The role of physiological changes occurring during prolonged seizures in the causation of epileptic brain damage has been investigated experimentally in baboons and rats. Prolonged drug-induced myoclonic seizure activity is associated with initial arterial hypertension and subsequent hypotension, increased venous pressure, early hyperglycaemia and subsequent hypoglycaemia, variable arterial hypoxia and lactacidosis, and hyperpyrexia.
Cerebral metabolic rate for oxygen and glucose is increased 2—3 fold throughout prolonged seizures provided the physiological status of the animal is well maintained.
Ischaemic neuronal change is found after seizures lasting 1.5—7 hours, involving the small neurones of the third cortical lamina, Purkinje and basket cells in the cerebellum, and pyramidal neurones in the endfolium and Sommer sector of the hippocampus.
Muscular paralysis and artificial ventilation minimise late physiological changes such as arterial hypotension and hyperpyrexia, and protect against cerebellar damage, but only slightly against neocortical and hippocampal damage. When arterial hypotension, hypoxia or hypoglycaemia lead to a reduction in the intensity of seizure discharge in paralysed, ventilated rats, there is also a reduction in hippocampal and neocortical damage.
Factors intimately related to the intensity and duration of the neuronal discharge are responsible for neocortical and hippocampal lesions.
Status epilepticus - brain damage - febrile convulsions - cerebral metabolism
