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We have elaborated the neuropsychiatric features of this disease, even though rare nowadays, because they are manifest almost uniquely as a chronic frontotemporoparietal meningoencephalitis and create a picture unlike that of most degenerative diseases discussed in Chap 39 with the possible exception of the newly popularized and imprecise category of frontotemporal dementia Also, it is well to remember that many of our ideas about the brain and the mind were shaped historically by this disease The blood serology is positive in nearly all cases The CSF is invariably abnormal, usually with 10 to 200 lymphocytes, plasma cells, and other mononuclear cells per cubic millimeter; a total protein of 40 to 200 mg/dL; an elevated gamma globulin; and strongly positive serologic tests The elevated gamma globulin in the CSF is produced intrathecally and has been shown to be adsorbed to T pallidum (Vartdal et al) Hence the gamma globulin (oligoclonal IgG) represents a speci c antibody response to this organism The pathologic changes consist of meningeal thickening, brain atrophy, ventricular enlargement, and granular ependymitis Microscopically, the perivascular spaces are lled with lymphocytes, plasma cells, and mononuclear cells; nerve cells have disappeared; there are numerous rod-shaped microgliacytes and plump astrocytes in parts of the cortex devastated by neuronal loss; iron is deposited in mononuclear cells; and, with special stains, spirochetes are visible in the cortex The changes are most pronounced in the frontal and temporal lobes The ependymal surfaces of the ventricles are studded with granular elevations protruding between ependymal cells (granular ependymitis) Meningeal brosis with obstructive hydrocephalus is present in many cases The prognosis in early treated cases has in the past been fairly good; 35 to 40 percent of patients made some occupational readjustment; in another 40 to 50 percent, the disease was arrested but left the patient dependent Without treatment there is progressive mental decline, and death occurs within 3 to 4 years Tabetic Neurosyphilis (Tabes Dorsalis) This type of neurosyphilis, described by Duchenne in his classic monograph L ataxie locomotrice progressive (1858), usually develops 15 to 20 years after the onset of the infection The major symptoms are lightning pains, ataxia, and urinary incontinence; the chief signs are absent tendon re exes at knee and ankle, impaired vibratory and position sense in feet and legs, and a Romberg sign The ataxia is due purely to the sensory defect Muscular power, by contrast, is fully retained in most cases The pupils are abnormal in over 90 percent of cases, usually Argyll-Robertson in type (see page 242), and the majority of patients show ptosis or some degree of ophthalmoplegia Optic atrophy is frequent The lancinating or lightning pains (present in over 90 percent of cases) are, as their name implies, sharp, stabbing, and brief, like a ash of lightning They are more frequent in the legs than elsewhere but roam over the body from face to feet, sometimes playing persistently on one spot like the repeated twanging of a ddle string, as Wilson remarked They may come in bouts lasting several hours or days Pins and needles feelings, coldness, numbness, tingling, and other paresthesias are also present and are associated invariably with impairment of tactile, pain, and thermal sensation The bladder is insensitive and hypotonic, resulting in unpredictable over ow incontinence Constipation and megacolon as well as impotence are other expressions of dysfunction of the sacral roots and ganglia In the established phase of the disease, now seldom seen, ataxia is the most prominent feature The patient totters and stag-
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gers while standing and walking In mild form it is best seen as the patient walks between obstacles or along a straight line, turns suddenly, or halts To correct the instability, the patient places his feet and legs wide apart, exes his body slightly, and repeatedly contracts the extensor muscles of his feet as he sways (la danse des tendons) In moving forward, the patient ings his stiffened leg abruptly, and the foot strikes the oor with a resounding thump in a manner quite unlike that seen in the ataxia of cerebellar disease The patient clatters along in this way with eyes glued to the oor If his vision is blocked, he is rendered helpless When the ataxia is severe, walking becomes impossible despite relatively normal strength of the leg muscles Trophic lesions, perforating ulcers of the feet, and Charcot joints are characteristic complications of the tabetic state The deformity of deafferented Charcot joints occurs in less than 10 percent of tabetics (the most common cause nowadays is diabetic neuropathy) Most often the hips, knees, and ankles are affected but occasionally also the lumbar spine or upper limbs The process generally begins as an osteoarthritis, which, with repeated injury to the insensitive joint, progresses to destruction of the articular surfaces Osseous architecture disintegrates, with fractures, dislocations, and subluxations, only some of which occasion discomfort The arthropathy has been observed to occur as frequently in the burned-out as in the active phase of tabes; hence it is only indirectly related to the syphilitic process Although the basic abnormality appears to be repeated injury to an anesthetic joint, the process need not be painless Presumably a deep and incomplete hypalgesia and loss of autonomic function are enough to interfere with protective mechanisms Sherrington reproduced the joint change in animals deprived of pain sensation Visceral crises represent another interesting manifestation of this disease, now rarely seen The gastric ones are the best known The patient is seized abruptly with epigastric pain that spreads around the body or up over the chest There may be a sense of thoracic constriction as well as nausea and vomiting the latter repeated until nothing but blood-tinged mucus and bile are raised The symptoms may last for several days; a barium swallow sometimes demonstrates pylorospasm The attack subsides as quickly as it came, leaving the patient exhausted, with a soreness of the epigastric skin Intestinal crises with colic and diarrhea, pharyngeal and laryngeal crises with gulping movements and dyspneic attacks, rectal crises with painful tenesmus, and genitourinary crises with strangury and dysuria are all less frequent but well-documented types In most cases now being seen, the CSF is normal when the patient is rst examined (so-called burned-out tabes) In the remainder it is abnormal, but less often than in general paresis Pathologic study reveals a striking thinness and grayness of the posterior roots, principally lumbosacral, and a thinness of the spinal cord due mainly to the degeneration of the posterior columns Only a slight outfall of neurons is observed in the dorsal root ganglia; the peripheral nerves are therefore essentially normal For many years there was an argument as to whether the spirochete rst attacked the posterior columns of the spinal cord, the posterior root as it pierced the pia, the more distal part of the radicular nerve where it acquires its arachnoid and dural sheaths, or the dorsal root ganglion cell The observations of our colleagues of rare active cases have shown the in ammation to be all along the posterior root; the slight dorsal ganglion cell loss and posterior column degeneration were found to be secondary The hypotonia, are exia, and ataxia relate to destruction of
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