Neurosyphilis / Modern Systematic Diagnosis and Treatment Presented in One Hundred and Thirty-Seven Case Histories

V. SOME RESULTS OF TREATMENT

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

SPASTIC HEMIPLEGIA in PARETIC NEUROSYPHILIS (“general paresis”), showing marked degenerative changes, a condition in which therapy could be theoretically of very little avail. Autopsy.

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.

COMMON THERAPEUTIC CONCEPTION

[M]VP =: TYPICAL PARESIS
MV[P] =: TYPICAL CEREBROSPINAL SYPHILIS
[M]V[P] =: TYPICAL SYPHILITIC ARTERIOSCLEROSIS

(M = Membranes, V = Vessels,

P = Parenchyma, [] = not involved)

Chart 21

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.

Bilateral pyramidal tract sclerosis, secondary to destruction of large motor (Betz) cells of motor (precentral) cerebral cortex—paretic neurosyphilis.

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.

NEUROSYPHILIS with total duration of symptoms twenty-two days. The comparatively MILD BRAIN LESIONS, INFLAMMATORY AND NOT DEGENERATIVE in type, suggest the possibility that therapy might have been successful. Autopsy.

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.

NEUROSYPHILITIC LESIONS

LESIONS OF THE SECONDARY PERIOD

(1) INTERSTITIAL ENCEPHALITIS OR MYELITIS
(“meningitis”)
(2) PARENCHYMATOUS ENCEPHALITIS OR MYELITIS
(“encephalitis,” “myelitis”)

LESIONS OF THE TERTIARY PERIOD

(1) CHRONIC INTERSTITIAL ENCEPHALITIS OR MYELITIS
(“gummatous meningitis”)
(2) CHRONIC PARENCHYMATOUS ENCEPHALITIS
(“dementia paralytica”)
(3) CHRONIC PARENCHYMATOUS MYELITIS
(“tabes dorsalis”)

“We have shown that the central nervous system is affected by syphilis at the same periods and in the same manner as are other internal organs. In addition the ‘parasyphilitic’ lesions are also of a typically syphilitic nature, being directly comparable to the parenchymatous affections found elsewhere in the body. They are ‘tertiary’ lesions differing only from the so-called ‘gummatous’ processes in the central nervous system in that their localization is in the parenchyma while that of the latter is in the interstitial tissues.”

McIntosh and Fildes, 1914

Chart 22

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.

Paretic neurosyphilis (“general paresis”) macroscopically normal, microscopically characteristic. Treatment does not have to face massive destructive processes already complete.

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.

PARETIC NEUROSYPHILIS showing very MARKED MENINGITIS, suggesting that therapy might have produced improvement. Autopsy.

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.

A high degree of chronic leptomeningitis. Pia mater thick, opaque, concealing brain. In paretic neurosyphilis (“general paresis”).

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:

“What is your name?”	“Baxter.”
“First name?”	After long pause, “Don’t know.”
“John?”	Pause of 7 seconds, “Yes, I think it is.”
“How old are you?”	“There are legs——there is a body——up to here——”
“Say the alphabet.”	Term not understood.
“Say the a, b, c.”	“Oh yes; a, b, c, d (long pause), e, f; I cannot say it, I did not have much education; I am not intelligent.” (In point of fact, the patient had a good grammar-school education, and had long worked as a clerk in a grocery store, with good wages.)
There was some speech defect.

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.

Some cases of PARETIC NEUROSYPHILIS (“general paresis”) have so much BRAIN ATROPHY that it is not possible to expect much improvement through antisyphilitic therapy.

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.

Perivascular exudate (low power) in atrophic cortex from case of general paresis.

Markedly atrophic cortex, but without local perivascular exudate.

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.

The THERAPY OF NEUROSYPHILIS has to face not merely variations in the degree of brain wasting and in the degree of meningitis, but also variations in the topographical distribution of lesions. Autopsy.

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

It is generally recognized that DIFFUSE NEUROSYPHILIS (“cerebrospinal syphilis”) frequently is cured through antisyphilitic therapy. Example. Mental improvement, in one month; recovery from paralysis, ten months.

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.

NON-PARETIC NEUROSYPHILIS

DIFFUSE NEUROSYPHILIS, MENINGOVASCULAR PARENCHYMATOUS, CEREBROSPINAL SYPHILIS

CASES SYSTEMATICALLY TREATED	13
CLINICAL RECOVERY, C.S.F. NEGATIVE	11
UNIMPROVED	1
UNIMPROVED, BUT C.S.F. NEGATIVE	1

Massachusetts Commission on Mental Diseases,
November, 1916

Chart 23

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.

The results of systematic, intensive, intravenous salvarsan therapy in atypical neurosyphilis (cases not certainly paretic, tabetic or the common types of meningovascular neurosyphilis) may be in our experience as good as the results of treatment in common meningovascular cases: example.

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.

	None	1 course	Repeated energetic
EFFECT OF EARLY TREATMENT ON THE DEVELOPMENT OF NEUROSYPHILIS

TOTAL CASES			4134
DEVELOPED GENERAL PARESIS			198 = 4.8%
DEVELOPED TABES DORSALIS			113 = 2.7%
DEVELOPED CEREBROSPINAL SYPHILIS			132 = 3.2%

			443 = 10.5%

EFFECT OF TREATMENT
NUMBER OF CASES	100	134	924
DEVELOPED G.P.	25 = 25%	31 = 23.1%	30 = 3.2%
DEVELOPED TABES	11 = 11%	16 = 11.9%	25 = 2.7%
DEVELOPED C.S.S.	3 = 3%	21 = 15.6%	71 = 7.6%

	Poorly treated 1880–84		Better treated 1895–99
NUMBER OF CASES	617		1139
DEVELOPED G.P.	60 = 9.7%		37 = 3.2%
DEVELOPED TABES	22 = 3.5%		16 = 1.4%
DEVELOPED C.S.S.	15 = 2.4%		28 = 2.4%

MATTAUSCHEK AND PILCZ

Chart 24

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.

The Argyll-Robertson pupil should not be used as a basis for a necessarily bad prognosis if treatment can be given.

Case 106. Frederick Stone was a business man of large interests. He had been in the hands of physicians for several years for a variety of disorders such as renal, respiratory, cardiovascular, and so on. No suspicion of syphilis had apparently been uttered by the physicians despite the fact that Mr. Stone readily stated that he had had a chancre thirty years before, and that he had received several years’ treatment of mercury and potassium iodid by mouth.

It appeared that a few years ago he had begun to have trouble with his nose, which was cauterized and operatively interfered with without satisfactory results. This nasal condition had later been diagnosticated as gummatous, and had improved considerably under a mild antisyphilitic treatment. However, this nasal condition had been considered and treated quite separately from the remainder of Mr. Stone’s troubles.

What brought him to attention was a sudden diplopia with ptosis. There was a paralysis of the external rectus of the left eye, as well as a drooping of the lid on this side. The left eye was much inflamed. The diplopia greatly bothered the patient, and there was also considerable pain in the left frontal region, confined chiefly to the distribution of the first division of the trigeminal nerve. According to the patient this headache was periodic. There was considerable tenderness to pinprick over the area and a diminution of sensory discrimination of fine touch. Both the pupils failed to react to light.

The remainder of the neurological symptomatic examination was surprisingly clear of disorder, nor was there anything in the history suggestive of tabes. There was ozena as well as evidence of the operative work upon nares and throat. Possibly the arteries were slightly hardened; blood pressure was 165 systolic. There was a large trace of albumin, and there were numerous hyalin casts in the urine.

Cases systematically treated			50
PARETIC NEUROSYPHILIS

(GENERAL PARESIS)


CLINICAL REMISSIONS			34		68%
	C.S.F. ALTERED TO NEGATIVE	4		8%
	C.S.F. ALTERED TO WEAKER	16		32%
	C.S.F. UNALTERED	14		28%

CLINICALLY UNIMPROVED			16		32%
	C.S.F. WEAKER	7		14%
	C.S.F. UNALTERED	9		18%

Massachusetts Commission on Mental Diseases
November, 1916

Chart 25

Mentally, there was a degree of depression and worry hardly out of keeping with the general situation. Despite the preservation of memory, Mr. Stone failed to do rather simple arithmetical calculations; this was the more remarkable as in his business he had to handle figures a great deal and had been doing so until recently. There was a slight tremor in his writing, as well as a certain difficulty in enunciating test phrases. Insomnia, irritability, and a feeling of nervousness and of being tired out, completed the picture.

A suggestion for diagnosis would be classically offered by the Argyll-Robertson pupils. Should not a patient with the Argyll-Robertson pupils have either tabes or paresis? However, in favor of tabes, besides the pupil, are to be counted merely the troubles with the eyes. In the direction of paresis we have to consider speech defect, to say nothing of less definite symptoms such as insomnia and increased irritability.

We are inclined to think, however, that the disease in this case is meningovascular. This diagnosis is suggested by the cranial nerve palsies and by the headache. Headache is much more rarely a phenomenon in the paretic type of neurosyphilis than in the meningovascular type.

In point of fact, the spinal fluid phenomena bore out the diagnosis of Meningovascular Neurosyphilis inasmuch as the globulin, albumin, cellular content, gold sol, and W. R.’s were all weakly positive.

1. How far can we regard the cardiorenal defects as syphilitic? Perhaps we may do so on the general principle of parsimony in scientific interpretation.

The diagnostic lumbar puncture led to an extremely severe exacerbation of the pains on the left side of the head. In fact, these pains could not be held in check by the exhibition of pyramidon. Mr. Stone regarded the pain as due to the lumbar puncture. However, there was no improvement in the pain in the prone position,—a feature characteristic of lumbar puncture pains. Upon administration of salvarsan, this local pain rapidly disappeared. In fact, there was a startling improvement; the ocular palsies disappeared in a few weeks, although these palsies had been present for several months before the administration of salvarsan. The blood pressure was reduced; the urine became negative. Perhaps the most startling feature of all (although of this we are not sure) was that the patient states he was accepted by a life insurance company although he had been twice refused previously.

Note in this case the 30–year interval between infection and generalized neurosyphilitic involvement. Note also the amenability of the process despite this duration. We are perhaps entitled also to note that a neurological examination careful enough to detect an Argyll-Robertson pupil should have been made by a number of examiners long before the particular crisis which we have sketched. It is also permissible to note that the rhinological work should not have been carried out independently of all other medical work.

2. What are the untoward results of lumbar puncture? It is true that there is always a possibility of setting up a septic meningitis by lumbar puncture, but this is a very remote possibility and with any reasonable care it is not to be considered. Lumbar puncture also has a considerable danger in cases of increased intracranial pressure. In cases of brain tumor where the tumor is located in the posterior fossa, sudden death may occur from withdrawal of spinal fluid. This is supposed to be due to the medulla being pressed down into the foramen magnum and causing paralysis of respiration. Therefore lumbar puncture should never be performed except with the greatest caution in a case in which brain tumor is suspected.

However, aside from these remote serious consequences which play very little rÔle in the ordinary procedure of lumbar puncture, certain unpleasant symptoms do frequently arise. These symptoms are chiefly headache and nausea, but, however, may go as far as vomiting. These symptoms occur almost entirely in the cases in which there is no abnormal condition producing increased spinal fluid pressure. Such unpleasant symptoms may last as long as four or five days; as a rule, however, last only for a period of a day or two.

3. What is the treatment of discomfort following lumbar puncture? It is a rule well worth observing that the patient after lumbar puncture should remain flat on his back without a pillow for 24 hours in order to avoid any unpleasant symptoms. If any symptoms do occur, it will be almost certainly when the patient arises, and in nearly every instance they will be overcome if the patient again assumes the prone position. Raising the foot of the bed so as to lower the head also helps. Veronal or bromides may be given but as a rule are not very satisfactory.

4. How permanent is the improvement obtained in the case of Mr. Stone likely to be? As a matter of fact, the patient discontinued treatment as soon as he felt well again, but after two months the pain returned to be again quickly dispelled by salvarsan. This improvement must be considered as only temporary. Under continued treatment there may be no further relapse. There is, however, evidence that much damage has been done to the body by the spirochetes, much of which is irreparable. It is even possible that further disintegration might occur even while undergoing treatment. Still treatment offers much in such a case and is to be highly recommended.

In DIFFUSE NEUROSYPHILIS, rendering the spinal fluid negative by treatment may mean neither cure nor disappearance of symptoms.

Case 107. Greta Meyer, a widow, 51 years of age, came voluntarily to the hospital, seeking medical aid for a marked depression. She was also suffering from a right hemiplegia. It appeared, according to Mrs. Meyer, that she was married at 16, and lived with her husband until 29, whereupon she left him on account of his alcoholism, his abuse of her, and the discovery through his physician that he was suffering from venereal disease. She had had two healthy children and there never had been miscarriages or stillbirths. Six years after the separation, namely at 35 years of age, and 16 years before resort to the Psychopathic Hospital, Mrs. Meyer developed certain red areas on her hand, and learned at a hospital that these were due to syphilis. She kept up treatment for these lesions for a year, until she seemed perfectly well.

She had, in fact, remained perfectly well for some 14 years, until at 49, a small tumor had appeared on the right side of the forehead, near the hair line. This tumor was firm and not sore. Medical treatment reduced it, leaving, however, a depression in the bone. One day, about a month after the appearance of the tumor, the patient lay down for a nap, and upon awaking found she could only with difficulty move her right arm and leg. Her face was not affected; she was not in pain; and there was no disorder of speech. In a few days she got much better and she had been improving for some time past through the administration of further medicine.

However, since the onset of the hemiplegia Mrs. Meyer had been very despondent. There had been ups and downs but she had rarely felt well. The depression was a mild one and in point of fact may perhaps be regarded as non-psychopathic, since at her age with her disability, there might well be a degree of sadness and unhappiness concerning the future. Mentally, there was no other disorder of note, and in particular no disorder of memory.

METHODS OF TREATMENT

I. BY MOUTH.
MERCURY
IODIDES
ARSENIC

II. INTRAMUSCULAR INJECTIONS
MERCURY
SALVARSAN, NEOSALVARSAN, OTHER ARSENIC PREPARATIONS
SODIUM NUCLEINATE
ANTIMONY

III. INTRAVENOUS
MERCURY
MERCURIALIZED SERUM
SALVARSAN, NEOSALVARSAN, ARSENIC
IODIDES

IV. SPINAL INTRADURAL
SALVARSANIZED SERUM (In Vivo—Swift-Ellis)
SALVARSANIZED SERUM (In Vitro—Marinesco-Ogilvie)
MERCURIALIZED SERUM (Byrnes)

V. CEREBRAL SUBDURAL AND INTRAVENTRICULAR
SALVARSANIZED SERUM (In Vivo)
SALVARSANIZED SERUM (In Vitro)
MERCURIALIZED SERUM

Chart 26

Physically, the patient showed a right-sided hemiplegia with excessive right knee-jerk, but without Babinski or other abnormal reflex phenomena. The extraocular movements were somewhat restricted in range but there was neither strabismus nor nystagmus.

The question arose whether the hemiplegia was of hemorrhagic or thrombotic origin. After all, at 51 years, hemiplegia is rather unlikely to be of a non-syphilitic arteriosclerotic origin; moreover, we had a clear history of syphilis. The serum W. R. proved positive as well as the spinal fluid W. R. The finding of 77 cells per cmm., excess albumin, and positive globulin test, taken in connection with the entire picture seems to warrant a diagnosis of Cerebrospinal Syphilis. If we proceed on statistical grounds, it might be regarded as more probable that the hemiplegia is Thrombotic in origin rather than hemorrhagic. It appears that syphilitic cerebral thrombosis rather characteristically occurs without preliminary symptoms, despite the fact that many cases do show headache, dizziness, and restlessness as prodromal symptoms.

1. What is the treatment indicated in the case of Mrs. Meyer?

It would appear that little or nothing can be done for the hemiplegia unless the claims of Franz with respect to reËstablishment of a degree of function in certain hemiplegics are substantiated. However, the indication of meningitic process as shown by the spinal fluid, suggests that the case is not a purely vascular one but may be regarded as meningovascular. (Possibly, also, we should regard the left frontal depression and scar as indicative of a non-parenchymatous and non-vascular process.) Accordingly, antisyphilitic treatment should be theoretically of some value.

In point of fact, the patient was given injections of mercury salicylate, mercury by mouth, and potassium iodid. Her psychopathic depression under this treatment, supported by proper hygiene and rest, diminished. However, six months later, the patient slipped on a wet floor and fell. Though the impact seemed hardly sufficient to cause a fracture, the pelvis was somewhat severely fractured. Very probably there was a syphilitic rarefaction of the bone. Six months later the patient’s depression was still in evidence, though somewhat less than upon admission. The blood serum remained positive but the spinal fluid had become entirely negative, both in respect to the W. R. and in respect to the other findings.

2. How may one explain the continuance of the depression after the spinal fluid had become entirely negative under treatment? It may be that while the active process had been stopped, as seems probable from the negative spinal fluid, that a permanent destruction of brain tissue may account for the depression. We recognize this readily in instances of vascular disturbance where (as also in this case) the active process being stopped, a residual defect remains.

3. Should treatment have been discontinued on reduction of the gumma? It cannot be too often emphasized that the disappearance of symptoms in cases of syphilis can not be considered as evidence of cure. The neurologist and psychiatrist see only too often cases of neurosyphilis occurring in patients who have been declared cured at some time previous because the symptoms then present had cleared up and remain in abeyance for years.

Contrary to various warnings, arteriosclerosis by no means absolutely contraindicates intensive salvarsan therapy.

Case 108. Victor Friedberg, 42 years of age, gave the following history. He acquired syphilis at 22 years. He had “adequate” medical treatment for two years with inunctions of mercury and mercury by mouth and potassium iodid. The only secondary symptoms were skin lesions of the legs; these disappeared upon treatment. Married, Friedberg has one child, apparently normal. There had been no miscarriages or stillbirths.

At about 34 years, there began to be shooting pains in the legs, occurring at first about once in three months, but later much more frequently. These pains were severe, lightning in character, lasting several days at a time, at which period his head would feel heavy; but there were no disturbances, crises, or difficulty in locomotion.

At 36 years of age, Friedberg waked up with pain one night, and found he was unable to move his left leg or hand, and he felt his mouth drawn to the left. Upon trying to get out of bed, he fell to the floor. In five hours, however, he was entirely recovered, able to get up and walk about, and to use his left arm quite normally. He went to sleep, but upon waking up after an hour, discovered that his left side was again paralyzed. After two weeks in a hospital, he was able to walk with a crutch. The arm remained helpless for about a year. Both arm and leg improved slowly for two years, after which time his condition had remained stationary. For four years past, there had been no more pain, but at 42—about two years before admission—the pains returned in his legs, back, and side. At that time he received four injections of salvarsan, mercury tablets, and potassium iodid. Three weeks before admission to the hospital, Friedberg again began having headaches, very much worse than formerly. At first these headaches were frontal, then occipital, and there was a feeling as if something were growling inside of the head. There was a feeling of pressure in front on the head and at the base of the nose.

Physically, Friedberg appeared somewhat older than his assigned age. There was a degree of general peripheral arteriosclerosis, but in general the physical examination was negative. Neurologically, there was a left hemiplegia with appropriate increase of the reflexes on that side, spasticity, Babinski reflex, and an Oppenheim; the pupils reacted properly; there was no Romberg reaction.

Mentally, Friedberg was entirely negative.

The W. R. of the blood serum was doubtful, as was that of the spinal fluid. There were but two cells per cmm. and there was neither globulin nor excess albumin in the spinal fluid.

The differential diagnosis might lie between cerebral hemorrhage and syphilitic thrombosis. Thrombosis is much more common as a result of syphilis than is hemorrhage. The occurrence of the thrombosis during sleep without premonitory symptoms is also characteristic in syphilis. Possibly there was a low-grade spinal meningitis at the bottom of the lancinating pains. Whether the headache is an arteriosclerotic effect or due to a meningitis not shown in the cerebrospinal fluid is doubtful. However, the absence of inflammatory products in the cerebrospinal fluid rather indicates that the headache is of arteriosclerotic origin. Autopsies, however, warn us that we may have a localized meningitis in various parts of the cranial cavity without the determination of any inflammatory products in the spinal fluid.

1. How shall we explain the doubtful (slightly positive) W. R. in the spinal fluid if the case is one of Vascular Brain Syphilis? The finding is not unusual in these cases. The W. R. producing body is recognized to be of a separate nature from the globulin and albumin bodies, and is probably also separate from the gold sol reaction producing bodies.

Treatment: The theory of treatment is that any spirochetes that may be still active in the body should be destroyed. Accordingly, although salvarsan can certainly have no effect in reproducing nerve tissue, it nevertheless seems indicated. It is frequently stated, however, that salvarsan is dangerous in cases of this group. We have not found this statement correct. In this case, there was a symptomatic improvement, as far as pain and discomfort went, under salvarsan and iodids.

2. What precautions should be taken in intensive salvarsan treatment of syphilitic arteriosclerosis? Treatment should be begun with very small doses of salvarsan, that is, about 0.1 of a gram and then the amount slowly increased. The injection should be given slowly so as not to put too great a load upon the cardiovascular system.

3. What rÔle does the mental attitude of the patient play in a case like that of Friedberg? It was quite evident that Friedberg was neurotic and that he had a syphilophobia. Consequently some of the symptomatic improvement may have been more results of assurances offered by the physician and knowledge that he was being treated, than results of salvarsan. In some cases mental anguish suffered by the patient is of more importance than the actual symptoms of the disease and this point must be always borne in mind in handling syphilitic patients.

Symptoms of intracranial pressure cured by antisyphilitic treatment.

Case 109. Mrs. Annie Rivers, a housewife 36 years of age, sought advice and treatment for severe convulsions which she had had during a period of several weeks. She left the hospital before being properly examined, and had several more convulsions, after which she was brought back in a state of marked confusion. The confusion shortly disappeared almost completely, and a good history was obtained.

It appears that the patient led a normal life and had had six children, the last of whom was born about four months before her coming to the hospital. The first symptoms appeared about a month after the birth of the child, when, one afternoon, Mrs. Rivers suddenly fell unconscious while ironing. She remained unconscious for nearly three hours. During this attack there were no convulsive movements or tongue-biting; and after the spell, she felt neither lame nor sore, but merely tired. This was Mrs. Rivers’ statement; but her daughter stated that the patient really did have convulsive movements. A week later came a second convulsion, followed by daze and stupor. This second attack lasted two hours.

About a week before entrance, the patient had remained in bed on account of dull grinding pain in the left side of the head, below the ear, and upon this day the patient vomited twice. In addition to the dull grinding pain, there were pains referred to the ear itself and to the left side of the head, especially over the left eye; there were no pains on the right side of the head. The next day the patient was better, but the day thereafter again remained in bed. The only other symptoms were cold feelings at times and bright spots in the field of vision.

No mental symptoms were observed in Mrs. Rivers except a bit of depression after her hasty retreat from the hospital the first time. Upon her second admission, however, after a week or ten days’ residence, apathy developed together with considerable amnesia for the same facts she had quite readily remembered a few days previously. Along with the apathy and amnesia developed considerable headache; and there were attacks of vomiting.

UNTOWARD SYMPTOMS OF THERAPEUTIC AGENTS

A. SALVARSAN

CYANOSIS MALAISE
RAPID PULSE
PERSPIRATION
RESPIRATORY DIFFICULTIES
FEVER
NAUSEA, VOMITING, DIARRHOEA
DERMATOSES
EDEMA
KIDNEY IRRITATION
LIVER IRRITATION
INTENSIFICATION OF SYMPTOMS
COLLAPSE

B. MERCURY

SALIVATION
FETID BREATH
EXCESS FLOW OF SALIVA
TENDERNESS OF TEETH—LOOSENING AND FALLING OUT
SPONGY GUMS—EROSION
METALLIC TASTE
NECROSIS OF BONES OF JAW
SORENESS OF PARETIC AND MAXILLARY GLANDS
SWELLING AND EROSION OF TONGUE AND MUCOUS MEMBRANES
GASTRO-INTESTINAL SYMPTOMS
ANEMIA
PAIN IN JOINTS
NEPHRITIS

C. IODINE

SKIN LESIONS
METALLIC TASTE
SALIVATION
CORYZA
URTICARIA (EVEN TO GRADE OF ANGIONEUROTIC EDEMA)
PAINS
CONSTIPATION
INVOLVEMENT OF JOINTS
FEVER
SOFTENING AND BLEEDING OF GUMS
EROSION OF MUCOUS MEMBRANES
GASTRO-INTESTINAL SYMPTOMS
ANOREXIA
WEAKNESS

Chart 27

On the physical side, it is interesting to note that the ophthalmoscopic examination upon Mrs. Rivers’ first admission to the hospital was entirely negative, whereas a week later, pronounced difficulty with vision appeared so that in a few days she was able to make out only very large type. The fundi now showed hazy and indistinct disc outlines, with small yellowish areas of fatty degeneration above the disc, reduction of arterial calibre, and dilated and somewhat tortuous veins (no projection of papillÆ), so that the ophthalmological diagnosis was chronic neuritis.

The physical examination otherwise was mostly negative. The skin presented irregular areas covered with silvery scales over the arms and chest, back, abdomen, and legs (the patient had had psoriasis several years before). Both pupils reacted to light and distance, though the right was slightly larger than the left and somewhat irregular. There was a slight tremor of the tongue and extended fingers. The reflexes were active, especially the knee-jerks; no abdominal reflexes could be obtained. The serum W. R. was positive, but the spinal fluid W. R. was negative. The spinal fluid showed but 3 cells per cmm., but there was a positive globulin test and an excess of albumin.

Diagnosis: After the symptoms had fully developed, it became clear from the optic neuritis, headaches, and vomiting that a condition of intracranial pressure existed. In view of the positive serum W. R., it is natural to conceive that the agent producing the intracranial pressure was a gumma.

It is, of course, possible that a marked degree of meningitis might be so localized as to produce the same symptoms. The diagnostician would crave a pleocytosis of the spinal fluid if a diagnosis of meningitis is to be made; and there was no such pleocytosis. On the whole, we do not feel that it is possible to make a diagnosis either of Meningitis or of Gumma.

Treatment: Treatment, however, caused a disappearance of all symptoms. The treatment consisted of but one injection of 0.3 gram of salvarsan, followed by a few injections of mercury; whereupon Mrs. Rivers became much brighter, recovered her vision, lost her headaches, ceased to have convulsions or vomiting spells.

1. Is salvarsan contraindicated in cases with involvement of the optic or auditory nerves? Such a contraindication exists according to prevailing opinion. In this particular case, a hemorrhagic retinitis occurred after the injection of salvarsan, but this retinitis disappeared along with the other symptoms. On the whole we believe that in many cases of optic or auditory nerve involvement salvarsan should be used. However, one should never lose sight of the possibility of untoward results and should advise such treatment only when other treatment seems inefficient.

TABETIC NEUROSYPHILIS (“tabes dorsalis”) may show very marked improvement as a result of intraspinous therapy.

Case 110. Mr. McKenzie^[18] was a retired merchant of 42 years whose complaint was that he tired very easily, could not make his legs go where he wished, was unsteady and felt a numbness in his legs. These symptoms had been in progress for a few months only when the examination was made. This disclosed Argyll-Robertson pupils, absent knee-jerks and ankle-jerks, Romberg sign, unsteady gait, moderate ataxia and dysmetria. The W. R. was negative in the blood serum but positive in the spinal fluid with 0.2 cc., and there were 107 cells per cmm. With the symptoms and signs it was therefore easy to make the diagnosis of Tabetic Neurosyphilis (“tabes dorsalis”).

The patient was given five intraspinous injections of mercuric chloride in blood serum (mercurialized serum) according to the method of Byrnes. The dose was 0.001 gm. of mercury. Two weeks after the first injection the cell count was 58 cells per cmm., the Wassermann was positive only with 0.4 cc. After the fourth injection there were but 18 cells and the Wassermann reaction was negative even with 1½ cc. of spinal fluids. The symptoms had improved to such a degree that the patient had no complaint whatsoever and considered himself cured.

1. What are the unpleasant results of intraspinous therapy? Frequently there is an exacerbation of symptoms and pain may be quite severe after intraspinous injections. This, however, lasts only a short period, that is, as a rule less than 24 hours. There may be other symptoms of cord irritation as retention of urine or lack of sphincter control. A rise of temperature is not unusual.

Treatment may alter the W. R. to negative in blood and spinal fluid in TABES DORSALIS.

Case 111. Ivan Rokicki was a baker, 43 years of age, who came complaining of exceedingly severe attacks of abdominal pain with vomiting. He described these attacks as having occurred periodically for a number of years, lasting sometimes as long as a week, during which time Rokicki could not eat or get relief short of large doses of morphine.

Upon his arrival, Rokicki was seen in one of his attacks; he was curled up with excruciating pain, and the abdomen was rigid, though it was impossible to produce additional pain by external pressure. There was spasmodic vomiting, frequently followed by slight relief from the pain, which however shortly recurred and caused the patient to cry out in his suffering. The condition was controlled by opiates but lasted a full week. The leucocytes remained normal and there was no rise of temperature. The attack ceased spontaneously.

Save for the pain, Rokicki’s mental examination proved entirely negative. Physically, Rokicki was fairly well developed and nourished. His pupils were slightly irregular: the left markedly larger than the right; both pupils failed to react to light, and the left pupil also failed to react in accommodation. There were no other reflex disorders evident to systematic examination, nor was there sensory disturbance or speech defect. The heart seemed somewhat enlarged but there were no murmurs; blood pressure: systolic 150; diastolic 110.

The correct symptomatic diagnosis in Rokicki’s case proved to be gastric crises, and this diagnosis must perforce be the first to entertain in view of the chronicity, the periodicity, the non-relation to diet, and the spontaneous cessation of the seizures. The observation of Argyll-Robertson pupils was naturally held to substantiate the diagnosis of Tabes Dorsalis.

The possibility of abdominal inflammation could be shortly dismissed on account of the absence of tenderness (the rigidity in this case was not accompanied by tenderness), fever, and other characteristic signs. There was no diarrhoea, such as is found in lead colic, and there was no other sign of plumbism. Jaundice was absent and there was no special radiation of pain from the abdomen. One had to think of gastric ulcer and hyperchlorhydria, and possibly malaria or gastroenteritis.

The pupillary reactions pointed to a syphilitic condition despite the fact that the lack of reaction to accommodation (over and above the Argyll-Robertson phenomenon) in the right pupil is not entirely typical. Accordingly, although there was no areflexia, Romberg sign, or ataxia, resort was had to the W. R. This however proved negative, in blood and spinal fluid; nor was there any globulin or excess albumin; there were 5 cells to the cmm., in the spinal fluid.

We are left, accordingly, with characteristic gastric crises; Argyll-Robertson pupils, slightly irregular; and a somewhat enlarged heart.

Upon investigation, it appeared, however, that a year before the attack above described, the patient had been examined and both blood and spinal fluid found positive to the W. R. At that time, treatment, consisting of intravenous injections of salvarsan and intraspinous injections of salvarsanized serum (Swift-Ellis), had been instituted. Whereupon the laboratory tests had become negative, as above stated, and there had been no alleviation of the symptoms.

1. How can Rokicki’s normal deep leg reflexes be explained? The abolition of the deep reflexes is of course due to lesions properly localized. It is probable that this particular case of tabes dorsalis is more truly “dorsal” than most cases; for most cases exhibit lesions involving regions lower than the dorsal. Both in these dorsal cases and in certain rare cases of cervical tabes, the deep leg reflexes are preserved. (See cases Green (30) and Halleck (31).)

2. What is the mechanism by which a characteristic gastric crisis is produced? The mechanism is unknown. Some endeavors have been made to meet gastric crises by surgery of the posterior roots, on the assumption that the irritation causing the pain was located either in the posterior ganglion or in the passage of the nerve through the meninges. In only a few instances, however, has the result been what was desired. In many instances the gastric crises and pain continued uninterrupted and in addition came discomfort due to the lack of sensation in the part supplied by the severed nerve. At present this treatment is seldom carried out.

3. Should antisyphilitic treatment be continued in such a case? As far as our present knowledge of syphilis goes one would hesitate to suggest further antisyphilitic treatment, feeling that the active process had been entirely stopped as suggested by the absence of any positive findings either in the blood serum or in the spinal fluid. We should perhaps conclude that there was no more activity in this case and that the crises were due to the changes that had already taken place in the nerve tissue and which could no longer be changed.

The literature is in doubt concerning (in fact is preponderantly against) the success of treatment in PARETIC NEUROSYPHILIS (“general paresis”). Our experience has yielded a number of apparently successful results through systematic intensive intravenous salvarsan therapy. Example.

Case 112. Albert Forest had always been a successful salesman, but in the middle of March, in his 46th year, he was arrested for grabbing a purse from a woman in front of a theatre and running down the street with it. In court, Forest acted strangely and he was sent to the Psychopathic Hospital for observation. Upon investigation, it appeared that his wife thought he had been showing mental changes for about a year. For example, he would embrace his wife on a street car, or refuse to pay her fare. He once attempted to hit his son on the head with a red-hot poker. Now and then he would become sleepy and stupid. He looked rather older than his age and had a coarse tremor of the hands. Otherwise, no change could be detected in the physical examination, either neurologically or otherwise. As for the manual tremor, Forest’s wife gave a history of considerable alcoholic indulgence on his part.

For several days, nothing abnormal could be detected in the man; and in particular, his memory for both remote and recent events was very good and his knowledge of current events was good. Simple arithmetic was easy to him.

One evening his temperature was found to be 104° F. and no cause could be discerned for this. The next morning, Forest was discovered in a stupor, with a complete right hemiplegia. The Babinski reflex, the Oppenheim reflex, and ankle clonus had appeared on the right side, and the right arm was spastic.

However, all symptoms of this paralysis had disappeared by four o’clock in the afternoon, and the paralytic phenomena were replaced with violence. The patient fought with the attendants and for some time remained extremely difficult to manage, being confused and subject to outbreaks of violence with destruction of furniture and other property about the ward.

Diagnosis. At first we were naturally inclined to dismiss the case with a diagnosis of alcoholism. The transient hemiplegia at once raised a considerable question of brain syphilis or of brain tumor.

The W. R. of the serum was doubtful. The spinal fluid yielded, besides marked excess of albumin and much globulin, also a “paretic” gold sol reaction and 75 cells per cmm. The W. R. was positive.

Treatment. The patient was given injections of salvarsan, 0.6 gram, twice a week, with potassium iodid. After a few weeks improvement followed, and after several months all the laboratory tests became negative, the patient was apparently perfectly normal mentally and was discharged from the hospital, and has remained well for 18 months without further treatment. The serum W. R. has continued to be negative.

1. What is the significance of the so-called “doubtful” W. R.? Where there is not a complete uniformity the results of the strong and weak antigens (see appendix on technique of Wassermann reaction) the result is reported as doubtful. In the majority of instances repetitions will give a strong positive reaction.

2. Is the case of Forest to be regarded as one of general paresis? Sometimes such cases are termed in the literature syphilitic pseudoparesis (see case Burkhardt (58)). The differential diagnosis of this group is entirely therapeutic. There are, unhappily, no laboratory tests which will suffice in the present stage of knowledge to differentiate a case of so-called pseudoparesis from general paresis. We are inclined to term the case one of General Paresis, with recovery, or, at all events, with remission.

Case 113. We present the case of Gussie Silverman, a housewife, 35 years of age, among other reasons, for its social interest. The case is, on the whole, sufficiently typical of General Paresis. Physically, for example, the pupils failed to react to light and accommodation and were unequal, the right being larger than the left. The knee-jerks were sluggish though equal. The ankle-jerks could not be obtained. The abdominal reflexes were not obtained. Otherwise, there was no reflex disorder.

From the laboratory point of view, the W. R. was positive in the blood and in the spinal fluid. There were 80 cells per cmm. and there were an appropriate globulin and albumin reactions. Mrs. Silverman was rather poorly nourished and had a slight edema of the ankles.

Mentally, she was found on admission to be markedly depressed. It appeared that during a recent pregnancy, terminated by the birth of a 7–months child, she had fainted several times a day, that since the confinement she had been very nervous, that she had been asking her husband not to send her away, that she had refused to leave the house, that she had become excited even to the point of injuring herself, especially at night, and that she would go so far as to scratch her husband, shortly afterward being very sorry for her performances. Before this last pregnancy there had been four others and the resulting children were all apparently in good health. Except for the fainting spells during the pregnancy, it would not appear that the story just told is at all characteristic of paresis.

However, in the hospital Mrs. Silverman could hardly be got to answer questions, continually saying, “You know what it is; I don’t have to tell you.” She claimed so marked a degree of confusion as not to know where she was and what she was doing. She would beg despondently that something be done for her, and iterate and re-iterate these claims. There appeared to be a marked degree of amnesia. Some one, she felt, had controlled her thoughts and made her do things she did not want to do and say things she did not want to say, things she did not know she was about to say. She said, “I feel like jumping around. I couldn’t believe myself as if I am me. Some one is making me jump around. I used to hear him talking. I don’t know who it is. I used to keep my eyes open and I couldn’t move. I feel only I would like to talk, and talk, and talk, and talk all the time. It seems to me that some one talks in me. I couldn’t sleep for five minutes. My God, I wish I could sleep! I used to feel something in my heart. I used to faint. It seems to me I used to see a funny thing. What it was I can’t tell. It used to talk to me, make me get out of bed, throw me about, make me do things. O, I don’t know what it was.”

These not entirely characteristic mental symptoms, together with the suggestive physical signs and the laboratory examination, caused treatment to be instituted; under which treatment (intravenous injections of salvarsan) she improved rapidly. Mental symptoms disappeared under the administration of 12 injections of salvarsan within two months. Moreover, the spinal fluid became entirely negative. Two and a half years have now elapsed since her discharge and she has shown no return of symptoms. The serum W. R. has always remained negative although there has been no treatment since leaving the hospital. There has, however, been no change in the reflexes, which remain as on admission. The 7–months baby has continued to be perfectly healthy. Its W. R. is negative, as are the W. R.’s of the husband and the other three children. It must seem surprising that a healthy child could have been born from a mother with generalized syphilis as in this case. However, perhaps there are more instances than we imagine like the case of baby Silverman.

1. May a patient be considered permanently cured although there has been no recurrence of symptoms for 2½ years and although the Wassermann has remained negative? One would hesitate to give a definite statement that the patient was cured until more time had elapsed. It is quite possible that spirochetes may be lurking in some portion of the body without causing the production of symptoms or Wassermann bodies and yet ready to break out at any time. This hypothesis has added weight from the recent work of Warthin already quoted. We advise examination of this patient at intervals of not longer than six months for a good many years.

2. Should the course under treatment cause us to change the diagnosis? It has often been stated that a differential point between cerebrospinal syphilis and general paresis is the reaction to treatment, that is, that a case which recovers could not be general paresis. Head and Fearnsides state that if six months after beginning of treatment the spinal fluid has become negative, the case should be considered as one of cerebrospinal syphilis and not general paresis. We do not feel ready to concur in this view as we know of no similar logic in medicine. We have many cases in which a spinal fluid has remained positive for six months and later become negative, so that where the symptoms shown are those of paretic neurosyphilis, we are inclined to consider the case such until such time as more definite evidence checked by post mortem examination causes us to change this point of view.

3. Do the reflexes change under treatment? The signs of spasticity often do disappear under treatment and also when there is no treatment. A few instances have been reported in the literature where Argyll-Robertson pupils are said to have altered to normal. It has never been our good fortune to see such a change nor have we seen an absent knee-jerk become normal, as has also been reported, except where it is the result of pyramidal tract disease superimposed upon the posterior column sclerosis causing a return of reflex. This, of course, is not to be considered as a return of the normal. (See Case 1.)

Some RESULTS of systematic intravenous salvarsan therapy are PARTIAL (e.g., clinical recovery and persistence of positive laboratory tests).

Case 114. Walter Henry was an undertaker in a small town. He was married and the father of two healthy children. In May, 1914, he began to lose his appetite. He felt restless and seemed to be losing his grip, and in August he repaired to a sanatorium, where he remained for two months. Shortly after leaving the sanatorium, he fainted one day, while digging a grave, during a spell of great heat. Since that time there had been numerous “weak spells,” with headaches and general debility, insomnia, and loss of weight.

In February, 1916, Mr. Henry came to the hospital for advice, but the trip from a distant part of the state was apparently such a strain for him that shortly after admission he collapsed. There were no convulsive movements in this collapse, but the patient was confused and his breathing was rapid and stertorous. The semi-stupor lasted for about 48 hours. Upon recovery from the stupor, Henry was found entirely disoriented, much confused, and laboring under the belief that he was digging a grave. After a time he again fell into a stupor and his temperature rose to 103° F.

The emaciation of this man was striking and unusual, but systematic physical examination showed no special disease. Neurologically, there were marked tremors, and there were purposeless movements of the arms. There was a marked speech defect. The pupils were dilated, regular, and equal, and reacted, though slightly, to light. Nothing abnormal was noted upon systematic examination of the reflexes.

The W. R. was strongly positive in the blood and in the spinal fluid; the gold sol reaction was typically “paretic”; there were 16 cells per cmm., globulin was present, and albumin was greatly increased.

The diagnosis General Paresis was accordingly made, and treatment instituted. Intravenous injections of arsenobenzol, at first, and later of diarsenol, were given, as a rule twice a week (usual dose, 0.6 of a gram). Mercurial injections and potassium iodid were also given. This treatment was continued as the patient began to improve. The improvement was of such a degree that at the end of four months, Mr. Henry returned to his home and his work. He had had 30 intravenous injections of salvarsan substitutes. Despite the treatment and the clinical improvement, the laboratory tests remained essentially unchanged. The W. R.’s of the blood and spinal fluid remained strongly positive, as well as also the globulin and albumin; the gold sol reaction was still “paretic”; the cells stood at one per cmm. The patient has continued antisyphilitic treatment since leaving the hospital, and has remained apparently well, with good insight into his condition.

1. What is the significance of a temperature of 103° in a paretic without signs of infection and a normal leucocyte count? Temperatures of this type are not infrequent in the course of general paresis. They are usually spoken of as “paretic temperatures.” Their meaning is not understood, but they are often stated to be due to a disturbance of the heat-regulating mechanism. Such temperatures may remain elevated for a considerable period of time, but the elevation may be very transitory. At times they vary, like septic temperatures.

2. What can be argued from the fact that the cell count became normal? If thorough antisyphilitic treatment is vigorously given, it will be found that in the vast majority of cases of neurosyphilis the cell count will return to normal. It matters not whether the treatment be intravenous or subdural. It is very difficult, however, to obtain this result in general paresis by the use of mercury alone. It cannot, however, be urged that this finding has any great prognostic significance as it occurs in the cases which do poorly as well as in those which recover symptomatically.

3. Is it safe to give large doses of salvarsan to a patient in a stupor? It is not a good plan to give a large dose to such a patient on account of the danger of sudden death. This is probably due as much to the strain put on the heart as it is to any effect on the nervous system, or specific arsenic effect. In this particular instance, a dose of 0.15 gm. was the initial injection and this was increased five centigrams per injection.

IMPROVEMENT IN PARETIC NEUROSYPHILIS (“general paresis”) may become evident only after several months of intensive treatment.

Case 115. Henry Ryan was a shipping clerk, 54 years of age, who was brought to the hospital following a convulsion. For a few months preceding this period, Mr. Ryan had been failing in his abilities. He had been very forgetful, showed no energy, and had become very irritable. He also complained of insomnia and of feeling nervous.

On admission to the hospital, the most striking feature in the mental situation was that he claimed that he had not slept a wink for three months, and each day he would solemnly affirm that he had not slept at all the preceding night, although the records might show that he had slept eight hours. Argument was of no avail against this conviction. In addition, his memory was very poor; he showed little knowledge of current events, and had no ability with arithmetical problems.

Neurologically viewed, the points of chief significance were contracted immobile pupils and a speech defect, especially noticeable on the repetition of test phrases. The whole picture was suggestive of general paresis, and this diagnosis was confirmed by the laboratory findings. It was found that the W. R. was positive in the blood and spinal fluid, that there was a pleocytosis, positive globulin reaction, excess of albumin, and a “paretic” gold sol reaction. Consequently, the diagnosis of General Paresis seemed justified, although the patient denied any knowledge of a syphilitic infection.

Treatment in this case consisted of intravenous injections of salvarsan, diarsenol, or arsenobenzol, whichever drug was most easily obtainable, given twice a week in doses of 0.6 gram each. In addition, he was given occasional injections of mercury salicylate as well as potassium iodid by mouth. Once or twice a week, 40 to 60 cc. of spinal fluid were withdrawn. Under this treatment for a period of three months, the patient showed no improvement whatsoever, either in his mental condition or in the laboratory findings. However, treatment was faithfully persevered in, and shortly after the three months, improvement began to be noticed. At first, the patient began to admit that possibly he may have slept a few winks some time during the previous six months, for he said he realized it was not possible for a man to live without sleep for that period. Then he began to admit that he might have slept a few hours during the night, and later that he was sleeping pretty fairly. His memory also showed improvement. His general attitude showed alertness, and he began to interest himself in his surroundings and in the events of the world, and finally he gained complete insight into his condition.

In the meantime, that is after three months of treatment, the laboratory findings began to grow weaker. The gold sol reaction was the first to decrease in strength, and after four months of treatment, it vacillated between negative and a mildly positive “syphilitic” reaction. Then the globulin and albumin became less in amount, and the W. R. began dropping off in the 0.1 and 0.3 cc. dilutions. As is usually true in those cases of neurosyphilis that receive adequate treatment, the cell count early dropped to normal. The W. R. in the blood serum, however, remained positive.

As the patient’s condition seemed so much better, he was allowed to leave the hospital at the end of five months. He took things easily for the following seven months, and then, after being out of employment for the period of a year, as his health continued good, he decided to return to work. Before doing so, he entered the hospital again for a lumbar puncture. At this time, it was found that the cell count was normal, there was a very faint trace of globulin, possibly a slight increase above normal albumin content, and a very mild gold reaction. The W. R. in the spinal fluid was negative including the 1.0 cc. dilution; the blood serum remained positive.

The patient then returned to his old position and has done satisfactorily for the past six months. During this entire time, he has been coming to the hospital for treatment: during the major portion of the time, about once in two weeks; of late, once in four weeks.

The significant point in this case is that improvement did not show itself until after more than three months of intensive treatment, and then the improvement was synchronous with a weakening of the spinal fluid tests.

It is further significant that his mental and physical condition was good before the tests had reached anything like normal; and that under treatment, these tests continued to grow weaker and weaker, until at the end of a year, they were practically negative.

The case further illustrates the enormous number of injections of salvarsan preparations that may be given to a patient without causing any appreciable damage to the general health or to the kidney function. Mr. Ryan has had more than 60 injections.

1. How soon after treatment is instituted does improvement usually occur in paretic neurosyphilis? In our experience improvement usually shows itself in from two or three months of treatment. Occasionally the improvement may be very marked shortly after treatment is commenced, that is, after three or four injections of salvarsan. This is not, however, the rule and as in the case of Ryan, it may be only after more than three months that improvement is seen. This means that in the treatment of these cases patience must be exercised and much work done.

2. What is the point of withdrawing large amounts of spinal fluid as in the case of Henry Ryan? It has been stated that the withdrawal of 40 or more cc., of spinal fluid while the patient is under treatment has the effect of reducing the intraspinous and intracranial pressure and thereby allowing the drug to diffuse into the nervous tissue better than it would do under ordinary conditions. How much truth there is in this contention it is difficult to say and there is as yet no experimental evidence to confirm this contention. As a matter of fact, the spinal fluid in cases of paresis is usually under increased pressure and it is at least plausible to conceive that a reduction of this pressure may give some symptomatic relief.

Evidence of the activity of syphilis outside the central nervous system may be seen in cases of neurosyphilis despite intensive treatment.

Case 116. William Rosetti was a speculator, 43 years of age, when he was brought to the Psychopathic Hospital on account of an outbreak in which he smashed a showcase at the store where his sweetheart was employed; he caused so much commotion that he was arrested.

On admission, he was very excited, talking loudly and at length. For some days it was very difficult to manage him, he was so active. At any moment, he would insist upon undressing and taking physical culture exercises. He was very euphoric and expansive, and had no insight into his condition.

Physically, he was a powerfully-built man and in very good physical condition except for an iritis and moderate thickening of the peripheral arteries. The neurological signs of importance were Argyll-Robertson pupils, and absent knee-jerks and ankle-jerks. With these findings in mind, a tentative diagnosis of General Paresis was made, and this was substantiated by the laboratory tests, which gave positive W. R.’s in blood and spinal fluid, globulin, excessive albumin, slight pleocytosis, and a “paretic” gold sol reaction.

When the patient’s mental condition was somewhat better, he gave a history of syphilitic infection 15 years before, for which he had had almost continuous treatment. As a matter of fact, treatment had been pretty strenuous because he had recurring skin lesions and iritis. It was practically impossible to get the skin lesions to heal with mercury, and it was not until salvarsan was introduced that a good result was obtained in this respect. After one or two injections of this drug, the skin lesion disappeared and has never returned. However, at least once a year, he has had attacks of iritis, and for this reason was still being treated for syphilis at the outbreak of his psychosis.

He was at once placed on more strenuous antisyphilitic treatment in the form of diarsenol, semi-weekly, aided by mercury injections. After a few months of this treatment, his mental condition improved so much that he seemed to be entirely normal. Treatment was continued, however, without any abatement, and it was of great interest to note at the end of five months of such treatment that, although mentally he seemed entirely well, he had an attack of iritis, which was considered as a sign of active syphilis. This would appear to indicate the great difficulty of getting results in certain cases of syphilis with any drugs at our command at present, as in the iritis we are dealing with a condition which as a rule reacts fairly readily to antisyphilitic remedies.

1. Are there different strains of spirochetes showing various degrees of malignancy? This question has been discussed at length in the literature but there is no satisfactory answer at the present time. We must always consider the reaction of the organism and the host; and it is true in syphilis, as in every other disease, that in some individuals it is more difficult to get any therapeutic results than in others.

2. Was the failure to obtain results by long years of treatment due to “drug fastness” of the spirochetes? It has been held that the organism of syphilis will develop an immunity after a time to mercury and arsenic preparations. This led Fournier to recommend intermittent treatment as more efficient than continuous treatment. Noguchi has shown that in test tube experiments, the spirochetes develop a tolerance to increasing doses of arsenic. It must be emphasized, however, that this finding has not been established for the conditions in vivo. Another explanation of the failure of treatment in certain instances has been offered by McDonagh, who describes a life cycle of the organism of syphilis under the name of cytorrhyctes luis, of which he believes the spirochete to be merely one form, the other forms not being affected by arsenic or mercury.

Some results of systematic intravenous salvarsan therapy in PARETIC NEUROSYPHILIS (“general paresis”) are partial in the sense that with clinical recovery the laboratory tests remain partially or less strongly positive.

Case 117. Annie Martin was a charwoman, 37 years of age. She had applied for relief at a general hospital, to which she was admitted on the suspicion of nephritis; but upon admission she became markedly excited and noisy, and spoke of seeing angels and hearing God speak to her. As the attendants were unable to quiet her, she was promptly transferred to the Psychopathic Hospital. She maintained that she had been sent to the Psychopathic Hospital through the spite of the general hospital doctors, and she claimed that other people were also attempting to work her harm for the purpose of taking her children from her. Visual and auditory hallucinations were marked, as was the patient’s loquacity, irritability, and flight of ideas. However, she seemed entirely oriented and her memory appeared to be intact. She was able to explain somewhat clearly her supposed condition. The voices told her that somebody was after her and that her soul belonged to the devil; that she was to be married but that her soul was to be damned. These voices probably belonged to priests. She was under the impression that she was going to be sent to an electric chair and said, “I think I am coming to the end and I want a pair of rosary beads before the end comes.”

This patient’s pupils were markedly unequal and entirely stiff to light and accommodation. Neurologically, however, there were no other symptoms. There was a slight trace of albumin in the urine and there were no casts.

The psychiatric diagnosis in this case would off-hand undoubtedly be dementia praecox. Yet the stiff pupils are almost proof positive of neurosyphilis. If further proof were necessary, it is found in the laboratory tests, which showed a positive W. R. of the serum and fluid, with a “paretic” gold sol reaction; there were 22 cells per cmm., there was excess albumin, and a positive globulin reaction.

Under intensive antisyphilitic treatment, there was a slow improvement. After several months, the patient was entirely free from mental symptoms; the spinal fluid tests became entirely negative except that the gold sol reaction has remained strongly positive.

1. Should treatment be continued in the case of Annie Martin in spite of the clinical recovery and the negative tests except the gold sol? We would again emphasize that it is unreasonable to suppose that a long-standing case of syphilis can be cured in a period of a few months of treatment and while the tests may become negative, it would seem foolhardy to stop treatment on this account. We do know that in many cases a Wassermann reaction remaining negative for many months may again become positive, indicating that the negative reaction did not mean cure but rather the absence of the Wassermann bodies in the circulation at the time the test was made.

2. What is the significance of the paretic gold sol reaction when the other tests have become negative? As previously stated, the gold reducing substance in the spinal fluid seems to be different from the substances which give the other pathological reactions. We should feel in this case that the process which was producing these gold reducing bodies had not been stopped, in other words, cure was not complete.

3. Should one make a diagnosis on the “paretic” gold sol reaction alone? The so-called paretic gold sol curve is not always indicative of general paresis or even of syphilis but may occur in non-syphilitic conditions as brain tumor, multiple sclerosis, etc. In our experience we have seen no case of untreated neurosyphilis in which the gold sol alone was positive, that is, in cases in which therapy has not changed the findings in the spinal fluid. In our experience the gold sol reaction has been fortified by one or several of the other tests as the W. R., globulin test, pleocytosis.

Some effects of systematic intravenous salvarsan therapy in PARETIC NEUROSYPHILIS (“general paresis”) are limited to the laboratory findings without clinical improvement.

Two examples of such limitation are offered: William Roberts (118) and John Silver (119).

Case 118. A bank teller, William Roberts, 39, was sent to the Psychopathic Hospital for a depression so marked that he had become entirely unable to work or care for himself. The story was that some money had been left him by his uncle, that Roberts could not prove his right to the money, and that depression, insomnia, and occasional periods of confusion had followed during a period of about five months.

On admission, Roberts appeared wholly disoriented and unable even to give his correct age. Attention could not be held, and the patient would slide off into statements like: “Oh, I made a mistake, I fooled a lot of people, I have a terrible disease, they are going to get it, they are going to get me,” etc., etc. There was great difficulty in thinking, and a marked reaction of fear. This cluster of phenomena certainly suggested very strongly the diagnosis of manic-depressive psychosis.

Neurologically, Roberts proved quite negative except that the tendon reflexes were very active and the pupils reacted somewhat sluggishly to light. The blood serum W. R. was negative. No history of syphilis could be obtained; nevertheless, Roberts kept dropping remarks about the terrible disease from which he was suffering. It seemed best to proceed to lumbar puncture, and the spinal fluid disclosed a positive W. R., globulin, increased albumin, pleocytosis, and “paretic” gold sol reaction.

The diagnosis of General Paresis was accordingly made. During the next year and a half, no improvement was made; a slight speech defect was developed, and tremors of the hand and tongue appeared.

The effect of treatment is particularly instructive. Only after 18 months in the hospital was intensive antisyphilitic treatment instituted; but after a few months of this treatment the W. R. of the spinal fluid had become negative, the cells normal in number, globulin absent, albumin present only in normal amount. Only the gold sol reaction remained positive. It is still of a paretic type. Treatment, however, did not succeed in altering the patient’s mental condition in the slightest. At the end of many months of treatment, we still confront a man showing marked psychic symptoms and a “paretic” gold sol reaction without other laboratory signs.

1. What is the significance of the practically negative tests in this case without clinical improvement? One must believe that the tests became negative as the result of treatment, and that this change in the tests was due to the clearing up of some inflammatory reactions which were present. This may mean that the syphilis had been reduced to inactivity or latency if not cured, or at least that there was no activity sufficient to cause a positive W. R. in the blood serum, whereas whatever activity was present in the brain was in such a region that it did not cause any reacting substances to be cast into the spinal fluid. This would not mean that there would necessarily be any return of function already lost, because this may be considered as a permanent loss which cannot be compensated for. As to these tests, we now feel that the case should remain stationary; that is, that no new symptoms will be added. However, we believe that it is somewhat premature with our present knowledge to make this claim very forcibly, and would rather suggest that this case be considered as demonstrating an interesting fact, the meaning of which can be learned only after a period of years.

2. Why does the gold sol reaction remain strongly positive when all the other tests become negative? As already pointed out, above (Case Martin (117)) there is no known rule about the disappearance of one or other of the abnormal findings in spinal fluid under treatment, and we can at present offer no explanation of this phenomenon. It does, however, illustrate how careful we must be in drawing any conclusions from tests in cases that are being treated.

Diminution in the spinal fluid tests may occur in treated cases of neurosyphilis without clinical improvement.

Case 119. John Silver, a man 29 years of age, presented classical symptoms of General Paresis: He had a convulsion shortly before his admission to the Psychopathic Hospital, his memory was poor, he was only partially oriented, he was very euphoric and expansive—thought he had millions, that he was the Czar of Russia, and so on. His tendon reflexes were very much increased and there was a marked speech defect. The W. R. of both blood and spinal fluid were strongly positive; the spinal fluid showed globulin, increased albumin, pleocytosis, and a “paretic” gold sol reaction. There was, therefore, no question about the diagnosis, and the patient was at once put under antisyphilitic treatment. This was continued for five months; slowly the intensity of the reactions in the spinal fluid diminished. At the end of the five months, there was the very slightest possible trace of globulin, with a doubtful increase in albumin, one cell per cmm., and a mild syphilitic gold sol reaction. The W. R.’s in the blood and spinal fluid, however, remained strongly positive. There was no mental improvement coincident with the weakening of the spinal fluid tests, and at the end of the five months, the patient had a series of convulsions in which he died.

This case is given as a contrast to Case Henry (114) in which clinical improvement occurred without diminution in laboratory tests; in the case of John Silver, marked diminution in the intensity of these tests had no prognostic significance. This was in keeping with the condition as shown in Case Roberts (118) where, while the gold sol was the only test to remain positive, the patient did not improve mentally.

1. What is the explanation of the lessening of the pathological elements in the spinal fluid under treatment? We have seen that the various findings may occur independently of one another, and we must admit that we do not know definitely what it signifies, or why one may be present or absent. It has been held by Head and Fearnsides that the findings in the spinal fluid represent conditions in the spinal cord and spinal meninges, or at the base of the brain only, and not conditions elsewhere. This is in keeping with our finding that the gold sol reaction in the spinal fluid post mortem very often differs from that in the ventricular fluids or cerebral, subdural, and subpial fluids. And further, we have found that during life the findings in paresis in the spinal fluid may differ markedly from those in the third ventricle, and that the change in the fluid in these two areas under treatment may not occur simultaneously.

Systematic intensive treatment of PARETIC NEUROSYPHILIS (“general paresis”), including intraventricular injections of salvarsan, may entirely fail.

Case 120. James McGinnis, aged 39, came to the hospital on a stretcher, semi-conscious, moaning, unable to reply to questions; there were signs of a right hemiplegia.

The next day, McGinnis cleared a little and became able to utter a few words. His wife said that he had been entirely well up to four years ago. At that time he was struck in the eye by the head of a hammer that flew off the handle. Diplopia had developed, but disappeared.

Only two years later did a marked change appear. McGinnis became careless as to personal appearance. Seemed absent-minded, apathetic and drowsy; he would fall asleep in his chair or while at work. He lost his position and became apprehensive, making not very strenuous efforts to find work, and finally consulted a physician. The physician told him that he had a sluggish liver and gave him calomel.

Six months later, McGinnis was restored to his position as foreman, and his work remained satisfactory for some six months. Then (about six months before coming to hospital), his speech became slow and somewhat unintelligible. He quit work, saying that his speech was going from him and that he might be considered to be drunk. His memory grew rapidly worse. There was improvement after a vacation and he returned to work, but continued to be ataxic, complained of vertigo, and fell down several times, though without loss of consciousness. On the very day of his admission to the hospital, in attempting to get out of bed, he fell, and psychotic symptoms at once appeared. There was slight improvement again with entire disappearance of all paralysis after a few days, a slow clearing up of the speech disturbance, and a certain return of memory.

Physically, there was little to note. Neurologically, the left pupil failed to react to light. The tendon reflexes were all very active, and more active on the left side. Other abnormal reflexes were absent. Improvement continued for a number of weeks, but the patient never recovered from his speech defect, and his memory remained impaired. Irritable at times, McGinnis was for the most part very happy and sure he would get well. The W. R. of the blood serum was negative, but the spinal fluid reaction was strongly positive, even down to 0.1 cc. The globulin and albumin amounts were excessive. There was a “paretic” gold sol reaction. There were 7 cells per cmm. The diagnosis of General Paresis was made.

Intravenous injections of salvarsan, arsenobenzol or diarsenol were made, and intramuscular injections of mercury, and potassium iodid by mouth were given. No real improvement occurred after a certain initial betterment; the spinal fluid yielded no changes. Diarsenolized serum according to the Swift-Ellis technique was then injected into the third ventricle. Under this treatment also there was no change for the better over a period of several months. The patient died suddenly after a series of convulsions, apparently from paralysis of respiration.

1. What are the causes of hemiplegia and confusion or unconsciousness? We must consider epilepsy, brain tumor, cerebral thrombosis, cerebral hemorrhage, multiple sclerosis, cerebral spinal syphilis, and general paresis.

MILD TREATMENT, often thought “adequate,” MAY FAIL, WHEN INTENSIVE TREATMENT PROVES SUCCESSFUL.

Case 121. Arthur Bright, a printer, had acquired syphilis in his 49th year, some six months before examination. He had been treated during these six months by three injections of salvarsan, injections of mercury, and mercury by mouth. He had been apparently cured until about a month before admission. He had fallen without warning from his chair in a convulsion accompanied by unconsciousness, which lasted about two hours. The patient had since been feeling rather peculiar. For instance, time seemed to flow too rapidly. Sometimes the patient had had difficulty in talking.

Physically, nothing abnormal could be found either in general condition or neurologically. The patient was, however, incontinent. Mentally, he was apathetic and unalert, even paying no attention to his outside physician when he came to visit him.

The diagnosis of cerebrospinal syphilis already suggested by his history was confirmed by the laboratory tests, which showed a positive serum and spinal fluid W. R., paretic gold sol reaction, 41 cells per cmm., an excess of albumin, and a positive globulin test.

1. What is the prognosis in cerebrospinal syphilis in the early secondary stage? The prognosis appears very good provided that intensive treatment be given and provided that no vascular insult or other focal destructive lesion occurs before treatment has had time to do its work.

2. Why did not the “effective” (?) treatment for the syphilis, dating from the primary lesion, succeed in staving off the cerebrospinal syphilis? It remains a question whether the treatment by three injections of salvarsan was efficient in this particular case. Of course, it may prove true that no treatment whatever in the present stage of knowledge will stave off cerebrospinal symptoms in certain cases.

Treatment: Bright was given intravenous injections of diarsenol twice a week, with occasional injections of mercury salicylate. After two weeks, the patient seemed markedly improved, and continued to improve rapidly. He was symptomatically well at six weeks. The spinal fluid had then become negative, although the serum W. R. had remained positive.

After discharge from the hospital, Bright returned to his work, but continued to take the diarsenol treatment weekly, and two months later the serum W. R. became negative.

Small injections of diarsenol at intervals of a month were continued, and Bright remained perfectly well for four months, when a peculiar seizure developed and lasted for several hours. This seizure consisted in a sort of somnambulism in which Bright stood up at a table, making marks on paper, and could not be persuaded to desist. After this seizure, Bright re-entered the hospital, again showed no mental or physical symptoms and no abnormalities of blood or spinal fluid.

3. What is the explanation of this seizure? It is possibly due to a small vascular insult, for which potassium iodid may be suggested with precautions as to hygiene and continued observation. He has since remained entirely well.

Another example where MILD MEASURES (though conceived to be “adequate”) SEEMED TO BE LEADING TO FAILURE; INTENSIVE THERAPY SUCCESSFUL.

Case 122. Levi Morovitz, a waiter, 39 years of age, came to the hospital with evidences of an old left hemiplegia, including the left side of the face (there was a left-sided Babinski, Gordon, and Oppenheim, and all the reflexes were fairly active; sluggish pupil reactions, Rombergism, and speech defect). Morovitz was much depressed, very slow in thinking processes, had a marked memory disturbance in general and apparently much deterioration mentally.

A history was obtained to the effect that Morovitz had acquired syphilis at about 33, but that he had received practically continuous treatment ever since at a dispensary. He had, in fact, received four injections of salvarsan a year before coming to the hospital. Of late, Morovitz had become much more cheerful and talkative, imagining he could do great things if he had money. He had begun to eat very rapidly and to be very nervous. His feet had begun to drag; a distinct speech defect developed, but from this he had recovered. About six weeks before entrance, Morovitz had a shock, which left him with the left hemiplegia above mentioned and with considerable headache.

Even while the preliminary examination was being performed, Morovitz developed a minor seizure without loss of consciousness. First came severe pain over the frontal region, which grew in severity so that the patient held his head in his hands. A bit later, twitching movements began in the thumb and in the fingers of the left hand, and the small muscles of the extensor group of the thumb and third finger showed contractions. These contractions grew more general and the excursions of the fingers greater, until finally every finger of the left hand became involved, whereupon movements of the same sort, though of smaller amplitude, began in the other hand. Finally the left arm began to jerk with alternate contractions of the biceps and triceps. The whole seizure lasted more than five minutes. During the seizure there was dizziness and pain in the head, chiefly on the right side.

Diagnosis: The attention is at once arrested by the data of the seizures described. It appeared that we had to assume an irritation of the right side of the brain, possibly due to vascular disease, or to brain tumor, or perhaps to syphilis. The shock with residual hemiplegia would be consistent enough with any of these diagnoses. However, the history seemed somewhat long for brain tumor. Nor were there any definite symptoms of intracranial pressure. “Adequate” treatment unfortunately does not rule out syphilis. The comparatively early age (39) of the patient makes it difficult to explain the vascular disease except on the basis of syphilis. Add to the hemiplegia the euphoria and grandiose ideas of a year’s duration, and we arrive at a diagnosis of neurosyphilis, probably Paretic Neurosyphilis.

The laboratory tests showed the W. R. of the serum and spinal fluid positive, 80 cells per cmm. in the fluid, large amounts of globulin and albumin, and a “paretic” type of gold sol reaction.

To be sure the Jacksonian seizure is not especially characteristic of paretic neurosyphilis, and even suggests a local irritation in the motor area, such as a localized meningitis, possibly of a diffuse gummatous nature.

This patient was put on intensive antisyphilitic treatment, namely, salvarsan twice a week and injections of mercury. He recovered rapidly. After a few months he left the hospital, and after treatment had continued for a year, he resumed his work by which time both blood and spinal fluid had become negative.

It must be recalled that this patient had from the time of his infection what has been considered good antisyphilitic therapy, in spite of which he developed after a period of years, the symptoms and signs of neurosyphilis in its most dangerous form. The conclusion must be drawn that however good such treatment is for the majority of cases, it was insufficient for Morovitz. That the early failure to cure was not due to any “drug fastness” of the spirochete or to any peculiarity of strain is proved by the result of more vigorous antisyphilitic treatment which caused an apparent if not a real cure. With our modern methods of treatment checked by Wassermann reactions and spinal fluid examinations, treatment is given according to the needs of the individual patient rather than according to general preconceptions. We have reason to believe that under these conditions there will be fewer cases developing late symptoms on account of insufficient treatment given even to patients who are willing to co-operate to the last degree.

The fact that Morovitz had no apparent symptoms for several years led to rather desultory treatment chiefly in the form of mercury by mouth. Previous to the time when the W. R. and lumbar puncture were available, the physician had no exact means of determining cure except the non-appearance of symptoms. But a period of years of quiescence before the outbreak of symptoms referable to the involvement of the nervous system is characteristic of syphilis. With this knowledge in mind it is evident that today the care of a syphilitic patient must be guided, in part at least, by examinations of the spinal fluid and W. R.

Salvarsan treatment may even occasionally be of value in simple FEEBLEMINDEDNESS due to congenital syphilis.

Case 123. The somewhat unattractive Robert Matthews was brought, at 5 years of age, to the hospital for backwardness of mind. It appears that the patient was born at term, with instruments, that he began to talk at a year, and to walk at 13 months, but that in point of fact, he had not talked intelligibly to date. Robert had never played with other children and is regarded by his parents as backward. In fact, Robert’s sister—a year his junior—is much brighter. Robert had had scarlet fever but without sequelae.

Examination by the Binet scale showed that, although he is actually 5½ years, he graded by the Binet scale at 4 and was regarded as feebleminded.

The physical examination showed a general adenopathy and prominent frontal bosses. In the study of the family history in the search for an etiology for the evident feeblemindedness, little or none could be found. There were no miscarriages or stillbirths; the parents were living and well. There was only the one sister above-mentioned, who is brighter than Robert.

The advantage of a routine W. R. is here well shown, for the W. R. in the serum was positive.

1. What is the prognosis of cases of syphilitic feeblemindedness? It would appear that every case is an individual problem.

2. What is the effect of treatment? Robert Matthews was given mercury protoiodid ? gr., three times a day, by mouth, for three months. The protoiodid was followed by ten injections of salvarsan, average: 0.15 gram, during six months. At the end of this period, the W. R. in the blood had become negative. A re-examination by the Binet scale, when Robert was 65
12 years of age, showed him to grade at 5?, so that one might conclude that Robert had shown more mental progress in a year than he had previously.

Note: The patient’s sister, 4 years of age, is attractive and bright, measuring beyond her actual age according to the intelligence tests. However, the girl was found to have a positive W. R. It may be that Robert and his sister illustrate the hypothesis of Mott: that the syphilitic virus becomes less potent as the years go on, and that the younger children in the family are less affected than the older. However, in our series, there are a number of instances in which this hypothesis is not substantiated.

3. What is the share of syphilis in the production of feeblemindedness? The percentage of syphilitic cases found in institutions is not high. A variety of cases have been proved to be congenitally syphilitic in the absence of a positive serum W. R.

Fernald^[19] has charted a comparison of cases diagnosticated “moron” (that is, feeblemindedness proper, in the narrower English sense) and “imbecile.” Fernald says that the morons have, as a group, many more bad family histories than have the imbeciles, to quote—“Only 70% of the [imbecile] group have bad family histories. This at first seems surprising, but when we consider that more of our syphilitic, traumatic, and sporadic cases tend toward the lower end of the feebleminded group, and when we remember that with such cases there is often a seemingly normal family tree, the drop in the curve appears logical.”

The situation with the idiots, of whom only 38 came into Fernald’s study, was similar; 12 out of 38, or 32%, of idiots, had good family histories. On these figures, how unfortunate it would be to dub feeblemindedness hereditary! It is true, however, that 68–70% of the idiots and imbeciles, judging by W. E. Fernald’s intensive study, do have bad family histories.

Goddard^[20] states that of all the causes of feeblemindedness, there is perhaps none for which there is less evidence than syphilis. Goddard found syphilis in 27 of his intensively charted cases of feeblemindedness, that is, in 9% of all his charts. He finds the majority of the syphilis cases occurring in relatives of the feebleminded to be in the hereditary group; for example, of 164 charts in the hereditary group, 17, or 10%, showed syphilis. In 34 charts in a group termed “probably hereditary” 3, or 9%, showed syphilis. Of 37 charts in the group termed “neuropathic” 4, or 11%, showed syphilis, whereas in 57 “accident” and 8 “no cause” groups, there were but 2 (4%), and one, or 13%, showing syphilis. However, Goddard concedes that much more careful studies are necessary if we are to give an exact evaluation of syphilogenic feeblemindedness.

The first ten of the Waverley Anatomical Series are shortly to be described in a forthcoming publication.^[21] Of these ten cases, four showed some slight evidence of chronic inflammatory changes, indicating the possibility of a syphilitic or similar infectious condition. These cases, be it remembered, were not cases of juvenile paresis, but cases of what, for the lack of a better name, may be called “ordinary” feeblemindedness.

If all or any of these processes are syphilitic, the syphilis is virtually extinct. The cases had not been treated for syphilis and were not regarded as syphilitic, though several of them showed a few stigmata somewhat suggestive of syphilis. The anatomical conclusion at this time is still doubtful.

As in the text case, the hypothesis of syphilis as a direct cause for simple feeblemindedness must be entertained for a few cases. In any event, it would not seem logical to let any institution for the feebleminded run without a Wassermann analysis of the population. In addition to the Wassermann data from the blood serum, osteological data from the X-ray have proved of occasional value for syphilis diagnosis in this as in other groups.

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