Plasma Cortisol Levels after Head Injury

King, Lionel R.; McLaurin, Robert L.; Lewis, Howard P.; Knowles, Harvey C.

doi:10.1097/00000658-197012000-00008

Cited by 48 publications

(28 citation statements)

References 18 publications

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“…20,33 In clinical TBI cases, HPA axis activation may be augmented above the stress response from physical stress independent of brain injury (i.e., peripheral orthopedic injury). 34,35 In experimental TBI, FPI and sham surgery both caused a peak HPA response; however, only FPI enhanced corticotrophin releasing hormone (CRH) messenger RNA (mRNA) expression in the hypothalamus, 36 which was also demonstrated by CRH mRNA in the amygdala. 37 Combined with the current results, the amygdala proves to be an exquisitely sensitive structure to glucocorticoids from robust and even mild stressors (exogenous or endogenous), and demonstrates resistance to recovery, providing a potential mechanism that could influence long-term functional outcome post-TBI and warrants future research to test causality.…”

Section: Discussionmentioning

confidence: 99%

Early and Persistent Dendritic Hypertrophy in the Basolateral Amygdala following Experimental Diffuse Traumatic Brain Injury

Hoffman

Paode

May

et al. 2017

Journal of Neurotrauma

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In the pathophysiology of traumatic brain injury (TBI), the amygdala remains understudied, despite involvement in processing emotional and stressful stimuli associated with anxiety disorders, such as post-traumatic stress disorder (PTSD). Because the basolateral amygdala (BLA) integrates inputs from sensory and other limbic structures coordinating emotional learning and memory, injury-induced changes in circuitry may contribute to psychiatric sequelae of TBI. This study quantified temporal changes in dendritic complexity of BLA neurons after experimental diffuse TBI, modeled by midline fluid percussion injury. At post-injury days (PIDs) 1, 7, and 28, brain tissue from sham and brain-injured adult, male rats was processed for Golgi, glial fibrillary acidic protein (GFAP), or silver stain and analyzed to quantify BLA dendritic branch intersections, activated astrocytes, and regional neuropathology, respectively. Compared to sham, braininjured rats at all PIDs showed enhanced dendritic branch intersections in both pyramidal and stellate BLA neuronal types, as evidenced by Sholl analysis. GFAP staining in the BLA was significantly increased at PID1 and 7 in comparison to sham. However, the BLA was relatively spared from neuropathology, demonstrated by an absence of argyrophilic accumulation over time, in contrast to other brain regions. These data suggest an early and persistent enhancement of dendritic complexity within the BLA after a single diffuse TBI. Increased dendritic complexity would alter information processing into and through the amygdala, contributing to emotional symptoms post-TBI, including PTSD.

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Section: Discussionmentioning

confidence: 99%

Early and Persistent Dendritic Hypertrophy in the Basolateral Amygdala following Experimental Diffuse Traumatic Brain Injury

Hoffman

Paode

May

et al. 2017

Journal of Neurotrauma

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“…T RAUMATIC BRAIN INJURY is the most common cause of death and acquired disability in children and young adults in the developed world (Sharples et al, dogenous alterations in the hypothalamo-pituitaryadrenal (HPA) axis occur following traumatic brain injury (Bouzarth et al, 1968;Chiolero and Berger, 1994;King et al, 1970;Koiv et al, 1997;Roe et al, 1998;Shohami et al, 1995;Woolf et al, 1990), and further evidence that suggests that brain injury may be exacerbated by elevation of circulating glucocorticoids (Masters et al, 1989;Sapolsky, 1985;Sapolsky, 1994;Sapolsky and Pulsinelli, 1985;White-Gbadebo and Hamm, 1993).…”

Section: Introductionmentioning

confidence: 99%

“…There appears to be a rapid but variable activation of the HPA axis in patients after head injury with some authors reporting an association between the severity of head injury and the extent of the HPA axis response (Bouzarth et al, 1968;King et al, 1970;Koiv et al, 1997), and others indicating that there is a relationship between plasma cortisol levels and patient outcome (Woolf et al, 1990). However, increased HPA axis responses have also been observed following extracranial trauma, again with a relationship between the severity of injury and plasma cortisol levels (Barton et al, 1987).…”

Section: Introductionmentioning

confidence: 99%

The Hypothalamo-Pituitary-Adrenal Axis Response to Experimental Traumatic Brain Injury

Grundy

Harbuz

Jessop

et al. 2001

Journal of Neurotrauma

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Alterations in the hypothalamo-pituitary-adrenal (HPA) axis following traumatic brain injury have not been documented in detail. We used fluid percussion injury (FPI) to evaluate the early changes in components of the HPA axis following experimental traumatic brain injury. Wistar rats were sacrificed at 2 or 4 h following sham or FPI surgery. In situ hybridization histochemistry was used to determine the expression of mRNAs of corticotrophin releasing hormone (CRH) and arginine vasopressin (AVP) in the hypothalamus and pro-opiomelanocortin (POMC) in the pituitary. A group of animals undergoing no surgery were used as control. Repeated blood sampling from an indwelling catheter demonstrated that plasma corticosterone (CORT) levels peaked 30 min following surgery in sham and FPI animals but there was no significant difference in CORT concentration between these groups at any time. Pituitary POMC expression was increased following sham and FPI surgery (compared with control non-operated animals) but with no significant difference between the two groups undergoing surgery. Hypothalamic CRH mRNA expression was significantly higher in animals undergoing FPI compared with sham surgery. Hypothalamic AVP mRNA expression was not significantly increased when compared with control nonoperated animals. These data indicate that the anaesthesia and/or surgery associated with FPI or sham surgery induces a generalised activation of the HPA axis. The selective increase in CRH mRNA in animals undergoing FPI may be due to specific effects of traumatic brain injury rather than a general stress response and may suggest an additional neurotransmitter role for CRH following head injury. The absence of an AVP response suggests that the effects of FPI may be mediated through the CRH-alone-containing subpopulation of neurons.

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“…Increased concentrations of NSE can be measured both in cerebrospinal fluid (CSF) and in peripheral blood after neuronal trauma (15). Serum cortisol is known to be elevated following head trauma (16) and prolonged hypercortisolaemia can lead to unipolar depression and dopaminergic, noradrenergic and thyroid dysfunction (17).…”

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confidence: 99%

Direct Hits to the Head during Amateur Boxing is Associated with a Rise in Serum Biomarkers for Brain Injury

Graham

Myers

Evans

et al. 2011

Int J Immunopathol Pharmacol

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Boxing exposes participants to the physiological response to high intensity exercise and also to direct body and brain trauma. Amateur boxing is increasing and females have also been included in the Olympics. The aim of this study is to assess the stress response and possible brain injury incurred during a match by measuring serum biomarkers associated with stress and cellular brain injury before and after combat. Sixteen male amateur boxers were studied retrospectively. The study population was divided into two groups: (a) a group that received predominantly punches to the head (PTH) and (b) a group that received predominantly punches to the body (PTB). Blood samples were taken before and five minutes after each contest. They were analysed for S-100B, neuron-specific enolase (NSE), creatine kinase (CK) and cortisol. The PTH group received direct contacts to the head (not blocked, parried or avoided) and to the body (n=8, age: 17.6 ± 5.3, years; height: 1.68 ± 0.13, meters; mass: 65.4 ± 20.3, kg). The PTB group received punches to the body including blocked and parried punches, but received no direct punches to the head, (n=8, mean ± SD, age: 19.1 ± 3.2 years; height: 1.70 ± 0.75, meters; mass: 68.5 ± 15 kg). Significant increases (P<0.05) were observed between pre-and post-combat serum concentrations in serum concentrations in PTH of S-100B (0.35 ± 0.61 vs. 0.54 ± 0.73, Jig.VI) NSE (19.7 ± 14 vs.31.1 ± 26.6, ng.ml") and cortisol (373 ± 202 vs. 756 ± 93, nmel.L"), Significant increases (P<0.05) of creatine kinase were recorded in both groups. This study demonstrates significant elevations in neurochemical biomarkers in boxers who received direct blows to the head. However, further work is required to quantify this volumetric brain damage and long term clinical sequelae.Children as young as 11 years of age are eligible to compete in boxing bouts that involve full contact blows to the head (1). Furthermore, female amateur boxing has also recently been included as an Olympic sport and is a testament to equality in sport and the assumed confidence in the safety of amateur boxing (2). The perception of safety surrounding the sport can be attributed to the lack of consensus in the scientific literature on the potential dangers involved in boxing (3-5), compounded by the assumed protection afforded by the mandatory use of headguards. This position is often assumed to be due to

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Plasma Cortisol Levels after Head Injury

Cited by 48 publications

References 18 publications

Early and Persistent Dendritic Hypertrophy in the Basolateral Amygdala following Experimental Diffuse Traumatic Brain Injury

Early and Persistent Dendritic Hypertrophy in the Basolateral Amygdala following Experimental Diffuse Traumatic Brain Injury

The Hypothalamo-Pituitary-Adrenal Axis Response to Experimental Traumatic Brain Injury

Direct Hits to the Head during Amateur Boxing is Associated with a Rise in Serum Biomarkers for Brain Injury

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