Endocrine Failure After Traumatic Brain Injury in Adults

Powner, David J.; Boccalandro, Cristina; Serdar, Muhiddin; Vollmer, Dennis G.

doi:10.1385/ncc:5:1:61

Cited by 100 publications

(91 citation statements)

References 78 publications

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“…As shown by the Bayly et al (2005) and Viano et al (2005b) studies, the hypothalamic-pituitary axis is particularly vulnerable to physical strain in concussion. Pituitary dysfunction can be associated with many of the same symptoms as seen by PPCS (Casanueva et al, 2006;Powner et al, 2006), yet this has not been systematically investigated in PPCS. This is particularly important because of some pituitary associated physical and neuropsychiatric symptoms are treatable.…”

Section: Confounding Factors That Must Be Considered In the Design Ofmentioning

confidence: 99%

Neuropsychology and clinical neuroscience of persistent post-concussive syndrome

Bigler

2007

J Int Neuropsychol Soc

363

248

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On the mild end of the acquired brain injury spectrum, the terms concussion and mild traumatic brain injury (mTBI) have been used interchangeably, where persistent post-concussive syndrome (PPCS) has been a label given when symptoms persist for more than three months post-concussion. Whereas a brief history of concussion research is overviewed, the focus of this review is on the current status of PPCS as a clinical entity from the perspective of recent advances in the biomechanical modeling of concussion in human and animal studies, particularly directed at a better understanding of the neuropathology associated with concussion. These studies implicate common regions of injury, including the upper brainstem, base of the frontal lobe, hypothalamic-pituitary axis, medial temporal lobe, fornix, and corpus callosum. Limitations of current neuropsychological techniques for the clinical assessment of memory and executive function are explored and recommendations for improved research designs offered, that may enhance the study of long-term neuropsychological sequelae of concussion. (JINS, 2008, 14, 1-22.)

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Section: Confounding Factors That Must Be Considered In the Design Ofmentioning

confidence: 99%

Neuropsychology and clinical neuroscience of persistent post-concussive syndrome

Bigler

2007

J Int Neuropsychol Soc

363

248

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“…This does not rule out the possibility of secondary seepage bleeding in cortical injuries, ventriculomegaly, or mechanical forces (compression and diffuse axonal injury caused by the impact), which then could induce chronic damage to the HP=BS region. Among the secondary effects of impact injury are edema formation (Roof et al, 1993), increased intracranial pressure (ICP) (Kita and Marmarou, 1994), and hemorrhage (Powner et al, 2006) in the vasculature of the HP and=or AP. It is important to note also that increased ICP is assumed to contribute to anterior lobe infarction (in the AP) through interruption of the hypothalamohypophyseal portal blood supply (Ceballos, 1966;Harper et al, 1986).…”

Section: Causes Of Gh Deficiencymentioning

confidence: 99%

“…In addition to the many acute focalized and systemic changes caused by the initial injury, TBI-induced long-term consequences can include more global alterations in the endocrine system as a result of the organism's systemic response to the injury at the level of the hypothalamus (HT) and the pituitary gland (Powner et al, 2006). The many reviews on the impact of TBI on the neuroendocrine system cite evidence for suppression of the stress, growth, and reproductive axes due to hypopituitarism with single or multiple hormonal deficiencies.…”

Section: Introductionmentioning

confidence: 99%

“…Other signaling mechanisms could include trans-synaptic (Koliatsos et al, 2004) as well as anterograde and retrograde neuronal degeneration from the site of injury to the more distal sites (Sorensen et al, 1996;Bechmann and Nitsch, 1997), also eventually affecting some of the endocrine functions. While we know something about the effects of TBI on endocrine function based on human studies (Ceballos, 1966;Agha et al, 2004aAgha et al, , 2004bAgha et al, , 2005aAgha et al, , 2005bAimaretti et al, 2004Aimaretti et al, , 2005bBondanelli et al, 2004;Herrmann et al, 2006;Powner et al, 2006;Schneider et al, 2006;Tanriverdi et al, 2006), there is still some uncertainty about the mechanisms by which long-term alterations in the endocrine system (like suppression of serum GH in TBI subjects) evolve over time, and whether such changes could be prevented by therapeutic interventions.…”

Section: Introductionmentioning

confidence: 99%

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Traumatic Brain Injury Causes Long-Term Reduction in Serum Growth Hormone and Persistent Astrocytosis in the Cortico-Hypothalamo-Pituitary Axis of Adult Male Rats

Kasturi

Stein

2009

Journal of Neurotrauma

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In humans, traumatic brain injury (TBI) causes pathological changes in the hypothalamus (HT) and the pituitary. One consequence of TBI is hypopituitarism, with deficiency of single or multiple hormones of the anterior pituitary (AP), including growth hormone (GH). At present no animal model of TBI with ensuing hypopituitarism has been demonstrated. The main objective of this study was to investigate whether cortical contusion injury (CCI) could induce long-term reduction of serum GH in rats. We also tested the hypothesis that TBI to the medial frontal cortex (MFC) would induce inflammatory changes in the HT and AP. Methods: Nine young adult male rats were given sham surgery (n ¼ 4) or controlled impact contusions (n ¼ 5) of the MFC. Two months postinjury they were killed, trunk blood collected and their brains and AP harvested. GH was measured in serum and AP using ELISA and Western blot respectively. Interleukin-1b (IL-1b) and glial fibrillary acidic protein (GFAP) were measured in the cortex (Cx), HT, and AP by Western blot. Results: Lesion rats had significantly (p < 0.05) lower levels of GH in the AP and serum, unaltered serum IGF-1, and significantly (p < 0.05) higher levels of IL-1b in the Cx and HT and GFAP in the Cx, HT, and AP compared to that of shams. Conclusion: CCI leads to a long-term depletion of serum GH in male rats. This chronic change in GH post-TBI is probably the result of systemic and persistent inflammatory changes observed at the level of HT and AP, the mechanism of which is not yet known.

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“…While mTBI has been shown to have unique effects on health and functioning [20][21][22][23], we focus on the overlap of mTBI with PTSD and depression because these most commonly present together, and cognitive complaints are important overlapping features of all three conditions [11][12][13][14][15][16]. We hypothesize that self-reported cognitive symptoms that adversely affect daily functioning at the level of moderate to very severe are more strongly associated with individual mental health disorders and with mental health disorders in conjunction with mTBI than with mTBI alone.…”

Section: Introductionmentioning

confidence: 99%

Association between mild traumatic brain injury and mental health problems and self-reported cognitive dysfunction in Iraq and Afghanistan Veterans

Seal¹,

Bertenthal²,

Samuelson³

et al. 2016

J Rehabil Res Dev

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Abstract-The Department of Veterans Affairs traumatic brain injury (TBI) screening program is intended to detect and expedite treatment for TBI and postconcussive symptoms. Between April 14, 2007, and May 31, 2012, of 66,089 Iraq and Afghanistan Veterans who screened positive on first-level TBI screening and later completed comprehensive TBI evaluation that includes the Neurobehavioral Symptoms Inventory, 72% reported moderate to very severe cognitive impairment (problems with attention, concentration, memory, etc.) that interfered with daily activities. This included 42% who were found not to have sustained combat-related mild TBI (mTBI). In contrast, 70.0% received a posttraumatic stress disorder (PTSD) diagnosis and 45.8% received a depression diagnosis. Compared with Veterans without mTBI, PTSD, or depression diagnoses, the lowest risk for self-reported cognitive impairment was in Veterans with confirmed mTBI only; a greater risk was found in those with PTSD diagnoses, with the greatest risk in Veterans with PTSD, depression, and confirmed mTBI, suggesting only a weakly additive effect of mTBI. These findings suggest that Veterans with multiple mental health comorbidities, not just those with TBI, report moderate to very severe cognitive impairment. Mental health treatment for conditions such as PTSD and depression (with or without TBI) may result in improvements in cognitive functioning and/or include assessment and support for Veterans experiencing cognitive problems.

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Endocrine Failure After Traumatic Brain Injury in Adults

Abstract: Severe TBI associated with basilar skull fracture, hypothalamic edema, prolonged unresponsiveness, hyponatremia, and/or hypotension is associated with a higher occurrence of endocrinopathy. Greater awareness of this possible complication of TBI and appropriate testing are encouraged.

Cited by 100 publications

References 78 publications

Neuropsychology and clinical neuroscience of persistent post-concussive syndrome

Neuropsychology and clinical neuroscience of persistent post-concussive syndrome

Traumatic Brain Injury Causes Long-Term Reduction in Serum Growth Hormone and Persistent Astrocytosis in the Cortico-Hypothalamo-Pituitary Axis of Adult Male Rats

Association between mild traumatic brain injury and mental health problems and self-reported cognitive dysfunction in Iraq and Afghanistan Veterans

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