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Hypernatremic dehydration was induced in rabbits during a 3- to 5-day period resulting in mean plasma sodium concentrations of 187 meq/liter. The animals were then rehydrated during a 4-h period by intravenous administration of a 2.5% glucose or fructose solution. The water content of four regions of brain sample showed a significant (P less than 0.05) increase in brain water content above normal in the rehydrated groups. Brain water content was significantly (P less than 0.01) greater in those animals with seizures compared with those without seizures, suggesting the importance of water intoxication in the pathogenesis of seizure activity. Changes in muscle Na, K, Cl, and water content were not similar to those of brain, indicating that muscle content of these substances was not an accurate reflection of the brain content specific time. The incidence of seizures was significantly (P less than 0.05) greater when glucose solution was used for rehydration (49%) compared with the use of fructose solution (25%). The mechanism(s) by which fructose resulted in a lower incidence of seizures is not known. The frequency of seizure activity was directly proportional to the rate of administration of intravenous solutions utilized to correct hypernatremia. In addition, the specific carbohydrate of the solution appeared to play an important role in the pathophysiology of the development of seizures.

This article discusses the management of seizure disorders, stressing selected aspects including (1) the pharmacology of drugs used in the control of seizures, especially the usefulness of measuring concentrations of anticonvulsants in blood in guiding therapy; (2) the treatment of prolonged seizures, particularly status epilepticus, in infants and children; (3) the use of the ketogenic diet as an adjunct in the therapy of epilepsy; and (4) the place of surgical treatment in the control of seizures resistant to medical management.

Herpes simplex virus was instilled in the conjunctival sac of six rabbits; four of these animals developed clinical evidence of encephalitis within 6–10 days and died of their disease within 1–4 days. In these animals EEG tracings showed the development of seizure discharges occurring on a background of irregular slow waves. These EEG changes appeared before definite clinical evidence of encephalitis in every animal. In the two animals which survived, no such changes were seen over a 6 week period following inoculation of virus.