An occasional complication of influenza, chickenpox, and a few other viral diseases in children under 14 years of age is Reye’s syndrome. After the initial infection has disappeared, the child suddenly begins to vomit persistently and experiences convulsions followed by delirium and a coma. Pathologically, the brain swells with injury to the neuronal mitochondria, fatty infiltration into the liver occurs, blood ammonia is elevated, and both serum glutamic oxaloacetic transaminase (SGOT) and serum glutamic pyruvic transaminase (SGPT) are elevated in the blood. Diagnosis is made by the measurement of the levels of these enzymes and ammonia.
The relationship between the initial viral infection and the brain and liver damage is unknown. Treatment is nonspecific and directed toward reducing intracranial pressure and correcting metabolic and electrolyte abnormalities. Some children who recover have residual neurologicaldeficits impaired mental capacity, seizures, and hemiplegia (paralysis on one side of the body). Mortality ranges from 10 to 40%. It is suspected that the use of aspirin or salicylate containing products to lower the initial viral fever increases one’s chances of acquiring Reye’s syndrome.
Another condition that involves the central nervous system and is associated with influenza infections is Guillain-Barré syndrome (some- times called French polio). In this disorder the individual suffers a delayed reaction (usually within 8 weeks) either to the actual virus infection or to vaccines against influenza. The virus or viral antigen in the vaccine damages the Schwann cells that myelinate the peripheral nerves and thus causes demyelination. As a result a prominent feature of this syndrome is a symmetric weakness of the extremities and sensory loss. Fortunately recovery usually is complete because the remaining undamaged Schwann cells eventually proliferate and wrap around the demyelinated nerves.
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