Case 81. Florence Fitzgerald, a woman 25 years of age, applied at the police station to be taken care of. She said she had been a prostitute for the last few months, was now ill, and wanted to reform. She appeared physically ill and was sent to the Psychopathic Hospital, where she remained at first almost mute, making answers chiefly by nodding the head. She gave the impression of daze or stupor, and in fact her condition was at first regarded as catatonic. This reaction, after a few days, changed and Florence became quite normal, giving a full account of her condition.

It seems that four months before going to the police station, she developed a chancre, which was locally treated. A careful physical examination showed a fine red macular eruption which was without much question a syphilitic roseola. The spinal fluid yielded a positive W. R. although other tests of the fluid were negative. Curiously enough, no physical sign of involvement of the nervous system could be discovered. We were inclined to regard the mental symptoms as partly due to the syphilitic intoxication, and partly due to a psychic reaction of the nature of defense. As for the positive W. R. in the spinal fluid, in early secondaries various observers differ as to the frequency both of the W. R. and of other changes, percentages being given that range from 25 to 90%. See case Caperson (45). It is of note that clinically there were symptoms referable to a syphilitic involvement of the nervous system; namely, marked headache and malaise. The headaches of the secondary period are frequently the result of meningeal involvement.

Case 82. Frederick Estabrook was a salesman, who, be it noted, had never had typhoid fever or any disease remotely resembling typhoid fever. He had acquired syphilis at 19; had married at 22; was the father of two healthy children (no miscarriages); had had a certain disturbance of bladder and rectum, but remained a successful salesman to the age of 28, when advancing tabes confined him to bed for a time. At 30, mental signs of Paretic Neurosyphilis developed, and death followed at 32, after an acute illness of a week.

The details of the history after the first symptoms at 28 are as follows:

At twenty-eight patient lost control of limbs and was confined to the house about two months, under medical care. Three months later he had regained partial control of his limbs but had lost all control of his sphincters. After another month he had returned to work, but did not work steadily and seemed to have lost ambition. In the summer of 1905, his mind became obviously altered. He grew indolent and extravagant and given to buying expensive and useless articles. Loss of interest in things followed, together with loss of memory for recent events, lack of insight into illness, delusions of persecution by wife, irascibility followed quickly by crying. Before admission to hospital, he was euphoric, drawling and tremulous in speech, sprawling in penmanship, alternately depressed and exalted in manner. Knee-jerks were absent, gait ataxic, pupils stiff to light.

The family history was negative with respect to insanity. All the family were reported as nervous. A brother died of peritonitis at twenty-eight, a sister of pneumonia under twenty. Another brother and sister are living. Father and mother died of heart trouble at about sixty-seven and sixty respectively.

The patient was at high school one year and was a fair student. Considerable tobacco was used, and some alcohol. Intoxication denied. There was no history of typhoid fever or other acute disease.

The patient on admission was sallow, poorly nourished, and flat-chested, with a slight lateral curvature. There was slight dulness over right apex in front and in right upper back. Voice sounds were increased over right apex in front and over whole right back. The right chest showed bronchial respiration throughout. The respiration in front of right chest was of an interrupted character. The liver seemed moderately enlarged. The urine showed a very faint trace of albumin. There were a few small nodes in right groin and a scar on dorsum of penis.

Neurological Examination. Slight swaying in Romberg position. Slight tremor of protruded tongue and extended fingers. Pupils irregular, left slightly larger than right. Left pupil reacted to light consensually, but not directly. Right pupil reacted very slightly to direct light, not consensually. Knee-jerks and Achilles jerks absent. Ankle clonus absent, abdominal and cremasteric reflexes brisk. Sharp and dull points were recognized in the legs with numerous mistakes. Vocal and facial tremor. Speech slow and drawling. Test phrases repeated well if care was taken. Consciousness clear. Orientation perfect. Calculating ability preserved. Many words omitted in writing. Penmanship clear but shaky.

Hallucinations absent. Memory of recent events poor. Associations of a logical or defining type. Patient denied various statements in commitment papers and had little or no insight into the mental side of his disease—slight euphoria.

After a month’s observation the patient was removed to a quiet ward and set to work a few days in the scullery. One night he began to yell as if assaulted and said later that he had an idea that he was going to die. Before three months had passed he had become untidy, disorderly, and imperfectly oriented.

The general degeneration continued rapidly. One week before death the temperature rose to 103 degrees F., and the patient succumbed to what seemed clinically like a bronchopneumonia. Unconsciousness two days before death.

Note with respect to history of typhoid.—Inquiries of his physicians, wife, employer, and brother tend to show conclusively that the patient never had a disease even remotely resembling typhoid fever.

The autopsy findings were as follows:

Acute conditions:

Hypostatic pneumonia, with early serofibrinous pleuritis and without lymph node swelling; enlargement of mesenteric lymph nodes; acute cerebrospinal leptomeningitis; multiple small hemorrhages of spleen.

Other findings:

Scar of penis; sclerosis of aortic arch (Heller’s type?) and slight coronary arteriosclerosis; calvarium thin and dense; dura mater thickened and adherent to calvarium; calcified arachnoidal villi; chronic cerebral and cerebellar leptomeningitis; atrophy of frontal lobes; granular ependymitis; sclerosis of posterior columns of spinal cord; emaciation; unequal pupils; slight parietal fibrous endocarditis, slight mitral sclerosis; gastro-intestinal atrophy; chronic cystitis; chronic abscess of prostate.

The description of the head findings is as follows:

Skin exceedingly loose, and the whole skull cap thinned. The diploë are absent. Adhesion with dura easily separated. The dura somewhat thickened, but not distended. Along the longitudinal sinus extensive calcareous granulations adhere to it. The longitudinal sinus does not contain blood, and the inner surface is normal in color. The pia is extensively thickened and opaque and a general subpial exudate exists which is more marked over the vertex where it lifts the pia from the brain surface to the extent of three centimeters in Rolandic, superior frontal, intraparietal, and mesial precentral sulci on each side. The arteries at base are free from atheroma. The temporal lobes are much bound down by adhesions, as is the cerebellum. Post mortem softening is evident. The hemispheres show no asymmetry, but the frontal convolutions are markedly atrophic. The corpus callosum is united to the cortex by old adhesions and has to be dissected away from it. Lateral ventricles contain some slight amount of cloudy fluid, and the pia along the vessels is opaque. Some granulations in ependyma. Brain weight, 1305 grams. Pons and cerebellum, 195 grams.

Cord.—Dura much thickened, and the pia corresponds to its appearance in brain with a like exudate. Cross sections of cord show sclerosis of posterior columns.

Bacteriologically the typhoid bacillus was cultivated from the meninges and from the swollen mesenteric lymph nodes. The blood was negative; the intestines were negative so far as lesions were concerned.

The microscopic examination confirmed the clinical diagnosis of General Paresis and of Tabes, since there was not only an extensive chronic encephalitis, with the usual lymphocytic and plasma cell deposit and irregular gliosis, but also a well marked posterior column sclerosis, not unusual save in its extreme degree.

It might be surmised that some difficulty would arise in distinguishing the effects of paretic meningoencephalitis from those of the more recent typhoidal process. The well-known tendency of typhoidal processes to escape polynuclear exudation, at least until frank necrosis has set in, gave rise to the idea that the two mononuclear pictures—that of general paresis and that of typhoidal processes—might be confusing.

The picture presented by the meninges was scarcely what might be expected. Although numerous mononuclear phagocytic cells are everywhere found, yet the predominant picture is that of a polynuclear exudation.

The polynuclear leucocytes occur in greatest numbers in the tissue spaces, especially in the meshes of the lumbar arachnoid and in the spaces of the frontal and paracentral pia mater. In the lumbar region of the spinal arachnoid wide fields occur in which the cells are almost one hundred per cent polynuclear leucocytes. In places phagocytic cells occur, and in a few fields, even in the open tissue spaces, the number of phagocytic cells may arise to fifty per cent. Edema is a considerable feature in the meninges. Fibrin is found chiefly in the cerebral meninges and appears in numerous delicate strands in the tissue spaces.