J. B——, a bright boy aged sixteen, was sent to me by F. H. Bosworth in April, 1883. He comes of nervous stock, his mother being subject to epilepsy, and his father is an eccentric man who manifests his mental peculiarities chiefly in a morbid restlessness and irascibility. There is a brother who is healthy. The attention of the parents was first called to the boy's condition by his recital of a sudden attack which occurred during the summer of 1882. While rowing upon a river he suddenly and completely lost the visual use of the right eye, so that in looking at a number of ducks swimming near his boat he failed to perceive those upon one side of the flock. This condition lasted for twenty minutes, and after a brief and severe pain over the right eye he became unconscious, the unconsciousness being preceded by a tingling and numbness of the hand, forearm, arm, and left side of the tongue. He has subsequently had eight or ten of these attacks, of which the following is an example: Usually without any bad feelings, physical or mental, he, while engaged in any duty or at any time, suffers a sudden unilateral blindness. This is never gradual, and not like the form of amblyopia in which the visual field is gradually reduced. There is some hemichromatopsia. It would seem as if the retinal anæsthesia was unequal, for while usually the loss is complete and universal, it sometimes happens that there is only a limited loss. Upon one occasion, while reading, he suddenly lost the printed matter of the right lower half of the page below a diagonal line extending from the right upper corner to the left lower corner. There is never diplopia. This deprivation lasts anywhere from ten to twenty minutes; meanwhile, a distal anæsthesia, coming very gradually, involves at first the fingers of the opposite hand, and successively extends to the forearm, arm, and other parts, as I have already mentioned. There seems to be analgesia as well as anæsthesia, for a pin may be run into the muscles without producing pain, and upon one occasion the gum was freely pricked without any discomfort to the patient. It invariably happened that the cutaneous sensory trouble occurred upon the side opposite to the hemianopsia and neuralgia, and in the greater number of instances the left side was that affected. The third stage of the attack consists in migrainous headache of a very severe kind, and which sometimes lasts for an hour or more. There is a subjective feeling as if the eye was pushed forward. This disappears with nausea and relaxation. More often he loses consciousness when the anæsthesia reaches its limit, which seems to be the extension of the anæsthesia to the gums. Occasionally there are slight convulsive movements upon the anæsthetic side. While the attacks involve the left side of the body as a rule, it happens that when there is primary left hemianopsia and right-sided anæsthesia the boy becomes very much confused in speech, and sometimes is paraphasic, the trouble being but transitory. He is sometimes unable to speak at all, though perfectly conscious and in possession of his faculties. No pupillary disturbance has been noticed at any time. Upon two occasions there was a swelling of gums and tongue, which was not only subjective, but perceived by the mother. Occasionally he sees prismatic colors and rays before the blindness, but this has been only once or twice. During his early life he had attacks of slight numbness of the hands and feet which were not thought much of, and he had headache as well. He has been a somnambulist.
MORBID ANATOMY AND PATHOLOGY.—The literature of the experimental physiology of epilepsy is enriched by the observations of a variety of careful students, among them Sir Astley Cooper, Kussmaul and Tenner, Brown-Séquard, Nothnagel, Schroeder Van der Kolk, Pitres, Hughlings-Jackson, and the followers of the localization school, as well as many others more or less distinguished.
The experiments of many of the early writers were directed for the purpose of ascertaining the relations of circulatory variations to convulsive seizures, and the most notable were those of Burrows and Kussmaul and Tenner. These latter produced compression of the carotid arteries, and instituted cerebral anæmia by free and exhausting hemorrhages. As a consequence, the emptying of the cerebral vessels was followed by a loss of consciousness and by epileptiform convulsions, and it was necessary to produce the same result to compress all the great afferent vessels of the brain. The experience of surgeons generally is, that ligation of the common carotid upon one side of the neck is sometimes very apt to produce an alarming anæmia, with occasional convulsions, and sometimes fatal consequences.
The experiments of Hall, Landois, Hermann, and others, as well as those of the writers just mentioned, show that carotid compression results in capilliary anæmia and venous hyperæmia, and that with cessation of this pressure there is a sudden congestion of all vessels. The susceptibility of the brain is greatest at its posterior part and between the optic thalami and the cord. When the bulb was subjected to sudden changes in its nutrition—such, for instance, as followed the experiments of Hermann, who ligated simultaneously the superior and inferior venæ cavæ of a rabbit—there were not only convulsions, but various cardiac and other disturbances which were undoubtedly due to central impairment of function. Kussmaul and Tenner conducted their experiments with watch-glasses luted into the cranium—a procedure which, however, at best, is unreliable.
Brown-Séquard some years ago in part established an important pathological truth, the theory of epileptic zones, and demonstrated in certain animals that bruising and injury of the great nerve-trunks, especially the great sciatic, would give rise to epilepsy, and that irritation of certain tracts would precipitate the paroxysms. He further announced that the progeny of animals in whom epilepsy had been thus induced very frequently inherited the epilepsy of the parent. By some it was held that such epilepsies were purely peripheral, and Brown-Séquard even believed in spinal epilepsy. His spinal epilepsic theory has, for the most part, been explained by the anatomical researches of Hitzig and the doctrine of interrupted spinal inhibition. In fact, many of the spinal epilepsies are examples of exaggerated reflexes.
The epileptiginous zone theory, which, while it induced many to believe that the disease might have its origin outside of the brain, gave rise to the false assumption that attacks with distal auræ were primarily non-cerebral, has been discarded, and most observers have arrived at the conclusion that even in these cases the first explosion is due to some cerebral cell-discharge.
Hughlings-Jackson's grand work has revolutionized the views held prior to his first published writings, about twelve years ago. He believes that any part of the gray matter may, through over-excitability, give rise to convulsive attacks.
The production of convulsions by cortical irritation is now an old story.
The experiment of Pitres and Frank33 bears upon the sensorial function of the cortex in showing that, when the cortex is irritated, epileptiform convulsions follow, but if the exposed surface be subjected to the ether spray the same irritation will only produce definite movements, but no convulsions.
33 Gazette des Hôpitaux, No. 38, 1883.