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The Probable Mechanisms of Brain Damage and Epilepsy in Febrile Convulsions, Singapore‐ Syndrome and Reye's Syndrome
Author(s) -
Aiyathurai Eric J.,
Boon Wong Hock
Publication year - 1989
Publication title -
pediatrics international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.49
H-Index - 63
eISSN - 1442-200X
pISSN - 1328-8067
DOI - 10.1111/j.1442-200x.1989.tb01299.x
Subject(s) - medicine , status epilepticus , epilepsy , hypoxia (environmental) , brain damage , lactic acidosis , cerebral edema , metabolic disorder , cerebral perfusion pressure , anesthesia , hypoglycemia , cardiology , cerebral blood flow , insulin , oxygen , chemistry , organic chemistry , psychiatry
Current knowledge suggests integration of cerebral perfusion and metabolism as enabling normal neuronal function, and their pertubations explaining the brain damage of hypoxia, hypoglycaemia, hypoperfusion and status epilepticus. Similar mechanisms appear operative in the viral encephalopathies and cause psychomotor dysfunction and epilepsy. A transient inhibition of plasma membrane glucose transport is central to the understanding of the metabolic abnormalities of these encephalopathies, the ensuing cell energy crisis resulting from neuroglycopoenia being evidenced by electroencephalographic changes, lactic and ketoacidosis, hyperuricaemia and ionic aberrations. Failure of Na+ and Ca 2+ pumps cause cerebral oedema and neuronal death respectively, the selective nature of the latter being due to α‐adrenergic vasoconstriction. Management with hyperglycaemia‐producing infusions and the judicious use of lactate and steroids can overcome the transport dysfunction and enable complete recovery. The temporal profile of the metabolic aberrations of febrile convulsions, which are the result of adaptation, provide a template supporting this mode of management of the severe encephalopathies.