Postictal hormonal changes

Prolactin shows more consistent postictal changes than other hormones. Postictal testing of hormones other than prolactin is not clinically useful at present, although some changes in hormone levels have been found.

Elevated postictal serum levels of the following hormones have been reported:

  • cortisol (after both bona fide and simulated generalized seizures)93
  • corticotropin, beta-endorphin, and beta-lipotropin (all products of a common precursor molecule, proopiomelanocortin)94
  • vasopressin94

All these hormones are secreted in response to stress, however, so their postictal elevation may not be specific to epileptic seizures.

Inconsistent findings of postictal changes in luteinizing hormone (LH) and follicle-stimulating hormone (FSH) have been found by different authors.94-96

No consistent significant postictal change has been seen in serum levels of growth hormone or thyroid-stimulating hormone (TSH).94,96

Melatonin, which has anticonvulsant properties, was measured in the saliva of persons with intractable temporal lobe epilepsy and healthy controls. The authors found that melatonin levels were decreased compared to controls at baseline, and measured melatonin increased threefold postictally.97

Interictal hormonal changes

The function of the hypothalamo-pituitary-adrenal axis may be altered chronically as well as acutely in seizure patients.93,94 Cortisol has been shown to be elevated interictally in some studies98 but not in others.99 Corticotropin is also elevated interictally in patients with temporal lobe epilepsy (TLE),98 a finding that appears to be related specifically to abnormal functioning of the anterior temporal lobe,98 where the amygdala is located, and to be limited to TLE that involves the amygdala. For instance, stimulation of the amygdala in TLE patients100 (as well as in animals)101 leads to a rise in serum corticosteroids and corticotropin. Stimulation of the hippocampus inhibits their secretion.100

Corticotropin is secreted by the anterior pituitary in response to corticotropin-releasing hormone (CRH) produced by neurons in the paraventricular nucleus of the hypothalamus. These neurons receive a direct input from CRH-containing neurons in the amygdala.102 Postictal and interictal elevation of corticotropin and cortisol after seizures is thus most likely due to activation of the hypothalamic-adrenal axis by the amygdala as a result of ictal and interictal epileptiform discharges.

What are the clinical consequences of this activation? Few have been appreciated to date, but that may be because they have not been specifically looked for. Three cases of reversible Cushing's syndrome and myopathy have been reported in patients with refractory complex partial seizures. The Cushing's syndrome and myopathy fluctuated in parallel with seizure exacerbations. They remitted with normalization of glucocorticoid levels upon treatment with ketoconazole, an inhibitor of adrenal steroidogenesis.103 Ketoconazole also successfully treated the seizures.

Experimental data suggest that interictal activation of the CRH-corticotropin-corticosteroid axis may lead to exacerbation of seizures104,105 and may also contribute to some of the chronic sequelae of poorly controlled chronic TLE associated with hippocampal damage, such as memory impairment.106 No clinical data exist to support this theory, however.

Adapted from: Klein P and Herzog AG. Endocrine aspects of partial seizures. In: Schachter SC, Schomer DL, eds. The comprehensive evaluation and treatment of epilepsy. San Diego, CA: Academic Press; 1997. p. 207-232.
With permission from Elsevier (

Authored By: 
Pavel Klein MD
Andrew G. Herzog MD
Reviewed By: 
Cynthia L. Harden MD
Sunday, February 1, 2004