The features of this form of epilepsy are (1) the expression of some hallucination (prodromal stage), or hemiopia; (2) supraorbital neuralgia; (3) aphasia, formication; (4) slight loss of consciousness, and little if any motor disturbance.
I may present two illustrative cases:
A few months ago I was consulted by a medical gentleman in regard to a patient who had for years presented a curious train of nervous symptoms, which afterward assumed a form leading me to think she might have sensory epilepsy. She would, in the presence of the gentleman who consulted me, who was a personal friend of the patient and a medical man, stop short in the midst of an animated conversation, look fixedly ahead, appearing momentarily lost, remaining abstracted for a short period, possibly a minute, and on recovering herself go on, finishing the sentence she had commenced before the seizure. At this time she constantly had hallucinations of a visual character, when she saw animals, birds, figures of men and women, who approached her, as well as a variety of other objects. A common hallucination, which had been repeated quite frequently, consisted in visions in which green leaves and white rabbits and other objects familiar to her in childhood figured extensively. Upon one occasion, while sitting in the drawing-room, opposite a door which communicated with the hall, she suddenly called her companion's attention to the hand of a man which she saw clasping the baluster rail. The hand was seemingly disconnected from the arm. She was somewhat agitated, and it was nearly half a minute before the vision was dismissed. Sometimes she would call attention to the hallucinations before the attack, but more often she became transfixed, apparently lost, and then recovering she described her visions minutely. She has apparently been able to foresee the attacks and ward them off by a strong voluntary effort. So far as can be learned, there is no hysterical element in the case, but her seizures are more frequent at the time of menstruation. In a private note it is stated that “the family history of the patient is very good, and she has always seemed remarkably healthy and robust, and has shown more than usual intellectual ability. She has appeared to persons generally to be of a contented, happy disposition.... At night, when she closed her eyes, she suffered from these hallucinations, especially after a day of fatigue. Her pupils are usually dilated, but her color undergoes no change during the seizure.”
The second case is one of a more complex type:
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 hassubsequently 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.
MORBIDANATOMY ANDPATHOLOGY.—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 wasnecessary 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 Frank33bears 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.
33Gazette 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 indicativeof 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 Kolk34in 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
34“On the Minute Structure and Functions of the Spinal Cord,” by J. L. C. Schroeder Van der Kolk,New Syd. Soc. Trans.
35TABLE.
35TABLE.
Nothnagel36is 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.”
36Ziemssen'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 onlynutritive 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.
Tamburini37reports a case of hemiplegic epilepsy with induration of the left optic thalamus and the left cornu ammonis, in which aphasia existed. Pfleger38and Henkes have also found the sole lesion to be induration of the cornu ammonis. Of Pfleger's3943 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.
37Sallanzani, Modena, 1879, viii. 550-557.
38Allg. Zeitschrift f. Psychiatrie, etc., Berlin, 1879, xxxvi. 359-365.
39Ibid., lxxvi., andArch. 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,40the bulb was found involved by tuberculous matter.
40Archives gén. de Méd., 1869, ii. 641et seq.
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 Bra41has 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.”
41Referred 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, andquite 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.
FIG. 27.
Lower face of right hemisphere
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 orcoarse 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 inArchibald 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 along-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:
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 somnolentstage 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.
The consideration of hysterical epilepsy may be found elsewhere, but it may do to briefly refer to some cases which do not present the phenomenon first described by Charcot and Bourneville. The ordinary hysterical attack is never attended by loss of consciousness, by any of the pupillary changes so constant in epilepsy, by the mobility of the pupil between the attacks which is present in a large number of true epileptic individuals. There are never the succeeding changes of color, and the seizures are commonly produced or attended by some emotional disturbance, or are associated with ovarian disturbance.
Epilepsy is occasionally simulated by malingerers, and sometimes the skill of the subject is so great as to even deceive the practised eye. Prisoners, soldiers, and litigants may counterfeit an epilepsy, and go through with great personal suffering to accomplish their purpose. “Clegg, the dummy-chucker,” whose remarkable case has figured in the medical journals, upon one occasion threw himself from an iron platform to the stone floor of the jail, nearly twenty feet below, to convince a suspicious physician of his honesty. The simulator rarely bears close watching. The dilatation and contraction of the pupil cannot be simulated, nor can the corneal or pupillary insensibility. The fraud cannot voluntarily change his color, as is the case in true epilepsy, and as a rule the thumbs of the impostor are never flexed, as they should be. Suggestions for a purpose are readily heard, and sometimes adopted, by the apparently unconscious man. Gottardi42lays great stress upon the use of the ophthalmoscope as a means of detecting simulated epilepsy. He calls attention to the frequency of retinal changes with facial asymmetry and other evidences that suggest cerebral disease or non-development. Gottardi has found that the pulse in true epilepsy is always lower after an attack, but it soon reaches its normal standard.
42Abstract inJournal of N. and M. Dis., Oct., 1881, p. 843.
The differentiation of idiopathic epilepsy from that due to syphilis is possible when we consider the element of pain. Besides the tibial pains of syphilis, the epilepsy thus produced is often preceded by intense frontal headache, while that of ordinary epilepsy follows the attack. The syphilitic epilepsy is not attended by so great or continued a loss of consciousness as the non-specific form, and the movements are apt to be most violent on one side or the other. The association of the attacks with various bodily signs, such as nodes, old scars, alopecia, erosions, etc., and in connection with possible cranial nerve-paralyses, will throw light upon its true character. The paralyses referred to seem most frequently to involve the motor ocularis, abducens, and patheticus. Syphilitic epilepsy, too, is quite irregular in its time of manifestation, and is not unrarely followed by aphasia; but the interparoxysmal mental state is one of extreme dulness, memory being blunted and there being a peculiar hebetude.
PROGNOSIS.—Within the past quarter of a century the ideas of the medical profession regarding the curability of epilepsy have certainly undergone a change. The statistics of Bennett and others show that since the introduction of the bromic salts the proportion of cures hasbeen decidedly increased. Nevertheless, the disease is a most discouraging and troublesome one to manage, and especially is this the case when it assumes the form of petit mal. The rapid recurrence of light attacks is, as has already been said, very apt to lead not only to mental enfeeblement, but is very often followed by very severe paroxysms.
Epilepsy of a more or less constant form, in which the seizures resemble each other, is far more incurable than that of variable type; for example, we find that unilateral seizures are much more apt to be associated with established cortical disease than when they are general and simply explosive manifestations. It has been held that a tendency to permanency is marked by a diminution in the extent of the interval. This is by no means true. I have had cases under observation for ten or twelve years in which attacks separated by intervals of six months or one year marked the course of the disease, in which frequent initial attacks were present. These cases I regard as very bad so far as prognosis is concerned. I much prefer a history of irregular and comparatively disorderly attacks. In female subjects the menstrual influence is not always a bad factor. When we are enabled to remove some production of an exciting cause in connection with the catamenia the prognosis is more hopeful; but an opinion must be expressed with great caution, especially in those cases beginning at an early age and not after the establishment of the menses. Traumatic cases are not always bad, but those in which the element of heredity plays a part most certainly are, Herpin and Gowers to the contrary; and though these cases for a time do well under treatment, its good effects are not constant. Individuals with misshapen heads, whose deformity suggests premature sutural ossification, are not susceptible to the influence of treatment, and all other osseous changes, such as exostosis, plaques in the dura, and bony growths, whose existence can only be guessed at or inferred from suggestive appearances elsewhere, give rise to a variety of epilepsy which is beyond the reach of drugs. With symptomatic epilepsies the case is sometimes different, for while the seizures which arise from the irritation of a cerebral tumor are almost as hopeless as the form I have just mentioned, we know from experience that the epilepsy of syphilis and other allied diseases, and those of toxic origin, with the exception sometimes of those occasionally due to alcohol or lead, are curable. The meningeal thickening of alcoholic origin or the encephalopathy of lead may be the pathological bases of very intractable paroxysms.
So far as age is concerned, it may be stated that many eclamptic seizures of young children which are due to well-recognized irritable causes are promptly cured if there be no hydrops ventriculi or preossification of the coronal sutures, and if the epileptic habit is not established. The epilepsies of six or eight years' standing are not encouraging from a therapeutic point of view, and those of advanced life developing in aged persons are equally unfavorable.
The treatment of epilepsy due to heat-stroke is by no means satisfactory, and, though the attacks are often separated by long periods, they are apt to recur in spite of drugs.
Gowers has prepared several valuable tables which show the influence of age upon recovery. He says: “The following table shows that age has a distinct influence on prognosis. The percentage of the unimprovedcases to the whole is 30 (43:143::30:100). The percentage of the cases commencing at each age arrested and unimproved is stated, and between brackets is indicated the excess of the arrested or unimproved cases at each period of life over the proportion for the whole 30 and 70 per cent. respectively:
Thus, the proportion of the cases commencing under twenty in which arrest was obtained is considerably less than the proportion of cases commencing over twenty, the difference amounting to about 13 per cent. The period of the first twenty years of life at which the disease commences has little influence, but the prognosis is little better in the cases which commence under ten than in those which commence between ten and twenty: arrest is more frequently obtained. The cases which commence in women at the second climacteric period are also obstinate, although not sufficiently numerous to be separately given.”
He also finds, from an analysis of the same cases, the fact noted by others, that the prognosis is favorable in inverse proportion to the duration of the disease.
Attacks which chiefly occur in the daytime are much more amenable to treatment than the nocturnal seizures, and especially is this the case in the tongue-biting form. Sudden blows upon the head or falls have been known in isolated cases to effect an amelioration in the patient's disease, but these examples are rare.
The existence of an aura is much better than if none existed.
Death from the attack itself is rare, yet in the large pauper institution with which I was connected for many years I have known of several cases. More often the death results from asphyxia resulting from a bolus of food which chokes the patient or from a fall in some dangerous place—into the fire or elsewhere. Accidental death from drowning is more common than any other form.
The status epileptica into which patients sometimes pass who have had many convulsions is occasionally a fatal termination of the malady, and is always a serious feature.
The influence of different epochs in life is worthy of consideration: of menstruation, of marriage, of pregnancy, and of the menopause there is much to be said. I have sufficiently spoken of the establishment of the menstrual flow, and I would only add another word of caution against giving a too favorable prognosis except in those cases of very recent origin. Marriage appears to have very little to do with changing the attacks, unless they be of an hysteroid character. I have never known epilepsy to influence the course of a pregnancy in any unfavorable way, and I think this has been the observation of others. Gowers refers to cases in which the attacks ceased during the time the mother was carrying the child.
The occasional bad influence of the pregnant state has been illustratedby a case reported by Terrillon.43This example was a woman who had been the victim of epilepsy of hereditary origin since her seventh year. At the commencement of menstruation her attacks became periodic, and recurred every two months, and she had several two or three days before the flow. Two pregnancies followed several years afterward. During the periods they were increased in number and severity, and occurred several times daily. She had more attacks at this period than in all the time after delivery.
43Annales de Gynécologie, June, 1881, p. 401.
I have found that the relief of uterine flexion or the establishment of menstruation has exercised a decidedly modifying influence for the better in several cases.
Sometimes the disease is interrupted by the menopause, but very often in my experience it has changed in type and been followed by mental degeneration.
The prognosis of the epileptoid mental state is serious in the extreme, and even when in early life the attacks are aborted or changed to perversion of the intellect or emotions existing as a complication, the hope of cure dwindles almost to nothing.
The spontaneous cure of epilepsy is rare. Its course, however, is more often interrupted by some intercurrent disease. Of 33 cases observed by Delasiauve in which there was some complicating disease, such as erysipelas, pneumonia, pleurisy, acute articular rheumatism, burns and contusions, scarlatina, erythema, or the condition of pregnancy, it was found that in 25 cases there was a decided improvement (une heureuse influence), and in 8 only was there no modification of the attacks. Axenfeld is disposed to believe that acute and febrile disorders more decidedly influence the course of epilepsy than those of a chronic nature. The influence of either may be small or may diminish the number of attacks without curing the disease.
TREATMENT.—The treatment of epilepsy depends so much upon the form of the disease that no arbitrary rule can be laid down upon general principles, and we must bear in mind the necessity for removing the exciting causes if possible, the preservation of the balance of cerebral blood-pressure and cell-equilibrium, and the nutrition of the cerebral mass. It may be our purpose to remove various toxæmic or cachectic states as well. As a minor division of treatment we must consider the abortion of the attack when auræ are detected. It has been the custom, I think among too many, to manage the disease in an empirical manner, depending upon some routine course of treatment, such as the indiscriminate use of the bromides, for example. I am convinced that the intractable character of the disease has come to be greatly exaggerated through failures attendant upon the wholesale use of the bromic salts, without regard to the indication in each particular case. It behooves us first to select a reliable bromide, and then to give it with relation to the time of the fit, its severity, and the condition of the individual. The importance of this has impressed me very often. An equally divided daily dose will not do a patient who has matutinal attacks the same good as will a large dose at night, and in certain anæmic individuals the bromides very often increase the attack. Then, too, the cases in which seizures of petit mal predominate are not benefited to the extent that those are in whichthe repetition of severe attacks is the feature. The bromide should always be well diluted and given when the stomach is empty or nearly so. The bromide of sodium is, to my mind, the most serviceable salt, and when given alone or combined with the bromide of ammonium is better than the potassic salt or the various others. It should be carefully kept in solution or in waxed-paper powders in a tight preserve-jar. As to its method of administration, I much prefer the use of a solution which shall combine other adjuvants which I will presently mention, and separate powders as well, which may be used to reinforce the dose. The latter are to be employed by the patient in the event of an unlooked-for series of attacks, and are to be used to the point of producing mild bromism at the time. In certain cases it is all-important to take into consideration the condition of the heart. In some cases where there is manifest and continued cerebral congestion, with full vessels and hard pulse, I have found that the combination with chloral or aconite was desirable. In other cases where the heart's action was irregular and weak my experience with digitalis and nitro-glycerin or with strychnine was most happy. In those cases that passed large quantities of clear urine of low specific gravity the action of nitro-glycerin and digitalis has been most prompt, and the same has been true of epilepsies of migrainous origin.
There have been various methods of using the bromide suggested which are more or less practical. The writers of a few years ago suggested the prompt production of bromism—a state in which the patient should be kept for a long time. This I strongly disapprove of, not only because the mental and physical depression is a very disagreeable and sometimes permanent condition, but because I have found that the attacks are often increased after a time, though at first they may have been suppressed. Others believe in giving the bromides at intervals, with periods when no medicine at all is administered.
For my own part, I am in favor of the establishment of a mild bromism which does not extend beyond a slight anæsthesia of the fauces or the appearance of slight acne. If I find it necessary to increase the dose, I give cod-liver oil, iron, and bark or some of the many preparations of the hypophosphites for a time; and they do not diminish the specific effects of the drug to any great extent. In the event of a series of attacks I direct the patient to take an extra dose at such time as will anticipate the seizure.
This treatment should be kept up for at least two or three years after the attacks have disappeared, and it may be even necessary to continue a bromide course in a small way for an unlimited period.
If there be an hysterical element, or if ovarian excitement is supposed to have anything to do with the attacks, the combination of cannabis indica is strongly recommended. This suggestion holds good in the cases where migraine is associated with the epilepsy, or the latter is an outgrowth of the former.
Next to the bromides of potassium and sodium I have been very successful with the nickel bromide. I find that it is retained with little trouble, producing no gastric derangement if taken after eating. A syrup prepared by most of the good pharmacists is preferable to any other method of administering the salt. Quite recently Leaman44has reportedtwo cases of severe epilepsy which were greatly benefited. His conclusion is that it does most good in the form of the disease when the attacks are separated by long intervals.
44Med. News, Apr. 18, 1885.
The bromate of potassium, which has been used by Weir Mitchell45and Hinsdale, may be worthy of a trial. It should never be given, however, in larger doses than five or ten grains thrice daily. These investigators found that thirty grains slowed the heart very considerably, and forty grains produced watery discharges from the bowels and drowsiness. In their hands, notwithstanding these disagreeable effects, it controlled the seizures. The hydrobromate of conia is a comparatively new remedy which has been recommended. My own experience does not support that of Wolfenden.46Severe cases were treated by him with benefit. The dose he recommends is half a grain, and not more than four and a half grains are to be given in twenty-four hours. Headache and dizziness attended its use.
45Med. News, Dec. 27, 1884, p. 718.
46Practitioner, June, 1884.
Erlenmeyer47is an advocate of the mixed treatment, and his best results have been obtained by combining the bromides of potassium, sodium, and ammonium in the proportion of 1:1:½. He thinks much greater permanency of effect follows such a combination. A curious result witnessed by this author is the fact that the acne produced by one salt given alone is apt to disappear when the combination is administered.
47Centralblatt für Nervenheilkunde, Psychiatrie, etc., No. 18, 1884.
A solution of hydrobromic acid, prepared after Fothergill and Wade's formula, is recommended by H. C. Wood of Philadelphia,48who presented the record of its use in twelve cases of obstinate epilepsy. It seems that in his hands large doses acted much better than when the bromides were given alone. He recommends ounce iij per diem. My own experience, which I detailed some years ago, was to the effect that it possessed no virtues whatever in ordinary doses. The solution is so difficult to take, and so disagreeable in every way, that many patients prefer almost any other treatment. It cannot be doubted that some cases of epilepsy are benefited by a change of treatment, no matter what, and possibly Wood's cases belong to this class.
48Med. News, Feb. 23, 1884.
Belladonna and ergot are remedies that have had many advocates, Trousseau being the most pronounced champion of the former. Their use in the lighter attacks is attended sometimes by the most happy results, but they cannot be said to have any permanent effect. The first is advantageous because of its power to diminish reflex excitement, and in those undeveloped infantile convulsions which are often grouped under the head of eclampsia its virtues are decided. Belladonna or its alkaloid may be given in combination with the bromides. Ergot or ergotin, in spite of its undeservedly bad reputation, may be given in large doses, one to two drachms of the tincture thrice daily, or five grains of the aqueous extract in the course of the day. Of chloral there is not much to be said. At one time it was thought to possess great virtues, especially in combination with the bromides, but subsequent experience has taught me that its use has many drawbacks, and only in exceptional cases is it to be recommended—viz. in those in which there is a disposition to excitement—either as a substitute for the attack or as a sequel.