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Psychoneuroendocrine Aspects of Temporolimbic Epilepsy

Part I. Brain, Reproductive Steroids, and Emotions

Received April 28, 1998; revised September 10, 1998; accepted October 6, 1998. From Harvard Neuroendocrine Unit, Beth Israel Deaconess Medical Center, Department of Neurology, Harvard Medical School, Boston, MA. Address reprint requests to Dr. Herzog, Neuroendocrine Unit, Beth Israel Deaconess Medical Center, 330 Brookline Ave., Boston, MA 02215.

The temporolimbic structures of the brain that subserve emotional representation are highly epileptogenic and play an important role in the modulation of hormonal secretion and mediation of hormonal feedback. Estrogen is highly epileptogenic and exerts energizing and antidepressant effects. Excessive estrogen influence produces anxiety, agitation, irritability, and lability. It can promote the development of anxiety manifestations (e.g., panic, phobias, and obsessive-compulsive disorder). Progesterone and its metabolites inhibit kindling and seizure activity. They have potent anxiolytic effects, possibly by virtue of their GABAergic activity. Excessive progesterone influence produces sedation and depression. Testosterone has two major metabolites: estradiol, which can exacerbate seizures, and dihydrotestosterone, which blocks NMDA-type glutamate transmission and may be responsible for antiseizure effects. Testosterone has energizing effects and increases sexual desire in both men and women. In excess, however, it may promote aggressive, impulsive, and hypersexual behavior. Hormonal effects tend to be exaggerated or idiosyncratic in the setting of an abnormal or anomalous temporolimbic substrate, especially temporolimbic epilepsy. This may reflect altered neuronal responsivity to hormonal exposure perhaps by virtue of changes in the number of dendritic spines and receptors.

Key Words: Epilepsy • Neuropsychiatric Disorders

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