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Cerebral capillaries and venules are packed with parasitized erythrocytes and the brain is dotted with small foci of necrosis surrounded by glia (Durck nodes) These ndings have been the basis of several hypotheses (one of which attributes the cerebral symptoms to mechanical obstruction of the vessels), but none is entirely satisfactory Also, it seems unlikely that a disorder of immune mechanisms is directly involved in the pathogenesis (see reviews by Newton et al and by Turner for a discussion of current hypotheses) Usually the neurologic symptoms appear in the second or third week of the infection, but they may be the initial manifestation Children in hyperendemic regions are the ones most susceptible to cerebral malaria Among adults, only pregnant women and nonimmune individuals who discontinue prophylactic medication are liable to CNS involvement (Toro and Roman) Useful laboratory ndings are anemia and parasitized red blood cells.

The CSF may be under increased pressure and sometimes contains a few white blood cells, and the glucose content is normal With Plasmodium vivax infections, there may be drowsiness, confusion, and seizures without invasion of the brain by the parasite Treatment Quinine, chloroquine, and related drugs are curative if the cerebral symptoms are not pronounced, but once coma and convulsions supervene, 20 to 30 percent of patients do not survive It has been stated that that the administration of large doses of dexamethasone, given as soon as cerebral symptoms appear, may be lifesaving, but most studies including those of our colleagues have expressed the view that corticosteroids are ineffective Exchange transfusions may confer a small bene t on survival in severe cases Trypanosomiasis This is a common disease in equatorial Africa and in Central and South America.

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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.

The African type ( sleeping sickness ) is caused by Trypanosoma brucei and is transmitted by several species of the tsetse y There has been an alarming increase in this disease in sub-Saharan Africa during the last two decades The infection begins with a chancre at the site of inoculation and localized lymphadenopathy Posterior cervical adenopathy is highly characteristic of CNS infection (Winterbottom sign); another sign of neurologic interest is pronounced pain at sites of minor injury (called Kerandel hyperesthesia) Later, episodes of parasitemia occur, and at some time during this stage of dissemination, usually in the second year of the infection, the trypanosomes give rise to a diffuse meningoencephalitis The latter expresses itself clinically as a chronic progressive neurologic syndrome consisting of a reversal or disruption of circadian sleep rhythm, vacant facial expression, and in some, ptosis and ophthalmoplegia, dysarthria, and then muteness, seizures, progressive apathy, stupor, and coma..

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