Role of Monoaminergic Systems of the CNS in Different Periods after Status Epilepticus and Its Relation to Cerebral Hemodynamics

Abstract

Changes in the monoaminergic mechanisms in the brain at different terms after status epilepticus are determined by diverse causes and depend on the role of monoamines in the implementation of specific postictal rearrangements in CNS. Two mutually aggravating pathways cause disorders of monoaminergic mechanisms in the brain in 24 h after epileptic status: high spike-wave activity accompanied by hypocirculation that form a vicious circle; the resulting deficiency of monoamine consolidates the self-sustaining epileptic circuit. Increased activity of monoaminergic mechanisms in 5 days after epileptic status is a result of compensatory-restorative reorganization of neuronal networks and is not accompanied by spike-wave activity and hemodynamics disorders, but high convulsive readiness persists. Disturbances of monoaminergic mechanisms in 30 days after epileptic status prolong convulsive readiness that can serve as a pathogenetic basis for delayed cerebral disorders.