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Published on: June 18, 2014
Circadian regulation of cortisol after hippocampal damage in humans
Tony W Buchanan1, Simone Kern, John S Allen
1Department of Neurology, University of Iowa, 200 Hawkins Drive, Iowa City, IA 52242, USA. tony-buchanan@uiowa.edu
Insights
Hippocampal damage in humans eliminates the cortisol awakening response, impacting the hypothalamic-pituitary-adrenocortical (HPA) axis. This suggests a specific role for the hippocampus in regulating basal cortisol secretion.
Area of Science:
- Neuroendocrinology
- Human Physiology
- Brain Function
Background:
- The hippocampus (HC) is known to influence the hypothalamic-pituitary-adrenocortical (HPA) axis.
- Animal studies show HC damage alters diurnal and stress-related HPA activity.
Purpose of the Study:
- To investigate the impact of hippocampal damage on basal cortisol secretion in humans.
- To determine if HC damage affects diurnal cortisol patterns.
Main Methods:
- Salivary cortisol was measured across a single day in patients with HC damage, brain-injured controls, and healthy controls.
- Quantitative MRI assessed hippocampal volumes in brain-injured patients.
Main Results:
- Bilateral and unilateral HC damage abolished the cortisol awakening response.
- The overall diurnal cortisol pattern remained unaffected in HC patients.
- No correlation was found between hippocampal volume and cortisol secretion.
Conclusions:
- Hippocampal damage in humans specifically abolishes the cortisol response to awakening.
- The hippocampus plays a unique role in controlling basal cortisol secretion, particularly the awakening response.
Background:
There is substantial evidence that the hippocampus (HC) regulates the activity of the hypothalamic-pituitary-adrenocortical (HPA) axis. Damage to the HC in animals produces a transient alteration in diurnal and stress-related HPA activity. This study was designed to examine the effects of HC damage on basal cortisol secretion in humans.
Methods:
Salivary cortisol was measured in 22 patients with HC damage (12 with bilateral damage and 10 with unilateral damage), 7 brain-damaged comparison participants, 10 healthy, age-matched comparison participants, and 6 of the patients' caregivers. Salivary cortisol samples were taken immediately after awakening, 30 min after awakening, at 8:00 am, 11:00 am, 3:00 pm, 6:00 pm, and at bedtime on a single day. Brain-injured patients underwent a structural magnetic resonance imaging scan to examine quantitative volumes of the HC.
Results:
Both bilateral and unilateral HC damage abolished the cortisol response to awakening documented in the comparison groups. Caregivers of bilateral HC patients showed a reduced response to awakening. The remainder of the circadian pattern was not affected in the HC patients; all groups showed a significant diurnal variation. There was no association between HC volume and cortisol secretion.
Conclusions:
Hippocampal damage in humans abolishes the cortisol response to awakening, whereas the remainder of the diurnal cycle is unaffected in these patients. These data suggest a unique role of the HC in the control of basal cortisol secretion.
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