Abstract
To assess the biological correlates of the precipitation of migraine attacks in the perimenstrual period, plasma β-endorphin (β-EP) and cortisol responses to naloxone (8 mg iv) and corticotropin releasing hormone (100 μg iv) were evaluated in both the follicular phase and the premenstrual period in 7 patients suffering from menstrual migraine and in 7 healthy, asymptomatic control volunteers. In the controls, naloxone evoked a significant release of both β-EP (F = 5.86, p <0.002) and cortisol (F = 4.43, p <0.008), independently of the menstrual cycle phase (F = 0.31 and 1.04, for β-EP and cortisol, respectively). Menstrual migraine patients, on the other hand, showed a significant hormone response only in the follicular phase, not in the premenstrual period. Corticotropin releasing hormone significantly increased β-EP and cortisol in both the controls and the menstrual migraine patients, independently of the menstrual cycle phase. In both the naloxone and corticotropin releasing hormone testings, the basal β-EP levels measured in the premenstrual period were lower than those observed in the follicular phase (p <0.02). These data demonstrate a cyclical, premenstrual dysfunction of the hypothalamic control exerted by opioids on the hypothalamus-pituitary-adrenal axis. Impairment of this fundamental adaptive mechanism (involved in stress responses and in pain control) could establish a causal relationship between menstrual-related migraine attacks and premenstrual opioid hyposensitivity.
| Original language | English |
|---|---|
| Pages (from-to) | 51-56 |
| Number of pages | 6 |
| Journal | Cephalalgia |
| Volume | 10 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - 1990 |
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ASJC Scopus subject areas
- Clinical Neurology
Cite this
Opioid control of the hypothalamus-pituitary-adrenal axis cyclically fails in menstrual migraine. / Facchinetti, F.; Martignoni, E.; Fioroni, L.; Sances, G.; Genazzani, A. R.
In: Cephalalgia, Vol. 10, No. 1, 1990, p. 51-56.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Opioid control of the hypothalamus-pituitary-adrenal axis cyclically fails in menstrual migraine
AU - Facchinetti, F.
AU - Martignoni, E.
AU - Fioroni, L.
AU - Sances, G.
AU - Genazzani, A. R.
PY - 1990
Y1 - 1990
N2 - To assess the biological correlates of the precipitation of migraine attacks in the perimenstrual period, plasma β-endorphin (β-EP) and cortisol responses to naloxone (8 mg iv) and corticotropin releasing hormone (100 μg iv) were evaluated in both the follicular phase and the premenstrual period in 7 patients suffering from menstrual migraine and in 7 healthy, asymptomatic control volunteers. In the controls, naloxone evoked a significant release of both β-EP (F = 5.86, p <0.002) and cortisol (F = 4.43, p <0.008), independently of the menstrual cycle phase (F = 0.31 and 1.04, for β-EP and cortisol, respectively). Menstrual migraine patients, on the other hand, showed a significant hormone response only in the follicular phase, not in the premenstrual period. Corticotropin releasing hormone significantly increased β-EP and cortisol in both the controls and the menstrual migraine patients, independently of the menstrual cycle phase. In both the naloxone and corticotropin releasing hormone testings, the basal β-EP levels measured in the premenstrual period were lower than those observed in the follicular phase (p <0.02). These data demonstrate a cyclical, premenstrual dysfunction of the hypothalamic control exerted by opioids on the hypothalamus-pituitary-adrenal axis. Impairment of this fundamental adaptive mechanism (involved in stress responses and in pain control) could establish a causal relationship between menstrual-related migraine attacks and premenstrual opioid hyposensitivity.
AB - To assess the biological correlates of the precipitation of migraine attacks in the perimenstrual period, plasma β-endorphin (β-EP) and cortisol responses to naloxone (8 mg iv) and corticotropin releasing hormone (100 μg iv) were evaluated in both the follicular phase and the premenstrual period in 7 patients suffering from menstrual migraine and in 7 healthy, asymptomatic control volunteers. In the controls, naloxone evoked a significant release of both β-EP (F = 5.86, p <0.002) and cortisol (F = 4.43, p <0.008), independently of the menstrual cycle phase (F = 0.31 and 1.04, for β-EP and cortisol, respectively). Menstrual migraine patients, on the other hand, showed a significant hormone response only in the follicular phase, not in the premenstrual period. Corticotropin releasing hormone significantly increased β-EP and cortisol in both the controls and the menstrual migraine patients, independently of the menstrual cycle phase. In both the naloxone and corticotropin releasing hormone testings, the basal β-EP levels measured in the premenstrual period were lower than those observed in the follicular phase (p <0.02). These data demonstrate a cyclical, premenstrual dysfunction of the hypothalamic control exerted by opioids on the hypothalamus-pituitary-adrenal axis. Impairment of this fundamental adaptive mechanism (involved in stress responses and in pain control) could establish a causal relationship between menstrual-related migraine attacks and premenstrual opioid hyposensitivity.
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U2 - 10.1046/j.1468-2982.1990.1001051.x
DO - 10.1046/j.1468-2982.1990.1001051.x
M3 - Article
C2 - 2317851
AN - SCOPUS:0025321916
VL - 10
SP - 51
EP - 56
JO - Cephalalgia
JF - Cephalalgia
SN - 0333-1024
IS - 1
ER -