Differential Response of Growth Hormone, Cortisol, and Prolactin to Seizures and to Stress

Culebras, Antonio; Miller, Myron; Bertram, Leelo; Koch, John C.

doi:10.1111/j.1528-1157.1987.tb03689.x

Cited by 48 publications

(30 citation statements)

References 19 publications

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“…1,2 Cortisol is released by activation of the hypothalamic-pituitary-adrenal (HPA) axis in response to a stressor. 3 People with epilepsy have higher basal levels of cortisol than people without; the level further increases after seizures, in adults, 4,5 but not in children. 6 Increased seizure frequency in people with epilepsy is associated with high cortisol levels.…”

Section: Introductionmentioning

confidence: 99%

The relation between cortisol and functional connectivity in people with and without stress‐sensitive epilepsy

et al. 2017

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SummaryObjective: The most common reported seizure-precipitant is stress. We recently showed a biologic basis for stress sensitivity of seizures: cortisol levels in people with stress-sensitive epilepsy correlated with focal interictal epileptiform discharges (IEDs) on electroencephalography (EEG). Here we aimed to determine whether the effect of cortisol on the epileptic brain is global or focal, and whether cortisol affects all brains or just those of stress-sensitive people. Because epilepsy is associated with changes in functional brain connectivity, we studied the relationship between cortisol and changes in global and focal (node-centered) functional connectivity measures for individuals with stress-sensitive and non-stresssensitive epilepsy. Methods: Seventeen people with epilepsy underwent long-term (>24 h) EEG recording. During the first 5 h after waking, saliva was collected every 15 min for cortisol measurements. Theta-band functional connectivity was assessed for every 15 min of the recording. We calculated the average phase-lag index (PLI) between all channels as a measure of global functional connectivity. We used network Strength, the averaged PLI per channel, as focal functional connectivity measure. We correlated cortisol, global, and focal functional connectivity (Strength) with IED frequency using linear mixed models. Analyses were split for people with and without stress-sensitivity of seizures. Results: Cortisol was negatively correlated with global functional connectivity in people with stress-sensitive seizures (estimate À0.0020; P < .01), whereas not in those without stress-sensitivity (estimate À0.0003; P = .46). This relationship occurred irrespective of the presence of IEDs on a channel (channels without IEDs and stress-sensitivity: estimate À0.0019; P < .01, non-stress-sensitive À0.0003; P = .41). Global and focal functional connectivity were negatively correlated with IED frequency, irrespective of stress sensitivity of seizures or channel type. Significance: People with stress-sensitive epilepsy have a whole-brain neuronal response to cortisol that is different from that of people with non-stress-sensitive epilepsy. This offers a basis for understanding seizure genesis in stress-sensitive epilepsy, which might require a different treatment approach.

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Section: Introductionmentioning

confidence: 99%

The relation between cortisol and functional connectivity in people with and without stress‐sensitive epilepsy

et al. 2017

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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: 71%

“…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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“…i) Melatonin-mediated restoration of a disrupted hypothalamic-pituitary-adrenal axisClinical data and experimental models have shown that the HPA axis is hyperexcited in 22 epilepsy (Culebras et al, 1987;Mazarati et al, 2009;O'Toole et al, 2014) and in depression (Cai et al, 2013;Chen et al, 2015) and that melatonin can correct glucocorticoid-induced HPA axis disruption (Konakchieva et al, 1998). Because stress responses are regulated by the hypothalamic paraventicular nucleus (Laryea et al, 2013), and MT2 receptors are present in this area (Lacoste et al, 2015), we may speculate that melatonin could correct HPA axis disruption by acting on these receptors.…”

Section: Molecular Mechanisms Linking Epilepsy and Comorbid Anxiety Amentioning

confidence: 99%

The role of the melatoninergic system in epilepsy and comorbid psychiatric disorders

Tchekalarova

Moyanova

Fusco

et al. 2015

Brain Research Bulletin

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Abstract\ud \ud There is emerging evidence of the beneficial role of the melatonin system in a wide range of psychiatric and neurologic disorders, including anxiety, depression, and epilepsy. Although melatoninergic drugs have chronobiotic and antioxidant properties that positively influence circadian rhythm desynchronization and neuroprotection in neurodegenerative disorders, studies examining the use of melatonin for epilepsy's comorbid psychiatric and neurological symptomatology are still limited. Preclinical and clinical findings on the beneficial effects of the melatonin system on anxiety, depression, and epilepsy suggest that melatoninergic compounds might be effective in treating comorbid behavioral complications in epilepsy beyond regulation of a disturbed sleep-wake cycle

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Differential Response of Growth Hormone, Cortisol, and Prolactin to Seizures and to Stress

Cited by 48 publications

References 19 publications

The relation between cortisol and functional connectivity in people with and without stress‐sensitive epilepsy

The relation between cortisol and functional connectivity in people with and without stress‐sensitive epilepsy

Paradoxical GH response to TRH during status epilepticus in man

The role of the melatoninergic system in epilepsy and comorbid psychiatric disorders

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