CARDIO-VASCULAR SYPHILIS AND CEREBRAL SYMPTOMS By P. G. GOLLERKERI, m.d. Pathology Department, Medical College, Rangoon The clinical results of a syphilitic infection have long been described in more or less definite three stages : primary, secondary and tertiary. This division into stages has been possible apparently because of a hypothetical tissue susceptibility of the various types of body tissues at different periods of the infection. We are taught that after the primary sore on the genitals or elsewhere?the lesion at the site of entry of the organism associated with trauma? the skin and mucous membranes follow with a rash, etc., in a regular sequence, and later, after a variable period, the so-called tertiary symptoms appear in the internal viscera. Anyone with a long clinical experience in a general hospital will have been struck by the number of syphilitics (as proved by the Wassermann reaction) who do not show or give any history of the disease going through the different stages. Often, syphilis in a patient is discovered when he develops signs or symptoms of an aortic aneurysm or of coronary artery damage with thrombosis. Ordinarily, however, a syphilitic does not die of his infection in the earlier stages, or even in the later stages, unless one of the vital organs is involved. A more severe secondary infection, such as tuberculosis, sets in, from the lowered vitality of the syphilitic infection, which kills him off. The writer still remembers the quaint aphorism that used to ' be dinned into him during his student days Syphilis is the bed on which tubercle is born'. In a general hospitalif a patient comes with symptoms of any disease that cannot be directly referable to a syphilitic infection, these symptoms get diagnosed and treated; and it is only when this treatment becomes unsuccessful, partially or



that syphilis is thought of. Many cases get involved in a serious major operation, avoidable at any rate in some of them. The clinical history and the subsequent post-mortem examination of a recent case admitted into the Rangoon General Hospital lends colour to the contention that a Wassermann reaction of blood should be a routine procedure with every admission with the slightest doubt about the diagnosis, before treatment is commenced.


J. A., aged 30 years, was admitted oil the morning of 20th June, 1939, for the treatment of persistent vomiting which started about 2 a.m. that day. On admission he complained of giddiness and vomited twice within the space of half an hour. Vomiting was effortless and projectile in character and seemed to have no relationship to food. Patient was quite conscious and was calling out for a receptacle whenever he felt the desire to vomit. He also complained of occipital headache. There was no histoiy of a previous attack of this kind, nor of injury or fall to account for these acute and sudden symptoms. The patient denied any history of venereal disease. With a provisional diagnosis of cerebral tumour he was admitted into the wards. Temperature 97.6?F., pulse 84 and respiration 20 at this time. In the ward, the patient preferred to lie curled up with the head tilted to one side, away from bright light. The eyes showed a right lateral deviation. Though conscious, he took no active interest in his clinical examination or in the surroundings. He was constantly groaning and looked dull and listless. The pupils were equal and reacted sluggishly to light. Abdomen showed some fullness, but was soft on palpation and tender on deep pressure. There was no enlargement of liver or spleen. A feeble peristalsis could be made out on auscultation of the abdomen. The knee and anklejerks were present. Two mornings later, the staff nurse reported that the patient would not talk or take his feeds, so that nasal feeding was resorted to. He showed at this time a left-sided hemiplegia which was not noticed the previous evening?possibly it came on in the course of the night. He had fewer attacks of vomiting now, though he was still apathetic and unconcerned with his surroundings. Temperature?97.2?F., pulse?94, and respiration?32. Routine stool examination was negative for protozoa, ova, cysts and cell exudates. Suspecting a cerebral neoplasm, the skull was re-rayed ' No abnormality to suggest the with the report presence of a new growth'. In the course of the next few days he seemed to be improving somewhat, having got over his paralytic symptoms and to some extent his gastric symptoms. On the seventh day of admission, it appears he took his feeds in the morning and was able to sit up in bed and use his limbs normally. Towards the evening? about six hours later?he suddenly became worse with intensification of his nausea and a definite left-sided hemiplegia. He died that night after a stay of about a week in the hospital. Post-mortem examination (about four hours after

death) that of a well-developed male, aged about 30 years. Abdomen somewhat distended, rigor mortis in the upper part of the body. On opening the abdomen distension with gas was noticeable chiefly in the colon and the stomach. A loop of jejunum about 18 inches long showed what looked iike a typical hemorrhagic infarction. The mesenteric vessels of this loop were standing out prominently against the pale fatty background. Cutting into the mesentery across the vessels, long worm-like clots were recovered intact from the lumens. The infarcted (?) loop was abruptly cut off on either side from normal looking intestine. No notable changes were seen in the spleen liver,







In the thorax except for a small solid area (about i inch across) in the upper lobe of the left lung, and predominantly a left ventricular hypertrophy nothing grossly abnormal was detected. The valves of the heart looked normal, and the aorta showed a smooth intima. The hypertrophy of the left ventricle wab put down to a possible dilatation of the aortic ring without any damage to the cusps themselves. The a solitary lung lesion was later proved to be hemorrhagic infarct histologically. The cranium was carefully opened up, as the clinical signs and symptoms pointed to a brain lesion (tumour ?). But for a little emptiness of the superficial vessels no gross change was noticeable anywhere. The brain was sliced through various points on the surface after noting the normal appearance and contents of the ventricles. No haemorrhagic focus, nor any softening could be detected in any of these sections. After collecting the blood serum from the cardial chambers for the Wassermann reaction an anatomical diagnosis of syphilis was provisionally made to explain the thrombotic phenomena in the intestine and lunS and the ante-mortem clinical symptoms. Fortunately* also the cerebro-spinal fluid drawn the day before his death was also available for the Wassermann reactionBoth the blood serum and cerebro-spinal fluid were put up the same day for the Wassermann reaction and the reports were ++ for blood and + + + + cerebrospinal fluid. _





to find any other direct evidence to explain the cerebral and the gastrointestinal symptoms, one has to fall back syphilis. Throughout the course of an untreated syphilitic infection, except for the tertiary be gumma, the various manifestations can the minute lesion around the



explained by capillaries from an irritation of the blocking by the treponema of the perivascular lymphatics01 Histologically, this perivascular inflammation

the smaller vessels is so characteristic that it .lS often the first hint of the diagnosis of syphilid Taking the cerebral symptoms first, the early symptoms were those of irritation and later of hemiplegia. Now, it is well known that when a vessel becomes narrowed, fr01*1 inflammation and later a fibrosis of its waW> the rate of flow of blood through such a channe becomes slowed down though the blood pressure tends to be greater at its mouth. This slowing down of a column of blood is probably the mos important prelude to thrombosis. Thrombotic phenomena in the coronaries and elsewhere?a whether from a syphilitic stenosis or from. degenerative sclerosis, have this primary slowing down of the stream for their development. ?*the vaso-motor nerves add to this organic. defe? in the vessel by a spasmodic constriction, a acceleration of the development of the sympto*11 is assured so that the onset would be sudde and acute. Ordinarily, a point in the diagn0-1 of a syphilitic thrombosis, in a vital orga like the brain, is the comparatively development of the signs than those oftn haemorrhagic lesion, though in both these signs, when fully established, may be the sam1 On the basis of a slow clotting of blood some of these cerebral vessels, the of giddiness and headache, of which tn * 1 patient complained, can be explained.




Dec., 1939]









the vessel segment got cut off from

occurred more or

probably when less completely

thrombosis and vaso-constriction

Producing severe amemia of the part supplied by the vessel. For the disappearance of the


one has to suppose that the blocked vessel became patent again to allow the required amount of blood to reach the region of *ts supply. This may easily happen if we suppose that the clot contracted sufficiently ^d the vaso-dilator mechanism again came into play to let it pass on to the venous side. Contraction of a blood clot is such a familiar Phenomenon in vitro but there is no reason this should not take place in vivo also. *he small infarct found in the lung could Possibly be a result of this arterial clot getting into the venous circulation, as Reasoned above, and reaching the lung filter through the branches of the pulmonary artery. The gastro-intestinal symptom of vomiting, described as effortless and projectile, is quite easy of explanation. The post-mortem finding ?f a loop of jejunum definitely cut off from the of the bowel in an infarction suggests that these were symptoms of a paralytic ileus. Acute intestinal obstruction brought about by of a loop or any part of the bowel (like the appendix) is well known to produce hese violent symptoms, which, with their spasmodic nature and absence of a definite ?cal history prior to onset, are apt to be mistaken for a symptom of central origin as lappened in this case. A ' cerebral tumour' ^vas the provisional diagnosis and attempts to substantiate this by rc-rays, etc., led to the Undoing of the clinicians in the correct diagnosis







But for

the Wassermann reactions of the blood and ante-mortem cerebrofluid (which was drawn only as a ^erapeutic measure to relieve pressure) the ante- and post-mortem evidence of syphilis is Very obscure. The aorta in tertiary syphilis in a young man shows the characteristic longindinal Assuring of the intima, so aptly likened 0 the crinkling of a tree bark. In the present ca^e the intima of the aorta was quite smooth and e myocardial hypertrophy of the left side was Put down to a dilatation of the aortic ring rather an to any defect in the cusps of its valve. In ?ne of the other internal organs was there any yphilitic stigma detectable with the naked eye.



A fatal


of cardio-vascular syphilis is escribed in which the signs and symptoms pointed to a tumour of the brain. of these symptoms is attempted from pathological evidence obtained at the Post~ ?r^ni examination. A case for a routine blood I ^0r syphilis, of all cases coming to a hospital v+i a ^aightforward diagnosis, is made out ,


pUte-mortem Applanation



foot of



(Continued from previous column) I am indebted to Mr. B. Veda of the final M. B. class of this college for parts of the clinical history of the case, and to Dr. U Ba Than, f.r.c.s.e., police surgeon, Rangoon m.b., General Hospital, for his kind permission to investigate the case post mortem. Since writing the above paper, the writer came across an editorial on the subject of spasm of the cerebral arteries in the British Medical Journal (1939, i, p. 1292), with obvious significance a propos the views expressed in this paper.

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