The cerebral spinalfluid shows an elevation of pressure and protein but no pleocytosis. Fourteen days following the mosquito bite the patient develops prodromal chills, spiking fever, which progresses to intense headache and muscle pain. The pathogenesis of cerebral malaria is a mechanical distortion of the bloodvessels due to rapid proliferation of the parasites, causing stagnation ofblood, or possibly some toxic effect on the vascular endothelium or an immune complex vasculitis. Treatment of cerebral malaria is with intravenous quinine. Glucocorticosteroids, used to treat cerebral edema, have been shown to prolong the coma and increase complications without affecting mortality and now appear to be contraindicated in cerebral malaria.
Viral meningitis produces a milder clinical syndrome than in bacterial meningitis.
The patient has a mild headache, less prominent meningeal irritation, and spinal fluid analysis reveals a elevated white blood cell count that is predominantly lymphocytic. Viral encephalitis is divided into two categories, infectious encephalitis, due to the direct effects of the virus, and parainfectious encephalitis, due to associated reactions in immune system affecting the central nervous system. Para-infectious complications include a perivenous inflammatory response and leucoencephalitis. Other post infectious syndromes include cerebellar ataxia, and peripheral nerve disorders, such as Guillain-Barre syndrome. The characteristic clinical course for herpes simplex encephalitis is an acute or subacute syndrome of headache, fever, behavioraldisturbance, seizures and progressive cortical dysfunction.