor centre and that of the centre for the muscles are co-ordinate—that both go on side by side, and are independent of each other.”
36 Ziemssen's Encyclopædia, vol. xiv. p. 268.
He by this theory explains the occurrence of those forms of petit mal in which there is loss of consciousness without convulsions, and, on the other hand, twitchings before the coma.
The best argument in favor of this hypothesis is in Jacksonian epilepsy, when monospasms exist oftentimes with a succeeding extension.