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coccal meningitis; in fully one-third of the patients, no cause could be established Charleston and colleagues reported a subgroup of these patients who were responsive to steroids; in 7 of 17 patients, medication could eventually be withdrawn without recurrence; four patients required treatment inde nitely; the remaining 6 died after many months or years The outcome and response to steroids in our cases and other reported series has been much the same These series excluded chemical or irritative meningitis, which should be considered if there has been spinal surgery or infusion of even apparently innocuous substances into the spinal space The special problem of chronic neutrophilic meningitis has been mentioned on page 622 It is usually attributable to Nocardia, Aspergillus, Actinomyces, or certain Mycobacterium species (see Peacock, cited in the preceding chapter) Our practice in the management of patients with chronic meningitis is to repeat the lumbar puncture several times in order to obtain cultures and cytology of CSF, using markers to detect uniform populations of B and T lymphocytes and tumor cells, a biochemical test that is sensitive to neoplastic meningitis (such as 2 microglobulin), PCR for ampli cation of herpesviruses, serologic tests for HIV, syphilis, Lyme disease, Brucella, etc; MRI of the brain and spinal cord with gadolinium should also be performed If hydrocephalus develops, it should be managed along the lines described in Chap 30 A trial of antiviral agents and broad-spectrum antibiotics seems reasonable, although we have had no success with them in our last several patients We resort to a biopsy of the meninges if the diagnosis has not been clari ed in 6 to 12 months or if a febrile meningitis persists for more than several weeks, but this practice has proved to be of limited value In Andersen s series, mentioned above, biopsy yielded a diagnosis in 5 of 25 patients Finally, if bacterial infection has been reasonably excluded, we try corticosteroids for several weeks or longer and then attempt to taper the dose while observing the patient and rechecking the CSF formula The CSF formula, in a number of other chronic or acutely recurring diseases of obscure origin, corresponds to that of aseptic meningitis: (1) The Vogt-Koyanagi-Harada syndrome, which is characterized by combinations of iridocyclitis, depigmentation of a hair strand (poliosis circumscripta) and skin around the eyes, loss of eyelashes, dysacusis, and deafness The course is quite benign, and the pathologic basis of the syndrome is not known (2) Mollaret recurrent meningitis, some (perhaps most) instances of which have been associated with HSV-1 (Steel) and some with HSV-2 infection (Cohen et al) These episodes of acute meningitis, with severe headache and sometimes low-grade fever, lasting for about 2 weeks, may recur for a period of several months or many years In a few such patients of ours, in whom no virus could be identi ed in the CSF, antiviral therapy met with little success, although corticosteroids seemed to reduce the severity of acute episodes, as mentioned above A proportion of these cases follow bouts of genital herpes (3) Allergic or hypersensitivity meningitis, occurring in the course of serum sickness and of connective tissue diseases, such as lupus erythematosus, and in relation to certain medications such as nonsteroidal anti-in ammatory drugs and intravenously administered immunoglobulin; and (4) Behcet disease, which is an important acute, recurrent in ammatory CNS disease It is essentially a diffuse in ammatory disease of small blood vessels and is more appropriately considered with the vasculitides (page 733) In summary, the history of the illness, the associated clinical ndings, and the laboratory tests usually provide the clues to the diagnosis of nonviral and chronic forms of aseptic meningitis It is.

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drawn or birth control pills are introduced suggests a more complex process than simply a small deep infarction perhaps something akin to Sydenham chorea Also, only about one-third of cases involve a stroke, and some have demonstrated hypermetabolism of the basal ganglia, also as in Sydenham chorea A connection between hemichorea and the antiphospholipid syndrome alone, without lupus, is tenuous in our view The use of phenytoin or other anticonvulsant drugs causes chorea in sensitive individuals A transitory chorea may occur in the course of an acute metabolic derangement such as hyperosmolar hyperglycemia, hypoglycemia, or hyponatremia Rarely, chorea complicates hyperthyroidism, polycythemia vera, lupus erythematosus or other forms of cerebral arteritis AIDS has emerged as a cause of a number of subacutely progressive movement disorders, initially asymmetrical in our experience, and chorea has been one manifestation The usual associations have been with focal lesions in or near the basal ganglionic stuctures such as toxoplasmosis, progressive multifocal leukoencephalopathy, and lymphoma, but a number of instances are not explained by any of these An inherited chorea with acanthocytosis of red blood cells has been well described, but the nature of the lesions of the basal ganglia is unknown (Chap 39) A paraneoplastic variety may combine several aspects of chorea with athetosis and ballismus or dystonia; in ammatory lesions are found in the striatum (Chap 31) Chorea may be limited to one side of the body (hemichorea) When the involuntary movements involve proximal limb muscles and are of wide range and inging in nature, the condition is called hemiballismus (see further on) A cerebral infarction is the usual cause A number of rare paroxysmal kinesigenic disorders, discussed later in this chapter, may have a choreic component The review by Piccolo and colleagues puts the frequency of the various causes of chorea in perspective Of a large number of consecutive neurologic admissions to two general hospitals, they identi ed 23 cases of chorea, of which 5 were drug-induced, 5 were AIDS-related, and 6 were due to stroke Sydenham chorea and arteritis were each found in 1 case In 4 cases no cause could be determined, and 1 case proved to have Huntington disease The anatomic basis of chorea is uncertain or at least inconsistent In Huntington chorea, there are obvious lesions in the caudate nucleus and putamen Yet one often observes vascular lesions in these parts without chorea The precise localization of lesions in Sydenham chorea and other choreic diseases has not been determined beyond a generalized disturbance in the striatum, which is evident on some imaging studies It is of interest that in instances of chorea related to acute metabolic disturbances, there are sometimes small infarctions in the basal ganglia or metabolic changes in the lenticular nucleus, as shown by imaging studies One suspects from their close clinical similarity that chorea and hemiballismus relate to disorders of the same system of neurons; however, the subthalamic nucleus is affected only slightly in Huntington chorea Athetosis This term stems from a Greek word meaning un xed or changeable The condition is characterized by an inability to sustain the ngers and toes, tongue, or any other part of the body in one position The maintained posture is interrupted by relatively slow, sinuous, purposeless movements that have a tendency to ow into one another As a rule, the abnormal movements are most pronounced in the digits and hands, face, tongue, and throat, but no group of muscles is spared One can detect as the basic patterns of movement an alternation between extension-pronation and.

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