Pathology.—The true pathology of idiopathic epilepsy is as yet an unwritten chapter in the history of the disease. We have reason to believe that the essential location of the conditions causative of the explosions which constitute epilepsy is in some part of the brain-cortex. The theory of interference with inhibition through irritation of the higher cells of the cortex, a theory elaborated in extenso by Hughlings-Jackson, is generally ac cepted, but not yet proved. This theory is not inconsistent with the experimental conclusions of Nothnagel tending to es tablish the fact of the existence of a lower convulsive centre in the floor of the fourth ventricle (pons).
If epilepsy can be caused by irritation or extirpation of certain portions of the cerebral cortex, we should find in the brains of epileptics certain manifest pathological changes, and some authors have described such alterations, consist ing essentially in proliferation of the neuroglia. Seventy brains from cases of epilepsy examined. Out of 50 of these which gave typical clinical pictures, 25 showed no change whatever in the cornu ammonis nor in the motor area of the cortex. In the other 25 cases the cornu ammonis was diseased on the right side II times, on the left 13 times, and on both sides once. The changes consisted of atrophy of the pyramidal cells in the third layer, which sometimes extended a considerable distance toward the ter mination of the gyms. Sometimes these cells had almost disappeared; in other cases they contained yellow pigment. In the stratum granulosum the cells were not uniformly atrophied, some apparently escaping the process. The inyelinated fibres proceeding from these cells showed a corresponding degree of atrophy. The subependymal layer, however, was in all cases normal. These atrophied struct ures were replaced by a dense net-work of neuroglia fibres, but a pathological formation of this tissue could not be de tected. There appeared to be no differ ence in the changes presented in the old and young cases; that is to say, old epileptics did not apparently show a more advanced stage of the process than those in whom the disease had existed for a very short time. No distinction could be observed in the clinical symp toms of the two groups; those with the cornu ammonis so altered having ap proximately the same type of symptoms as the others. Three of the cases never had grand seal, and, therefore, the sclero sis cannot be ascribed to excessive dis charge of motor impulses. Bratz (Arai)? f. Psychiatrie, B. 31, H. 3, '99).
The study of the morbid anatomy of epilepsy has so far been equally incon clusive. The abnormal conditions noted have varied with different observers even with the vastly-improved laboratory technique employed within recent years.
The tuberous or hypertrophic sclerosis, found chiefly upon the convexity of the convolutions, by Barthez and Rilliet; the "gliosis" invading the normal cellular tissue, as described by Chaslin; the vacu olation of cortical cells with increase of spider-cells, found by Bevan Lewis; the hyperplasia of neurogliar tissue, with re duction in size and deformity of the cells, as observed by von Geison; these are all interesting and perhaps impor tant; but numerous and insurmountable objections exist in each instance to their final acceptance.
Epilepsy is the dynamical expression of an inhibitory insufficiency, not in dicative of an overproduction of nerve energy, nor disc to a molecular irrita bility per se. The cause of the inhibitory insufficiency is to be sought in the end bulbs of the collateral processes of vari ous cortical neurons. This defect con sists most probably in a structural in completeness, or a numerical deficiency, in the collaterals referred to. These defective collaterals may favor recur rences of convulsions in two ways:— 1. By impairing connection with the neuron (inhibitory storage).
2. By increased resistance to overflow currents, causing a temporary charge of motor axis-cylinders. Langdon (Jour. Nerv. and Ment. Dis., Sept., '96).
In the majority of deaths in status epilepticus there was found vascular le sions and extravasation of blood into the cortex and the medulla, with de struction of adjacent nerve-elements. When these lesions occur in the medulla they are often the direct cause of-death. In other cases they cause damage to the circulatory and respiratory systems, paresis of the limbs, and psychical dis turbance, according to the positions in which they occur in the brain. Weber (Wiener med. Woch., No. 4, '99).
The mental changes in epilepsy are analogous, if not commensurate, with the defective motility. However, to es tablish an adequate coefficient between the occurrence of fits and the degree of dementia is a difficult and complex prob lem. As to treatment, the writers con clude that they have in this study ade quate evidence for the present empirical treatment of the disease in which the individual is given first attention. This consists, largely, to overcome hereditary tendencies and exclude toxic and auto toxic agents, in giving the patient a thoroughly detailed plan of diet, exer cise, recreation, baths, and sedatives. comprised in the administration of bro mides. In the light of the pathogenesis, the histo-pathological changes and their sequence, which result in more or less important impairment of normal cere bral functions, the importance of the earliest treatment is obvious; the dis ease is also too profound in its changes for anything less than the most compre hensive attention.