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treated, the symptomatic varieties would in most instances be prevented Since asymptomatic neurosyphilis can be recognized only by the changes in the CSF, it is axiomatic that all patients with syphilis should have a spinal uid examination 6 Clinical syndromes such as syphilitic meningitis, meningovascular syphilis, general paresis, tabes dorsalis, optic atrophy, and meningomyelitis are abstractions, which at autopsy seldom exist in pure form Since all of them appear to have a common origin in a meningitis, there is usually a combination of two or more syndromes, eg, meningitis and vascular syphilis, tabes and paresis, etc Even though the patient s symptoms may have been referable to only one part of the nervous system, postmortem examination usually discloses diffuse changes, in both brain and spinal cord, which were of insuf cient severity to be detected clinically 7 The clinical syndromes and pathologic reactions of congenital syphilis are similar to those of the late acquired forms, differing only in the age at which they occur All the aforementioned biologic events are equally applicable to congenital and childhood neurosyphilis 8 The CSF is a sensitive indicator of the presence of active neurosyphilitic infection The CSF abnormalities consist of (a) a pleocytosis of up to 100 cells per cubic millimeter, sometimes higher, mostly lymphocytes and a few plasma cells and other mononuclear cells (the counts may be lower in patients with AIDS and those with leukopenia); (b) elevation of the total protein, from 40 to 200 mg/dL; (c) an increase in gamma globulin (IgG), usually with oligoclonal banding; and (d) positive serologic tests The glucose content is usually normal In congenital (but not adult) neurosyphilis, the earliest changes in the CSF, consisting of pleocytosis and an elevation of protein, may occur in the rst few weeks of the infection, before the serologic tests become positive Later, the CSF changes may vary With either spontaneous.

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or therapeutic remission of the disease, the cells disappear rst; next the total protein returns to normal; and then the gamma globulin concentration is reduced The positive serologic tests are the last to revert to normal Frequently the CSF serology remains positive, despite repeated courses of therapy and the subsidence of all signs of in ammatory activity When this occurs, it may be safely concluded that the syphilitic in ammation 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 nonspeci c or nontreponemal (reagin) antibodies and speci c treponemal antibodies The common tests for reagin are the Kolmer, which uses a complement xation technique, and the Venereal Disease Research Laboratory (VDRL) slide test, which uses a occulation technique These reagin tests, if positive in the CSF, are 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 signi cant 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 reagin tests), it is essential to employ tests for antibodies that are directed speci cally against treponemal antigens The latter are positive in the serum of practically every instance of neurosyphilis The uorescent treponemal antibody absorption (FTA-ABS) test is the one in common use and is more than adequate for the majority of clinical situations The T pallidum immobilization (TPI) test is the most reliable, but it is expensive, dif cult to perform, and available in only a few laboratories.

These de cits are also demonstrated most clearly in the parkinsonian patient The prevailing posture is one of involuntary exion of the trunk and limbs and of the neck The inability of the patient to make appropriate postural adjustments to tilting or falling and his inability to move from the reclining to the standing position are closely related phenomena A gentle push on the patient s sternum or back may cause a fall or start a series of small corrective steps that the patient cannot control (festination) These postural abnormalities are not attributable to weakness or to defects in proprioceptive, labyrinthine, or visual function, the principal forces that control the normal posture of the head and trunk Anticipatory and compensatory righting re exes are also manifestly impaired This occurs early in the course of progressive supranuclear palsy and later in Parkinson disease A point of interest is whether akinesia and disorders of postural xation are invariable negative manifestations of all extrapyramidal diseases and whether, without them, there could be any secondary release effects such as dystonia, choreoathetosis, and rigidity The question has no clear answer Akinesia and abnormalities of posture are constant features of both Parkinson and Wilson diseases; they seem to be present also in Huntington chorea and in the athetosis of cerebral palsy, but one cannot be sure of their existence in hemiballismus

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