Hypothalamo-pituitary-adrenal axis abnormalities in depression: a review and a model

1989 ◽  
Vol 19 (2) ◽  
pp. 331-336 ◽  
Author(s):  
Bruce G. Charlton ◽  
I. Nicol Ferrier
Keyword(s):  
Hpa Axis ◽  
Future Experiment ◽  
Hormone Regulation ◽  
Corticotropin Releasing Hormone ◽  
Releasing Hormone ◽  
Adrenal Axis ◽  
Recent Advances ◽  
Wide Range ◽  
Pituitary Adrenal Axis

SynopsisA wide range of abnormalities of the hypothalamo-pituitary-adrenal (HPA) axis has been described in depression. This paper reviews recent advances in the understanding of this system, and draws them together to construct a model for the purposes of further research and discussion. It is proposed that there are two fundamental changes which both originate in the hypothalamus: an increased secretion of corticotropin-releasing hormone, and a neurally mediated adrenal hyper-responsivity to ACTH. The resulting changes in hormone regulation would be expected to produce all the characteristic HPA axis abnormalities commonly seen in depression. The model makes several predictions which could be tested by future experiment.

Opioid Control of the Hypothalamus-Pituitary-Adrenal Axis Cyclically Fails in Menstrual Migraine

Cephalalgia ◽  
1990 ◽  
Vol 10 (1) ◽  
pp. 51-56 ◽  
Author(s):  
Fabio Facchinetti ◽  
Emilia Martignoni ◽  
Loridine Fioroni ◽  
Grazia Sances ◽  
Andrea R Genazzani
Keyword(s):  
Menstrual Cycle ◽  
Follicular Phase ◽  
Menstrual Migraine ◽  
Cycle Phase ◽  
Corticotropin Releasing Hormone ◽  
Menstrual Cycle Phase ◽  
Releasing Hormone ◽  
Adrenal Axis ◽  
Hypothalamus Pituitary Adrenal Axis ◽  
Pituitary Adrenal Axis

To assess the biological correlates of the precipitation of migraine attacks in the perimenstrual period, plasma b-endorphin (b-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 b-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 b-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 b-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 b-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.

Sign in / Sign up

Export Citation Format

Share Document