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habits. He could not articulate a word distinctly, though he appeared to make attempts to do so, and was constantly uttering a sharp, prolonged cry, and at the same moment clapping his hands violently together. He evidently understood what was said to him, as when he became more docile he came when called by name.

On the evening of his admission he was attacked with a convulsive seizure, and when I saw him some four or five minutes after, he was just emerging from the fit, being quite unconscious, breathing heavily, the outer angles of the eyelids and of the mouth were twitching in a direction upwards and outwards, as well as both arms and legs, which were also slightly convulsed, but at longer intervals and in a lesser degree. These spasms soon subsided, and by next morning the little fellow had entirely recovered from their effects.

The second attack he had since coming here occurred some months ago, on the day after his mother had visited him, and was reported to have been in all points similar to that which he previously had. The next attack, and the one I wish to draw particular attention to, happened in the beginning of last August. I witnessed, I may say, the whole of the fit, as I happened to be entering the ward as he fell. He first became quite unconscious, lying on his back with his eyes directed upwards. As the convulsion came on, the outer angle of the left eyelid was drawn upwards and outwards, both eyes simultaneously moving in the same direction. Almost at the same moment the left angle of the mouth was drawn in the same direction, by the action evidently of the zygomatic muscles. As the spasm proceeded from above downwards, the left arm was jerked up and drawn across the chest, and the left leg was bent and drawn towards the body by the muscles passing from the trunk to the thigh, and at the same time the whole left side of the body was jerked upwards, and partially rotated from left to right. During the time these convulsions lasted, the entire right side of the body was perfectly motionless, not one of the muscles of either the face, arm, or leg twitching in the slightest degree. The spasms were throughout clonic, the contractions subsiding almost instantly, and recurring again with as short an interval. The pupils were widely dilated, the right one reacted to the influence of a candle held close to the eye. These unilateral left-sided convulsions lasted, from being almost momentary in the face, for about seven or eight minutes elsewhere, the intervals gradually growing longer and the spasms less severe, the pupils at the same time becoming smaller and resuming their natural size. The twitching of the eyelid and mouth continued for some minutes after that of the arm and leg had subsided, in a few minutes more the patient returned to consciousness, and in a little time was as bright and lively as before, there being no drowsiness or stupor, as is generally the case after ordinary epileptic attacks.

On October 9th he had another seizure at about 10.30 in the morning. The spasms commenced in the left side in a similar manner to the last, and after a short time subsided; however, after a few minutes' interval, they recommenced, and this time both frontal muscles were first affected; the right orbicularis next began to work, and gradually the entire right side became severely and momentarily convulsed, the spasms being more or less irregular, and the left side not being engaged. This attack lasted until two o'clock in the afternoon, when it subsided, and the lad was as well as ever again. Since then he has had one other "right-sided” seizure, which differs from the others in that it was followed by hours of sleep, though occurring in the morning as before.

On the pathology of this interesting case few practical remarks can be offered. All that can be said must of necessity be more or less theoretical. The history and symptoms pointing to “hydrocephalus,” I would feel inclined to place the case-in Dr. Ireland's classification under the head of “ hydrocephalic idiocy." I say from the history and symptoms, as although there is now no decided enlargement of the head, yet from the peculiar cry and mental restlessness, taken with the initial symptoms, the presence of effusion at one time or another may be fairly suspected. In several cases recently published, in which effusion was found both in the arachnoid and lateral ventricles, there was no increase in the size of the head, and this, I think, may be explained in this way: that as general development takes place, the head also naturally increases in size, but the brain, from being pressed upon by the fluid present, does not undergo any corresponding development, a space is naturally left within the cranium, which the effusion can occupy; and therefore the bones of the cranium, not suffering the same amount of internal pressure as they did before, will, after the lapse of several years, present an almost natural appearance, the abnormal expansion which would otherwise have taken place being compensated for by the diminished internal pressure. The convulsive seizures are evidently a symptom of disease, and the question which first, and most naturally, demands our attention, is to what are they due, and where is the lesion to which they owe their origin? As Dr. Hughlings Jackson has well said, all cases of convulsions and paralysis should be regarded “as experiments made by disease on particular parts of the nervous system of man.” They are the exact homologues of the artificial experiments made by the physiologist, who, when he wishes to determine the exact distribution of a nerve, both stimulates and destroys it. Indeed, this double method of study is essential to a correct understanding of these cases of nervous disease, as a “destroying” lesion of a circumscribed portion

of the cerebrum may produce no obvious effects, while a “discharging" lesion of the same portion may produce very striking results. As an illustration of this, I may cite the case of a celebrated mathematical professor at Oxford, who up to the time of his death was occupied over the most abstruse problems, and yet on a necropsy being made, one hemisphere of the brain was reduced to a mere sac of pus, thus showing that such extensive disease may exist without the development of correspondingly severe symptoms. In fact, in all cases the convulsions, or paralysis, as the case may be, are only symptoms of the disease, and that not constant ones, as the disease itself may be present, and yet there may be no symptoms to declare its presence, or mark its progress.

Taking now the foregoing case as an example, I would say that the attempt to localise the movements present in the “fit” in some portion of the brain, is more easily done, and with a better chance of correctness, by adopting Dr. Hughlings Jackson's suggestion, and comparing the convulsions present with the paralysis present in a case of hemiplegia. Keeping in view the “left-sided fit,” we see that the convulsions followed the saine course, and were in the same ratio, as the palsy in a case of left hemiplegia. Now, knowing as we do from the recorded results of many cases of this disease that the “destroying lesions” causing the paralysis are situated in or near the corpora striata and optic thalami, or the surrounding convolutions, we may, with a fair show of reasoning, localise the site of the " discharging lesion” giving rise to the convulsions, and affecting similar groups of muscles supplied by the same nerves, in somewhere about the same region of the organ. To some it may seem a thing almost impossible that the cerebral convolutions those organs from time immemorial considered to be solely for the evolution of ideas--can ever give rise to movements, but it has now been, by the march of scientific inquiry, put almost beyond the region of uncertainty that sudden discharges give proof that sensori-motor processes are the anatomical substrata of ideas. Granting now, from the results which this comparison affords, that the locus of origin of the convulsions lies in some of the convolutions of the corpus striatum, we have next to inquire what is the nature of the discharging lesion causing these convolutions, a task even more difficult than the last, as here we are entirely in the region of speculation. Are the convulsions the result of a local irritation from a collection of fluid, tumour, &c., or are they due to simple instability of the grey matter? If effusion does or did exist, they may be the effects of its present or past existences.

It may next be interesting to inquire whether the muteness, or rather the loss of expressing words, coming on as it did immediately before the convulsive seizures, is in any way connected with them, or depending upon the same cause. It certainly appears to be so. We have the mother's statement that the boy was beginning to speak well, when, as the head began to affect him, he ceased to do so, and became foolish.” Is the loss of speaking power “ ataxic” from inability to bring into co-ordinate action the muscles requisite for articulation ? or is it “amnesic” from loss of memory of words, the former being low down in the scale of sensori-motor processes, the latter being high up in that scale ? The difference between these forms is more of degree than kind, the one gradually merging into the other, and both being in the same series of nervous processes. It appears to me, from observation of the case-particularly from noticing the attempts at articulation the boy makes when pressed, as, for instance, when shown any familiar object, such as his cap, food, &c., and repeatedly asked to name it, that the defect is of the “ataxic” degree, and not from loss of memory for words. Now any injury done to the corpus striatum or convolutions close to it, according to the temporary or permanent character of the lesion, causes loss of co-ordinating power in the muscles of articulation, and as I have before showed that the anatomical origin of the convulsions may probably be in the same region, may it not be that the latter, and the defect of speech, are due to the same pathological conditions; the “discharges” giving rise to the former being of a temporary character, while the lesion which has caused the latter is of a more permanent character? Here, then, we must leave this case, until, should it be the will of Providence to remove the boy, a post mortem examination may render the case pathologically complete.

Case of Syphilitic Caries and Perforation of Calvarium

Encysted Abscesses in Cerebral Hemisphere, discharge of one of these externallyAlternation of Epileptic Convul

sions and Purulent Discharge. By James HOWDEN, M.D. J. S., admitted 5th Oct., 1871, from Dundee, æt. 51, a gardener and weaver, married, Protestant. He has been under treatment in the Dundee Infirmary for an injury to his head, and has, within the last few days, become insane, the cause of the insanity being alleged to he the injury to his head. He is stated to be epileptic, and dangerous to others.

The medical certificates state regarding him, that he suffers from almost complete loss of memory, does not know his own name, the day of the month, or year; he thinks he is only three weeks old, and again that he is 300 years old; he is restless, and occasionally outrageous.

On admission, his bodily condition was bad, and several bruises were observed on different parts of body and head. A day or two after admission his memory had returned, but he was constantly asking to be ripped open.

Nov. 6th.-He is now apparently sane. A large abscess has formed in the left temporal fossa, otherwise he is in good health.

1872. January 2nd.—The abscess mentioned in last entry was opened, and a quantity of pus escaped. Sometimes the discharge was copious, at other times it ceased. Later on another abscess formed over the coronal suture.

He knows everything going on around him, answers questions slowly but correctly. He then began to have epileptic fits, when the discharge from his head stopped, but they ceased on the recurrence of the discharge. Latterly, after the fit he became unable to speak or swallow, but always rallied, until about the 10th of January, when he had fit after fit for a day or two, and died comatose on the 13th.

Sectio.—15th January, 1872, at 2.30 p.m. Temp. 46o. Height, 5ft. 9 in. Rigor mortis slight. An inch and a half above the inner angle of the left eye there was a fistulous opening in the skin covering the frontal bone. Two-and-three-fourth inches above the outer angle of the same eye, at the junction of the frontal and temporal bones, was a second fistulous opening, and about four and three-quarter inches from the first, and an inch above the left ear, was a third opening.

On reflecting the scalp, caries of the bones was observed immediately below the fistulous openings in the skin. A probe was passed through the bone in all of them, resting on a soft membranous-like substance; on removing the calvarium, its inner surface presented three orifices lined by a milky-white membranous structure, the lower orifice being open. The dura mater on the left side was adherent to the brain-substance over its anterior third, and to the membranous structure lining the orifices previously mentioned. On removing the dura mater the pia mater presented much venous congestion.

On section of the left hemisphere, a cavity filled with fætid pus was opened into in the anterior lobe. This cavity was situated anterior to the ventricle, and was about two inches in diameter, and lined by an irregular pinkish membrane. There was no communication between this cavity and the ventricle, but it appeared to communicate anteriorly through the grey matter, dura mater, bone, and scalp. At the back part, and under the left ventricle, another cavity the size of a walnut was found also filled with pus.

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