Case 55. Daniel Falvey, 44 years of age, was an almshouse transfer to the Danvers State Hospital in the year 1904, when the principle of state care was adopted in Massachusetts. As in most of the almshouse transfers of that day, little could be discovered as to antecedents. He had been a mill-worker from the time of his immigration in 1890, at 30 years of age. He had been somewhat alcoholic. There was a shock some 17 months before his death, which occurred about seven weeks from the date of transfer.

Not only was he unable to walk unsupported, but when supported there was a slight dragging of the left leg and the gait was noted to be somewhat propulsive. The tongue and hands were tremulous, and the left grasp was somewhat weaker than the right. Both knee-jerks were increased although neither more than the other. There was no sensory disorder.

Although but 44 years of age, Falvey presented the appearance of a much older man. His heart was somewhat enlarged and there was a degree of peripheral arteriosclerosis. On the whole, no special attention was attracted to this case clinically and he was regarded as an example of arteriosclerotic dementia, like many another among the transfers. However, we owe to Dr. H. M. Swift the important observation of the Argyll-Robertson pupils. The case was studied long before the Wassermann method was available, and is here reported merely to call attention to the fact that the stiff pupils may have other neural origin than neurosyphilis.

The autopsy material in the case was worked up by one of the authors.^[11] The autopsy had been performed by Dr. A. M. Barrett, who found on section through the brain stem at the anterior border of the pons a mass springing from and continuous with the pineal gland, lying in the third ventricle and the aqueduct of Sylvius. Upon further study, this mass was found to begin posteriorly in the pineal body itself, from which the mass could hardly be told in the gross except by an injected border.

This mass proved upon microscopic examination to be a psammoma, which histologically resembled a glioma rather than a sarcoma. Throughout the mass there was a variable content of fibrillary intercellular substance having the histological reactions of neuroglia fibrillæ. The histological details (mitosis, large giant cells with multiple nuclei, etc.) do not here concern us. We deal with a neoplasm springing from the pineal gland growing on the posterior half of the third ventricle, the anterior orifice of the aqueduct of Sylvius, and the space between the velum interpositum as far back as the posterior corpora quadrigemina. There is no evidence in the body of old syphilis; although it is possible that the stiff pupils were neurosyphilitic, it seems probable that they were related to the pineal tumor. At all events, there are in the literature evidences that the pineal-quadrigeminal group of tumors and other lesions may bring about pupillary disturbances. On this account, we here include the case. The tumor hardly led to an error in diagnosis since neither neurosyphilis nor brain tumor was at all expected clinically.

1. Can alcoholism produce identical results? See Case Murphy, (60), one of alcoholic pseudoparesis.

2. What is the nature of stiff pupils? A pupil is called stiff in the sense of the Argyll-Robertson pupil if it fails to react to illumination either of itself or of the other eye and at the same time if it reacts properly in convergence and accommodation. Of course the stiffness of a blind eye must not be regarded as an Argyll-Robertson pupil. In a case of right-sided Argyll-Robertson pupil, therefore, the left pupil reacts properly both to direct illumination of itself and to illumination of the right eye, but the right eye fails to react to illumination of either eye. Such an Argyll-Robertson right pupil will remain of the same width both in darkness and in light. Clinicians agree that the Argyll-Robertson is diagnosticated rather too frequently than too seldom, and this by reason of the fact that a sluggishness of light reaction is interpreted as stiffness. The sign, as is well known, has come to be regarded as almost pathognomonic of tabetic or paretic neurosyphilis. Nonne, however, has found among 510 cases of alcoholism, nine instances of Argyll-Robertson pupil and 19 cases of sluggish light reactions. The pathological anatomy of this sign is still doubtful although a number of schematic accounts are available; among hypotheses, one may think of an elective effect of the tabetic or paretic degeneration upon reflex collaterals. The explanation would then resemble that for absent knee-jerks and kindred reflex disorders. We should then hypothesize a loss of the finer processes of the terminal arborizations about the cells of the nucleus of sphincter nucleus iridis. However, the situation of the sphincter iridis has not yet been absolutely determined.

When a pupil is said to be entirely stiff it means that it reacts neither to light nor accommodation. This condition not infrequently follows the partial stiffness or Argyll-Robertson reaction.

3. Is the Argyll-Robertson pupil more tabetic than paretic? This has been claimed at times, but in point of fact, the Argyll-Robertson pupil is very frequent in paresis, and so also are posterior column changes. According to statistics of Bumke, 36% of tabetics fail to show the Argyll-Robertson pupil, and 38% of paretics. When, however, finer methods, such as those standardized by Weiler, with photographic records, are employed, the number of cases without at least a tendency to the Argyll-Robertson pupil becomes much smaller.

In connection with the important question as to the classical Argyll-Robertson pupil and pupillary sluggishness to light, it may be inquired what are the ocular signs in neurosyphilis? Joffroy has tabulated the signs in 300 general paretics as follows:

Case 56. There was no great difficulty in setting up a diagnosis of general paresis in the case of James Burns, a mechanic of 31 years of age, who came voluntarily to the Psychopathic Hospital for treatment. The point in Burns’ case was that the spinal fluid proved entirely negative in all respects despite the fact that the serum W. R. was positive, and despite the following facts of history and mental examination.

The patient claimed syphilitic infection seven years before, namely, at 24 years of age, and also claimed that he had infected his wife, who was in fact at the time undergoing antisyphilitic treatment. He complained of insomnia, worry, depression, hypersensitivity to noises (such as those made by his own children), thoughts of suicide, and amnesia. The amnesia, however, might be regarded as subjective since our tests failed to show amnesia. Nor was there any diminution in arithmetical ability. Despite the patient’s claim that he had been “way off in his way of thinking,” there appeared to be no delusions. Beyond a certain flightiness in conversation, we could hardly get any evidence of psychosis unless of the neurasthenic order.

Physically, however, the left pupil failed to react to light though it was found to react to distance, and the right pupil exhibited a diminution of its reaction to light. There was no ataxia of gait, yet there was a complete Romberg reaction. There was a moderate tremor of the hands and of the tongue. Otherwise there were no reflex disorders upon systematic examination, nor was there any demonstrable disorder in the rest of the physical examination.

1. What is the diagnosis in the case of James Burns? On the whole we agree with Nonne, that negative spinal fluid findings (of course, in the absence of treatment) preclude the diagnosis of general paresis. The symptoms might possibly be explained, however, by means of a localized syphilitic involvement of the cerebrum, no cells or products of inflammation having penetrated to the spinal fluid. According to Head and Fearnsides, this condition may be found especially in the anterior or middle fossa. Accordingly, going upon these views of Nonne and of Head and Fearnsides, we should be entitled to make, perhaps, a diagnosis of cerebral syphilis.

2. What is the significance of the Argyll-Robertson pupil in James Burns? Nonne states that if one follows cases with Argyll-Robertson pupil over a sufficient period of years, they one and all eventuate in active symptoms of cerebrospinal syphilis (not necessarily of the cortical type), and this despite the fact that the pupillary change may have been present a number of years before any other symptom had developed.

Case 57. We borrow the main features of a remarkable case examined at the Danvers State Hospital clinically by Dr. H. W. Mitchell and reported elaborately by Dr. A. M. Barrett. This case, whom we shall call John Summers, acquired syphilis at about the end of the third week in May, 1902, and consulted a physician on June 12, at which time a characteristic initial lesion of syphilis was plain. Summers was excessively alcoholic at times and was not seen by a physician again until July 2, just after an alcoholic debauch. At this time there was ulceration of the primary lesion, and a papillary eruption had developed over the arms, chest, abdomen, and legs. Mercurial treatment and mixed treatment were given. Arthritis occurred but disappeared with increased dosage.

About six months after infection, the patient developed severe headaches, hardly controllable by treatment. Amnesia and a certain stupidity, with neglect of personal habits, and even of eating, developed, whereupon Summers was admitted to the Danvers Hospital, December 11, 1902. He weighed 124 pounds, was extremely feeble, with dull and expressionless face, coarse purposeless movements of arms; left pupil larger than right; right external strabismus and ocular ptosis; increased knee-jerks, crossed adductor reflex, coarse tremors of arms and hands; and extreme clouding of consciousness. It was doubtful whether the pupils were stiff to light or not.

The patient died on the ninth day, December 18, in a state of coma. After admission, his stupor had become more marked; there had been incontinence of urine and fæces, and the patient could be aroused only by loud tones. Difficulty in swallowing had developed; the right-sided ptosis had become more marked, and muscular twitchings had developed on the right side. When the left leg was pinched, there was twitching of the left leg and arm. There was slight spasticity of the right arm and leg. An examination upon the day of death definitely showed a lack of reaction of the pupils to light.

Dr. Barrett was able to find in the literature a case of Bechterew which histologically resembled his own case, but though in the instance reported by Bechterew the first symptoms developed within the year following infection, death did not occur until two years later.

In view of a total duration of symptoms clearly not over seven months, it is interesting to inquire how far microscopic brain changes could have proceeded. Neither calvarium nor dura mater showed changes. There was a slight haziness of the pia mater over the convexity, but the pia mater over the base (especially below the cisterna and from thence spreading out over the pons and into the fissure of Sylvius) was not only hazy but definitely thickened and hyperæmic. The thickening was most marked about the root of the right third nerve (corresponding with the eye findings in life). There was also a macroscopic thickening of the left Sylvian artery. Section of the brain showed nothing abnormal except a small area among the pyramidal fibres of the right side of the pons, where there was a single hemorrhagic area about 7 mm. in diameter around which there were small punctiform hemorrhages. (Compare twitchings of left leg and arm upon stimulation of left leg, and note also the muscular twitchings and slight spasticity of right leg and arm noted just before death.) This case was examined and reported upon in 1905. We learn from Dr. Barrett that a re-study of the case with modern methods has failed to demonstrate a spirochetosis.

The meninges show infiltration and destructive and proliferative changes of the blood vessels. Condensed extracts from Dr. Barrett’s full report follow:

There were local variations in the severity of the meningitis. The sulci showed the most marked infiltration. The slighter degrees of exudation were made up largely of lymphocytes with a few plasma cells, occasionally large mononuclear cells, and rarely a polymorphonuclear leukocyte. Where the exudation was more extensive, the large mononuclear cells became more common and the polymorphonuclear leukocytes increased in number. The large mononuclear cells were often phagocytic, containing from one to six leukocytes. The exudate was always most abundant about the blood vessels. The plasma cells were always most numerous in the adventitia of the veins, here greatly outnumbering the leukocytes. The polymorphonuclear leukocytes were relatively infrequent except where there were necrotic areas, which areas were usually continuous with an infiltration of a vessel wall.

As to vascular changes, the media was not often involved, nor was the adventitia so often affected as the intima. Such lesions as appeared in the intima and adventitia were infiltrative rather than proliferative. The elastica of the blood vessels proved to show but slight changes.

A characteristic change was the endarteritis,—of a focal nature with a few large mononuclear and lymphocytic cells pushing the intima inward at the edge of a lesion. In the more marked portion of the focal process, the thickness of the intima was greatly increased by proliferation. Great numbers of large mononuclear cells could be seen between the intima and the elastica. About these cells and interlacing among the other elements of the proliferating tissue was an excess of connective tissue fibres.

The meningeal veins were more often diseased than the arteries; there was adventitial infiltration with lymphoid and plasma cells; sometimes the vein walls had become necrotic and infiltrated with polymorphonuclear leukocytes.

It will be remembered that the left Sylvian artery was grossly thickened, and microscopic section of this vessel showed a partial thrombosis.

The brain showed diffuse and focal changes. The diffuse process was one of nerve cell degeneration and proliferative changes in the neuroglia and blood vessels, and no section of the many examined proved to be free from such changes, although in the majority of instances, these diffuse changes were slight. The cortical layers showed more of these diffuse changes than did the white substance. Barrett considered that the glial cell changes were more delicate indicators of the cortical changes than the nerve cell changes. He found rod cells, satellitosis, superficial gliosis, and a large gamut of changes in the neuroglia. There were two rather characteristic nerve cell changes: a shrinkage change going on to almost complete destruction, and a type of cell swelling, also apparently proceeding to complete destruction.

Among focal changes, there were four main types: Areas of encephalitis, having the general appearance of granulation tissue, areas of simple necrosis or softening, apparently directly related to vascular changes near by, hemorrhages, and certain foci regarded as gummatous.

Save for pial infiltration and a few vascular changes, there was very little change in the medulla and spinal cord. There was a hypertrophic gliosis of the margin of the medulla and cord throughout, and a focal lesion of well marked gliosis at one point in the bulb. There were no fibre degenerations in the medulla or cord, nor were there any coarse fibre degenerations in the cortex itself except in one locus, the left gyrus rectus. This case is of peculiar value in showing to what extent lesions may proceed in a period of six to eight months after primary infection.

Of course the case is in one sense entirely atypical. The lesions were not confined to the nervous system. Aside from the maculo-papular eruption and ecchymosis of the skin, there was a diffuse hemorrhage of the inner half of the conjunctiva of the left eyeball, a small hemorrhagic focus in the mitral valve, a caseous nodule, one cm. in diameter, in the apex of the left lung whose tuberculous or syphilitic nature is left in doubt; a broad milk-colored patch of thickening of the capsule of the liver. It is to be noted that there were no gross lesions of the aorta.

Case 58. Peter Burkhardt had been an efficient highway inspector, but in his forty-fifth year he had begun to be unable to do his work satisfactorily. His wife had become somewhat afraid of him. He had had somnolent spells in his chair and had squandered money. The mental symptoms had lasted for some six months, but had become more marked during the month preceding admission. Burkhardt would at times fail to recognize his friends.

The general physical condition of Burkhardt was very good. The pupils were irregular and reacted sluggishly both to light and to accommodation. The knee-jerks and ankle-jerks were absent. There were no other neurological disorders upon systematic examination. There was a speech defect. Mentally, little could be determined except a certain sluggishness.

History and physical examination at once suggested general paresis. The serum W. R. was doubtful, but the spinal fluid reaction was positive, as was the gold sol reaction (which was “paretic”); the globulin and albumin were greatly increased; there were 48 cells per cmm. Antisyphilitic treatment, consisting of salvarsan twice a week and potassium iodid by mouth, was followed by a rapid mental improvement. After two months, Burkhardt was discharged apparently normal, with all the blood and spinal fluid tests negative. He has been taken back into the highway service.

1. What is the proper definition of pseudoparesis? Fournier termed pseudoparesis certain cases that looked like paresis but were not syphilitic in origin. Of these cases the most characteristic group is that of alcoholic pseudoparesis. It is clear that there will be no difficulty in the definition of a disease pseudoparesis whose entity is presented in the adjective that precedes the term (e.g., alcoholic pseudoparesis). According to this usage, a case of pseudoparesis would be one in which the symptoms and possibly some of the signs somewhat resemble the symptoms of paresis itself but for which another etiology could be fairly established.

2. Are there any cases of syphilitic pseudoparesis? We are of the opinion that the term should be dropped. It is true that there are cases which clinically look like general paresis and exhibit the appropriate laboratory signs of general paresis but seem to differ from paresis in their course even when they receive no treatment whatever. In the present phase of doubt as to the classification of paretic and non-paretic forms of neurosyphilis, it seems to us of doubtful utility to characterize a case as pseudo simply because it differs in its course, particularly as the literature has always duly recognized that a number of cases of general paresis have had long courses and sometimes very long remissions.

There is also another group of cases that have been termed cases of pseudoparesis, namely: certain cases of neurosyphilis which clinically look like general paresis and seem to be following its classical course but are interrupted by treatment. Here again it seems to us doubtful whether the designation pseudo should be attached to this group of cases, particularly while the whole therapeutic question in the paretic group of neurosyphilis cases remains sub judice. Accordingly we are tempted to include in the group of paretic neurosyphilis cases that either get well of themselves, or get well under treatment, or pursue a very long course, or are subject to very long remissions. But we make this decision in terminology without prejudice to the therapeutic question and it is open to any critic to throw these cases into an atypical non-paretic group of neurosyphilis cases.

3. How shall we explain the absence of ataxia of case Burkhardt when knee-jerks are absent and when, therefore, we are entitled to conclude a certain degree of spinal disease? As stated in connection with case Sullivan (16), the absence of knee-jerks is not a warrant for terming a case—paresis of the tabetic form. The fact is that the lesion in paresis tends to be intraspinal, just as the higher brain lesions tend to occur within the brain substance. The meninges are relatively spared both within the cranium and within the spinal canal. The characteristic degeneration of posterior nerve roots which we find in tabes dorsalis is not necessarily found in general paresis even when there are somewhat extensive spinal lesions. Accordingly the absence of sensory returns by way of the posterior nerve roots which characterizes tabes dorsalis is not necessarily a phenomenon of general paresis. The mechanism by which the knee-jerks are lost depends upon histological detail. They may be lost when under tabetic conditions the posterior roots are severely diseased and when under paretic conditions only intraspinal collaterals or a small portion of fibres are affected. The whole question hinges upon where and to what degree the various reflex arcs are cut in the disease. The tabetic phenomena are, as so commonly stated, intradural; that is, the sensory or gangliospinal neurones at certain levels are affected all the way in from the points at which they pierce the dura mater. The affection of these and other neurones in general paresis is an intraspinal and parenchymatous affection.

Case 59. Bridget Curley was a case that was discharged from the Psychopathic Hospital, recovered, after 26 days in hospital. The symptoms so resembled those of alcoholic hallucinosis that the diagnosis was made despite the fact that the patient consistently denied the use of intoxicants. There was, in fact, no proof that she drank alcohol. The case was, however, not clearly one of alcoholic hallucinosis or of any other well-defined form of mental disease. A provisional diagnosis of manic-depressive psychosis, manic phase, had, in fact, also been made.

The illness had begun with depression and inactivity, Bridget’s friends accounted for these conditions on the ground that a lover had departed for Ireland. A few days after the depression began, Bridget became dizzy and refused to give a boarder his breakfast, stating that she had lost her memory and had begun to hear bells ringing and people talking. She then became greatly excited and was brought to hospital, where the prolonged baths quieted her.

It seems that Bridget had had stomach trouble and headaches at the top of her head or sometimes in her temples. Physical examination showed the left pupil to be larger than the right, a slight tremor of the lips, a slight systolic murmur at the apex, slightly irregular pulse, and moderate edema of ankles. The blood serum was negative to the W. R., but lumbar puncture was executed and the fluid showed a positive W. R.

The patient was tested by the Binet and other methods, and although 35 years of age, seemed to be by the mental tests hardly over 11 years old. She was inclined to be feverish, somewhat restive, and pugnacious; rather slow of speech, sometimes refusing to answer and grimacing. Her pugnacity was, however, easily controllable, and the excitement was largely at night. This excitement subsided rapidly in the course of a few days.

1. What is the diagnosis in this case? The following diagnoses and suggestions for diagnosis were made at the staff meetings:

• Unclassified mania.
• Manic-depressive psychosis, manic phase.
• Toxic delirium.
• Dementia praecox.
• Bacterial infection of the brain.
• Unclassified delirium.
• Acute delirium.
• Infectious psychosis.
• Acute confusional psychosis.
• Psychopathic personality by use of alcohol.
• Mental deficiency with atypical mental state.
• Syphilitic paranoia.

2. Is this a case of syphilitic paranoia? The so-called syphilitic paranoia of Kraepelin is a rare and uncertain type of syphilitic mental disease. Delusions and hallucinations are prominent. As a rule, the onset is stated to be slow and insidious, or at any rate there are a variety of indefinite prodromata. Jealousy is a prominent feature, sometimes attended with marked sexual excitement. Auditory hallucinations and ideas of persecution are particularly in evidence. The most striking feature in Kraepelin’s group was a sudden occurrence and equally sudden disappearance of violent excitement, with or without external cause. Thus, an excitement would be produced by a few words spoken, and immediately after, the phase of excitement would pass and the patient would become entirely friendly and accessible once more, as if nothing had happened. About half of Kraepelin’s cases showed a positive serum W. R. He does not report lumbar puncture findings, and grounds the existence of disease upon certain autopsied cases. The speech and writing disorder of paresis as well as the characteristic disorientation for time and muscular weakness of general paresis were absent in the group. It appears that most cases of the group have hitherto been placed in dementia praecox.

To demonstrate this proposition, the cases of Francis Murphy (60) and David Collins (61) are in point, being sharp foils to one another.

Case 60. A laboring man about 44 years of age was brought to the Psychopathic Hospital one summer day, in a stupor. This patient, Francis Murphy, had been at his regular work as axeman in the Park Service, when he suddenly fell in a heavy convulsion. He was carried to a general hospital, still in convulsions, and ether was administered to quiet the movements. The convulsions shortly ceased, but the patient’s consciousness failed to clear; hence his transfer to the Psychopathic Hospital.

Here he remained much disturbed and was placed in a room with a mattress on the floor. On this mattress he would crouch on all fours for a considerable time, looking fixedly downward as if at an object on the floor, unresponsive to questions but compliant with efforts to place him on his back. He gave the impression of daze and either disorientation or confusion.

Within twenty-four hours the patient became more tranquil and consciousness became clearer, but the patient was at a loss to bring to memory either recent or remote events. However, he replied to questions, giving some different story each time he was approached. Curiously enough, the patient seemed very contented and good-natured and would even laugh foolishly at times, saying that he felt fine and all ready to go out to work.

The general impression conveyed by Francis Murphy at once suggested the possibility of neurosyphilis. Convulsions, perhaps initial in middle age, with a post-convulsive stupor, followed by a partial clearing up, with persistent amnesia and a suggestion of fabrications with euphoria, bore out the suggestion.

The physical examination strengthened the impression of neurosyphilis. Well developed and nourished, florid, with a manual tremor and sweating of the palms, the patient was in general without physical symptoms. Neurologically, however, whereas the left pupil was larger than the right and reacted properly to light, the right pupil was a bit contracted, somewhat irregular, and either reacted not at all to light or very slightly so (reacting perfectly to accommodation). The knee-jerks could be obtained only with reinforcement, and several other reflexes could not be elicited (triceps, radial, ulnar, periosteal, Achilles, umbilical). Moreover, the heel-to-knee test was poorly performed; some of the common tests phrases were very poorly repeated; there was marked tremor in writing; and the paragraphia seemed to be not merely peripheral, for syllables were left out in words and ordinary words spelled incorrectly (psychographic disturbance).

We do not care here to insist that the right pupil was really an example of the Argyll-Robertson phenomenon since the slightest tinge of doubt is important if a positive diagnosis is practically equivalent to asserting syphilis. Practically, however, the right pupil was regarded as an Argyll-Robertson pupil under hospital conditions (flash-light reaction). Argyll-Robertson pupil, areflexia, speech disorder, writing disorder, memory disorder, conduct disorder, and euphoria, all with a history of convulsions, certainly warranted the tentative diagnosis of neurosyphilis.

As usual, resort was made to the W. R. in the serum and in the spinal fluid. One of the first results to come through from the laboratory was the absence of globulin, normal albumin, negative gold sol reaction, and a cell count of two cells per cmm. in the spinal fluid. Later the W. R.’s were returned negative for blood and spinal fluid.

In the meantime, an illuminating change had occurred in the patient, for two days later,—three days after the first convulsion in the park,—the patient had apparently quite recovered; his consciousness became nearly clear; he could remember every event up to the time of the convulsion, and his memory came back in appropriate degree for both remote and recent events.

The patient, it appeared, had for some time been drinking more and more heavily. In recent days, he had been taking five or six whiskeys and a half dozen beers daily on the average, and often much more. About ten years before, the patient narrated, there had been a convulsion at a ballgame, and this convulsion the patient himself called a “rum fit.”

Here, then, is a case of Alcoholic Pseudoparesis. Without the W. serum test and without the spinal fluid examination, it is probable that the diagnosis of general paresis might have clung to the patient for some time on account of the apparent Argyll-Robertson pupil, which had to be accepted as such on the flash-light data. In point of fact, in this case the pupil later reacted more normally to light, and the speech and writing disorders measurably cleared up.

1. Can alcohol produce the Argyll-Robertson pupil? The majority of neurologists would today answer, Yes.

2. If in the case of Francis Murphy, the W. R. in the blood had happened to be positive on account of a non-neural syphilitic infection (spinal fluid negative), would the diagnosis general paresis be warranted? Probably the diagnosis general paresis would have been made. If the patient had been lost to observation, he might well have been regarded as an atypical paretic with prodromal convulsions.

3. Would positive globulin and excess albumin in the spinal fluid alone or in association with a positive serum W. R. warrant the diagnosis general paresis or neurosyphilis? The chances are that most neurologists would advocate proceeding to treatment in any case of positive serum reaction, whether or not there was globulin or excess albumin; but the positive globulin and excess albumin would probably not warrant the diagnosis general paresis or neurosyphilis in the absence of excess cells and the characteristic gold sol reaction and W. R. in the fluid.

4. Is the case of Francis Murphy one of alcoholic epilepsy (as suggested by Murphy’s own phrase, “rum fits”)? It must be remembered that epileptics become alcoholic and that epileptic convulsions increase or become more severe with alcoholism. On the other hand, the literature indicates that alcoholism can produce convulsions, as can many other factors. The literature also indicates that there is a condition of epilepsy in which the convulsive tendency sets in as a result of alcoholism in a patient not previously disposed to epilepsy; it appears also that sometimes, though very rarely, the epilepsy continues after withdrawal of alcohol, and even after giving up the habit. Francis Murphy appears to have had but two spells of convulsions, both of them following heavy bouts with alcohol. There is so far, then, no warrant for calling Francis Murphy’s case one of alcoholic epilepsy.

5. Does the use of alcohol by a subject destroy the value of the W.R.? It has been held by some that alcoholism interferes with the accuracy of the W. R. This has not been our experience and for the present we are of opinion that the results have the same value in alcoholics as in non-alcoholics. The next case (Collins, 61) is one in which a positive W. R. occurred in an alcoholic. When dealing with paretic neurosyphilis it is especially true that the W. R. is disturbed very rarely, if at all, by toxins or drugs, except antisyphilitic drugs.

Case 61. David Collins was a steamfitter of about 43 years of age, picked up at 6.45 a.m. in the midst of convulsions and talking incoherently, in a state apparently of fairly clear consciousness. On arrival at the hospital, the patient was able to tell how he had always been a hard drinker, and how during the past week of unemployment he had taken large quantities of poor whiskey,—perhaps an average of a pint a day. Collins also told how he had had delirium tremens several times, but he said the present spell was quite unlike delirium tremens. There was no disorientation or impairment of memory, and the patient did not in any wise suggest a mental case a few hours after admission.

It appears, according to Collins, that he had obtained some work the night before, and had quit work about 6.30, whereupon he stepped into a barroom, took one drink of whiskey, left the barroom, walked down the street, and suddenly lost track of the world, coming to consciousness in a carriage with two policemen, but remaining, as he said, “dopy,” inattentive, and confused. After a meal, however, the patient began to feel better and soon felt quite all right.

The physical examination was quite negative except that neurologically there was lingual and manual tremor, a speech defect, apparent only with test phrases, unsteadiness of handwriting, left knee-jerk greater than right, a left-sided Babinski reflex, and a difficulty in executing rapid successive movements (dysdiadochokinesis). This degree of neurological disorder in our experience warrants lumbar puncture as well as a serum test. The lumbar puncture shortly disclosed a positive globulin and excess albumin, and the returns from the W. R.’s were positive for both spinal fluid and blood serum. The data of the gold sol reaction were not available on account of technical difficulties. However, it appears that the diagnosis of neurosyphilis could hardly be avoided in this case.

David Collins differs from Francis Murphy, then, in showing a positive blood and spinal fluid reaction for syphilis as well as a positive globulin and excess albumin. As above remarked, it is probable that the positive globulin and excess albumin would not warrant more than a suspicion of neurosyphilis taken by themselves.

Unfortunately, we were unable to persuade the patient to submit to treatment, and from the patient’s point of view possibly his decision, not to submit to treatment, was a good one since he has had no symptoms of any sort for a period of 18 months since his episode. However, as abundantly elsewhere demonstrated, we feel that the patient is wrong, and that the physicians are right in urging treatment.

1. Is not the convulsive episode an alcoholic phenomenon in David Collins entirely separate from the patient’s general and neurosyphilis? Possibly; however, an outbreak of neurological symptoms with spontaneous recovery is not only consistent with the diagnosis of syphilis, but somewhat characteristic of neurosyphilis. We suspect that another attack will occur in David Collins.^[12] We shall from time to time make use of the social service to suggest his going under treatment, and shall employ his record of contact with a public institution to drive in our suggestion. Still it is clear that there are numerous cases in the community that are not accessible to social service initiated from a public institution. Accordingly, educational propaganda is necessary for salvage of the middle- and upper-class victims of syphilis. It is a little unfortunate that the ethics of the private practitioner make such salvage of middle- and upper-class persons not very likely. Might it not be that an extension of state medicine to this field would incidentally increase the amount of successful private practice?

2. What may be the cause of such a convulsive episode as that of David Collins? It would appear that the convulsions of general paresis and of neurosyphilis in general often occur without gross structural lesions of the brain. It may be suggested that vascular irritation or parenchymal irritation by spirochetes, acting in appropriate parts of the central nervous system, can produce such convulsions.

3. What is the significance of the unilateral phenomenon in David Collins (left knee-jerk greater than right; left-sided Babinski)? The current explanation of hyperreflexia is that somehow inhibitory impulses from upper portions of the nervous system have ceased to influence the local arcs that mechanize reactions like the knee-jerk and the normal plantar reflex. The phenomena are commonly found in cases with pyramidal tract disorder, and in the case of David Collins one may suspect, therefore, that there was a central disorder affecting the right pyramidal tract above its decussation. One might suspect that the convulsions were initiated by a lesion (whether gross or microscopic in range) in the right side of the cerebrum; but whether in the white matter or in the gray matter must be left doubtful. The clearing up of all symptoms suggests either that the lesion was microscopic in range or that the phenomena were transient and functional.

4. Can the dysdiadochokinesis be used to indicate cerebellar lesion in David Collins? Possibly; but it does not appear that the difficulty in executing successive movements was unilateral. It seems impossible to bring into close topographical relation the basis for the Babinski and left-sided hyperreflexia, and the basis for the dysdiadochokinesis. Alcohol is sometimes asserted to exert an especial effect upon the cerebellum.

5. Must we suppose structural lesions, either (a) of the nature of cell losses demonstrable microscopically, or (b) of the nature of secondary degenerations demonstrable by Weigert myelin sheath methods, in the case of David Collins? It appears that we do not need to assert the existence of such lesions.

6. Could the hyperreflexia and the Babinski reaction be due to local spinal cord disease? Possibly; but the existence of other neurological symptoms (lingual and manual tremor, speech defect to test phrases, ataxic handwriting, and dysdiadochokinesis) makes it probable that there were lesions, or at any rate disordered functions, within the cranium; and there appears to be no basis for asserting local spinal cord disease.