Frequently, the CSF serology remains positive, despite repeated courses of therapy and the subsidence of all signs of inflammatory activity. When this occurs, it may be safely concluded that the syphilitic inflammation in the nervous system is burned out and that further progression of the disease probably will not occur. If treatment restores the CSF to normal, particularly the cell count and protein, arrest of the clinical symptoms almost always occurs. A return of cells and elevation of protein precedes or accompanies clinical relapse.
Serologic diagnosis of syphilis This depends on the demonstration of one of two types of antibodies: nonspecific or nontreponemal (regain, RPR) antibodies and specific treponemal antibodies. The common tests for reagin, which uses a rapid complement fixation technique, and the venereal disease research laboratory (VDRL) slide test, which uses a flocculation technique. The reagin tests, if positive in the CSF, are virtually diagnostic of neurosyphilis. Serum reactivity alone demonstrates exposure to the organism in the past, but does not imply the presence of neurosyphilis. However, serum reagin tests are negative in a significant proportion of patients with late syphilis and in those with neurosyphilis in particular (seronegative syphilis). In such patients (and in patients with suspected false-positive test in the serum) it is essential to employ tests for antibodies that are directed specifically against treponemal antigens. The latter are positive in the serum of practically every instance of neurosyphilis. The fluorescent treponemal antibody absorption (FTA-ABS) test is more than adequate for most clinical situations. The
T. pallidum immobilization (TPI) test is the most reliable, but it is expensive, difficult to perform, and available in only a few laboratories.
Principal Types of Neurosyphilis
In this condition, there are no symptoms or physical signs except, in rare cases, abnormal pupils, which are light-unreactive but constrict as part of the near response (accommodate with convergence) (Argyll Robertson pupils, Chap. 13). The diagnosis is based entirely on the CSF findings, which vary, as mentioned above.
Symptoms of meningeal involvement may occur at any time after infection but typically does so within the first 2 years. The most common symptoms are headache, stiff neck, cranial-nerve palsies, convulsions, and mental confusion. Occasionally, headache, papilledema, nausea, and vomiting—as a result of the presence of increased intracranial pressure—are added to the clinical picture. The patient is afebrile, unlike the case in tuberculous meningitis. The CSF always has a lymphocytic reaction, more so than in asymptomatic syphilitic meningitis. Obviously, the meningitis is more intense in the symptomatic type and may be associated with hydrocephalus. With adequate treatment, the prognosis is good. The symptoms usually disappear within days to weeks, but if the CSF remains abnormal, it is likely that some other form of neurosyphilis will subsequently develop if treatment is not continued.
As indicated earlier, this clinical syndrome is now probably the most common form of neurosyphilis. Whereas in the past, strokes from syphilitic meningitis accounted for only 10 percent of neurosyphilitic syndromes, their frequency is now estimated to be 35 percent. The most common time of occurrence of meningovascular syphilis is 6 to 7 years after the original infection, but it may be as early as 9 months or as late as 10 to 12 years. It is therefore the main manifestation of what has been termed “secondary syphilis.”
The CSF almost always shows some abnormality, usually an increase in cells, protein content, and gamma globulin, as well as a positive serologic test.