Noradrenergic and/or serotonergic deficits, as well as other abnormalities, may contribute to predisposition to some
epilepsies and depressions. Evidence for this hypothesis stems from several sources. Epidemiological investigations are intriguing but incomplete. Pharmacological studies show that noradrenergic and/or serotonergic transmission are both
anticonvulsant and
antidepressant. Therapeutically pertinent investigations show that
antidepressant drugs have
anticonvulsant properties, whereas
antiepileptic drugs are effective in the management of
affective disorders. Additional investigations demonstrate that
seizures, whether spontaneously occurring or therapeutically induced, protect against depression. Through studies of innate pathophysiology, noradrenergic and serotonergic deficits have been identified in individuals with depression and in animal models of
epilepsy, as well as in some humans with
epilepsy.
Vagal nerve stimulation, a treatment already known to be effective in the
epilepsies, is presently under investigation for effectiveness in
affective disorder. New evidence suggests that
vagal nerve stimulation exerts at least some of its
therapeutic effects through its capacity to increase noradrenergic and serotonergic transmission. Finally, emerging evidence supports the concept that some genetic mammalian models of the human
epilepsies exhibit analogous manifestations of depression.