The Hormonal Responses to Generalized Tonic-Clonic Seizures

Abstract

We studied the hormonal responses to a generalized tonic-clonic convulsion in 20 patients with idiopathic or posttraumatic epilepsy (6 patients) or alcohol-withdrawal seizures (14 patients). We found an increase shortly after the seizure in plasma levels of ACTH, beta endorphin, beta lipotropin, prolactin, and vasopressin, and a later increase in plasma cortisol. There was no significant change in levels of growth hormone, luteinizing hormone, follicular stimulating hormone, or plasma renin activity. An increase in plasma ACTH level was accompanied by a rise in beta lipotropin and beta endorphin, and followed by a rise in plasma cortisol. In 2 patients there was no postictal increase in plasma prolactin, despite changes in other hormones. There was no difference in the nature or time course of the hormonal changes in patients with alcohol-withdrawal seizures and those with seizures from other causes. The mechanisms subserving these changes are unknown. Nonspecific stress influences the release of certain hormones, but the absence of a significant growth hormone response suggests that this was probably not responsible for our findings. It is possible that the generalized neuronal discharge of a seizure stimulates the hypothalamus either directly, through specific neurotransmitter changes, or through the release of other substances. One possibility that we are investigating in experimental animals is that endogenous opioids are involved, especially in the release of prolactin.

Delayed hypokalemic paralysis following a convulsion due to alcohol abstinence

“…Although serum K does not usually change significantly in alcohol withdrawal or abstinence, 11 there are other physiological changes, including sympathetic overactivity, 10,11,13 adrenoceptor or dopaminoceptor hypersensitivity, 14 hyperactive glutaminergism, downregulation of c-aminobutyric acid receptors, decreased adenosine transporter sites, an activation of the hypothalamus-pituitary-adrenal axis and increased atrial natriuretic peptide. These are usually proportional to the magnitude of the withdrawal symptoms.…”

“…[9][10][11] The serum K is usually normal or increases slightly in the postictal period, 9,10 but may occasionally decrease due to glucose influx from glycogenogenesis. [10][11][12] Nevertheless, symptomatic hypokalaemia or hypokalaemic paralysis is rarely reported as a complication of convulsion. Therefore, the mechanisms of excessive postictal K fluxes causing acute symptomatic hypokalemia and subsequent paralysis should be discussed.…”

Changes of serum adrenocorticotropic hormone and cortisol levels during sleep seizures

“…There were two patients whose ACTH and cortisol levels did not change after administrated with the highest admissible dose of bemegride, the highest admissible dose of bemegride did cause changes in the EEG, but did not provoke clinical seizures. It has been known that seizures are associated with changes in hormone levels [8,9] , but its exact relationship to electroclinical events was obscure. The present study is hardly to assess the causality between pre-ictal neuronal activity and ACTH: whether the preictal neuronal activities stimulate the CRH release and cause the seizure or the gradually decreased ACTH levels during the night trigger the CRH release and induce the pre-ictal and ictal neuronal activities.…”

Induction of Pituitary Adenylate Cyclase-Activating Polypeptide mRNA in the Medial Parvocellular Part of the Paraventricular Nucleus of Rats following Kainic-Acid-Induced Seizure

“…Seizure is known to cause autonomic, neuroendocrine and stress responses as well as intensive recurrent neuronal discharge and neurochemical changes [14, 15, 16, 17, 18]. Activation of the HPA axis has been demonstrated in temporal lobe epileptic patients [15], and seizure is shown to induce the expression of several hypothalamic genes in the PVN including CRH [19, 20, 21]which may play an important role in the interaction among autonomic, neuroendocrine and stress responses to seizure [14, 15, 16, 19, 20, 21].…”

“…Activation of the HPA axis has been demonstrated in temporal lobe epileptic patients [15], and seizure is shown to induce the expression of several hypothalamic genes in the PVN including CRH [19, 20, 21]which may play an important role in the interaction among autonomic, neuroendocrine and stress responses to seizure [14, 15, 16, 19, 20, 21]. Therefore, we raised the possibility that seizure may induce the expression of the PACAP gene in the mpPVN.…”