Chapter XI: Introduction (3)

Mr. Twist had sought advice at our out-patient department in his thirty-third year. The records show that at that time he was somewhat depressed, and his speech was even then, according to his own statement, stammering. However, we found the W. R. at that time to be negative in the blood serum. It appeared that his mother had died of consumption; his father was said to have committed suicide. A brother had once recovered from an attack of depression, presumably an attack of manic-depressive psychosis. Accordingly, we thought at the time that the case was probably one of manic-depressive psychosis. Moreover, our routine serum W. R. failed to indicate any syphilitic process. As for the so-called stammering of speech, this appeared to be a matter of the patient’s own recollection rather than of our observation. In any event, the patient had gone into the country and appears to have entirely recovered; falling, again, however, into mental difficulties after a short period, and finally arriving at the hospital in the above-mentioned classical condition.

The W. R. in the blood serum proved again negative. The test was repeated a number of times; also, after salvarsan had been given. The salvarsan did not act provocatively, and the blood serum has remained consistently negative.

In cases of syphilis the W. R. is at times negative. Swift claims that in such cases an injection of salvarsan will often produce a positive W. R. if the blood is tested on several days following the injection.

The spinal fluid, however, did show a positive W. R. as well as a gold sol reaction of a “paretic” type. There were at the first examination 194 cells per cmm., there was a moderate excess of albumin, and a positive globulin test. In short, there was no question of any other diagnosis than GENERAL PARESIS.

1. How can the negative W. R. of the blood serum be explained? It is
difficult or impossible to explain this. Figures differ as to the
percentage of cases of general paresis with negative blood serum;
perhaps 3 to 5% of these cases yield a negative serum W. R.

It is important to note the long preparetic period: at least a year
and a half. Could our diagnostic methods be sharpened a trifle,
such cases as these could be obtained early in this preparetic
period and it might then be safe to promise good therapeutic
results.

2. What is the nature of the preparesis of Dana? When Dana’s brief
paper on preparesis was written, there was of course hardly any
idea that cases of paretic neurosyphilis could be cured or would
recover, except possibly vanishingly few _curiosa_ about which
there would always rage a diagnostic question. Accordingly, Dana,
having found certain cases that seemed to him to have early signs
of paresis but had apparently been cured by treatment, proposed to
call them cases of preparesis. His idea was that he would thereby
not offend those who held that general paresis was theoretically a
fatal disease. With modern work and the display of more and more
atypical cases of neurosyphilis, and the observation of relatively
numerous cures or remissions under treatment, the designation of
preparesis for a separate entity, or even for a sub-form of
neurosyphilis, becomes superfluous.

3. What is the percentage of cases of paretic neurosyphilis that
show a negative serum W. R.? Among the best figures are those of
Müller, who found that of 386 examples of paretic neurosyphilis,
379 showed all reactions positive, or 98.5%.

4. What is the meaning and value of the so-called provocative
salvarsan injection? In practice, there may be a series of
negative W. R.’s in the blood serum before a positive reaction is
finally obtained, owing to technical difficulties or biological
peculiarities. Where intensive work is being done upon the
neurosyphilis problem, it is beyond question desirable to make the
W. R. test upon at least three separate samples of blood drawn at
intervals, for the second or third test may prove positive. This
situation makes the interpretation of the so-called provocative
salvarsan injection exceedingly doubtful; that is, the reaction
might have been positive on repetition without the injection of
salvarsan. The present case, as above stated, failed to yield a
serum W. R. even after repeated tests and the “provocative.”

5. What is the significance of the irregular pupils in this group?
Paretic neurosyphilis shows inequality of the pupils in a high per
cent of cases. Irregularity of outline of the pupils is commonly
thought to be an important sign and to suggest neurosyphilis. It
is true that many cases of pupillary irregularity are syphilitic,
but the sign is of little or no differential value since
congenital malformations and relics of old injuries and adhesions
may produce effects identical with those of neurosyphilis.

=DIFFUSE (that is, meningovasculoparenchymatous[5]) NEUROSYPHILIS is
typically associated with six positive tests (serum Wassermann
reaction, fluid Wassermann reaction, spinal fluid gold sol reaction,
pleocytosis, positive globulin, excessive albumin); but one or more,
and frequently several, of these tests are likely to run mild as
compared with the tests in PARETIC NEUROSYPHILIS (“general
paresis”). The clinical course of the diffuse (and especially the
meningovascular) cases is likely to be protracted, with a good
prognosis as to life (barring fatal vascular insults).=

=Case 14.= We shall present the case of John Jackson, a surveyor, 31 years of age, suffering from a left hemiplegia, with this in mind: To exhibit difficulties in diagnosis in the presence of an embarrassment of symptomatic riches.

The patient arrived at the hospital, in the first place, because he had been threatening a woman who lived next door to him. He believed that this neighbor had been talking about him and circulating reports against him. Excited by these ideas, he had threatened to cut her throat.

Now the occurrence of hemiplegia in adult life before the approach of senium is always suspicious of syphilis, and this suspicion we naturally entertained from the beginning. However, there was upon the scalp a crooked linear furrow about six inches long, running from the vertex to the right parietal eminence. Another furrow about an inch long was present upon the forehead. These furrows appeared to be of a bony nature and were not tender. There was evidence of an old decompression operation on the right side of the head; there were also large scars on both sides of the neck, evidently the result of old operations; and there were numerous palpable glands—the largest about the size of a lima bean—all firm and not tender.

Station in syphilitic hemiplegia. Syphilitic pigmentation of skin.
]

It seems that at the age of eight, according to the patient’s mother, Jackson had received a head injury and had remained unconscious for three weeks. Upon recovery, he had to relearn both to walk and to talk; however, he was able to begin school where he left off. He became more nervous and irritable after the accident than previously. Nothing further had developed until, at about 25 years of age, a tubercle was discovered in his eye (the right pupil was smaller than the left, reacting more slowly; right iris bound down by adhesions, with white opacity of anterior chamber). For two years, 25 to 27, the patient was under medical treatment for tuberculosis, and at the conclusion of this period numerous glands were removed from the neck and diagnosticated tuberculous. However, the neck did not heal and he carried bandages upon it for two years.

At 28, the patient’s mother described the occurrence of a slight shock, with head retraction, for a minute or two, and inability to speak. Thereafter there had been five or six similar attacks, less severe, and without loss of speech. The attacks were never accompanied by convulsive movements. Then occurred a paralytic stroke, leaving the patient with a left hemiplegia, which had somewhat improved. Mentally, the patient had gone down hill, becoming less alert and more apathetic, and to some extent amnestic. One had to consider, accordingly, the somewhat doubtful possibility of post-traumatic and post-operative conditions, and the question of tuberculosis (possibly errors in diagnosis; the lungs showed no evidence of tuberculosis).

=Physically,= the signs of a left hemiplegia were appropriate. Spasticity on the left side was found; there were Babinski, Gordon, Oppenheim reflexes and ankle clonus on the left side (all absent on the right). Speech defect was present. =Mentally,= aside from the delusions noted at the beginning of our analysis, a striking feature was the patient’s childishness. While reciting delusions, the patient was overactive and evinced a somewhat childish interest. Arithmetically, Jackson had preserved a fair ability but his apathy and lack of interest interfered with tests, and possibly also with the exercise of memory. As above noted, we were compelled to maintain the suspicion of syphilis throughout despite the attractive hypotheses of traumatic and post-decompressive effects and cerebral tuberculosis. A history of the acquisition of syphilis an unknown number of years before admission entered to strengthen the suspicion of the syphilitic nature of the mental symptoms.

TYPICAL LABORATORY FINDINGS IN NEUROSYPHILIS (NONNE, 1915)
─────────────┬─────────┬─────────┬─────────┬───────────────┬───────────
DIAGNOSIS │ W. R., │ W. R. │ SPINAL │ PHASE I, │PLEOCYTOSIS
│ BLOOD │0.22 CC. │ FLUID, │ GLOBULIN │
│ SERUM │ BLOOD │ 1.0 CC. │ │
│ │ SERUM │ │ │
─────────────┼─────────┼─────────┼─────────┼───────────────┼───────────
PARESIS OR │POSITIVE │POSITIVE,│POSITIVE,│POSITIVE, │POSITIVE,
TABOPARESIS│ IN │ 85–90% │ 100% │ 95–100% │ ABOUT 95%
│ ALMOST │ │ │ │
│ 100% │ │ │ │
│ │ │ │ │
TABES (not │POSITIVE,│POSITIVE,│POSITIVE,│POSITIVE, │POSITIVE,
combined │ 60–70% │ 20% │ 100% │ 90–95% │ 90%
with │ │ │ │ │
paresis) │ │ │ │ │
│ │ │ │ │
CEREBROSPINAL│POSITIVE,│POSITIVE,│POSITIVE │POSITIVE almost│POSITIVE
SYPHILIS │ 70–80% │ 20–30% │ ALMOST │ always; │ ALMOST
│ │ │ ALWAYS │ NEGATIVE only│ ALWAYS
│ │ │ │ EXCEPTIONALLY│
─────────────┴─────────┴─────────┴─────────┴───────────────┴───────────
CHART 8

Syphilitic thrombosis. Contours of brain preserved.
]

The W. R. proved positive in blood and spinal fluid. The gold sol reaction was of the syphilitic type; 37 cells were found per cmm.; there was a slight amount of globulin and a slight excess of albumin.

We made a diagnosis of CEREBROSPINAL SYPHILIS rather than general paresis on account of, first, the slow course of the disease; second, the vascular type of the cerebral insult, hardly typical of paresis; and third, the mild spinal fluid reaction. Treatment will hardly cure the hemiplegia, at least so far as restoration of cerebral tissues lost in the insult is concerned. We were perhaps entitled to consider that, as in the cases of Petrofski (17), O’Neil (19), Robinson (45), the meningitic process could be arrested. Unfortunately, our treatment of 20 injections of salvarsan over a period of 10 weeks, followed by a number of months of bi-weekly injections of mercury salicylate, proved incapable of making any change in the mental and physical picture or in the laboratory findings.

1. Can we explain the apparently poor reaction to treatment of the
cerebrospinal syphilis in the case of Jackson by supposing a more
deep-seated involvement than the meningovascular involvement
indicated by the hemiplegia and the signs in the fluid? Autopsied
cases in our experience show focal parenchymatous involvements
that have not caused obvious clinical symptoms at any time during
the course of the disease. These symptomatically silent lesions
may have been present.

2. What is the comparative prognostic value of seizures in paretic
neurosyphilis and in such a meningovascular case as that of
Jackson? Paretic seizures are often and indeed characteristically
recovered from. Moreover, autopsies in paretic neurosyphilis
characteristically show no gross focal destructive lesions to
correspond with the seizures. The paretic seizures are apparently
more irritative than paralytic. However, the seizures of the
meningovascular group of neurosyphilis are also, though less
commonly, recovered from, so that the differential diagnosis on
the basis of the outcome of seizures is not safe. Rarely paretic
neurosyphilis itself also develops seizures from which no recovery
is made.

3. What is the relation of neuropathic heredity to neurosyphilis?
The family history of John Jackson is undoubtedly poor, since his
father died of diabetes and a paternal uncle was insane; and on
the mother’s side, the grandmother died of tuberculosis and an
aunt died insane. This general question was more interesting in
the days before the syphilitic nature of general paresis and of
allied diseases was known. However, we may still hold perhaps that
not only syphilis but also various intoxications, especially
alcoholism, do flourish upon a neuropathic soil. This question,
like that of Krafft-Ebing’s celebrated claim of the relation
between syphilization and civilization, needs revision in the
light of more extensive applications of the W. R. in larger and
larger groups of persons under various community conditions.

=The SIX TESTS (serum Wassermann reaction, fluid Wassermann
reaction, pleocytosis, gold sol reaction, globulin, excess albumin)
are likely to run STRONGER in PARETIC NEUROSYPHILIS (“general
paresis”) than in DIFFUSE (especially meningovascular)
NEUROSYPHILIS; in particular, the gold sol reaction is likely to
prove “paretic” rather than “syphilitic.” The clinical course of
paretic neurosyphilis (“general paresis”) is likely to terminate in
death within a few years.=

=Case 15.= Pietro Martiro was a well developed and nourished man, 30 years of age, who had been doing erratic things and acting peculiarly for a few weeks before entering the hospital. In the hospital, Martiro proved to be very excitable and given to violence. He had marked delusions of grandeur, saying he was worth many millions of dollars, was the greatest singer in the world, the greatest athlete in the world, and the like.

=Physically=, there was no disorder except overactivity of some reflexes. The diagnosis of GENERAL PARESIS offered no difficulties, and it was confirmed by the laboratory tests (positive serum and fluid W. R., “paretic” gold sol reaction, 42 cells per cmm., an excess of albumin, and a positive globulin test).

=Treatment=: The perfect physique of this case and the extremely brief clinical duration (a few weeks) would naturally suggest a probably favorable outcome. However, cases with marked delusions of grandeur have very frequently proved to be cases with extensive brain tissue loss as shown in certain studies with Danvers material.

In any event, the treatment in this case proved unavailing. Enormous doses of salvarsan, twice a week, aided by mercury and potassium iodid, were given. Although other cases had been helped by such intensive treatment, Martiro went steadily downhill, nor was there the slightest diminution in the intensity of any of the spinal fluid reactions. After 50 injections of salvarsan over a period of 30 weeks without improvement, treatment was discontinued. A few months later, the patient died.

=PARETIC NEUROSYPHILIS (GENERAL PARESIS)=

=PHYSICAL SYMPTOMS=

EARLY HEADACHE
VISUAL DISORDER
HYPALGESIA
ADIADOCHOKINESIS
ATAXIA
NASOLABIAL FLATTENING
VOCAL CHANGE
SPEECH DISORDER
WRITING DISORDER
LOSS OF MANUAL DEXTERITY
PUPILLARY CHANGES
REFLEX CHANGES
SEIZURES
LATE: PARALYSIS, CONTRACTURE

CHART 9

=PARETIC NEUROSYPHILIS (GENERAL PARESIS)=

=MENTAL SYMPTOMS=

INTAKE IMPAIRED
CONSCIOUSNESS CLOUDED
FATIGUABILITY INCREASED
HALLUCINOSIS RARE
AMNESIA—RECENT! CHRONOLOGY AND STORAGE IMPAIRED. FABULATION
OVER-SUGGESTIBILITY
JUDGMENT IMPAIRED
FANTASTIC DELUSIONS
INSIGHT INTO ILLNESS NIL
EARLY IRRITABILITY OR HEBETUDE
QUICK SHIFTING EMOTION
CHARACTER CHANGE
CONDUCT SLUMP

CHART 10

1. What is the duration of paretic neurosyphilis (“general
paresis”)? If we omit the doubtful, early, and prodromal stages
and count the beginning of the disease with the occurrence of
definite symptoms, we find (Kraepelin) that almost half the
patients with pronounced paretic signs die within the first two
years of their disease. Kraepelin’s observations upon 244 cases
are as follows:

Year: 1 2 3 4 5 6 7 8 9 10 14
Cases: 51 63 52 41 22 4 5 2 2 1 1

The average duration of the disease in months has been calculated
as varying from 24 to 32 months. Juvenile paresis runs a slower
and more insidious course. The duration of paresis, according to
many observers, diminishes with the increasing age of the patient.
It is now held that a combination of tabes with paresis does not
prolong the duration of the paresis. As noted above in the
discussion of Case Harrison (9), our conceptions of the
characteristic duration of paretic neurosyphilis must alter with
the increase of our knowledge due to the early application of
laboratory tests.

2. What is the significance of the term _general paresis_? The case
of Martiro is, of course, a good instance to show that the term is
sometimes a misnomer. The characteristic generalized motor
incapacity denoted by the term _general paresis_ is shown in
patients in the institutions for the chronic insane in their last
few months of life. The term _paresis_ is perhaps to be preferred
to the term _paralysis_ because the paralysis is not complete but
partial; but perhaps the best reason is that the word _paresis_ is
a shorter word. When the mental side is to be emphasized, the term
_paralytic dementia_ is employed. In this book we have used the
term _paretic neurosyphilis_ to mean a more precise statement of
the etiology of general paresis (general paralysis, paralytic
dementia). The lay term, _softening of the brain_, like the terms
_metasyphilis_ and _parasyphilis_ is in the present phase of our
knowledge to be eschewed.

Euphoria in paretic neurosyphilis (“general paresis”). The head, arms
and trunk were shaking with mirth; hence, the indistinct outlines of
the photograph.
]

3. If this fatal case be typical of general paresis (for more
favorable results, see Part V), what is the toll of deaths from
this disease in the community at large? A striking statement may
be quoted from Dr. Thomas W. Salmon’s “Analysis of General
Paralysis as a Public Health Problem:”

“With the information in our possession at the present time, we
are able to state that not fewer than 1000 persons in whom general
paralysis is recognized die in New York State every year. Let us
compare this with the lives lost from some other important
preventable diseases. It means that _one in nine_ of the 6909 men
who died between the ages of 40 and 60 in New York last year died
from recognized general paralysis and that _one in thirty_ of the
5299 women who died in the same age-period died from this disease.

“The number of deaths from general paralysis in New York last year
about equalled the number of deaths from typhoid fever. The
following table gives the number of deaths due to the ten most
important specific infectious diseases. Of course, deaths in
measles, typhoid fever and scarlet fever will be found also under
the names of some of the complications of these diseases, but it
should be remembered that these primary diseases are not
invariably fatal as general paralysis is. Many of the patients
with measles who died from bronchopneumonia would have recovered
but for this complication, while the paretics with
bronchopneumonia would have died even if this complication had not
arisen. No attempt is being made to compare the _prevalence_ of
general paralysis with that of other diseases—we are trying only
to estimate its share in the _mortality_.

“1. Tuberculosis (all forms) 16,133
2. Pneumonia 9,302
3. Bronchopneumonia 7,217
4. Diphtheria and croup 1,854
5. Influenza 1,381
6. Measles 1,071
7. Typhoid Fever 1,018
_General paralysis (recognized)_ 1,000
8. Scarlet fever 837
9. Whooping cough 818
10. Syphilis 782”

=PARETIC NEUROSYPHILIS (GENERAL PARESIS)=

=CHARACTERISTICS=

AMNESIA
QUICK SHIFTING EMOTIONS
CHARACTER CHANGE
CONDUCT SLUMP
NERVOUS DISORDERS
SPEECH DISORDERS
PUPILLARY CHANGES
REFLEX CHANGES
SEIZURES
CEREBROSPINAL FLUID PICTURE

CHART 11

=SYPHILITIC PSYCHOSES=

SYPHILITIC NEURASTHENIA
GUMMA
SYPHILITIC PSEUDOPARESIS
APOPLECTIC CEREBRAL SYPHILIS
SYPHILITIC EPILEPSY
SYPHILITIC PARANOIA
TABETIC PSYCHOSIS
HEREDITARY
PARESIS

KRAEPELIN, 1910

CHART 12

=TABOPARETIC NEUROSYPHILIS (“taboparesis”) is CLINICALLY a
combination of the symptoms of TABES DORSALIS and those of GENERAL
PARESIS. The COURSE of TABOPARESIS is likely to be from a
characteristic tabes dorsalis (often of years’ standing) to a
characteristic general paresis; the ultimate paretic picture is
likely to retain various characteristics of tabes. The LABORATORY
TESTS in the paretic phase are characteristic of ordinary
(non-tabetic) general paresis. The PROGNOSIS, after the paretic
phase has arrived, is apt to be that of general paresis.=

=Case 16.= Joseph Sullivan, a waiter, 50 years of age, sought assistance at the Psychopathic Hospital voluntarily. His complaint of severe and lancinating pains in the legs, difficulty with his gait, and a feeling of constriction about the waist, was forthwith suggestive of tabes dorsalis. He was a rather poorly nourished, white-haired man, with a drooping of the left side of the face. The pupils reacted sluggishly to light, the right somewhat better than the left. A marked Romberg reaction could be demonstrated. Ataxia in walking was marked. There was some incoördination of the hands, considerable tremor, and writing was poorly performed. The ankle-jerks and knee-jerks were absent. On the whole, the diagnosis of TABES DORSALIS was clear enough.

The most appealing situation was =mental=. Sullivan was exceedingly apprehensive about his condition on the ground that it was growing progressively worse; if it was to get worse, Sullivan feared he would commit suicide. From his own account, he had become irritable, quick-tempered, and often unreasonable. As usual in these cases, the question arose whether the depression was psychopathic or natural.

=TABETIC SYMPTOMS AND SIGNS IN ORDER OF THEIR FREQUENCY=

=ANALYSIS OF 250 CASES=

PER CENT

1. ROMBERG SIGN 96.4 2. ABSENT KNEE-JERKS 90.0 3. LANCINATING PAINS 88.4 4. STAGGERING GAIT 87.2 5. ARGYLL-ROBERTSON PUPIL 80.0 6. ATAXIA IN UPPER EXTREMITIES 68.2 7. SPHINCTER DISTURBANCES 67.6 8. SENSORY DISTURBANCES 58.2 9. VISUAL DISTURBANCES 43.6 10. PARESTHESIA AND NUMBNESS OF FEET AND LOWER EXTREMITIES 42.8 11. GIRDLE SENSE 31.2 12. PTOSIS OF EYE-LIDS 23.2 13. PARESTHESIA OR NUMBNESS IN HANDS OR UPPER EXTREMITIES 13.6 14. STRABISMUS 12.0 15. VISCERAL CRISES 12.0 16. LOSS OF SEXUAL DESIRE 11.5 17. CHARCOT JOINTS 9.2 18. VERTIGO 4.0 19. MAL PERFORANS 3.2 20. PAIN IN JOINTS 2.8 21. RECTAL TENESMUS 2.8 22. MENTAL DEGENERATION (other than paresis) 2.4 23. HEMIPLEGIA 2.4 24. VESICAL TENESMUS 2.0 25. DIFFICULTY IN ARTICULATION 2.0 26. DEAFNESS 1.2 27. ANOSMIA 0.8

BALDWIN LUCKE.

CHART 13

While in the hospital things shortly came to a crisis. In the midst of a fit of depression, Sullivan attempted suicide by beating his head against the wall. Whether this attempt could be regarded psychopathic, however, remained in question. Sullivan had been drinking very heavily although he had stopped about six weeks before admission, fearing that the alcohol was causing a development of symptoms. The remedy was almost worse than the disease because he then became more nervous, lost his appetite, and had a marked insomnia.

According to the patient’s own history, he had had several attacks of gonorrhœa and a syphilitic infection at the age of 19; that is, some 31 years before admission to the hospital. However, the first _neurological_ symptoms of which the patient was aware came about 27 or 28 years after infection, namely, 3 or 4 years before admission, when facial paralysis developed. At that time, he had suddenly felt a peculiar sensation in the throat and became unable to swallow for a time. His voice remained hoarse and low for some time, and his face began to droop. The lancinating pains and the ataxia also dated back several years.

1. How shall we evaluate the mental symptoms? The prognosis of tabes
dorsalis is relatively good so far as life is concerned, and it
might even be possible for Sullivan by training to remain capable
of being a waiter. The manual incoördination was not marked, and
possibly the manual tremor was in part due to alcohol.
Accordingly, the mental symptoms, such as emotional lability and
memory defect, were in the foreground of attention. In point of
fact, the laboratory examinations showed positive W. R. in the
serum and the spinal fluid, which latter also contained 60 cells
per cmm., positive globulin, and an excess of albumin. THE
DIAGNOSIS MADE WAS THAT OF TABOPARESIS, meaning thereby a tabes
associated with appropriate symptoms of a mental nature.

2. How shall the term _taboparesis_ be used? Some use the term, as
we feel erroneously, for instances of general paresis which happen
to show crural areflexia (absence of knee-jerks). We feel that the
best usage of the term is for instances in which well-defined
symptoms of tabes (as well as of paresis) are present, namely,
characteristic ataxia, lightning pains, and the like. If the term
is used more loosely, as above mentioned, then practically every
case of general paresis might perhaps be termed _taboparesis_,
since almost every case of paresis does show involvement of the
cord as well as of the cerebrum. Such involvement may lead to
hyperreflexia, hyporeflexia, or areflexia according to the
localization of the process. In true taboparesis, in which there
is a commingling of the features of tabes with those of paresis,
we should find the posterior roots of the spinal cord affected.
The spinal lesions of paresis itself are more apt to be
intraspinal; that is, confined to the nervous system within the
pial investment.

3. Bearing in mind that Sullivan was a waiter, what shall be said
about the infectivity of these cases? It is counted as a rule as
negative, since there are no open spirochete-bearing lesions. The
longer the period since infection the less, as a rule, is the
chance of contagion in syphilis; and as tabes and paresis occur
fairly late in the disease, the infectiousness at this stage is
practically negligible.

4. Of what differential value is the insight shown by Sullivan into
the nature of his symptoms? Kraepelin remarks that a genuine
insight into the nature of the disease does not as a rule occur in
paresis. At the beginning of the disease, there may sometimes be a
correct understanding of the nature of the disease and of its
probable outcome; but the presence or absence of insight into the
fact of mental disease is by no means a differential sign of
practical value.

5. What is to be said of the occurrence of depression and excited
states in paretic neurosyphilis? A variety of classifications of
sub-forms of paretic neurosyphilis have been propounded.
Kraepelin, for example, deals with four: the demented, depressive,
expansive, and agitated forms, but remarks that the division is
merely convenient for exposition. The institutional intake does
not accurately represent the distribution of cases. Under
psychopathic hospital conditions with the relatively easy resort
to such institutions, the number of quiet cases increases; under
the less advanced conditions in Heidelberg, Kraepelin took in 53%
demented paretics as against 56% at Munich (73% women) under the
easier conditions of admission. The admissions of demented
paretics varied from 37 to 56%. The variations depend much upon
the facility with which the cases can be brought to institutions.
Where admission is beset with various legal restrictions, the
quiet and demented cases are more apt to be treated for long
periods at home. The depressive type of paretic neurosyphilis
forms a much smaller group, according to Kraepelin, as only about
12% of his Heidelberg admissions were of this type, and still
fewer of his Munich admissions. Other authors give percentages as
high as 16 and 19. The so-called expansive group is larger,
Kraepelin finding 30% of his Heidelberg cases to be of this group,
and 21 to 22% of his Munich cases. The rarest sub-form of paretic
neurosyphilis is the agitated form: 6% of Kraepelin’s Heidelberg
admissions; 14% among males and 5% among females in his Munich
admissions, where the diagnosis of agitated paresis was entered on
somewhat broader lines. French authors (Sérieux and Ducaste) have
enlarged the number of sub-forms of paretic neurosyphilis as
follows: Expansive 27%; sensory 24%; demented 24%; persecutory 3%;
depressive 2%; circular 7%; hypochondriacal 7%; and maniacal 6%.

=DIFFUSE (meningovasculoparenchymatous) NEUROSYPHILIS may look
precisely like PARETIC NEUROSYPHILIS (“general paresis”) at certain
periods of clinical and laboratory examination.=

=Case 17.= The police found Gregorian Petrofski crouching on his knees on a Boston sidewalk, attempting to take pickets off a fence. Petrofski knew little English; he said that he had slept in Poland the night before. He did not appear to be alcoholic.

When he was examined, through an interpreter, he told how he had been in America two days, and in Boston two years; that he was at the present time in Poland, and that his brother had brought him to the hospital and left him there.

The =physical examination= showed Petrofski to be well developed and nourished. His pupils were somewhat dilated and reacted somewhat slowly to light and accommodation. =Neurologically,= there was nothing else abnormal found upon systematic examination although, through lack of coöperation, sensory and coördination tests proved difficult if not impossible. There was a large ulcer on the under surface of the glans penis, with several small smooth scars on the upper surface. There was a purulent discharge from the external meatus. There were exostoses of both tibiae.

The initial diagnosis had to consider uremia and diabetes, which could be easily excluded on examination. Alcoholism was excluded through absence of alcohol on the breath. There remained such diagnoses as epilepsy, some post-traumatic condition, or meningitis, to say nothing of the hypothesis of syphilis raised by the tibial exostoses and the lesions of the penis. The hypothesis of trauma was given up, as well as epilepsy and meningitis upon the data of the lumbar puncture. The spinal fluid proved to be clear but with enormous amounts of globulin and albumin, 80 cells per cmm., a “paretic” gold sol reaction, and a positive spinal fluid W. R. (the serum W. R. was also positive). Accordingly, it was clear that the case was one of neurosyphilis.

Treatment was instituted with injections of mercury salicylate, a grain and a half twice a week, and potassium iodid. After some weeks, diarrhoea and salivation with marked symptoms of mercury poisoning set in; the treatment was suspended, but later re-instituted. In a few weeks Petrofski was apparently quite well, the spinal fluid tests had all become negative, as had the serum W. R.

Petrofski now began to pick up a good deal of English, and gave a consistent narrative of his past life, although the period just prior to and during his early stay in the hospital has remained blank. Without further treatment Petrofski has remained well for over a year.

1. Does the “paretic” gold sol reaction mean general paresis? In
connection with this general question, a brief summary of the
significance of the gold sol reaction in this group may be made.
(1) Fluids from cases of general paresis in the vast majority of
cases will give a strong and fairly characteristic reaction,
especially if more than one sample is tested. (2) Very rarely
general paresis fluid will give a reaction weaker than the
characteristic one. (3) Fluids from cases of syphilitic
involvement of the central nervous system other than general
paresis often give a weaker reaction than the paretic, but in a
fairly high percentage of cases give the same reaction as the
paretics. (4) Non-syphilitic cases may give the same reaction as
the paretics; these cases are usually chronic inflammatory
conditions of the central nervous system. (5) When a syphilitic
fluid does not give the strong “paretic reaction” it is
presumptive evidence that the case is not general paresis, and
this test offers a very valuable differential diagnostic aid
between general paresis, tabes, and cerebrospinal syphilis. (6)
The term “syphilitic zone” is a misnomer, as non-syphilitic as
well as syphilitic cases give reactions in this zone, but no fluid
of a case with syphilitic central nervous system disease has given
a reaction out of this zone, so that the finding may be used
negatively; and any fluid giving a reaction outside of this zone
may be considered non-syphilitic. (7) Mild reactions may occur
without any evident significance, while a reaction of no greater
strength may mean marked inflammatory reaction. (8) Tuberculous
meningitis, brain tumor, and purulent meningitis fluids
characteristically, though not invariably, give reactions in
higher dilutions than syphilitic fluids. (9) The unsupplemented
gold sol test is insufficient evidence on which to make any
diagnosis, but used in conjunction with the W. R., chemical and
cytological examinations, it offers much information, aiding in
the differential diagnosis of general paresis, cerebrospinal
syphilis, tabes dorsalis, brain tumor, tuberculous meningitis, and
purulent meningitis. (10) We believe that no cerebrospinal fluid
examination is complete for clinical purposes without the gold sol
test.

=FREQUENT SYMPTOMS IN DIFFUSE AND VASCULAR NEUROSYPHILIS=

=(“CEREBRAL” AND “CEREBROSPINAL SYPHILIS”)=

PUPILLARY DISORDER
HEADACHE
VERTIGO
INSOMNIA
DROWSINESS
CHANGE IN DISPOSITION
Irritability Slow thinking
SEIZURES
PARALYSES
Permanent Transient
APHASIA
HEMIANOPSIA
SENSORY DISTURBANCES
GASTRIC CRISES
SPHINCTER DISTURBANCES
INTRACRANIAL PRESSURE SYMPTOMS
POLYURIA, POLYDIPSIA, GLYCOSURIA
MÉNIÈRE’S SYNDROME
NYSTAGMUS

CHART 14

See Appendix B for technical details.

2. What is the relation of the tibial exostosis to neurosyphilis?
The syphilographers have always stressed the tibial lesions in the
diagnosis of syphilis. Although not so much attention has been
paid to these and kindred osseous lesions in neurosyphilis, yet we
have frequently found such lesions and they afford an important
auxiliary means of diagnosis.

=A POSITIVE SERUM Wassermann reaction with a NEGATIVE FLUID
Wassermann Reaction may be found in NEUROSYPHILIS, particularly in
VASCULAR NEUROSYPHILIS: the remaining signs in the fluid, although
frequently positive, may even be negative.=

=Case 18.= Frederick Wescott was a promoter, an elderly looking man of 60 years. His health had been failing for 18 months. There had been shortness of breath, dizziness, a tired feeling, inability to “get the words he wanted,” and forgetfulness of names. About eight weeks before examination, Wescott had had a convulsion, following which he had been unable to express himself at all well. This convulsion was not accompanied by loss of consciousness. Besides a marked motor aphasia, there was agraphia.

=Physically=, Wescott showed arteriosclerosis and a blood pressure of 135 systolic, but, except very lively knee-jerks, no other reflex disorders or anomalies were discovered. In particular, the pupils reacted fairly well.

There was, perhaps, no special reason to implicate syphilis in the case, yet Wescott gave a history of syphilis at 35 years. The W. R. of the blood serum proved positive; that of the spinal fluid was negative, and the albumin was but slightly increased; there was a very slight amount of globulin, and there were 16 cells per cmm. in the fluid. The gold sol reaction suggested syphilis.

We felt entitled to make a diagnosis of SYPHILITIC CEREBRAL ARTERIOSCLEROSIS, regarding the convulsion or seizure eight weeks before as due to a vascular insult. The laboratory picture in the spinal fluid in Wescott’s case seems to be rather characteristic of this group of syphilitic arteriosclerotics.

1. What is the reason for the negative spinal fluid W. R.? The
theory would be that the syphilitic lesion is localized in the
vascular system and that the parenchyma is only secondarily, if at
all, involved. The W. R. producing bodies are accordingly not
found in the fluid.

2. How frequently are several of the spinal fluid tests negative,
while others are positive? Whereas, clinically speaking, the five
tests in the spinal fluid (W. R., globulin reaction, excess
albumin, pleocytosis, and gold sol reaction) are each indicative
of a pathological condition in the central nervous system, yet a
specially intensive study of the distribution of these tests has
shown that they are prone to occur independently. Consequently, we
must concede that they do not all represent the same inflammatory
products and chemical conditions. The W. R. producing bodies, the
gold sol reaction producing bodies, as well as the globulins and
albumins, have been proved to be separate. Special work has also
shown that _these tests disappear under treatment at different
rates_. There is, unfortunately, no doubt that the rate and
intensity, presence or absence, and the order of disappearance of
these tests in either treated or untreated cases, do not at all
parallel the clinical conditions of the patients.

3. What is the prognosis in vascular neurosyphilis, such as in the
case of Wescott? The prognosis is identical with that of cerebral
arteriosclerosis in general, that is to say, bad, but with
frequent periods of improvement. In the neurosyphilitic type of
arterial disease thromboid formation is frequent. Where the lesion
is chiefly perivascular infiltration, rather than disintegration
of the vessel wall, improvement may very well occur as a result of
treatment. Wescott showed slight improvement under treatment. He
has already lived two years since his first convulsion, and three
and a half years since the onset of symptoms.

=DIFFUSE NEUROSYPHILIS (so-called “cerebrospinal syphilis”) is often
marked by SEIZURES.=

=Case 19.= Agnes O’Neil, an unmarried woman of 28 years, was first examined five weeks after the initial symptoms. It appears that she had had certain seizures, with unconsciousness and twitching of the limbs (otherwise not well described), followed by confusion of mind and sometimes by a weakness of the left side and a difficulty in speaking. Headache had been almost constant, as well as pains in the arms and legs.

=Physically=, both in general and =neurologically=, there were no signs or symptoms; mentally, we could discover no symptoms. Syphilis was denied, although possible exposure to syphilis was admitted.

The =diagnosis= of some form of organic brain disease was clear with the picture of convulsions followed by slight aphasia with headaches and limb pains. With onset at 28, the most frequent cause for such epileptiform seizures is certainly syphilis. Examination of the blood and spinal fluid showed a positive W. R., in both. The albumin was also somewhat increased. The clinical picture suggested a fairly generalized meningitic involvement.

The =prognosis= in such cases of generalized meningitic involvement is in general good, and this principle was illustrated in the O’Neil case, in which the symptoms soon disappeared under intensive antisyphilitic treatment. In fact the spinal fluid W. R. became negative in the course of four weeks. The blood serum W. R., however, has remained positive despite eight months of active treatment.

=CONDITIONS IN WHICH CONVULSIONS OCCUR=

NEUROSYPHILIS
HYSTERIA
EPILEPSY MAJOR (GRAND MAL)
EPILEPSY MINOR (PETIT MAL)
DEMENTIA PRAECOX
TOXIC CONDITIONS:
Asphyxia, Uremia, Alcohol, Absinthe, Lead, Mercury, etc.
ORGANIC BRAIN LESIONS
Apoplexy, Meningitis, Intracranial Growths
STOKES-ADAMS DISEASE
MALINGERING
DISSEMINATED SCLEROSIS

CHART 15

1. Are certain cases of syphilitic epilepsy really cases of
Jacksonian epilepsy? As a matter of nomenclature, Jacksonian
cortical epilepsy is usually the result of a focal and
circumscribed irritative lesion in the cortex. Gumma, local
syphilitic meningitis, and syphilitic vascular lesions, as well as
scars consequent upon the latter, are among the causes of
Jacksonian epilepsy, along with such other focal lesions as
trauma, tumor abscess, tubercle, and the like. Even non-syphilitic
Jacksonian epilepsy has been observed from time to time in cases
of diffuse intracranial pressure. Jacksonian attacks also have
been found in so-called genuine epilepsy. Accordingly, we must not
conclude from the occurrence of Jacksonian convulsions, even
though in a proved syphilitic case, that the convulsions in
question are surely due to a focal lesion, for they may be due to
diffuse syphilitic lesions.

2. What is the significance of aphasia in Agnes O’Neil? Aphasia is
not a characteristic symptom in ordinary Jacksonian epilepsy, but
the aphasia is another sign of focal lesion and forms an added
argument against the diagnosis of genuine or idiopathic epilepsy.
See also discussion of aphasia in paretic neurosyphilis under Case
Levenson (22).

3. What is the behavior of the serum W. R. and the spinal fluid W.
R. under systematic treatment? Sometimes, as in this case, the
serum W. R. remains positive and the fluid W. R. becomes negative;
but in other equally well-defined cases, the reverse holds true,
and the serum W. R. reaction becomes negative whereas the spinal
fluid reaction remains positive. The obvious conclusion is that we
cannot always be sure even by faithful tests of either the serum
or the fluid alone, whether the treatment has succeeded in
abolishing the laboratory signs.

4. Can this case be regarded as one of cure? Not by the definition
adopted in this book or by the syphilographers who take into
account not only the nervous system but the body which contains
it. To be sure, the spinal fluid of Agnes O’Neil is now entirely
negative and she is clinically free from symptoms; yet from the
broad standpoint of syphilis therapy in general, this patient is
not cured, as is evidenced by the positive serum W. R.

=PARETIC NEUROSYPHILIS (“general paresis”) is often marked by
SEIZURES.=

=Case 20.= Lester Crane, a plumber, 37 years of age, came to the hospital with a slow and defective speech. Moreover, there seemed to be some mental disorder since his answers to questions were not always relevant. It appeared that he was seeing bugs on the wall.

=Physically=, Crane was a well developed and nourished man, with overactive knee-jerks and a Babinski reaction on the left side.

It developed that there was an impairment in hearing. The pupils reacted well both to light and to distance. The patient was very restless and smiled in a silly fashion. His memory was decidedly defective in all spheres, and he was very slow in the intake of ideas.

The plumber’s wife said that, at about the age of 23 or 24, he had a spell of confusion lasting two or three days, with peculiar conduct, unintelligible talk, and a good deal of weeping. The medical diagnosis at that time took into account the fact that Crane was a plumber and was “lead encephalopathy.”

However, according to his wife, Crane had acquired chancre at about 26 years, was treated mercurially for about three years and declared well. He had remained well up to about 18 months before entrance, when, without previous warning, the patient had a convulsion with the continuous movements for about half an hour. He was semi-conscious for about 18 hours and vomited continuously. There was amnesia for the whole affair on regaining consciousness. In a week’s time, Crane was entirely well. But six weeks later there was another convulsion. Upon removal to a hospital, the diagnosis of general paresis was made, and the patient was given the Swift-Ellis intraspinous treatment. This seemed to be very successful, and the patient discontinued treatment after 14 weeks (during which time there had been seven treatments) on the ground that he was entirely well.

However, after discontinuing treatment, there was another convulsion in about a month, and further convulsions occurred once a month. For six months, however, the patient took no treatment, but finally returned to the hospital and was given mercury. This treatment appeared to suspend convulsions again for three months, but at the expiration of six months, the patient had three convulsions in one day, and several more during the following days. After the last of these convulsions, there had been numbness on the right side of the body and considerable headache.

The diagnosis of PARETIC NEUROSYPHILIS (“general paresis”) is borne out by the laboratory tests. The W. R. of the blood serum was, to be sure, negative, but the W. R. of the spinal fluid was positive, and there was a “paretic” type of gold reaction, together with other laboratory signs.

The case well demonstrates that group of paretic cases in which convulsions periodically occur, leaving the patient worse after each convulsion. Treatment with salvarsan was instituted, and mercury and iodid was given by mouth. During the period of eight months which have now elapsed since the beginning of this treatment, there have been no convulsions; there has been a great improvement in the memory, the hearing has improved, the W. R. in the spinal fluid is much less intense, the gold sol test has become negative, and the other tests are all less intense.

The patient, however, has not been entirely well, for in place of the generalized convulsions, he has had minor seizures, beginning as a rule with a tingling sensation in the right hand, extending up the arm, down the trunk and leg, and through the right side of the face, with a bitter sensation on the right half of the tongue. The patient maintains that this sensation is absolutely confined to the right half of the body (in this connection we may recall case Morton (1), in which there was also a hemiplegia together with other apparently hysterical symptoms at several times during the long course of a disease with abundant structural correlations). During these minor seizures, the patient is unable to talk, although he does not lose consciousness and is entirely aware of everything going on about him. These attacks have of late been growing somewhat less frequent.

=LOSS OF DEEP REFLEXES=

NEUROSYPHILIS
NEURITIS
(alcohol, diabetes, diphtheria, lead, arsenic, tubercle,
cachexia, etc.)
Peripheral nerves sensory or motor
PERIPHERAL NERVE PALSIES
TEMPORARILY FROM COMPRESSION BY TOURNIQUET
FRIEDREICH’S ATAXIA
SUBACUTE COMBINED DEGENERATION OF POSTERIOR AND LATERAL COLUMNS
Posterior column disease
FOCAL LESION IN GRAY MATTER OF CORD
INFANTILE PARALYSIS (ACUTE ANTERIOR POLIOMYELITIS)
PROGRESSIVE MUSCULAR ATROPHY
(chronic anterior poliomyelitis)
Anterior cornua of cord
AMYOTROPHIC LATERAL SCLEROSIS
SYRINGOMYELIA
THROMBOSIS OF ANTERIOR SPINAL ARTERY
LANDRY’S PARALYSIS
Anterior cornua and peripheral motor nerves
MYOPATHIES
(pseudohypertrophic and atrophic types)
MuscLe itself
AMYOTONIA CONGENITA
FAMILY PERIODIC PARALYSIS
(during attacks)
INCREASED INTRACRANIAL PRESSURE
(especially hydrocephalus and tumors of posterior fossa)
PNEUMONIA
IMMEDIATELY AFTER ATTACK OF MAJOR EPILEPSY
(post-epileptic coma)
TOXIC COMA
(uremia, morphine, etc.)
DURING SPINAL ANESTHESIA
COMPLETE TRANSVERSE LESION OF CORD

PURVES STUART

CHART 16

1. What is the cause of the negative serum W. R.? It is claimed that
3 to 5% of all cases of general paresis yield a negative blood
serum. In this particular case, there had been considerable
treatment, including some Swift-Ellis treatment, so that it may be
that this treatment had reduced a formerly positive blood serum W.
R. to a negative one.

2. What is the nature of the typical seizures of general paresis?
The most frequent seizures are epileptiform and bear a general
resemblance to cortical epilepsy; but more rarely these seizures
resemble the ordinary epileptic attack or consist of a violent
general shaking of the whole body. A variety of initial minor
disorders usher in the attacks: the temperature is often
increased. The attacks are over after one or at most after a few
hours. Kraepelin speaks of one that lasted 14 days. Sometimes a
_status paralyticus_ develops, suggestive of the _status
epilepticus_. Another rarer form of characteristic seizure is the
apoplectiform, which can hardly be told from an ordinary stroke,
and may be followed by the usual post-apoplectic phenomena. A good
many of the strokes leading to sudden death in middle life are
probably cases of neurosyphilis although often set down as early
arteriosclerosis of a non-syphilitic nature. Besides the
epileptiform and apoplectiform seizures, there are certain
seizures of a less definite and complete nature, ranging from
simple fainting spells, dizzy spells and petit mal attacks, to
various special forms of irritative muscular contractions and
temporary speech disorders. Sometimes these attacks occur with
complete preservation of consciousness. Transient paresthesias,
visual field defects, and especially attacks of vomiting, which,
according to Kraepelin, may precede paresis by years (of course in
this connection gastric crises of tabes must be thought of), may
be counted as sensory seizures.

3. What is the proportion of paretic cases developing seizures?
Figures vary from 30 to 90%. According to Kraepelin, seizures
occurred in 30 to 40% of his cases at Heidelberg; he was of the
impression that treatment in bed had reduced the number of
seizures. 65% of paretics admitted to Munich (under very free
conditions of admission) were determined to have shown seizures
before their admission to the hospital. Seizures are said to be
somewhat more frequent in men than in women. These paretic
seizures are not due to either hemorrhages or vascular plugging—at
least in the vast majority of cases—and must be ascribed to the
effects of microscopic injuries.

4. What is the effect of seizures upon the future course of paretic
neurosyphilis? The current idea as expressed, for example, by
Mercier, is that “immediately after each crisis the patient is
much worse than he was before it, and thereafter there is some
improvement, but he never improves up to the point at which he was
before the occurrence of the crisis.” That is, “The course of the
disease is one of sudden plunges, each deeper than the last, each
followed by a gradual recovery that is less complete than the
recovery from the previous plunge.”

5. During what period of the disease are seizures most common? Late
in the disease many cases have convulsions, even though there were
none for the first year or two. In other cases the convulsion is
the first indication of paresis.

=DIFFUSE (non-paretic) NEUROSYPHILIS (“cerebrospinal syphilis”) is
often marked by APHASIA.=

=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.

=CONDITIONS IN WHICH SPEECH DEFECT IS FOUND=

NEUROSYPHILIS
HYPOGLOSSAL PARALYSIS
FACIAL PALSY
PARALYSIS OF PALATE (POST-DIPTHERITIC)
BULBAR PALSY
PSEUDOBULBAR PALSY
MYOPATHY—FACIO-SCAPULO-HUMERAL TYPE OF LANDOUZY AND DEJERINE
MYASTHENIA GRAVIS
FRIEDREICH’S ATAXIA
LARYNGEAL TABES
ALCOHOLIC INTOXICATION
POST HEMIPLEGIC
LENTICULAR DISEASE
BILATERAL ATHETOSIS
MULTIPLE SCLEROSIS
DEAF MUTISM
PARALYSIS AGITANS
CHOREA
STAMMERING
TICS
HYSTERICAL APHONIA

CHART 17

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.)