Cases 99–103 show the Variety of Structural Lesions that Treatment has to face.

Case 99. James McDevitt arrived at the Danvers Hospital, July 20, 1906 (saying that he came to be “thawed out”), and died less than six months later: January 12, 1907. He was 34 years of age. He had been a shoe-worker after leaving school, had worked eight years with the General Electric Co., and had then become a bartender. He had, however, stopped work in September, 1905, and we may safely say that mental symptoms had begun insidiously at about that time. His symptoms, if there were any, had been masked by a heavy alcoholism, but an obvious change had appeared in November, 1905. The patient lost ambition, smoked and loafed about his room, and developed speech disorder. He denied venereal disease, nor was there any superficial evidence of such.

Physically, the patient showed little or no disorder except acne of the trunk, patches of eczema on the left lower chest, and numerous brownish scars along both tibiae.

Neurologically, the Romberg position was maintained, but the gait was very unsteady on attempts to walk a straight line; fingers, tongue, and face were tremulous, and finer movements were performed with marked incoördination. No direct or consensual light reactions could be obtained in the pupils, which were dilated and irregular.

The condition of the reflexes is important on account of the autopsy findings. The abdominal and cremasteric reflexes were prompt, and the knee-jerks equal and very lively. Achilles and normal plantar reactions were present; there was no clonus; the arm reflexes were very brisk.

The mental symptoms need not detain us. Consciousness was clear; orientation for time, place, and to some extent for persons, was imperfect. Arithmetic had been largely forgotten. Handwriting was irregular and scrawling, and in places unintelligible. Although the patient claimed that his memory was intact, it was decidedly imperfect. He remarked that John D. Rockefeller, a Chicago king, was President; the General Electric Works had almost 50,000 people at work; and in fact Lynn was one of the largest cities in the state, having over 12,000 people. The height of patient’s room was estimated at 25 feet. There was a slight euphoria. There was never any doubt of the diagnosis of Paretic Neurosyphilis (“general paresis”).

Five months after admission, slight convulsions developed, after which the patient was more dull and demented; he became bedridden. More convulsions followed, leaving the right arm and hand useless. There were clonic spasms of the muscles of both lower legs. Decubitus developed and death occurred.

We may set the total duration of symptoms in the case of James McDevitt at a little over a year; nor is there any evidence of previous or prodromal symptoms beyond a total period of about 15 months, unless we may regard his leaving the General Electric Works to become a bartender some nine years before death, as a symptomatic change of character. In any event, it is of note that the autopsy showed singularly few lesions. Death was due doubtless to complications following decubitus, and there was a slight acute splenitis. The kidneys showed some parenchymal change. The aorta showed many patches of sclerosis, with calcification or ulceration throughout its length. These changes were not characteristic of syphilitic disease. There was considerable coronary arteriosclerosis and a slight mitral valvular sclerosis. There was a brown atrophy of the heart muscle, somewhat surprising in a man of 34 years. The brain was practically normal, weighed 1200 grams, and showed convolutions normal in size, relation, and arrangement. There was no sclerosis grossly evident in the blood vessels. The pia mater appeared to contain a considerable excess of clear fluid. The calvarium was of normal thickness and showed diploë and the dura mater failed to show adhesions. There were no macroscopic signs of lesion in the spinal cord.

Microscopically, the lymphocytosis, plasmocytosis, and phagocytosis of the perivascular spaces, (relative?) increase in blood vessels, the gliosis, and evidence of nerve cell destruction, taken together warranted the diagnosis of Paretic Neurosyphilis. It was plain that the nerve cell destruction was best marked in the inner layers of the cortex. The microscopic study of the spinal cord showed that there was very possibly a slight sclerosis of the posterior columns in the lumbar region, but this was so slight that it could hardly be noted in the myelin sheath stains (Weigert). Very sharply marked, on the other hand, were the bilateral pyramidal tract lesions in the lumbar and thoracic regions, less marked at the cervical levels.

Without attempting to analyze carefully all these findings, it is interesting to note in this case a foil to the usual spinal cord picture of paretic neurosyphilis. The spinal cord, ordinarily normal, or perhaps more usually affected by a degree of posterior column sclerosis, in this case showed such well marked pyramidal tract sclerosis that we may perhaps place the case in a subordinate group of Spastic Paretic cases of Neurosyphilis. The source of the pyramidal tract disease lodges, however, in the cortex cerebri itself, being part and parcel of the lesions mentioned above as affecting more directly the inner layers of the cortex. Many of the so-called giant, or Betz, cells had undergone a complete destruction. It will be remembered that clonic spasms of the muscles of the legs appeared in the fortnight preceding death, and that there had been convulsions for about six weeks before death. There was no evidence at the autopsy why the right arm and hand should have become useless, whereas the left upper extremity remained normal. This case, then, forms an exception to the ordinary paretic neurosyphilis group in that the brunt of the microscopic process was borne by the inner layers of the cortex. The cells of origin of the pyramidal tract fibres had been cut in this lesion, and had become subject to partial or complete destruction. Note, however, that the lesion remained a microscopic one and that the marked convulsions were not related to gross lesions, thereby following the rule for paretic seizures.

From the standpoint of possible treatment, it is of course true that few organs of the body showed grave lesions save in the calcified and ulcerated aorta, which conceivably might have become quiescent under appropriate treatment. But, although the brain was almost if not quite normal in the gross, and although its membranes showed practically no lesion, treatment would not have been very promising. To be sure, the exudate might have been cleared away if the spirochetes responsible therefor had been destroyed by treatment. Yet the destruction of the giant cells of origin of the pyramidal tract fibres to such an extent as in this case could hardly have been compensated for by any known process. So far as we are aware, the destruction of considerable numbers of the smaller association elements of the brain is subject to the compensation of other elements of the nervous system, which conceivably might be re-educated or newly educated to perform certain processes. The histological picture in a case like that of McDevitt accordingly leads to the hypothesis that so well marked a spastic paresis, even in the presence of otherwise favorable signs, would be of especially baneful portent therapeutically.

Case 100. Jacob Methuen, 35, was a carpenter from Newfoundland. He was working upon a certain Thursday with his brother, who noticed that Jacob was lifting the tools about in an unusual manner and talking strangely to his fellow workmen. He fell asleep, going home in the street car, and said afterward that he felt dazed and peculiar. He talked all kinds of nonsense to his wife upon arrival. Methuen remained in bed next day, fancying he was going to die, calling his family together, and saying good-bye to them. He remained in bed all through the next day, but on Sunday appeared better,—more active, and in fact quite natural. He slept only an hour Sunday night, calling to his wife that it was time to get up. On Monday he began to be irritable to his wife, and accused her of flirting with his brother and intending to elope with him. He struck his wife several times, and when two brothers came to watch him, accused them both of trying to steal his wife, and struck them. Tuesday he remained in bed until late at night, when he arose and tried to assault the family.

It seems that another brother of the patient had died but eleven days before his admission to the hospital and five days before the onset of Jacob’s symptoms. Since his brother’s death he had been dwelling upon religious matters, and in fact the day after his brother’s death, he waked up during the night, saying that he was too happy to sleep, that he heard the Master’s voice, and at times the devil’s voice; that there was to be a modern miracle and his spiritual life from now on would be different.

Eleven days after admission to the hospital, Methuen died, making a total duration of symptoms, beginning at his brother’s death, of 22 days.

Physical examination showed a man 5′ 9″ tall, weighing 149 pounds, rather pale and poorly nourished, with a somewhat enlarged heart and no evidence of venereal disease.

Neurologically there was a slight facial and digital tremor, but otherwise no symptom or reflex disorder except that the tendon reflexes were generally increased; the knee-jerks especially were very vigorous. There was no speech defect. His handwriting was fairly legible.

The patient was very noisy and uncontrollable, tearing clothing and biting, striking the attendants, refusing food, talking rapidly, loudly, and incoherently. His manner suggested auditory hallucinations but no positive evidence of these was obtained. His clothes could not be kept on him. The following is a sample of his reactions: As the examiner entered, the patient stood stark naked and glaring. He started to talk as follows: “Methuen,—I, Saviour, come to life and ought to die—— Now I lay me—— Now I die—— The heart beats—— No, I ain’t going to die—— I am going out soon. I want my clothes—— You can’t hold me; I am strong.” (Struggles violently with the attendants.) “I am God. God. I know you, you can’t fool me.——I am here——I can do you all. How many doctors are there here?” (Struggles violently. Looks at examiner.) “He is writing something. Sir, you can’t fool me in a million years. Do you understand that, doctor? You can’t fool me. Write all the prescriptions you want to. Ten thousand years; you hear that, doctor? Ten thousand years. You can’t fool me; ten thousand years. Ten thousand years are but a day for the spirit of the Lord,” etc., etc.

The excitement continued unabated. The patient became entirely disoriented, and finally almost unable to move. He lay in bed trying to talk and muttering broken gibberish, still attempting to struggle to the extent of his limited strength.

The autopsy showed no sign of lesion (brain weight 1380 grams), unless, perhaps, the occipital regions were slightly firmer than the rest of the brain. Death was apparently due to a bilateral pneumonia, bronchial type. There was an acute splenitis. The only chronic lesions of the body were a bilateral chronic adhesive pleuritis and a slight sclerosis of the arch of the aorta.

Microscopically there was a distinct though mild degree of lymphocytosis of the perivascular spaces in many regions. Somewhat extended search failed to reveal plasma cells, and it is certain that if plasma cells existed, they must have occurred in very small numbers.

Here, then, was a case of Diffuse Neurosyphilis (with brain picture consistent) with symptoms lasting but 22 days and with an appearance of acute mania. It is to be noted that this case arrived at the hospital on the eleventh day of his symptoms. The case occurred long before the development of the temporary care system in Massachusetts. It is probable, or at any rate possible, that he would have been brought to the hospital far earlier, say, upon the sixth day, had the modern temporary care system been installed at that time. The routine W. R. examination would then have been made. With more effective hydrotherapy, it is possible that the patient’s life might have been prolonged and that treatment might have been effective. So far as we can see, the case would have been a singularly good one for treatment despite the practical unmanageability of the case under ordinary home treatment, and even under hospital conditions where modern hydrotherapeutic appliances are not available.

Case 101. We report the case of John Baxter, a boat tender of 48 years, because this particular victim of Paretic Neurosyphilis seems to have had the most markedly thickened and altered meninges in our whole series. Of course, the therapeutic theory upon which we now proceed in the treatment of non-paretic and possibly even of paretic neurosyphilis is that, other things being equal, the meningitis can be removed by treatment, or in the course of treatment, so that the degree of ultimate recovery rather depends upon the condition of the brain substance itself than upon the condition of the meninges. Here, at all events, is an example of the most highly meningitic neurosyphilis that we have seen.

Curiously enough, two of Baxter’s brothers were also patients at the hospital at which Baxter died, and a number of the other members of the family are reported as “nervous.” It seems that at 35 Baxter began to drink heavily and had never given over the habit of alcoholism.

Upon admission to the hospital, in fact, he showed a sufficiently typical picture of delirium tremens. His consciousness was clouded, he had vivid visual hallucinations and was very apprehensive.

His heart was enlarged to the left; the pulse, 120, was of increased tension and irregular; there was peripheral arteriosclerosis; the teeth were poor; the tongue coated; and the mouth foul. The urine showed a trace of albumin and rare hyalin casts.

Neurologically, the gait was somewhat unsteady, there was an extreme tremor of the whole body, including the tongue and fingers. The Romberg sign was negative although there was marked swaying. The pupils were equal and reacted normally; the knee-jerks were markedly exaggerated, the arm reflexes somewhat exaggerated. The remainder of the reflexes upon systematic examination were negative.

Upon arrival, Baxter was put to bed, but he barricaded his door and fought with the attendants. The tremor increased, the hallucinations were both visual and auditory. After a few days, Baxter became so weak that he could not move. He refused to eat for a period of two days, explaining in whispers that he did not wish to be poisoned; a voice had told him the food was to be poisoned. The voice was of agreeable tones, probably belonging to a lady; it did not speak, but sang to him. The clouding of consciousness failed to clear up, as in delirium tremens, so that, though patient was admitted March 3d, it was hardly possible to speak freely with him until more than a month later, April 9th. A good-natured conversation would run as follows:

Soon the hallucinatory phase passed, and the patient remained in a cloudy and disoriented state, inaccessible, rarely speaking, and gradually failing physically. Death occurred about three months after admission (pulmonary symptoms).

In estimating the duration of the process in John Baxter, we must take into account that he left the grocery business and became a hard-working but poorly-paid boat tender at about 35 years, at the same time that the alcoholic habit began.

The autopsy showed that death was due to bronchopneumonia with pleurisy. There were in the body a variety of chronic lesions, such as gastritis, colitis, epididymitis, splenitis, parietal and valvular endocarditis, prostatitis, chronic appendicitis, and some mesenteric lymphnoditis. The heart was somewhat hypertrophied. There was a slight diffuse nephritis with cysts, emaciation, and decubitus. The calvarium was thick and somewhat dense. The dura was thickened and adherent, and the pia mater,—as above stated, the most thickened and altered pia mater in our series,—is described as everywhere thickened, of a brownish gray and white color, especially over the vascular lines, and as showing small white areas of deeper thickening scattered over the surface, but most markedly over the sulci, and not as a rule over the crowns of the gyri. There were also yellowish brown spots with a suggestion of fibrin over the lateral aspects of both hemispheres. The vessels at the base were not remarkable in the gross. The brain weighed 1220 grams, and appeared to be of darker color than usual.

Case 102. Theodosia Jewett, dead at 58 years, showed the most remarkably wasted brain in a long series of victims of paretic neurosyphilis. We present her case to emphasize what therapy must face in certain instances, but would recall the fact that exceedingly few such wasted brains have come to our attention in cases dying in the institutions of Massachusetts.

Mrs. Jewett, a housewife, whose parents died of shock, and one of whose two brothers also died of shock, was a normal child and schoolgirl, and worked as dressmaker until she was married, at 24, to a grocer, by whom she had two children. At the age of 46, Mrs. Jewett began to suffer from so-called “nervous prostration.” The attack lasted some two years, but there were no psychotic symptoms beyond worry and insomnia. The menopause occurred at 52, at which time the first signs of psychosis appeared, namely, a forgetfulness concerning familiar matters, such as sewing, cooking, and the like. At 55, this amnesia had become so marked that Mrs. Jewett could neither write nor tell time. She, however, was a perfectly quiet and easily manageable patient, often subject to drowsiness in the day.

Six months before her admission to the hospital, she began to suffer from insomnia, failed to recognize her surroundings, and had a number of crying spells. Restlessness had begun a month before admission; auditory hallucinations developed in the form of imaginary conversations with dead persons. A certain loquacity set in, and for a week before admission, Mrs. Jewett became somewhat resistive.

Physically, the patient was sallow, poorly nourished, with pale mucous membranes, peripheral arteriosclerosis, no teeth, muscular feebleness, tremor of hands and tongue, and active knee-jerks. Mentally, the patient was depressed, talked to herself, assumed a supplicating position, suddenly altered her attitude, and was very tremulous. Her talk was low, mumbling, and incoherent, for the most part composed of answers to her own questions. Sometimes there was a curious difficulty in speaking, such that the lips moved but no sound emerged; but for the most part there was no difficulty in uttering words. The patient either could or would not write. Only when the attention was secured by speaking to her sharply was she apparently able to understand questions, and the answers to these sharp questions came spasmodically and as if interrupting her own thoughts. Nor was it ever possible to obtain a repetition of the same answer.

The patient died in exhaustion, with pulmonary symptoms three weeks after admission.

The autopsy which was performed 3½ hours after death showed the following points of interest:

The heart weighed 210 grams. There was marked thickening of the aortic valve. The coronaries were slightly thickened.

The lungs were slightly adherent to the chest wall at the apices and posteriorly. The right lung was consolidated in the lower two lobes posteriorly and the bronchi exuded pus; the left lung was not remarkable. There was a chronic splenitis.

The liver showed fibrous changes, was a brownish-red in color, mottled with yellow.

Combined weight of the kidneys 195 grams. The capsules were adherent, tearing the cortex when stripped.

The diploë were well marked. The dura was not adherent. The pia was slightly thickened and raised from the cortex by a large amount of subpial fluid (showing atrophy of the cortex). The pial vessels were injected, more markedly so on the left side. The arachnoid villi were reported as moderately developed, especially along the longitudinal fissure.

The brain was rather soft in all regions. The weight was 1045 grams. According to Tigges’ formula the weight of the brain should be approximately 8 times the body length in centimeters. The length in this case was 158 cm., therefore, according to this formula the weight of the brain should have been 1464 grams. The difference of more than 400 grams is evidently a loss to be accounted for by atrophy, a very heavy loss.

1. Was the “nervous prostration” at 46 of syphilitic origin? One cannot give a categorical answer to this question. The high incidence of shock in the family suggests poor stock in which a psychoneurosis is not an unusual phenomenon. The presence of syphilis might act as a debilitating factor or agent provocateur, if it were not to cause any demonstrable brain lesion. As pointed out in the case of Harrison (9), however, it is not unusual in neurosyphilis to find a history of symptoms occurring years before the final breakdown and symptoms frequently not recognized as of neurosyphilitic nature.

2. Does the fairly long duration of the psychosis (at least 3 years) explain the marked atrophy? Cases having symptoms even much longer than three years at times show relatively very little atrophy, so that this factor in itself cannot be said to explain the tremendous destruction of tissue.

Case 103. To bring out this point we may instance the case of Alfred Weed, a victim of Paretic Neurosyphilis, dying at the age of 48 years after a course of about seven years. The following is an abstract of the clinical history:

A. W. suffered from lues some 24 years before his death at Danvers Insane Hospital in 1907. There is no account of insanity in his family. The patient had been undergoing mental changes for six years before death. At the age of 42 began to take interest in socialism and spiritualism. Would become excited at times and was observed to talk to himself. At times it seemed that he was reacting to visual hallucinations. After eight months he became depressed and apprehensive and developed delusions of poisoning.

On admission to the Danvers Insane Hospital in June, 1902, the subject was found to be ataxic, falling in the Romberg position. Pupils were equal but of pin-point size. There was tremor of the facial muscles. The knee-jerks were absent. Speech was ataxic. Memory defective. Depressed. Thought he was to be punished. Refused to eat.

Later in the year of admission, patient became more negativistic. He refused to have his clothes brushed. His answers were slow. Mental arithmetic was correctly but slowly done. During January, 1903, the patient was apt to be active and talkative for a time, and then his attitude would suddenly change to one of silence, resistivement and untidiness. From time to time he would be querulous and sulky. In August, 1903, the patient became weaker and could walk with assistance only. Paralysis developed in the left facialis region and in the left external rectus. Pupils were still small, but the left had become smaller than the right. Light reaction tests unsatisfactory. Knee-jerks could not be obtained.

In December, 1903, the patient was untidy and helpless, lying with his thighs and legs flexed. The limbs were spastic on passive motion. In 1905, the pain sense of the legs was found lost and the pupils were small and stiff. The protruded tongue was deflected to the right. The right labial fold was more prominent than the left. Knee-jerks remained absent. Ataxia was extreme.

The Neurological Findings may be summed up as follows:

1.

Ataxia of the legs.

2.

(Probable) Diminished sensibility in the legs.

3.

Pupils small and stiff. Left smaller than the right.

4.

Paralysis of left facialis.

5.

Paralysis of left external rectus.

6.

Tongue protruded to right.

7.

Right elbow jerk greater than left.

8.

Knee-jerks absent.

The cause of death was bronchopneumonia. The walls and valves of the heart showed a few chronic changes. There was a marked splenitis and an atrophy of the liver. The kidneys showed numerous depressed scars. The arch of the aorta was somewhat sclerotic. The following is a full description of the head findings which we present by way of comparison with other cases. Note especially the cerebellar, dentate, and olivary changes. Note also the fact that palpable sclerosis is demonstrable over a far larger area than atrophy, so that we may almost safely conclude that the process of induration sometimes precedes that of atrophy. One gets the impression from the extent of visible atrophy and tangible induration in this case, that a possible therapy would have not merely to clear the perivascular spaces of cells and spirochetes, but would also need to arrest the indurating and wasting process. Nor could any therapy deal effectively with the superior frontal and upper central atrophy of the cerebrum of this case, or with the olivary and cerebellar lesions.

Head: Hair thin at vertex. Scalp normal. Calvarium thin and dense. Dura mater slightly adherent to calvarium at vertex. Sinuses normal. Arachnoidal villi well developed. Pia mater of anterior and central regions contains an excess of fluid. The pial veins well injected.

The pia mater exhibits one unusual lesion: Faintly yellowish brown spots of miliary and slightly larger size are scattered irregularly in clusters over the vertex. These miliary pial macules are observed especially over the posterior third of the left superior frontal gyrus (a group of twelve or more). Two are seen in the pia mater of the right superior frontal gyrus. One is seen in the upper part of the left post central gyrus. The upper end of the right postcentral gyrus contains three macules.

Besides these brownish macules, the pia mater also shows focal white thickenings which resemble the more frequent appearances of chronic fibrous leptomeningitis. The white thickenings are of irregular size but are, as a rule, larger than the macules above mentioned. They occur, as a rule, over the sulcal veins and are most frequent in the anterior region.

The vessels at the base are normal. There is no evidence of pial thickening at the base of the brain. Brain weight, 1265 grams. There is visible atrophy of both superior frontal gyri and of the upper two-thirds of both central gyri. The extent of palpable sclerosis surpasses that of visible atrophy. Palpable increase of consistence is shown by the prefrontal, orbital (more marked on left side), frontal, central, hippocampal and occipital regions. The temporal cortex is of normal or slightly reduced consistence.

Section of the cerebral cortex shows everywhere preservation of the cortical markings. The sclerosed areas show a diminution in depth of the cortex, which is more marked in the left prefrontal region. The white matter of the centrum semiovale of the prefrontal and occipital regions on both sides shows an increase of consistence. The cerebellar cortex also shows variations in consistence. The clivus and lobus cacuminis and the posterior half of the inferior surfaces of both cerebellar hemispheres are firmer than normal. The laminæ of the left clivus are a trifle narrower than those of the right. There is visible extensive atrophy of the laminæ on both sides of a fissure in the middle of the left lobus cacuminis. In the coördinate portion of the right cacumen there is a similar process which is less marked. The dentate nuclei are firm. The olives show an increase of consistence, equal on both sides. The left olive shows on section a crowding together of its folds in the middle part of the upper limb.

Spinal cord was not remarkable.

Summary:

• Adhesive pachymeningitis
• Chronic fibrous leptomeningitis
• Miliary pial macules
• Cerebral atrophy
• Cerebral sclerosis
• Cerebellar atrophy and sclerosis
• Bronchopneumonia
• Chronic splenitis
• Nephritis
• Aortitis

Case 104. John Edwards, a man of 28 years, well developed and nourished, with general enlargement of glands and skin lesions, came to the hospital in a stuporous condition, with evidences of a complete hemiplegia.

According to the wife, Edwards had had a chancre of the lip about a year before, for which he had been treated with an intravenous injection, presumably of salvarsan, and also presumably with mercury. The lip lesion had then disappeared. For a month before admission, Edwards had had headache and dizziness, for which he was given pills and drugs. There had also been difficulty with speech and numbness of the left arm as far up as the elbow, but this paresthesia had quickly disappeared. The hemiplegia was of only a few days’ duration. After a feeling of nausea and vomiting, the patient had fallen with left-sided paralysis. Afterwards, he had shown mental peculiarities, eventually becoming noisy, hard to manage, and appropriate for hospital care.

The physical examination showed a variety of increased reflexes, including ankle clonus on the left side.

The question might arise whether this case was one of hemorrhage or thrombosis, and the facts about the onset of the hemiplegia are inadequate for a decision. However, at so early an age, the probability of syphilis is large and the history of labial chancre was quite suggestive. If we may conclude neurosyphilis, the diagnosis of thrombosis rather than rupture of blood vessel is likely. The laboratory tests bore out the diagnosis since the W. R. of serum and fluid both proved positive; the gold sol reaction was syphilitic; there were 176 cells per cmm.; there was excess albumin, and a positive globulin reaction.

The outcome in such a case is dubious. If death does not occur soon, recovery is not impossible under treatment. At all events, a considerable improvement is likely.

Edwards was given bi-weekly injections of salvarsan, intramuscular injections of mercury salicylate, and doses of potassium iodid, averaging 100 grains, three times a day. Under this treatment, he slowly recovered and became mentally clear after a few weeks. The paralysis seemed complete and permanent. Even after three or four months, there was absolutely no change in the condition, and Edwards was quite unable to move either arm or leg. Meanwhile, the spinal fluid had become practically negative to all tests.

Treatment was somewhat optimistically continued and was rewarded at the end of ten months with marked improvement such that the patient was able to stand on the paralyzed leg and move the arm to a certain degree. This improvement is still continuing. The spinal fluid and the serum have remained negative to laboratory tests.

Note: A period of six months is commonly regarded as that period in which improvement in paralysis is to occur if there is to be any improvement. There was certainly not the slightest improvement in the paralysis of this case before eight or nine months of treatment had elapsed, and it took ten months to secure the marked improvement mentioned.

1. What is the significance of the prodromal symptoms? The headache and dizziness should have been viewed with great gravity. They are characteristic in Meningovascular Neurosyphilis.

Moreover in this case there had also been difficulties with speech and other transient symptoms which should have called attention far earlier to the possibility of neurosyphilis.

2. What is the significance of the high cell count: 176 per cubic millimeter? Such high cell counts are frequent enough in diffuse neurosyphilis, but low cell counts are frequent also. But although the high cell count taken alone is of lesser significance, the fact that the high cell count in this case is associated with a “syphilitic” gold sol reaction is of far greater significance for diagnosis. These associated findings are characteristic of meningovascular neurosyphilis.

3. What kind of recovery may be expected in successful examples of treatment in meningovascular cases? Recovery with defect. It will be noted that ten months elapsed before any marked improvement occurred on the paralyzed side. We could not expect a complete recovery from this paralysis.

4. Was inadequacy of treatment following the chancre responsible for the early cerebrospinal involvement? In this connection one must remember that such neural involvements occur occasionally even during active treatment (neurorecidives). The discontinuance of treatment after a short period, in this case less than a year, is always a risk to say the least. And this is true even though the W. R. becomes negative, for trouble of a neurosyphilitic nature may occur later; this when both blood and spinal fluid have previously been found negative. The old rule of following and treating a syphilitic for several years despite the disappearance of symptoms is still a good rule.

Case 105. Henri Lepère, a machinist, 48 years of age, came voluntarily to the Psychopathic Hospital for a gradually failing memory and inability to work. He had had indigestion for four years (epigastric distress, nausea, no vomiting). He was still suffering from epigastric distress and from headaches. At times he had had difficulty in walking.

Physically, Lepère looked older than he was; he was very poorly developed and nourished, and seemed very weak. There was a slight visceroptosis.

Neurologically, there was considerable speech defect, particularly well marked in test phrases. The pupils were contracted and gave the Argyll-Robertson reaction. Neurologically there were no other signs.

Mentally, there was a depression with worry; but it was a question whether these phenomena were not entirely natural. The special complaint was of failing memory.

The Argyll-Robertson pupil also prima facie signifies neurosyphilis. Lepère, in fact, admitted syphilitic infection at 23. The gastric symptoms at once suggested tabes. The knee-jerks and ankle-jerks were, to be sure, preserved; however, this is not very unusual in tabes. The amnesia and aphasia naturally suggested paresis. Without resort to laboratory findings, accordingly, the diagnosis of taboparetic neurosyphilis (“taboparesis”) was suggested.

The serum W. R. proved positive, but the spinal fluid W. R. very slightly so (yielding only moderate reaction with 1 cc., 0.7 and 0.5 cc., and a negative reaction with 0.3 and 0.1 cc.). Globulin was moderate, and albumin was found in only moderate excess. There were 21 cells per cmm. in the spinal fluid. The gold sol reaction was that which we regard as typical of syphilis or tabes. If we were to rely upon the weakness of the fluid W. R. and the nature of the gold sol reaction, we should be inclined to favor the diagnosis of Diffuse Neurosyphilis (“cerebrospinal syphilis”) rather than resort to the diagnosis of paretic neurosyphilis.

Salvarsan treatment was attended by the rapid disappearance of headaches and gastric symptoms and by a rapid gain in weight and feeling of well-being. Salvarsan was continued twice a week for two months, whereupon Lepère returned to work. He has been successfully at work now for seven months without return of symptoms. Four months after beginning of treatment, the spinal fluid was examined and found entirely negative. Nevertheless, the serum W. R. has remained positive despite eight months of salvarsan treatment.

1. What is the meaning of the titrations in the spinal fluid Wassermann reaction? When Plaut originally applied the Wassermann reaction to spinal fluids, he used 0.2 of a cc. of spinal fluid. With this amount of fluid he found that cases of general paresis gave a positive reaction in about 100% of the cases while this positive reaction was only given by 40 to 60% of the cases of cerebrospinal syphilis and tabes dorsalis, hence he promulgated a differential point that a negative reaction in spinal fluid indicated that the case was not general paresis. Hauptmann later showed that if 1 cc. of spinal fluid were used, a positive reaction would occur in practically 100% of the cases of general paresis, cerebrospinal syphilis and tabes. Therefore, at present, we use the different titers of spinal fluid from which we draw the following conclusions: If the reaction in the untreated case is negative with 0.1 and 0.3 of a cc. and positive with the 0.5, 0.7 and 1 cc. dilutions as in the case of Lepère, we are probably dealing with non-paretic neurosyphilis. With this method of titration we are also better able to watch the progress of treatment as the dilutions of 0.1 and 0.3 cc. become negative first.

2. How soon can one expect improvement after commencement of salvarsan therapy in cases of diffuse neurosyphilis? The time relation of results in treatment varies with each individual case. In the case of Lepère gastric symptoms that had been present for a number of months disappeared as if by magic after the first injection of salvarsan. As a rule, it is true that the more acute the symptoms the quicker their disappearance but this does not hold for all cases, as in this particular instance the long-standing symptoms disappeared very rapidly. The symptoms often disappear very much more rapidly than the laboratory, tests change.

3. How can the mental symptoms (depression and failing memory) of which patient complained be explained? In the first place, as has been stated, it is doubtful if these are more than subjective and the result of the patient’s feeling of discomfort and pain. However, it is also possible that there may be intracranial involvement of the meninges or of the brain itself. And, if such were the case, the improvement might be the result of the treatment.