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 {489} 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 Frank[33] 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.
[Footnote 33: _Gazette des Hôpitaux_, No. 38, 1883.]
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 {490} 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 Kolk[34] 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]
[Footnote 34: “On the Minute Structure and Functions of the Spinal
Cord,” by J. L. C. Schroeder Van der Kolk, _New Syd. Soc. Trans._]
[Footnote 35: TABLE.
--------------------+-----------+-----------+-----------+----------
Different | Hypo- | Corpus | |
Epileptics. | glossus. | olivare. | Raphé. | Vagus.
--------------------+-----------+-----------+-----------+----------
Table A—tongue | 0.306 | 0.315 | 0.315 | 0.237
biters | | | |
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.
--------------------+-----------+-----------+-----------+----------]
Nothnagel[36] 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.”
[Footnote 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.
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 {491} 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.
Tamburini[37] reports a case of hemiplegic epilepsy with induration of
the left optic thalamus and the left cornu ammonis, in which aphasia
existed. Pfleger[38] and Henkes have also found the sole lesion to be
induration of the cornu ammonis. Of Pfleger's[39] 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.
[Footnote 37: _Sallanzani_, Modena, 1879, viii. 550-557.]
[Footnote 38: _Allg. Zeitschrift f. Psychiatrie, etc._, Berlin, 1879,
xxxvi. 359-365.]
[Footnote 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.
[Footnote 40: _Archives gén. de Méd._, 1869, ii. 641 _et seq._]
{492} Convulsions have very frequently been noted in association with
imperfect cerebral development, and Echeverria laid great stress upon
the hyperplastic increase in volume of certain parts of the brain.
Marie Bra[41] has thus summed up her conclusions relating to the
morbid anatomy of epilepsy:
“1. The mean weight of the brains of epileptics is less than the
physiological mean.
“2. The cerebellum is greater than the physiological mean.
“3. There frequently exists an asymmetry between the lobes (not
peculiar to epilepsy). The increase of weight is sometimes found on
the right and sometimes on the left side. Equality is the exception.
“4. In no form of mental disease (excepting perhaps general paresis,
which is accompanied also by epileptiform crises) have we met with so
marked and constant a variation between the weights of the hemispheres
as exists in epilepsy.”
[Footnote 41: Referred to by Axenfeld.]
Drasche, Green, Greenhow, Löbel, and others have detailed cases in
which tuberculous deposits were undoubtedly the causes of the disease.
Kussmaul and Tenner, Hoffman, and others have held that a stenosis of
the superior part of the vertebral canal may explain, through pressure
upon the cord, the genesis of the attack, and Kroon found asymmetry of
the medulla oblongata.
The microscopical changes that have been found in brains where no
gross lesion was apparent are by no means distinctive. I have myself
examined the brains of many epileptics with discouraging results. The
varying granular cell-degeneration, capillary dilatation, and
exudative changes are common enough. In several cases of cortical
epilepsy I found more or less advanced degeneration of the great cells
in limited regions.
By far the most important and exact changes are those observed in the
cases of sensory epilepsy. I have elsewhere collected some continental
cases. In brief, areas of occipital softening or degeneration have
been discovered in those cases with hallucination, sensory
expressions, and hemiopia. In one case attended by hallucination of
smell the autopsy disclosed the following:
M. M——, was a stout Irish woman about forty years of age. She had
suffered from a light form of epilepsy dating from the tenth year, and
resulting, as she stated, from a fall, when she struck her head and
was unconscious thereafter for some hours. No scar was visible,
however. No satisfactory history could be obtained regarding her early
life and the first paroxysms. In the beginning these were rather
frequent, and she had as many as four or five a month. They afterward
diminished in number and severity, and for many years she had but
three or four in the course of the year. They were not very severe,
and she was enabled to pursue her work as a housemaid, but did not
keep her places for any great length of time. She rarely bit her
tongue, but usually frothed at the mouth and became livid and
convulsed for a short time. There was no history of one-sided spasms.
As I have stated, I could gain no accurate account of the previous
attacks, except that she nearly always had an aura of a peculiar
character, which was a prominent feature of the seizure and very
pronounced. She suddenly perceived a disagreeable odor, sometimes of
smoke, sometimes of a fetid character, and {493} quite uncomplicated
by other sensory warnings; and afterward became unconscious, and
remained so for two or three minutes. She was invariably able to
describe her sensations when she recovered, which she always did when
I asked her, comparing her warning to the smell of burning rags, to
the smell from a match, and, as she expressed it, it sometimes rose up
in her head and choked her. She was under my observation for one or
two years, but eventually developed phthisis, and died, her attacks
occurring from time to time until her death.
Besides well-marked tuberculous lesions in the lungs, there was little
of interest so far as the visceral examination was concerned. The
brain was removed and its peculiarities were carefully observed. A
great quantity of fluid was found, especially at the dependent
portions of the membranes and in the ventricles, while the dura was
thickened and pearly in spots. There was a condition that might be
likened to a low grade of hemorrhagic pachymeningitis, and at the base
of the brain old plastic changes were found, there being adhesions,
especially in the region of the middle lobes, but more particularly on
the right side and near the median line. The brain as a whole was
small, and weighed forty-one ounces and a fraction. The sulci were
deep and gaping, and the convolutions were distinct. There was no
atrophy of the fore-brain convolutions, and no other pathological
appearance was presented except that found in the meninges, but at the
lower part of the temporo-sphenoidal lobe of the right side an
appearance was found of an exceedingly interesting nature. At this
point a decided shrinkage of tissue was discovered, with depression
and adhesion of the pia, the induration involving the uncinate gyrus
and parts of the adjacent convolutions, as represented in the drawing.
No induration or softening of the great motor tracts was observed, and
the optic thalamus and parts adjacent were uninvolved, as was the
cord. An attempted microscopic examination, undertaken some months
subsequently, was unsatisfactory, because of the bad condition of the
brain, the preserving fluid having been improperly made. The olfactory
nerves were not involved. The third frontal convolution was examined,
but no disease was found there. Consequently, it is to be inferred
that no lesion of the external root of the olfactory nerve existed.
[Illustration: FIG. 27. Lower Face of Right Hemisphere.]
DIAGNOSIS.—Having spoken of epilepsy as in most instances a
symptomatic disorder, it would be proper to confine this section to
the differentiation of the simpler and more classical form of the
idiopathic disorder from certain purely eclamptic attacks or those due
to cerebral tumor or {494} coarse degeneration. The epileptic attack
itself is to be considered from its time of happening, its duration,
the element of unconsciousness, its associations, and the antecedent
history of the individual. It may be confounded with the similar
phenomenon dependent upon cardiac weakness, uræmic poisoning, toxic or
alcoholic saturation, etc.
Of course, when we find recurring seizures with a certain amount of
what Carter-Gray calls quasi-periodicity, preferring perhaps the
night, the early morning, or only the daytime, we are almost sure of
epilepsy. This supposition is strengthened by the association with
attacks of petit mal. The duration of an attack, which may be from a
few seconds to several minutes, is also a guide, for in certain toxic
and other paroxysms the rule is for a succession of attacks to occur.
The question of consciousness is one that has drawn forth a great deal
of discussion, especially with reference to medico-legal cases. I
think the majority of clinicians are agreed that loss of consciousness
is an absolute belonging of epilepsy, yet there are cases in which the
lapse is scarcely perceptible. It is a dangerous precedent to
establish, for the convulsive symptoms in such cases are taken from
the epileptoid category. It is quite true that there are many
hemi-epilepsies in which the intellectual condition is one that may
easily be mistaken. I have seen numerous cases in which an apparent
conservation of consciousness remained throughout a slight monospasm,
but I do not feel at all sure of this; and in cases of aborted or
masked epilepsy there is a dual mental state which would readily
deceive the lay observer. The case of Mrs. S—— is an example of this
kind. After the obvious subsidence of the dramatic and conspicuous
feature of the fit she remained for hours and days in a state of
undoubted transposition, performing acts which required something more
than a high degree of automatism—going to the table, talking about
certain subjects which were suggested, with apparent ease, but not
connecting them intelligently with her surroundings, as she would
before and after the epileptoid state. After a time she apparently
resumed her normal state, but was entirely unconscious of the
happenings of her previous hours or days, not even recollecting her
simplest actions. Julian Hawthorne's hero in _Archibald Malmaison_,
though not drawn by a physician's pen, suggests the state of which I
speak, and it has the merit of being based upon one of the elder
Forbes Winslow's interesting cases.
When we find paroxysmal attacks occurring in individuals with atypical
heads, thick swollen lips, scarred tongues, and irregular teeth, we
may strongly suspect the patient to be epileptic. To these we may add
the appearance of the eyes, the fishy, lack-lustre expression which
betokens old epilepsy. The hands are clammy and the skin mud-colored;
the hair is dry and coarse; and the body often has a death-like odor.
In children, certain mental peculiarities are to be inquired into.
Unnatural brightness or dulness—what may be called the clumsy
organization—is often present, and the muscular use is often
imperfect. We find that there is often but little nicety in walking,
in using the hands, in speaking, or after learning to write there is
an incapacity, with ever so much teaching, to develop a character or
style. Such children can never become ambidextrous. These little
points may seem trifling, but to the physician who carefully studies
his cases they may prove of great help. The history of the nights may
often lead to the discovery perhaps of a {495} long-existing nocturnal
epilepsy. Incontinence of urine, blood upon the pillow, nightmares,
morning headache, and petechiæ betoken unsuspected night attacks; and
Le Grand du Saulk mentions the case of a young Englishman who
committed a purposeless crime and was discovered to be epileptic, the
diagnosis being confirmed by an antecedent history of nocturnal
seizures, and subsequent watching resulted in the discovery of many
night attacks.
As to special conditions with which the epilepsy may be confounded, I
may refer to cardiac weakness. It not rarely happens that simple
fainting attacks are confounded with those of an epileptic nature.
Such is the case more often in heat-prostration, when some rigidity
attends the loss of consciousness. The duration of such a state, the
condition of the pulse and color, however, will easily clear up any
doubts upon the part of the observer. The existence of a cause should
also be considered, and the fact that usually the epileptic paroxysm
is sudden, while a feeling of depression and feebleness precedes the
fainting attack, should be remembered. I may present in tabular form
the points of difference:
EPILEPSY. | SYNCOPE.
|
Loss of consciousness sudden. | Loss of consciousness follows
| feeling of faintness.
|
Period of complete unconsciousness | Unconscious throughout, no
usually short. | convulsions.
|
The existence of auræ of a | The existence of preliminary
well-defined type. | vague prostration, nausea, and
| irregular heart action.
|
Often involuntary discharge from | Quite rare or never.
bowels and bladder. |
|
Patient usually falls into heavy | After slight weakness patient
sleep or is indifferent after | is anxious and worried, and
convulsion. | quickly seeks relief.
The difficulty of diagnosis, however, is only in cases of petit mal.
There are light forms of auditory vertigo that may resemble
vertiginous epilepsy. In the former there is never loss of
consciousness, and the patient refers to the rotary character of the
vertigo. A history of antecedent attacks, tinnitus, aural disease, and
a certain constancy which is not a feature of petit mal, may be
mentioned.
There are cases, however, which are puzzling, and come under the head
of auditory epilepsy rather than auditory vertigo; and in these there
is a multiplicity of expressions, the auditory symptoms predominating.
Of uræmic convulsions it is hardly necessary to speak. There is a
previous history of renal disease which the microscope and less
delicate tests will reveal, and clinically there is antecedent
headache, some stupidity, and not unrarely thickness of speech and
somnolence. There are some cases, however, which are obscure. I have
known patients with chronic renal disease—such as waxy kidney, for
instance—to develop a species of epilepsy, the paroxysms recurring
from time to time and behaving very much as the idiopathic disease
would; and their occurrence would mark some imprudence in diet or
exposure, and their disappearance an improvement in the patient's
general condition. The attacks were not classical, inasmuch as there
seemed to be but one stage of violent clonic convulsion, preceded by
intellectual dulness, and followed by a semi-comatose condition which
was far mere profound than the somnolent {496} stage of epilepsy. The
movements were not accompanied by a great degree of opisthotonos or
pleurosthotonos.
Alcoholic and absinthic epilepsies are usually preceded and followed
by symptoms indicative of profound saturation.