Loss of Cortisol Circadian Rhythm in Patients with Traumatic Brain Injury: A Microdialysis Evaluation

Llompart‐Pou, Juan Antonio; Pérez, Gerardo; Raurich, J. M.; Riesco, M.; Brell, Marta; Ibáñez, Javier; Pérez-Bárcena, Jon; Abadal, J. M.; Homar, J.; Burguera, Bartolomé

doi:10.1007/s12028-010-9399-1

Cited by 36 publications

(21 citation statements)

References 13 publications

(18 reference statements)

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“…The similarities in morning versus evening cortisol data suggest disruptions in diurnal rhythms. This finding is consistent with other recent data demonstrating data suggesting that diurnal cortisol variation is disrupted after both TBI (Llompart-Pou et al, 2010) and critical illness (Paul and Lemmer, 2007). The rapidly declining serum progesterone levels for both men and women provide a rationale for why both gender groups may benefit from acute progesterone therapy after severe TBI (Wright et al, 2007;Xiao et al, 2008).…”

Section: Fig 5 (A)supporting

confidence: 91%

Acute Serum Hormone Levels: Characterization and Prognosis after Severe Traumatic Brain Injury

Wagner

McCullough

Niyonkuru

et al. 2011

Journal of Neurotrauma

143

155

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Experimental traumatic brain injury (TBI) studies report the neuroprotective effects of female sex steroids on multiple mechanisms of injury, with the clinical assumption that women have hormonally mediated neuroprotection because of the endogenous presence of these hormones. Other literature indicates that testosterone may exacerbate injury. Further, stress hormone abnormalities that accompany critical illness may both amplify or blunt sex steroid levels. To better understand the role of sex steroid exposure in mediating TBI, we 1) characterized temporal profiles of serum gonadal and stress hormones in a population with severe TBI during the acute phases of their injury; and 2) used a biological systems approach to evaluate these hormones as biomarkers predicting global outcome. The study population was 117 adults (28 women; 89 men) with severe TBI. Serum samples (n = 536) were collected for 7 days post-TBI for cortisol, progesterone, testosterone, estradiol, luteinizing hormone (LH), and follicle-stimulating hormone (FSH). Hormone data were linked with clinical data, including acute care mortality and Glasgow Outcome Scale (GOS) scores at 6 months. Hormone levels after TBI were compared to those in healthy controls (n = 14). Group based trajectory analysis (TRAJ) was used to develop temporal hormone profiles that delineate distinct subpopulations in the cohort. Structural equations models were used to determine inter-relationships between hormones and outcomes within a multivariate model. Compared to controls, acute serum hormone levels were significantly altered after severe TBI. Changes in the post-TBI adrenal response and peripheral aromatization influenced hormone TRAJ profiles and contributed to the abnormalities, including increased estradiol in men and increased testosterone in women. In addition to older age and greater injury severity, increased estradiol and testosterone levels over time were associated with increased mortality and worse global outcome for both men and women. These findings represent a paradigm shift when thinking about the role of sex steroids in neuroprotection clinically after TBI.

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Section: Fig 5 (A)supporting

confidence: 91%

Acute Serum Hormone Levels: Characterization and Prognosis after Severe Traumatic Brain Injury

Wagner

McCullough

Niyonkuru

et al. 2011

Journal of Neurotrauma

143

155

View full text Add to dashboard Cite

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“…22 Here we found no evidence of circadian disruption as indicated by the amount of activity counts and vRW exercise during the light inactive period suggesting that HPA circadian rhythm has recovered by this later period.…”

Section: Griesbach Et Alcontrasting

confidence: 58%

Recovery of Stress Response Coincides with Responsiveness to Voluntary Exercise after Traumatic Brain Injury

Griesbach

Tio

Nair

et al. 2014

Journal of Neurotrauma

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We have recently shown that there is a heightened stress response after a mild traumatic brain injury (TBI) during the first 2 post-injury weeks. This corresponds to the same post-injury period when exercise does not increase brain-derived neurotrophic factor (BDNF) and autonomic dysfunction becomes evident with exercise. Here we determined stress and autonomic responses to voluntary and forced exercise at a post-injury time window when exercise has been found to elicit beneficial effects. Rats underwent a mild fluid percussion injury and were exercised at post-injury days 28-32 and 35-39. Cardiac and temperature autonomic function were evaluated. Hippocampal tissue was obtained immediately after exercise for analysis of BDNF. In contrast to the sub-acute period, corticosterone and adrenocorticotropic hormone responses to exercise were normalized in the TBI group. Irrespective of injury, forced exercise markedly stimulated the corticotrophic axis and did not increase BDNF. BDNF levels were increased with voluntary exercise in all animals. Rats exposed to forced exercise had lower activity levels during periods of non-exercise. This effect was more pronounced in the TBI rats. Cardiac and temperature autonomic responses to delayed exercise also recuperated. Rats with TBI that underwent forced exercise, however, had higher core body temperatures during experimental manipulations, thus suggesting that exposure to a potent stressor facilitates responsiveness to environmental stimulations.

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“…Several authors have reported that TBI causes circadian deregulations, including altered homeostatic mechanisms such as the regulation of blood pressure, heart rate, body temperature [46], hormonal cycles [47], and the sleep-wake cycle in patients [48,49]. Recently, it has been shown that the expression of circadian genes is disrupted in the suprachiasmatic nucleus and hippocampus of rats that are subjected to TBI [50].…”

Section: Resultsmentioning

confidence: 99%

Does the Neuroprotective Role of Anandamide Display Diurnal Variations?

Martínez-Vargas

Morales-Gomez

González‐Rivera

et al. 2013

IJMS

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The endocannabinoid system is a component of the neuroprotective mechanisms that an organism displays after traumatic brain injury (TBI). A diurnal variation in several components of this system has been reported. This variation may influence the recovery and survival rate after TBI. We have previously reported that the recovery and survival rate of rats is higher if TBI occurs at 1:00 than at 13:00. This could be explained by a diurnal variation of the endocannabinoid system. Here, we describe the effects of anandamide administration in rats prior to the induction of TBI at two different times of the day: 1:00 and 13:00. We found that anandamide reduced the neurological damage at both times. Nevertheless, its effects on bleeding, survival, food intake, and body weight were dependent on the time of TBI. In addition, we analyzed the diurnal variation of the expression of the cannabinoid receptors CB1R and CB2R in the cerebral cortex of both control rats and rats subjected to TBI. We found that CB1R protein was expressed more during the day, whereas its mRNA level was higher during the night. We did not find a diurnal variation for the CB2R. In addition, we also found that TBI increased CB1R and CB2R in the contralateral hemisphere and disrupted the CB1R diurnal cycle.

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Loss of Cortisol Circadian Rhythm in Patients with Traumatic Brain Injury: A Microdialysis Evaluation

Abstract: In our series, circadian variability of cortisol evaluated by serum and cerebral microdialysis samples seems to be lost in TBI patients.

Cited by 36 publications

References 13 publications

Acute Serum Hormone Levels: Characterization and Prognosis after Severe Traumatic Brain Injury

Acute Serum Hormone Levels: Characterization and Prognosis after Severe Traumatic Brain Injury

Recovery of Stress Response Coincides with Responsiveness to Voluntary Exercise after Traumatic Brain Injury

Does the Neuroprotective Role of Anandamide Display Diurnal Variations?

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