On convulsive seizures / by J. Hughlings Jackson.

  • John Hughlings Jackson
Date:
[1890]
Catalogue details

Licence: Public Domain Mark

Credit: On convulsive seizures / by J. Hughlings Jackson. Source: Wellcome Collection.

Provider: This material has been provided by King’s College London. The original may be consulted at King’s College London.

    32/50 (page 30)
    50 Lecture III. After-Effects of Epileptiform Fits.—Paralysis due to Cortical Ex- haustion.—Analysis of a Case.— Variations in Degree and in Range of Post-epileptiform Paralyses.—Hemiplegia, Post-epilep- tiform and from Destruction of Motor Part of Internal Capsule contrasted.—Post-epileptiform Defects of Speech.— The Negative and Positive Elements of these Defects.—The Psychical and Physical.— The Concern of the Right and of the Left Half of the Brain in Speech. I have now to consider the After Effects of excessive nervous discharges in cases of epileptiform seizures. This part of our sub- ject is of extreme importance; the presumption is that from the study of the comparatively simple post-epileptiform conditions we shall obtain a basis for the interpretation of post-epileptic conditions. It is for this reason that I go into some detail as to the former. There is not rarely after epileptiform seizures local temporary paralysis;51 and sometimes aphasia with it. For the present I speak of paralysis only. In this inquiry we have no direct con- cern with paralysis, temporary or permanent, owing to destruc- tion (by clot, softening, or any other pathological process) of any part of the brain, not even if the malady set in with a convulsion. I must particularly mention cases in which there are both (1) permanent paralysis—for example, imperfect hemiplegia; and (2) occasional epileptiform seizures, the convulsion beginning in some point of the muscular region paralysed and involving part or the whole of it, and sometimes also parts beyond that region. In these cases the two opposite functional states—destruction of some nervous elements which represented complex movements, and high instability of some others which still represent other complex movements of the same muscles—are side by side in one part of the cortex (or the latter of cortex and the former of fibres passing down from it). After a paroxysm in such a case there may be temporary increase of the paralysis. For my present purpose, which is only an attempt to explain the nature of the sequence (paralysis after convulsion), I shall exclude these cases, and deal only with what I may call uncomplicated cases—that is, with those in which there is only paralysis immediately when epilepti- form seizures have ceased, such paralysis being temporary (un- less, of course, the fits recur at short intervals). Something has to be said, however, regarding certain of the so-called uncompli- cated cases. In some cases in which there is no discoverable paralysis in the intervals of the fits, except for a short time after one, there may be indirect evidence of a negative functional state of a few fibres of the second segment of the kinetic route. That evidence is foot clonus and exaggerated knee-jerk on the same side as that in which the convulsion occasionally starts. I mean, of course, cases in which these abnormal tendon reactions are producible at all times, although in a greater degree just after a fit. It may be that severely careful tests would show some quasi-trifling paralysis 51 ThiB paralysis was long ago described by Todd under the name “ Epileptic Hemiplegia.