Epileptic but Not Psychogenic Seizures Are Accompanied by Simultaneous Elevation of Serum Pituitary Hormones and Cortisol Levels

Rao, Marie Luise; Stefan, H.; Bauer, Jürgen

doi:10.1159/000125088

Cited by 101 publications

(52 citation statements)

References 29 publications

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“…In one study, 19 6 patients with ES had attenuation of mean PRL concentration to 17.5 Ϯ 3.6% of mean peak postictal PRL by 2 hours after seizures. The 2-hour postictal PRL levels were similar to the baseline PRL measured at the same time on the subsequent seizurefree day.…”

mentioning

confidence: 96%

“…One Class I and nine Class II studies compared serum PRL changes following ES and psychogenic NES (table 1). [14][15][16][17][18][19][20][21][22][23] Of these 10 studies, all except one study 15 ascribed psychogenic etiologies to the NES. The terminology of NES was used in one study that did not elaborate on etiology.…”

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confidence: 99%

“…Two Class II studies 14,19 examined the time course of PRL attenuation following ES. In one study, 19 6 patients with ES had attenuation of mean PRL concentration to 17.5 Ϯ 3.6% of mean peak postictal PRL by 2 hours after seizures.…”

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confidence: 99%

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Use of serum prolactin in diagnosing epileptic seizures

Sandstrom

Anschel²

2005

Neurology

213

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Abstract-Objective:The purpose of this article is to review the use of serum prolactin assay in epileptic seizure diagnosis. Methods: The authors identified relevant studies in multiple databases and reference lists. Studies that met inclusion criteria were summarized and rated for quality of evidence, and the results were analyzed and pooled where appropriate. Results: Most studies used a serum prolactin of at least twice baseline value as abnormal. For the differentiation of epileptic seizures from psychogenic nonepileptic seizures, one Class I and seven Class II studies showed that elevated serum prolactin was highly predictive of either generalized tonic-clonic or complex partial seizures. Pooled sensitivity was higher for generalized tonic-clonic seizures (60.0%) than for complex partial seizures (46.1%), while the pooled specificity was similar for both (approximately 96%). Data were insufficient to establish validity for simple partial seizures. Two Class II studies were consistent in showing prolactin elevation after tilt-test-induced syncope. Inconclusive data exist regarding the value of serum prolactin following status epilepticus, repetitive seizures, and neonatal seizures. Recommendations: Elevated serum prolactin assay, when measured in the appropriate clinical setting at 10 to 20 minutes after a suspected event, is a useful adjunct for the differentiation of generalized tonic-clonic or complex partial seizure from psychogenic nonepileptic seizure among adults and older children (Level B). Serum prolactin assay does not distinguish epileptic seizures from syncope (Level B). The use of serum PRL assay has not been established in the evaluation of status epilepticus, repetitive seizures, and neonatal seizures (Level U). NEUROLOGY 2005;65:668-675 Prolactin (PRL) release from the pituitary is controlled by the hypothalamus via a PRL inhibitory factor, now believed to be dopamine.1 It has been hypothesized that ictal epileptic activity in the mesial temporal structures may propagate to the hypothalamus, altering the hypothalamic regulation of PRL release. 2Trimble first demonstrated that generalized tonicclonic seizures, but not nonepileptic seizures (NESs), could raise serum PRL.3 Despite subsequent confirmatory findings, the sensitivity and specificity of serum PRL assay for diagnosis of epileptic seizures (ESs) remain uncertain. Utility of PRL assays for diagnosis of seizures depends upon the study design, standard of seizure classification, and criteria for abnormal PRL elevation. Additional uncertainty arises from the circadian fluctuations of serum PRL, demonstrating surges of 50 to 100% prior to awakening from sleep, although PRL serum levels otherwise are stable during the waking state.4 PRL concentrations usually are higher in females than in males, 5 and higher in persons with epilepsy than in healthy individuals. 6 In a study that measured baseline PRL every 20 minutes over 24 hours in 20 healthy controls and 17 people with epilepsy, 5 no female had baseline PRL exceeding 700 U/mL, and no ...

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Use of serum prolactin in diagnosing epileptic seizures

Sandstrom

Anschel²

2005

Neurology

213

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“…In order to broaden our understanding of how status epilepticus affects hormonal release we have extended our analysis to include GH and cortisol, two other hormones related to the pituitary. The literature on GH levels in connection with epilepsy and single epileptic seizures is sparse, and partly conflicting results have been reported (1,6,(21)(22)(23). To our knowledge, there is no previous information on GH levels in humans with status epilepticus.…”

Section: Journal Of Endocrinology (1999) 140mentioning

confidence: 99%

“…Serum cortisol levels are known to rise after single epileptic seizures (22,23) and seem to remain elevated for up to 12 h after cessation of clinical seizures in status epilepticus in man (28). There seems to be a time factor involved in the GH response to corticoids in man.…”

Section: Journal Of Endocrinology (1999) 140mentioning

confidence: 99%

Paradoxical GH response to TRH during status epilepticus in man

Lindbom¹,

Al²,

Tomson³

1999

European Journal of Endocrinology

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Information on GH in relation to epilepsy is sparse, and to our knowledge there is no information on GH levels during status epilepticus in man. We studied GH in serum in six patients during status epilepticus, and in a control group of six seizure-free patients with epilepsy, before and after injection of TRH. The baseline GH values before TRH administration were within the normal range in all patients. After injection of TRH all patients with status epilepticus showed a paradoxical peak-shaped increase of GH to at least twice their baseline levels within 45 min after the injection (median basal GH value 1.5 mU/l and median peak GH value 6.5 mU/l, mean increase 330%). No uniform reaction to TRH was observed in the control group (median basal GH value 2.7 mU/l and median of the highest value within 45 min 5.2 mU/l). A paradoxical peak reaction of GH to TRH was significantly more frequent in the status epilepticus group compared with the control group (P = 0.008, Fisher exact probability test). TRH is not considered a GH-releasing hormone in humans during normal conditions, but a paradoxical response of GH to TRH, similar to that observed during status epilepticus, has been reported in various other pathological conditions, such as acromegaly, liver cirrhosis, mental depression and hypothyroidism. Our results of GH release after TRH administration in patients with status epilepticus suggest an altered regulation of GH as a result of the long-standing epileptic activity.

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