In those cases which are the outgrowth of migraine the pathological condition is probably an exaggerated tendency to angio-spasm, the original impaired vascular tonus in the beginning giving rise simply to pain and lesser troubles, while after repeated changes of calibre not only nutritive alterations ensue, but hyperexcitability of the bulbar convulsion centres as well.
The labors of those who have endeavored to connect epilepsy with cerebral-tissue alterations have been attended by nothing very definite or positive, so far as pathological explanation is concerned. The post-mortem appearances have varied widely, and the only conclusion to be reached is that which shows that almost any morbid gross alteration of the cerebral mass may be symptomatized by convulsions, but such a production of paroxysmal trouble is much more likely to be the case, and in a more definite manner, when the cortical motor-centres are subject to destructive disease or irritative pressure. This is even not always the case, for numerous cases of injury of the paracentral lobe have been recorded with no showing of resulting convulsions. The long list of autopsies which I will not here consider show that an epilepsy may owe its origin to the pressure of a spicula of bone, or to the pressure exercised by depressed fragments of the same—to tumors or adventitious products, meningitis, cortical encephalitis, vascular degeneration, ventricular œdema, contusio-cerebri, and many other morbid processes which result in rapid or tardy degeneration. Of course, in such cases the genesis of the disease depends not so much upon the nature of the lesion as the location. The fruitful collections of cases of Ogle and Jackson are full of examples of limited growth or disease involving the cerebral cortex, while numerous cases collated by other writers show disease of the bulb or various peripheral parts which have been closely connected with the growth and behavior of the affection.
Several able pathologists have independently and repeatedly found that sclerotic degeneration of the hippocampal folds often existed. Delasiauve and Lébert first observed this lesion, but many modern authorities—among them Meynert, Nothnagel, and Charcot—who have also found this appearance, regard the change as of purely secondary, and consequently unimportant, character.
Tamburini37 reports a case of hemiplegic epilepsy with induration of the left optic thalamus and the left cornu ammonis, in which aphasia existed. Pfleger38 and Henkes have also found the sole lesion to be induration of the cornu ammonis. Of Pfleger's39 43 autopsies, atrophy and sclerosis of the cornu ammonis were found twenty-five times, and it was noted that the extent of the morbid change bore relation to the violence and frequency of the seizures.
37 Sallanzani, Modena, 1879, viii. 550-557.
38 Allg. Zeitschrift f. Psychiatrie, etc., Berlin, 1879, xxxvi. 359-365.
39 Ibid., lxxvi., and Arch. de Neurologie, No. 2, 1880, p. 299.
In many examples, especially where the disease has been found to be unilateral and associated with more or less hemiatrophy, the autopsy disclosed a corresponding hemiatrophy of the brain. Many such cases are reported. I have frequently found epilepsy in association with cerebral hypertrophy, and as a symptom of cerebral tuberculosis it has long been recognized, and numerous cases are reported in which for a long time the paroxysms were the only manifestations of the condition. In one of these cases, reported by Luys,40 the bulb was found involved by tuberculous matter.
40 Archives gén. de Méd., 1869, ii. 641 et seq.