Case 21. Martha Bartlett, a woman of 40 years, was brought to the Psychopathic Hospital aphasic, or at least unable to talk distinctly enough to be understood, or even to give name and address. The police had found her wandering aimlessly about the streets. Although she was well-dressed, she was mud-bespattered and apparently had not changed her garments for several days. It shortly developed that the patient, although unable to express herself either in words or by writing, could understand everything that was said to her and could indicate by the monosyllables yes or no whether she agreed or disagreed with statements made. It was thus determined that she was pretty well oriented. She was able to understand both speech and printed words. Although she approximated more than is at all common a pure type of motor aphasia, it appeared that there was a slight involvement on the sensory side, especially in the sphere of visual imagery.

Neurologically, the patient showed moderate strabismus, slight deviation of the tongue to the right, and considerable tremor on protrusion of the tongue. The right side of the palate hung lower than the left. The ankle and arm reflexes were possibly more active on the left side, and the left grasp was somewhat better than the right. Both knee-jerks were active, but again the reflex on the left side was more active than the right. No other abnormalities of reflex were determined. There was no Rombergism but the gait was somewhat ataxic. For the rest, the physical examination was normal. The blood pressure was 120 systolic, 85 diastolic.

The ready suspicion was that the case was one of apoplexy of slight degree with post-apoplectic phenomena. Upon investigation, this suspicion was confirmed since it appeared that Mrs. B. had been apparently quite well until about six months before admission, when without particular warning she began to act strangely and promptly fell into a series of convulsions. These convulsions would begin with twitchings of the face, and then spread throughout the body. There would be a period of unconsciousness for two or three hours. It is not certain how many of these convulsive seizures the patient had. At all events she is reported to have recovered therefrom completely, remaining well for three months; whereupon, suddenly, while visiting a friend, she suffered a paralysis of the left side of the body. She remained dazed and had hospital treatment for about a week. Ever since this left-sided paralysis, the aphasic condition above described has persisted.

Such a phenomenon has often been dismissed in the past as due to an early arteriosclerosis, but most neurologists and internists of today would look beyond the diagnosis of mere arteriosclerosis and consider syphilis. The only suggestive feature in the case, aside from the post-apoplectic reflex disorder and spastic phenomena, is the irregularity and diminished light reaction of the pupils. Our suspicions were confirmed by the positive serum W. R. The W. R. of the spinal fluid proved, however, to be negative. There was a moderately strong gold sol reaction of the syphilitic type. There was a slight excess of albumin, and there was an exceedingly slight amount of globulin. There was but one cell per cmm.

On the whole, it would seem best to consider the case of Mrs. Bartlett to be one of Cerebral Arteriosclerosis of Syphilitic Origin, and a case in which there is no evidence of meningitis or meningoencephalitis.

1. What is the explanation of the negative spinal fluid W. R.? It may be that none of the W. R. producing bodies have gone over into the spinal fluid. It has been shown by the work of Weston that the W. R. producing body is not identical with the bodies responsible for the other tests in cerebrospinal syphilis. Moreover, it has been clearly shown that these several tests of the spinal fluid do not run at all parallel with one another. Especially is it true that the chemical tests do not correspond at all with the degree or nature of the pleocytosis. On the whole, when involvement of the nervous system is entirely vascular, it is not only theoretically proper but also practically common, to find a spinal fluid negative to several tests.

2. Omitting consideration of the syphilitic gold sol of this case, what conclusion could be drawn from the albumin and globulin findings? It would not be warrantable to assume syphilis since it is a common finding after cerebral hemorrhage due to non-syphilitic arteriosclerosis to find excess albumin and also globulin in the spinal fluid. Occasionally, also, pleocytosis occurs in cases of cerebral hemorrhage even when the hypothesis of an active meningitis can be excluded. We may recall in this connection the pleocytosis in so-called meningitis sympathica of certain brain tumors. (See also the case of Milton Safsky (48), a case of brain tumor in which there was an excess of albumin, a large quantity of globulin, and a pleocytosis of 146 cells per cmm.)

3. What can be expected from treatment in these cases of vascular cerebral syphilis? The condition offers very little opportunity for therapeutic results. However, antisyphilitic therapy is indicated to prevent if possible further progress of the lesions. Since the lesions are, however, vascular, and since it must remain a question how far these vascular lesions are due directly to spirochetal action, and since in any event it may be difficult to reach the spirochetes thus active, perhaps it is best to place most reliance on potassium iodid. In any event, potassium iodid should be given. Salvarsan and mercury are also indicated. It is common to warn against administration of large doses of salvarsan in this type of case on the ground that further vascular ruptures may be produced. (See Friedberg, 108.)

4. If we conclude that the aphasia of the Bartlett case is due to vascular disease, can we conclude a relation between this vascular disease and vascular tension? It is not safe to draw such a conclusion. The Bartlett case itself showed low blood pressure. To be sure, some cases of neurosyphilis show high blood pressure from which one draws the à la mode clinical conclusion to the effect that the kidneys are probably involved in the arteriosclerosis; but other cases do not show a high blood pressure but may in fact show a low blood pressure. The vascular disease doubtless responsible for the aphasia in the Bartlett case is probably not at all an effect of blood pressure conditions, but is, on the contrary, an effect of local syphilitic vascular lesions.

Case 22. Meyer Levenson, a traveling salesman of 36 years, had for the last two or three years been undergoing a change of disposition, quite interfering with his work. He had begun to take unreasonable aversions to people, had become irritable and emotionally depressed, and often fell to weeping without cause.

About nine months before hospital observation, it seems that a trunk-cover had fallen on Levenson’s head, and there is some question as to whether he did not have a convulsion at that time. However, a month later he had a definite seizure, followed by speech disorder, a slight paralysis, and a staggering gait. Four weeks later, however, he had gotten over these post-convulsive difficulties and had gone back to work.

At his work, he became tired easily, his gait and speech did not seem entirely normal, and there was a considerable memory disorder. After five more months, another attack of a convulsive nature, with twitching of hands and face and tongue-biting occurred, and the attending unconsciousness remained for two days. Again improvement followed, though without ability to return to work. Four (?) months later there were several severe convulsions and Levenson would remain unconscious for a day or two at a time. Restlessness, irritability, and irrational talking followed.

Physically, the patient was fairly well developed and nourished; blood pressure 168 systolic, 68 diastolic; pupils reacted very sluggishly to light. There was a marked motor aphasia, which the patient recognized as a speech difficulty. On the whole, however, Levenson was very euphoric and was entirely sure that he was improving and would surely get well.

Shortly after entrance, Levenson had a severe convulsion, with unconsciousness. The movements were mainly on the right side of the body, and there was a post-convulsive weakness of the right side for several days, followed by a slow recovery of strength.

The course of the disease—convulsions followed by improvement—is very characteristic of a paretic onset. The laboratory findings were in all respects confirmatory. It was rather striking that a permanent motor aphasia followed the convulsions in this case, since the seizures of paresis do not in the vast majority of cases leave permanent paralyses. The course of the disease continued to show convulsions, which would in each instance leave him at a lower terrace of capacity than had been before shown. The patient died four years after the onset of symptoms of a general asthenia. With the exception of the permanent motor aphasia, this case might be regarded as a fairly typical one of general paresis.

1. What is the general nature of speech disorder in paretic neurosyphilis? Speech disorder is, along with the pupillary changes, one of the most important clinical symptoms in paretic neurosyphilis. There are aphasic and articulatory disturbances. The aphasia that accompanies paretic seizures is of a transient nature as a rule. A case with such long-standing motor aphasia as shown by Levenson is not common. Paraphasia, with incorrect naming of objects, may last longer. The so-called “sticking” phenomenon is often observed.

Word-deafness is said to be rarer but is difficult to test on account of the patient’s dementia. Agrammatism (incapacity to form correct sentences) is sometimes observed. But the most characteristic disorder is in the syllabic composition of words. Syllables are left out (“medaltricity” for medical electricity), or fused (“exity”), or doubled (“electricicity”). Besides the central speech disorders of which the above are examples, there are disorders in articulation, which at first occur as a consequence of paretic seizures or in states of excitement, but later become permanent. These are divided into paretic and ataxic disturbances.

2. What is the structural basis of these forms of aphasia? It is believed that they are due to microscopic changes, not to coarse destructive lesions.

Case 23. Thomas Donovan, a merchant 44 years of age, acquired syphilis according to his own story at the age of 31, and he was at that time treated at a well-known watering-place with mercurial injections. Later he continued treatment under his family physician, and at 34 was pronounced cured. However, four years later—that is seven years after his initial infection and in his 38th year—he had his blood examined and it proved positive. He was accordingly treated by salvarsan and his W. R. became negative. The story did not end there, however, for at 43, mental symptoms appeared of the nature of depression and a diagnosis of paresis was made. He was released from the institution against advice at that time, and without treatment, made a partial recovery.

A sudden outburst of violence brought Mr. Donovan to the Psychopathic Hospital; he was very surly, combative, and difficult to manage, standing 6′ 2″, and weighing 210 pounds. He was oriented only fairly well and his surliness was streaked with humor. He facetiously said that the Psychopathic Hospital was the largest hospital in the country, and that it was, in fact, a horse hospital; that he had come because he liked the surroundings, not to make money; that he was the healthiest man in the world, never having been sick; that the Psychopathic Hospital was a club, for which you have to get somebody to propose your name. There was amnesia and no knowledge of current events. He regarded the food as poisoned, refused to eat, and was very irritable and untidy.

Physically, there were few abnormalities, but the pupils failed to react either to light or accommodation, and the knee-jerks and ankle-jerks were absent. There was a slight Rombergism. There was a marked speech defect to test phrases. Both serum and spinal fluid W. R.’s were positive; the fluid showed 41 cells per cmm., there were large amounts of globulin and albumin, and the gold sol reaction was of the “paretic” type.

Salvarsanized serum was injected intraventricularly through a trephine opening in the right frontal region. Injections were made through the corpus callosum into the third ventricle. There was progressive symptomatic improvement after each of four injections. In fact, after the fourth injection the patient was allowed to leave the hospital despite the fact that there was only a slight improvement in the spinal fluid findings. The speech defect had entirely disappeared. (Speech defect, according to many authorities, including Kraepelin, is of very grave diagnostic significance.) His memory returned. Mr. Donovan is now able to handle figures rather extraordinarily well. He now has a good insight into his delusions and tells stories about them with great humor.

1. What is the definition of a remission in general paresis? Remissions form a foil to seizures; just as seizures mark a sudden advance in the severity of the disease or may even lead to death; so remissions may cause a sudden cessation of both mental and nervous phenomena in the disease. Whereas the seizures occur most often, according to Kraepelin, in the demented types of paresis, the remissions occur in all cases except in the terminal phase. Kraepelin quotes Hoppe as observing pronounced remissions of long duration in 17% of male and 15% of female paretics. Gaupp observed marked improvement in less than 10%, and very marked improvement indeed in only 1% of his cases. Kraepelin states that such improvements are most frequent in agitated and especially in expansive forms of paresis, and that they are rarer and less complete in the depressive and demented forms. Sometimes the improvement occurs over night, although the full extent of the remission becomes complete only gradually, perhaps in the course of months. The sensorium clears, the disorientation disappears, the delusions retreat, and the former delusions are treated as dreams and imaginations. There is often a good deal of persistent uncertainty as to events during the height of the disease. The nervous disorders are far more obstinate than the mental. Still, both speech and writing may often greatly improve.

Cotton in New Jersey found, among 127 cases of paresis diagnosticated by modern methods during seven years, that remissions occurred in but five, or about 4%, lasting from a half to three years.

2. Does a remission ever amount to a cure? The classical case quoted in this connection is one observed by Tuczek. This case developed a picture of paresis in 1876, at the age of 36; and a remission, or cessation, of symptoms, occurred in 1878; but in 1883, at 43 years, the patient developed a tabes without any trace of mental disorder, which tabes gradually advanced. By the middle of 1898, when the patient was 58, certain symptoms of excitement and confusion occurred, which led to death with dementia, 22 years after the beginning of the disease. Nissl pronounced the cortex to be undoubtedly the characteristic cortex of a paretic. This observation seems to indicate that a clinical remission tantamount to a clinical recovery may occur without the death of the spirochetes engaged. This observation is to be held in mind in connection with all therapeutic work with neurosyphilis.

Nonne states that during his clinical experience of 19 years he had followed 10 cases of paresis with apparent recovery; but of these ten cases, four had to be thrown out by Nonne because the apparent recoveries turned out to be only long and almost complete remissions, finally issuing in characteristic dementia. Of the remaining six cases, perhaps two should hardly be counted as paretic and Nonne rather preferred to term them cases of syphilitic dementia in the sense of a non-paretic cerebral syphilis. At the end, therefore, of his review of observations, Nonne found himself with four cases of true recovery from paresis.

Spielmeyer holds that there is no theoretical reason why paresis might not be cured, since all the different changes that have been described in the disease can be halted, and many of them can be repaired. In particular, he reminds us that the acute infiltrative process, the neuroglia reaction, and the phagocytic action of the large mononuclear cells are distinctly removable processes. (See discussion below under Section V, for apparent cures and remissions occasionally secured under treatment.)

Case 24. Michael O’Donnell, a laborer of 48 years, came home, one day, at 5:30, complaining of severe headache. His wife told him he should lie down and, taking him by the arm, tried to help him to the bed. At this moment, O’Donnell lost control of both left arm and left leg, and fell, unable to move but with consciousness preserved. The wife noted that the left side of his face was drawn up and that he drooled. He was at once carried to a general hospital, remaining there for about three weeks, talking at random in a delirious manner and tied in bed. Two intraspinous injections of salvarsan were given, and O’Donnell showed considerable improvement and went home.

However, upon his return from the hospital, he became very wilful, would not remain in bed, and on one occasion actually took the mattress from the bed, carried it to another room, and then returned to his own room and slept upon the springs. He became irritable and emotional, insisted upon going to the hospital, did not go there but upon returning home insisted that he had been there. That night, O’Donnell left the house only partly dressed.

It appears that O’Donnell had been excessively alcoholic, but that before August 15, when he sustained the left-sided hemiplegia above mentioned, there had been no symptoms except that in February he had once been very dizzy. It appears that there had been another dizzy spell, three nights before the paralysis, accompanied by a fall and unconsciousness for about 15 minutes.

O’Donnell was brought to the Psychopathic Hospital some six weeks after the paralysis, complaining merely of a slight headache and desirous of treatment. There were no mental symptoms of any sort. Physically, O’Donnell was in general not abnormal (there was a slight pre-systolic murmur and a blood pressure of 190 mm. systolic). The pupils were slightly irregular, the left larger than the right; both reacted sluggishly. Both ears were moderately deaf; the tendon reflexes of the left arm and leg were somewhat more lively than those on the right. The systematic neurological examination otherwise revealed no abnormalities. The urine was negative. The serum W. R. was positive but the spinal fluid reaction was negative. There were but 2 cells per cmm., and there was a very slight trace of albumin.

1. How shall we account for O’Donnell’s transient paralysis? We might invoke brain tumor, alcoholic pseudoparesis, or some form of neurosyphilis. The diagnosis of brain tumor seems quite untenable in view of the absence of premonitory symptoms and in the absence of intracranial pressure. As for alcoholic pseudoparesis it is true that the patient was excessively alcoholic.

However, against these two diagnoses and in favor of the diagnosis of Neurosyphilis, are the positive serum W. R. and the pupillary reactions (although these are short of the true Argyll-Robertson phenomenon). Dizziness with retention of consciousness and associated with the paralyses mentioned suggests rather a subcortical than a cortical lesion. We are inclined to regard this lesion as probably Thrombotic, and to place it possibly in the region of the internal capsule. We are inclined to regard the phenomenon as purely vascular and as not in this case associated with an encephalitis. We are, however, not entirely satisfied with the diagnosis.

2. What shall be said as to treatment? A full-blown left-sided hemiplegia may be produced even when the thrombotic lesion is itself exceedingly small. It is common to explain this on the basis that there is an area of collateral edema about the small necrotic, thrombotic, or hemorrhagic area responsible for the lesion. In short, numerous neurones are functionally rather than structurally affected, or at all events capable of early restitution of function.

3. What is the prognosis in such cases? It appears that now and again patients run for several years without further trouble, both with and without treatment. We are inclined, however, to advocate treatment rather than absence of treatment for a variety of reasons. In the first place, vascular lesions may at any time become associated with meningitic lesions, and treatment by salvarsan may perhaps be counted on to head off this process; secondly, the treatment with iodids may possibly aid in the resolution of a local thrombotic process.

4. What are the prodromal symptoms of cerebrospinal syphilis? According to Nonne, headache, dizziness, sleeplessness, mental symptoms of the irritability group, loss of capacity as to mental work, whether severe or not, and loss of capacity for difficult thinking; also impairment of memory. Nonne does not regard these phenomena as characteristic of syphilitic vascular disease, and calls attention to the fact that in every organic disease the same subjective symptoms occur. The triad—headache, dizziness, and impairment of memory—is for example now counted as a prodromal symptom complex for arteriosclerotic apoplexy (Cramer). Of course, apoplectic attacks occur without such preliminary symptoms: particularly, according to Nonne, the nocturnal attacks.

5. Can the fleeting paralysis be of service in differentiating the diffuse from the paretic form of neurosyphilis? Probably not. In both forms transient paralyses occur as well as the permanent ones. In general, however, the transient paralyses are more frequent in paretic neurosyphilis, whereas the permanent ones occur more often in diffuse neurosyphilis.

Case 25. Richard Lawlor^[6] was admitted to the Psychopathic Hospital, October 29, 1914, being sent there from a general hospital where he had gone on account of a self-inflicted wound of the wrist, apparently made in a period of depression with suicidal intent. Routine notes follow.

Family History. Paternal grandparents both died of heart disease. Maternal grandfather died at seventy-two of dropsy. Moderately alcoholic. Maternal grandmother died of shock at fifty-six. Father died at age of forty, after an illness of eight years, from heart disease. Father all his life was subject to fainting spells and headaches. The only paternal cousin died at thirteen months of brain fever. Mother, aged forty-seven, is, to say the least, eccentric. Says “she has several times been given up from tuberculosis.” Two maternal uncles died of tuberculosis, one from rupture, one from heart disease. One uncle who “doesn’t know anything after he has a teaspoonful of liquor.” Several other uncles and aunts whose history is not obtained. Patient is mother’s only child. Mother was twice married. There were several miscarriages by both husbands; patient child by first marriage.

Past History. Patient born thirty-two years ago, full term, normal delivery and development. Measles, mumps, and chickenpox in childhood. Subject to headaches since seven or eight years old. Kicked in the face by horse at seventeen or eighteen, not considered serious. Hit by a baseball three or four years ago, leaving him hard of hearing on left side. Married ten years ago; no children because he says his wife needed an operation. He denies venereal disease by name and symptoms. For past ten years has had attacks of depression lasting but a short time, but quite severe. Never caused him to quit work as a barber and he felt better when working. His married life he says was fairly happy except for his wife’s extravagances, and on this account he left her a little over a year ago, and she has applied for a divorce, which he is willing that she should have, but does not wish to give her alimony. He admits moderate alcoholism.

Present Trouble. Patient states that since he left his wife a year ago he has felt sorry a number of times. He has wished he had her back. He has felt lonely. He has had six or eight periods of depression in that time similar to those he has had for many years, lasting two or three days, and sometimes a week. These were always precipitated by some cause for worry. In these attacks he feels nervous, sleeps poorly, has little or no appetite, sweats during his work and everything looks black. Several times in these attacks he has had suicidal ideas. Ten months ago he considered taking corrosive sublimate. For a little over a week before entrance to hospital he had been out of work and had been “sporting.” The day before entrance he had a telephone message from his lawyer which upset him somewhat and he walked the floor all night. He had just been shaving when the idea of suicide came to him. He sat down a minute when suddenly the thought “to hell with the world” came to him; he took the razor and slashed his wrist. He does not remember drawing the razor across his wrist. As soon as he saw the blood he felt sorry, called his mother, and was taken to an emergency hospital and then sent to the Psychopathic Hospital.

Physical Examination. Patient is a well developed and nourished man thirty-two years of age. Head is normal as to size and shape; there are no scars or marks of injury. Hair and skin not remarkable in any way. Ears negative to external examination. Teeth well kept; two missing, several gold fillings. Tongue very slightly coated. Throat negative. Tonsils easily visible without evidence of inflammation or exudation. Neck, no thyroid enlargement, no abnormal pulsations, no adenopathy. Chest, symmetrical, expansion good, resonant throughout. Breath sounds transmitted normally. No râles or rubs heard. Heart, no enlargement or cardiac dulness. Sounds of good quality, no murmurs heard. Rate regular. Pulses equal, regular and synchronous, and of good volume and tension. Systolic blood pressure 130, diastolic 65. Abdomen, flat, soft and tympanitic throughout; no masses; no tenderness. Liver edge not felt, below costal margin. Spleen not palpable. Extremities negative, except for incised wound on left wrist.

Neuromuscular Examination. Pupils are large, round, regular, equal and react readily to light and accommodation. No nystagmus, strabismus or ptosis. No weaknesses or paresis of facial muscles. The tongue projects medially and shows no tremor. The triceps and biceps reflexes are readily elicited, and are quite active, as are the knee-jerks and ankle-jerks. On one occasion it was thought that the tendon reflexes were slightly more active on the left than on the right. This was never confirmed; always afterwards found equal. There was no tremor of extended hands. Abdominal reflexes not elicited. Cremasteric present on both sides. The plantar response is flexor. There is no Babinski, Gordon or Oppenheim. No Romberg. Coördination tests well performed. No speech defect. No sensory disturbances. Urine examination negative.

Wassermann reaction in the serum: Positive, with cholesterinized antigen; negative, with syphilitic fetal liver antigen.

Wassermann reaction in fluid positive on two occasions. Examination of spinal fluid, November 4: globulin +++, albumin ++, 100 cells per cubic millimeter; large lymphocytes, 8 per cent; small lymphocytes, 90 per cent; plasma cells, 0.7 per cent; endothelial cells, 1.3 per cent. November 11, globulin +++, albumin +++, cells 18 per cubic millimeter. November 26, globulin ++, albumin ++, cells 92 per cubic millimeter; large lymphocytes, 13.1 per cent; small lymphocytes, 82.1 per cent; plasma, 1.2 per cent; endothelial, 3.6 per cent.

Gold sol, November 4, 5555432100.

Gold sol, November 26, 3332100000.

Mental Examination. On entrance to hospital patient seemed slightly depressed and a bit irritable. This condition lasted two days, after which he was agreeable and apparently entirely over his depression. Even during his mild depression, however, he talked freely. There was no evidence of retardation. He told his story readily. Orientation was intact. Memory excellent. Educational knowledge well retained. There was no evidence of any hallucinations or delusions.

1. Was Richard Lawlor insane?

There was, then, on the mental and physical examination nothing to make a definite suggestion of a psychosis, and the most one could think of was a psychoneurosis or a cyclothymia of at least ten years’ duration. The findings in the cerebrospinal fluid and the Wassermann reactions, however, give us material for thought. Certainly one cannot call the man insane; all who saw him agreed on this point.

2. If Richard Lawlor should some day develop mental symptoms, what would be the genesis of the new psychosis? Though writers such as Fildes and McIntosh, and Swift, have suggested an anaphylactic or hyperallergic explanation for the development of symptoms after a normal interval; such a hypothesis could hardly obtain in the present case. The hyperallergic hypothesis for the development of tertiary neurosyphilis would run to the effect that in the secondary stages there had been a definite disease of the nervous system, which, however, absolutely cleared up, leaving no inflammatory vascular or parenchymatous relics of its existence. Nothing would on this hypothesis remain except a hypersensitisation of the tissues. In some later period of the now clinically normal person, one or more spirochetes from a lesion outside the nervous system are carried into the nerve tissues and there set up an anaphylactic or hyperallergic reaction. It is obviously difficult to prove the correctness or incorrectness of the hyperallergic theory without numerous examinations of the spinal fluid, in clinically normal persons after the secondaries have passed. The present case, so far from demonstrating a normal fluid, demonstrates a highly pathological fluid, even though there are absolutely no clinical symptoms which could be regarded as of nervous origin. The burden of proof at the present time would seem to lie with those who claim hyperallergy in neurosyphilis. We prefer on present evidence to think that at the conclusion of the secondaries a disease process often remains in the nerve tissues despite clinical quiescence.

3. What is the prognosis in the case of Richard Lawlor? The prognosis re neurosyphilis is doubtful. We have, however, boldly termed the condition PARESIS SINE PARESI, meaning thereby to suggest that the patient is in considerable danger of the efflorescence of a true diffuse or paretic neurosyphilis. We have no means of telling, however, whether the positive symptoms would be those of a paretic or a non-paretic neurosyphilis. As data accumulate regarding these cases of paresis sine paresi, we may be able finally to come upon some case in which trauma shall bring out the clinical symptoms of neurosyphilis. For discussion of this matter, see the case of Bessie Vogel (52) in Part III of this book.

4. Should Lawlor have been brought to a psychopathic hospital? It is a safe working rule to have any person who attempts suicide observed. A large percentage of suicides occur in psychotic individuals and a suicidal attempt is not infrequently the first recognized abnormality. Immediate observation is a necessary safeguard against another more successful attempt.

Case 26. John Morrill, 49, an operative in a mill town in Essex County, Mass., was described as a “Saturday night and Sunday drinker,” with a history of very serious long sprees at the age of 43. It seems that he had had what was called “sciatica” at 35, and was treated in hospital for seven weeks at that time. The nature of this sciatica is in doubt, but there was a history of syphilitic infection at 36 years (scar of glans).

Morrill had been married twice, and two of the children were dead; one daughter was described as “very nervous,” but there were four children under ten years of age, all regarded as perfectly healthy.

Morrill had been a mill operative of average capacity, was industrious, and had supported his family despite alcoholism. The syphilis had been treated with reasonable thoroughness.

Aside from alcoholism, there had been no symptoms up to two months before admission to Danvers Hospital. Then there had been insomnia, fatigue, agitation, eruption on foot, loss of ten pounds in weight, hypochondriacal fears, apprehensiveness for the future of the children, incoherent talk; and just before admission, his talk was described as foolish. He had taken to running away and hiding in bushes by a pond and in the cellars of other people’s houses.

The patient was of medium height and weight, with thin grayish hair and grayish irides; musculature was slender. The face was blank in expression, the teeth poorly preserved with atrophy of gums, the tongue coated, and the breath foul. There was a gummy secretion of the eyelids, an area of brownish branny eruption over both clavicles, a number of depressed scars over the limbs and back, and another area of scaly eruption on the right heel and the sole of the foot. The heart area was increased, and the sounds were faint at the base, with the first sound accentuated at the apex. The urine showed a trace of albumin.

Neurologically, the Romberg position was maintained with a general tremor and fluttering of the eyelids. In complicated movements, the patient was slightly ataxic. The pupils were irregular, the left being much larger than the right. There were no light reactions to be obtained in window light. The reaction to accommodation was present, though slight. Vision was poor, ¼-inch capitals could not be read by left eye at reading distance. The knee-jerks were diminished equally; the Achilles jerks were absent; the other reflexes were normal. Upon the sensory side, the patient gave a history of pains in the legs at irregular intervals for several years. These pains he described as of a darting character. There was little or no sensory disorder, although the outer surface of the right leg required a deeper pressure to elicit sensation. There were no disorders of muscle sense.

If Morrill was to be trusted, he had been born in Ireland, and had come to the United States at the age of 17. He married at 18; there had been seven pregnancies by the first wife, with one stillborn child; one child had died at five weeks. The four children by the second wife were healthy. The first signs of neuritis had occurred at 45 and had received the diagnosis neuritis, although no connection between the neuritis and the syphilis had been noted.

The patient entered the hospital July 26, 1904, and was discharged, improved, January 5, 1905. He returned a little more than a year later, January 15, 1906, and died March 21, 1906. The total duration of the disease from the onset of mental symptoms may therefore be stated as somewhat under two years. When the patient appeared at the hospital the second time, he showed a positive Romberg sign, an unsteady gait, an ataxia that still was moderate, and somewhat more marked tremors, involving fingers, tongue, and face. He was now unable to read ½-inch type with the left eye. The knee-jerks, formerly diminished, were both exaggerated, the left slightly more so. The Achilles reaction, not obtained formerly, now appeared on the right side. The pupils reacted as before. The sensory loss had become more marked, since sharp and dull points could hardly be distinguished. Deep pinpricks were not felt in the leg, and heat could not be told from cold.

The speech in 1904 had been somewhat defective (“truly rural” rendered as “tooly lualal,” “sifted soft thistles” as “thoft thsistles”), and there had been little further development of the speech defect. The handwriting had lost appreciably in legibility and had become much more tremulous. During the first period of hospital observation Morrill had what might possibly have been visual hallucinations, but it was impossible to tell whether his story of seeing his wife and children trying to get in through the window was hallucinatory or a matter of fabrication. Memory was decidedly imperfect and few details of recent events could be produced. The association of ideas was almost a so-called “flight” of apprehensive, fearful ideas, loosely connected, incoherently expressed, and dealing chiefly with his work and his children. Judgment was imperfect; the height of the room was estimated as 24 feet, but the height and weight of persons were estimated with fair accuracy, and also the length of small objects, whose lengths were doubtless remembered rather than estimated. The estimate of time elapsing during a medical examination was accurate, but the estimate of longer durations involving over-night memories was hopelessly imperfect. Emotionally, there was a dulling of sensibility, an appearance of suspicion and apprehensiveness; the patient fancied himself to be in a hopeless condition as a result of syphilis, but at the same time accompanied his statement of his hopelessness with laughter. A sample of his hypochondriacal ideas: “I am all gone; I am good for nothing; I am all gone now; I can’t drink now; can’t write or talk at all; worse than when you saw me first; nothing in my inside; all wrong through me again; I aint got no swallow now; I can’t die even; my heart aint much good; I can’t hear it beat; I don’t think it flutters; no life in these hands; they are all cold and dead” (pointing to his arms and moving them about). During such a portrayal the patient laughed in a silly way.

During the second hospital stay, Morrill was at first restless, sleepless, profane, imperfectly oriented for time, possibly for place, and also for the attendants. A few weeks later he became stuporous and confused, and his feebleness and physical exhaustion were finally ended by death, March 21, 1906. Death was preceded by a semi-comatose condition; a left otitis media had developed.

At the autopsy, it appeared that death was due to an early bronchopneumonia associated with acute splenitis and doubtless related to the otitis media of the left side. The body at large showed, aside from these acute lesions, a few chronic lesions, including slight scars of the left apex, and chronic adhesive pleuritis, chronic diffuse nephritis, and aortic and coronary syphilis. The aorta showed slight linear and nodular markings, with a single small dark ulcer in the upper thoracic region, but the aorta did not show the characteristic scarring which syphilitic aortas often show. The femoral marrow was of a dark red chocolate color. The thyroid appeared to be smaller than normal. A slight sacral decubitus had developed.

The description of the head (E.E.S.) is given in full on account of the encephalitic lesions shown. These encephalitic lesions may be summed up as follows:

Local cerebral atrophy and sclerosis of the frontal, orbital, and central regions, especially of the left operculum and left supramarginal gyrus.

Extension of sclerosis to hippocampal gyri with effacement of substantia reticularis alba.

Slight chronic internal hydrocephalus.

Granular ependymitis (especially of floor of 4th ventricle).

Compensatory edema of frontal and central pia mater.

Cerebellar sclerosis (culmen monticuli, lobus culminis, lobus cacuminis).

Spinal sclerosis (grossly evident in the posterior columns of the upper thoracic region and of the lumbar enlargement).

The details are as follows:

Head:—Bald on top. Hair gray. Scalp normal. Calvarium thin, deeply excavated by arachnoidal villi to right of vertex. Diploë absent. Dura closely adherent in bregmatic region. Dura of usual thickness. Sinuses contain cruor clot. Arachnoidal villi slight. Pia mater hazy and over sulcal veins porcelain white over all of vertex except occipital poles and over flanks (notably left). Thickened also around circle of Willis, over culmen monticuli and in posterior cerebellar notch. Edema of pia corresponding to atrophy of frontal and central regions. Cerebral atrophy most marked in orbital surfaces of both frontal lobes, in left area of Broca, and in left supramarginal region. The ascending branch and the ascending ramus of the posterior limb of the left Sylvian fossæ both readily admit the thumb by reason of atrophy of adjacent substance. Induration corresponds closely with atrophy, but is not more marked about the left Sylvian fossa. There is sclerosis of both hippocampal gyri, with loss of the substantia reticularis alba. The culmen monticuli and lobus culminis are firmer than the clival regions, and the lobus cacuminis is again slightly firmer than the clival region. Cerebellum a little softer than usual. Pia strips with usual readiness from all regions. The subpial region of the frontal lobes is a trifle grayer than that of the rest of cerebrum. Ventricles slightly dilated. Surfaces evenly sanded. Floor of fourth ventricle shows numerous coarse, closely set granules. Brain wt. 1200 grms. Cord shows a slight increase of consistence over one or two upper thoracic segments and in lumbar enlargement corresponding with a slight graying out of posterior columns. In places there is a suggestion of graying out also in lateral columns. A few calcified plaques in posterior lumbar pia.

Analysis of these details shows a number of lesions that characterize paretic neurosyphilis (among others, granular ependymitis, frontal atrophy, chronic leptomeningitis), but the lesions are more than merely frontal, extending as they do back as far as the postcentral regions on both sides, and even as far as the left supramarginal gyrus. The cerebellar involvement although frequent, can hardly be said to be characteristic in paretic neurosyphilis. The spinal involvement is characteristic of a case which is probably to be regarded as one of taboparesis; that is, of paretic neurosyphilis following a number of years after the establishment of tabetic neurosyphilis. The aorta is almost constantly affected by sclerosis in paretic neurosyphilis. The absence of diploë in the skull is not infrequent and the adherent dura mater is often found.

Microscopically, the tissues showed the characteristic lesions of Paretic Neurosyphilis; nerve cell destruction, fibrillar and cellular gliosis, lymphocytic and plasma cell deposits about the small vessels.

1. What are the clinical evidences of syphilis outside the nervous system? The brownish branny eruptions of the skin, the depressed scars and the scaly eruption on right heel and sole are very suggestive of syphilis. Such clinical evidences of syphilis are very important in systematic examination. Although the laboratory tests are of the utmost assistance in the diagnosis of syphilis, the clinical signs should not be neglected, and no physician should rest satisfied with laboratory signs alone. X-ray diagnosis of bone conditions sometimes succeeds when all other methods have failed.