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The Anatomical Facts and Clinical Varieties of Traumatic Insanity

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Abstract

Considering the meager knowledge of unmistakably reliable facts of etiology in mental disease, traumatism would seem to furnish unusually clean-cut conditions of interference with the mechanism of sensory-motor plasticity. Yet both as to frequency and the nature of the actual conditions there is a great uncertainty. Some writers include—bowing to the crude sense of the word—all mental disorders in whose etiological constellation any kind of traumatism plays a role, even a surgical operation on a totally indifferent organ, or a fracture of an ankle (curiously enough they are not consistent enough to include the puerperal cases); also, insolation is frequently included. In this study, I shall consider chiefly those disorders which are the direct and obvious result of some traumatic interference with the brain. Theoretically, trauma figures prominently among the distinguishable types of possible disturbances of the cerebral functions, through the role it may play in disorders of growth and of nutrition, inflammation and tumor-formation, and in derangement of blood- and lymph-circulation. Even in the “psychogenic” disorders, trauma has its place in the form of mental shock. In most of these directions, one would expect to deal with a very definite entity, a welcome and solid ground in this period of rather too verbose explanations by auto-intoxication.

Unfortunately the simplicity is only apparent. There seem to be so many ways for the nervous system to suffer from trauma, even if we limit ourselves largely to the brain.

The most important ones are collisions with other objects, falls, or a meeting with projectiles. Both types produce direct local and more general effects. It further seems quite important to consider the sensory effect—the variable extent of fright, and the emotional consequences of loss of work and litigation.

In order not to mix together a large mass of heterogeneous material we shall try to maintain clearness and distinctions by limiting ourselves as closely as possible to the effects of concussion and actual direct traumatisms.

What effects can traumatism have on the structure of the nervous system? We might distinguish:

1.

The direct focal and the more diffuse destruction of the nerve-tissue or of parts of it; and the reaction of the tissues.

2.
b.a.

The immediate effects—edema.

b.b.

The scar formation.

3.

The distinctly diffuse commotions in which the general reaction and the psychic elements preponderate, including the remote reactive results of exaggerations of vasomotor and emotional responsiveness. A brief review of some effects of trauma will give us the material on which to make the distinctions.

Simple Contusions.—The general arrangement of the cranial cavity furnishes special opportunities at the point of maximum impulse and a point opposite it; further at points where the unevenness of the base or the existence of the tentorium leads to focal contusions. Such disorders are seen in patients falling, in epileptic convulsions for instance, chiefly at the tips of the temporal lobe, at the base of the frontal lobes and, as Duret showed, in the central gray matter surrounding the 3d and 4th ventricle. The probable reason for this localization is the great unevenness of the base of the cranium. Tillmann claims further that lacerations are produced in the brain itself at the points at which tissues of different specific weight meet—this would be the case in the ventricular linings and in the pia owing to the difference in the specific weight of the cerebro-spinal fluid and the tissue, and especially at the juncture of gray and white matter. The hemorrhages, as such, are as a rule not very copious unless the meningeal arteries burst, or where an already affected blood-vessel yields—sometimes several days after an injury in the so-called delayed apoplexies (Bollinger). The statement that the ventricles were filled with blood should be taken with caution considering the rough method of a usual brain-autopsy. Since we know of intracranial hardening with 10 per cent formalin before the brain is handled, these findings have been rare.

Many of the lesions are really a hemorrhagic infiltration of contused brain-tissue, such as we have met with in Case 1, a patient with typical senile dementia., who fell accidentally in the ward, backward on the occiput. He was unconscious one-half hour, but the third day he died in coma with bronchopneumonia. No fracture. Over the right parietal lobe and all around the occipital poles, and especially around the right cerebellar hemisphere there were subdural clots; also a few in the left frontal and both temporal fossae; moreover there were deep hemorrhagic contusions of the fusiform gyri less marked on the right.

Case 1. L.H.S. Born 1831. Father and two aunts were insane. No accurate history is available. In 1898 the patient is said to have had a sunstroke. He then stopped working. During the last months he has become very perverse; he would get up and build a fire in the night thinking it was day, and go out on the street and sometimes stay out all night; he would get excited and did not let his wife have wood and coal. He wandered away from his home to an adjoining town and walked six miles to his daughter's, saying he was going home. The physicians found him exhausted and restless; slow in answering and talking irrelevantly; he walked about the room, went to the window and looked out and laughed.

The patient was admitted January 12, 1900. He was restless, walking about the hall, saying little except: “I guess I will go home this evening.” He was inclined to resist his bath but submitted to the rule; at supper, however, he refused to eat because he was offended at having been bathed. When he is requested to do something he is very contrary and irritable and inclined to fight. He requires to be pushed into the dining room; then he is too angry to eat; he walks about the room; refuses to be seated, takes off his coat without any reason except “it is none of your business.” He requires constant watching lest he take off his clothes and shoes; but January 14 and 15, the attendant has to undress him. After the interview he refuses to leave the room.

Physically he claims to feel well; he is rather tall, somewhat emaciated and sallow; he has varicosities of the legs, thickened and tortuous radials, beginning arcus senilis, no heart lesion; a barrel-shaped chest and scaphoid abdomen. The hands and forearms shake and the tongue has a gelatinous tremor, and the gait is relatively slow and tottering.

In conversation the patient is suspicious and evasive and irritated by questions and unable to grasp the whole situation, takes the examination for a “mess of lawyers,” frequently answers “None of your business.” Or to the question, where are you, he says “Don't you know? Well, I won't tell you; well I would give up my business,” and when he was told it was the Worcester Insane Hospital, he said: “I would like to know why.” The date was given as Friday, in “November, ain't it,” 1890, 1889 or 1890. The localization in time both of remote and recent events is very defective and variable. “I shall be 70 the 30th of this month, November. I was born in Boston, and went to school for a year; I had two brothers and two sisters; the youngest sister is only three years old”; and the brothers' age he does not remember. His father is living in S. and 73 years old. When the discrepancy was pointed out he said: “Can't you take a record from the Bible?” When did your father die? “Well, he is living and was living—and you want to get me mixed up in a scrape—well, I had just as lief as not.” He says his wife is in B., Mass. (correct) and he has four children; two days later he says his wife lives in S., Vermont, and that she is 26 years old, that he has no children and can't tell “exactly” when he was married, “I think 6 years ago.” January 15, he takes this place for the Horticultural Building in Boston. He thinks he has been here not more than three or four weeks (two days). He mentions no definite delusions or complaints.

January 17, 1900, the patient fell on the floor on the back of his head. He immediately straightened out and stopped breathing until the attendant performed artificial respiration. He remained unconscious about half an hour, then became gradually clear, and in about three hours said to the attendant he was all right. He fell asleep, but at 4 a.m. the physician found him lying flat on his back with open mouth, fixed eyes, deep breathing and slight rattling. There were no symptoms of paralysis, no difference of pupils. During the examination there were several hiccoughs. Nothing was found in heart or lungs. No fracture of the skull was detected. The temperature was 100.2°; pulse, 80; respirations, 15. At 9 a.m. there was much flickering of the muscles of the thigh and leg on both sides and on the right an occasional contraction of the muscles. The toes are in dorsi-flexion which is increased on plantar stimulation and especially hard to overcome on the right; cutaneous and tendon reflexes about normal. There is withdrawal from pricks only at the sole of the feet, hardly at all in the arms and hands, slightly in the face. Forward movement of the jaws stops rattling. Towards evening he could be roused partially by calling his name and he swallowed fairly well, but he became more and more comatose and the temperature rose to 105° in the course of two days. He died at 11 p.m., January 19, 1900.

Autopsy. No fracture of the skull was found, but several hyperostoses on the inside of the frontal bones, especially marked on the left and several others in a depression just behind the bregma. To these regions the dura is firmly adherent. The inside of the dura appears free in the frontal part; over the right parietal and all around the pole of both occipital lobes there are, however, marked clots inside the dura and a rather large blood clot on the right cerebellum and a more limited membrane over the left. Only in the left frontal fossa is there a small clot and in either temporal fossa several diffuse membranes and a few small clots. The blood-vessels are hard at their exits from the canals only. There are marked contusions especially of the region of the fusiform lobe on the left and a little less under the right third temporal gyrus. Brain as a whole weighs 1,260 g. The floor of both temporal lobes proves greatly contused to the ventricle.

The lungs weigh 450 and 570 g, with thickened pleura at the apex, are slightly edematous, and there are bronchopneumonic foci in both lower lobes. The left pleura has several ecchymoses and a small amount of fluid in the cavity. The heart weighs 250 g and has a decided thickening of the edges of the mitral flaps, with small rough nodules; no atheroma of the aortic valves or the beginning of the aorta, but a number of ulcers in the descending aorta.

The kidneys have a few small cysts and weigh 100 and 104 g; old adhesions of the ascending colon and omentum to the abdominal wall; 12 gallstones.

Walter B. Cannon of Harvard Medical School (“Cerebral Pressure Following Trauma,” American Journal of Physiology, Vol. 6, pp. 91–121) lays much stress on the swelling of the injured tissues as a source of immediate rise of intracranial pressure. I consider this one of the most important contributions to this problem, and an excellent explanation of many otherwise mysterious “molecular changes.” [On this ground of changes of osmotic relations, we understand why Polis found animals previously made anemic more endangered by concussion.—Author]

Whether the cranium is fractured or not means relatively little. It would seem, however, that for chances concerning life, a relatively extensive destruction of the skull is rather more favorable than otherwise. I can present a photograph of the skull and brain of a patient (Case 2, M.), who was kicked by a horse at the age of 7; pieces of bone were removed. The patient had more or less persistent frontal headache and slight deafness on the left side; but no mental defect. She married, brought up a family (the children suffer from frequent headaches) and has been perfectly well. At the age of 75, she had a shock with sensory aphasia, a renewed attack at 77, and a few weeks before death she was admitted in a condition of depression and dementia; the autopsy showed a shrinkage of the middle part of the left first temporal gyrus, accounting for the terminal aphasia, and no other macroscopic brain lesion traceable to the injury, notwithstanding the huge defect of 10 by 2 cm in the skull.

The following types of residuals of injury and their consequences deserve mention. We find rather frequently an incrimination of depressions of the skull. Our series does not happen to include any such case. A few are mentioned by Starr (Brain Surgery, pp. 267–271), and in my therapeutic remarks.

In two of our patients, residuals of subdural hemorrhage proved to be of decided importance. One case has only been examined operatively, the other by autopsy. Both give valuable hints for operative treatment even where there is no depression.

The first case showed a clot in process of organization and was considerably benefited by operation. The second case showed an ossified plate and spur over the left frontal lobe, besides the effects of a fall in the terminal status epilepticus.

Case 3. F.T., mill operator, married, about 38 years old, of cheerful, sociable disposition, about January, 1897, was struck on the head by a 57 lb. weight. He was not knocked down, but there was a hematoma of the scalp. Since then the patient has had attacks of headache and dizziness, a few times he vomited his coffee in the morning. His character changed; formerly jolly and active in social enterprises (theatricals), he became silent and non-responsive, at times he wandered away for several hours at a time and would stone the friends who followed him; about June his work became less efficient owing to the headaches; he thought the workmen put things in his way; it was their fault that he could not do things. About June 25, he had a violent outbreak, in which he nearly succeeded in killing his wife with an axe and smashed furniture. July 2, he had to be committed; in an attack of headache he again had become excited, complained of being full of electricity and that his wife and children might injure him; the pictures on the wall bothered him; he ordered everybody out of the room.

Under observation he showed on admission (July 2, 1897), and for nearly three weeks a condition of sulky delirium with vehement blind outbreaks; he would get up and rush to the window and smash the glass, or clutch the steam-pipe and shake it violently to “shake out the steam.” He talks deliriously in German, says he sees faces, one piece of furniture on the ceiling, another hanging from the window, the children all topsy-turvy, and breaking all the windows—“That won't do, Mary.” In the struggle with attendants the patient broke a rib and was restrained in bed. He was inaccessible to conversation till July 23, when he began to listen and to give an account of his headaches and the injury. He still would lie on the floor, was indifferent or sulky, diffident, urging unreasonably to go home. July 28, he gave a patient 15 cents with which to buy tobacco, and when he did not get it, he said “fool me,” had a violent outbreak and began to beat his head against the wall, and had to be restrained. He is found in great distress. “Help me, help me, for heaven's sake, help me—take off the fetters, take off—take off—the—the—the—, these fearful flies eat me up—I—I—I don't do any thing. I am one of the best of men.” Can't you be reasonable? “I am reasonable.” You must stay in bed. “I can't stay in bed; the bed oppresses me. I will never leave my bed—I want to go home to my wife and to my baby (the patient has five children living); I do not cry; I do not cry—my baby—my baby—my children, children, children, etc.”; quite inaccessible to reason. He complains of fearful dreams; one morning he kept shouting: “Everything is dry in the garden,” one night he was “dead in the lower world.” At times his good-will can be held for a few moments, but he rapidly drifts into shouting, clamoring for his wife, or he makes a sudden assault. August 2, disclaimed all memory of assaulting the physician two days before, was much surprised, and said quickly if he did so he was sorry. The next day he was lying on his back with the bed sheet drawn tightly from the feet to the head, the ends tucked under him, the hands folded in prayer; he could not be diverted.

The first physical examination was essentially negative. The patient was a short man of tremendous muscular power without any nervous or other symptoms.

The further observation showed that relatively quiet periods with fair orientation but unreasonable general attitude would, with or without attacks of severe headache (which yielded slightly to phenacetin 0.80, but were aggravated by acetanilid), show sudden outbreaks either of fault-finding, or a blind attack without warning, or dream states. A nocturnal noise upstairs started him to claim the next day: “The ceiling is coming down; I am oppressed.” He complains that he cannot understand the people, that he has forgotten all he learned at school, cannot learn to read English. At times he keeps a promise to abstain from violence, but is easily irritated again. “If you want to kill me now, kill me; I cannot stand this now any longer; I don't know what this means; I want to go to my children.” He claims he can work in the mill. At times he has a summary remembrance of his troubles. Thus, on December 9, he admitted “I fought with the attendants but I do not remember why.” “That is an old affair, I had rather not speak of it. It is not my nature to speak so freely of my own affairs. I do not remember why I struck; they laughed at me, and I got tired of it.” “I would like best if I could shut my eyes.”

A renewed examination of the head showed nothing but very slight lateral nystagmus on extreme turning of eyes, and on tapping the scalp with a hammer a painful spot over the right parietal protuberance. The headaches are mostly right-sided. A permission for an exploratory operation was obtained, and it was carried out by Doctor Homer Gage as follows, on December 27, 1897:

The shaving of the scalp exposed a small scar over the right parietal prominence near the “painful” spot; the usual incision was made with this scar in the center; the skull was found intact, both the external and the internal plate. The dura appeared somewhat bluish and, on incision, brownish fluid escaped, and brown, half gelatinous material was found. A second trephine opening was made further forward and the same material of partially organized clot was exposed. It seemed possible to remove practically the whole through the somewhat enlarged opening. The pia appeared normal. The fluid contained small hematoidin needles and very few leukocytes. Its amount was difficult to judge, the thickness of the layer was hardly more than 5 mm, and the whole mass probably not more than 25 or 30 cc. The wound healed perfectly smoothly.

The patient did well. December 30, in the evening he was sulky, irritated by “foolish” questions; he had rather severe headache, but was relieved by phenacetin 0.80. It reappeared a little for a few days only. The patient remained rather diffident and impatient, and only once (January 28, 1898), when being photographed he burst out suddenly: “Ich will nicht, ich will nicht; ich will nach Hause gehen”; he took off his coat as if for a fight and started against the photographer. He attributed the outbreak to his impatience.

On his discharge, January 30, 1898, the patient was unappreciative. He did well until March, 1898, when, after an alcoholic excess, he broke up the furniture in the house and threatened the family; and in December, 1898, he was arrested for disturbing the peace (intoxication) and sentenced to three months in jail. Since then he has done well when abstaining from drink.

Summary. Traumatism without marked primary results, except hematoma of the scalp. Change of character; sulkiness, irritability; intolerance to alcohol, attacks of headache with violent outbreaks with only summary remembrance. Removal of an old subdural clot over the right frontal lobe. Disappearance of headaches and outbreaks of violence; but residual susceptibility to alcoholic excitement.

…………………………………………

The question whether there is such a thing as traumatic insanity is easily answered on the basis of our material. We admit the term as a generic one. Where we have collected the facts, we do, however, well to give a brief descriptive designation for the mental pictures, and, in addition, an expression of the relative importance of the etiological factors. Psychiatry will never progress unless its diagnoses mean to be summaries of the available facts arranged according to their pathological or nosological bearing, instead of the traditional ill-defined terms. And where our nomenclature is hazy, or a record made with insufficient regard for differentiations, nothing short of a concise rendering of the findings in plain language should be considered good enough, instead of a term which has too many connotations and may be used differently by writers and readers. In the absence of such accounts a reclassification of the statistics in the literature has no sense.

Summarizing our experience concerning clinical distinctions, we should discourage the hope for a strict classification, but suggest as salient types and as a means to keep order among the facts:

1.

The direct post-traumatic deliria with the following subdivisions.

2.
b.a.

Preeminently febrile reactions.

b.b.

The delirium nervosum of Dupuytren, not differing from deliria after operations, injuries, etc.

b.c.

The delirium of slow solution of coma with or without alcoholic basis.

b.d.

Forms of protracted deliria usually with numerous fabulations, etc. (with or without alcoholic or senile basis).

3.

The post-traumatic constitution.

4.
d.a.

Types with mere facilitation of reaction to alcohol, grippe, etc.

d.b.

Types with vaso-motor neurosis.

d.c.

Types with explosive diathesis.

d.d.

Types with hysteroid or epileptoid episodes with or without convulsions (such as most reflex-psychoses).

d.e.

Types of paranoiac development.

5.

The traumatic defect conditions.

6.
f.a.

Primary defects allied to aphasia.

f.b.

Secondary deterioration in connection with epilepsy.

f.c.

Terminal deterioration due to progressive alterations of the primarily injured parts, with or without arteriosclerosis.

7.

Psychoses in which trauma is merely a contributory factor.

8.
h.a.

General paralysis with or without traumatic stigmata.

h.b.

Manic-depressive and other transitory psychoses, catatonic deterioration and paranoiac conditions, with or without traumatic stigmata.

9.

Traumatic psychoses from injury not directly affecting the head.

…………………………………………

ACKNOWLEDGMENTS

[Based upon observations accumulated from 1896–1902 at the Worcester Insane Hospital, with the much-appreciated help of its staff.—Author]

These excerpts from “The Anatomical Facts and Clinical Varieties of Traumatic Insanity,” by Adolf Meyer, are reprinted from the American Journal of Insanity, vol. 60, no. 3 (January, 1904), pp. 373–380 and 438–439, by permission of the American Journal of Psychiatry.
Introduction copyright © 2000 American Psychiatric Press, Inc.