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ment may be found on the contrast-enhanced MRI, as described by Sherman and Stern and by Christoforidis et al The intensity of enhancement may be reduced after the administration of corticosteroids for several days There is indeed a wide variety of changes that has been described on MRI Positron emission tomography may be helpful by demonstrating increased activity that corresponds to a brain or cord lesion and also by revealing increased activity at the site of involved pulmonary lymph nodes Radionuclide scanning with gallium67 shows uptake in the chest, spleen, salivary or lacrimal glands in almost half of patients and can be a useful ancillary test Test material for the formerly popular Kveim-Siltzback skin reaction (a homogenate of spleen or lymph node from patients with known sarcoid) is no longer generally available It has also been found that sarcoid can give rise to a noncaseating epithelioid granuloma at the site of a Mantoux test (for tuberculosis) placed on the skin of the forearm (a skin biopsy is necessary to demonstrate it), but we do not know the validity of this test The latency in development of the granuloma (up to 6 weeks), during which time corticosteroids cannot be given, and a limited rate of positivity (less than two-thirds of patients) also reduce this test s usefulness (see Mankodi et al) Delayed hypersensitivity skin reactions to other antigens are frequently depressed Mild anemia, lymphocytopenia (occasional eosinophilia), slightly elevated sedimentation rate, hypercalcemia, and hyperglobulinemia are common ndings in active disease Serum levels of angiotensin-converting enzyme (ACE) are increased in two-thirds of the patients but seem to us to be less helpful in the diagnosis of CNS involvement It is not clear if the concentration of ACE in the spinal uid is expected to be increased in CNS sarcoid Obviously, evidence of primary sarcoidosis in the mediastinum and lungs should be sought in these cases by chest x-ray and CT scan The differential diagnosis of what has been termed neurosarcoidosis is quite broad and includes multiple sclerosis as well as a number of other entities such as Sjogren syndrome, systemic lupus, lymphoma, isolated angiitis of the CNS, intravascular lymphoma, leprosy, cryptococcosis and other fungal infections that cause abscesses and meningitis, toxoplasmosis, brucellosis, syphilis, Wegener granulomatosis, and, of course, tuberculosis Treatment Administration of corticosteroids is the main therapy, but it has not been subjected to scrutiny in an adequate trial Cyclosporine can be used when the patient cannot tolerate steroids or as an adjunctive treatment to reduce the dose of steroid Other immunosuppressive drugs have not proved to be as effective; methotrexate, cyclophosphamide, chloroquine, and radiation of focal lesions have found favor in various clinics, but again, the results are dif cult to judge The major problem is in knowing when to treat the patient, because the disease may remit spontaneously in about half the cases The recent onset of neurologic symptoms, indicating an active phase of the disease, or a disabling syndrome such as myelopathy are the most certain indications for steroid therapy One approach is to use prednisone in divided daily doses of 40 mg, given for 2 weeks, followed by 2-week periods in which the dose is reduced by 5 mg, until a maintenance dose of 20 to 10 mg on alternate days is reached Therapy should be continued for at least 6 months and in many cases is required for several years
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the advent of penicillin In the United States, for instance, the rate of rst admissions to mental hospitals because of neurosyphilis fell from 43 per 100,000 population (in 1946) to 04 per 100,000 (in 1960) However, in more recent years, the number of reported cases of early syphilis has increased, both in nonimmunocompromised individuals and particularly in HIV-infected ones One may logically anticipate an increase in late syphilis, including neurosyphilis, as these patients live longer Notable also is the shift in clinical presentation of neurosyphilis from parenchymal damage, now quite rare, to one of chronic meningovascular disease, particularly in patients with AIDS Congenital syphilis represents a special problem, which is discussed with developmental diseases in Chap 37 Etiology and Pathogenesis Syphilis is caused by Treponema pallidum, a slender, spiral, motile organism The biologic characteristics of this organism and the natural history of the disease it produces are described in Harrison s Principles of Internal Medicine, which may be consulted as an introduction to the following discussion In this chapter, only the basic facts regarding the neurosyphilitic infection are enumerated The following ones have been well established by clinical and postmortem observation; without knowing them, it is not possible to treat patients with syphilis intelligently (Fig 32-5) The treponeme usually invades the CNS within 3 to 18 months of inoculation with the organism If the nervous system is not involved by the end of the second year, as shown by completely negative CSF, there is only 1 chance in 20 that the patient will develop neurosyphilis as a result of the original infection; if the CSF is negative at the end of 5 years, the likelihood of developing neurosyphilis falls to 1 percent 2 The initial event in the neurosyphilitic infection is a meningitis, which occurs in about 25 percent of all cases of syphilis Usually the meningitis is asymptomatic and can be discovered only by lumbar puncture Exceptionally, it is more intense and causes cranial nerve palsies, seizures, apoplectic phenomena (due to associated vascular lesions), and symptoms of increased intracranial pressure As a corollary, the occurrence of these symptoms in a young adult should always suggest the possibility of neurosyphilis and requires examination of the CSF 3 This meningitis may persist in an asymptomatic state and ultimately, after a period of years, may lead to parenchymal damage In some cases, however, there is a natural subsidence of the meningitis a spontaneous regression 4 All forms of neurosyphilis begin as a meningitis, and a more or less active meningeal in ammation is the invariable accompaniment of all forms of neurosyphilis The early clinical syndromes are meningitis and meningovascular syphilis; the late ones are vascular syphilis (1 to 12 years), followed later by general paresis, tabes dorsalis, optic atrophy, and meningomyelitis The latter are pathologic sequences that result from chronic syphilitic meningitis The intermediate pathologic stages whether by transformation of a persistent asymptomatic syphilitic meningitis or a relapsing meningitis to the late forms of parenchymal neurosyphilis are unknown 5 From a clinical point of view, asymptomatic neurosyphilis is the most important form of neurosyphilis If all cases of asymptomatic neurosyphilis were discovered and adequately 1
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