Early and Longtime Modifications of Temperature Regulation after Severe Head Injury

Behr, Robert; Erlingspiel, D.; Becker, Alexander

doi:10.1111/j.1749-6632.1997.tb51774.x

Cited by 14 publications

(4 citation statements)

References 22 publications

(24 reference statements)

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“…57,58 Post-traumatic hyperthermia can persist from weeks to months and correlates with negative outcome in several clinical studies of patients with TBI. [59][60][61] Post-traumatic hyperthermia is characterized by the loss of the diurnal temperature variation, is relatively resistant to antipyretic medications, and occurs secondary to hypothalamic thermoregulation center dysfunction. 61 In a rat model of severe TBI induced by lateral fluid percussion, the authors reported a significant inflammatory response in the periventricular nucleus of the hypothalamus that was characterized by astrogliosis and the infiltration of microglia/macrophages 1 week after brain injury, suggesting hypothalamic dysfunction.…”

Section: The Potential Clinical Relevance Of Disseminated Brain Inflamentioning

confidence: 99%

Dissemination of brain inflammation in traumatic brain injury

et al. 2019

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Traumatic brain injury (TBI) is recognized as a global health problem due to its increasing occurrence, challenging treatment, and persistent impacts on brain pathophysiology. Neural cell death in patients with TBI swiftly causes inflammation in the injured brain areas, which is recognized as focal brain inflammation. Focal brain inflammation causes secondary brain injury by exacerbating brain edema and neuronal death, while also exerting divergent beneficial effects, such as sealing the damaged limitans and removing cellular debris. Recent evidence from patients with TBI and studies on animal models suggest that brain inflammation after TBI is not only restricted to the focal lesion but also disseminates to remote areas of the brain. The dissemination of inflammation has been detected within days after the primary injury and persists chronically. This state of inflammation may be related to remote complications of TBI in patients, such as hyperthermia and hypopituitarism, and may lead to progressive neurodegeneration, such as chronic traumatic encephalopathy. Future studies should focus on understanding the mechanisms that govern the initiation and propagation of brain inflammation after TBI and its impacts on post-trauma brain pathology.

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Section: The Potential Clinical Relevance Of Disseminated Brain Inflamentioning

confidence: 99%

Dissemination of brain inflammation in traumatic brain injury

et al. 2019

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“…The on-court risk to players is especially significant for illnesses involving gastrointestinal distress (eg, vomiting and diarrhoea) and/or fever. Notably, a history of concussion may increase the risk for exertional heat illness during training and competition, secondary to autonomic nervous system dysfunction,32 33 although this has not been examined until now in tennis. Sickle cell trait should also be considered a possible contributing clinical risk/complicating factor for vascular dysfunction, exertional rhabdomyolysis and collapse related to red blood cell sickling during strenuous practice or play in the heat34–36; although this has not been reported or explored in tennis either.…”

Section: Clinical Conditions Medications and Caffeinementioning

confidence: 99%

Hydration and thermal strain during tennis in the heat

Bergeron

2014

Br J Sports Med

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Competitive tennis in the heat can prompt substantial sweat losses and extensive consequent body water and electrolyte deficits, as well as a level of thermal strain that considerably challenges a player's physiology, perception of effort, and on-court well-being and performance. Adequate hydration and optimal performance can be notably difficult to maintain when multiple same-day matches are played on successive days in hot weather. Despite the recognised effects of the heat, much more research needs to be carried out to better appreciate the broader scope and full extent of the physiological demands and hydration and thermal strain challenges facing junior and adult players in various environments, venues and competition scenarios. However, certain recommendations of best practices should be emphasised to minimise exertional heat illness risk and improve player safety, well-being and on-court performance.

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“…Posttraumatic hyperthermia (PTH), also known as neurogenic fever, is a syndrome that persists for weeks to months after brain injury and has been reported in 4% to 37% of patients with moderate to severe TBI (Sazbon and Groswasser, 1990;Meythaler and Stinson III, 1994;Childers et al, 1994;Thompson et al, 2003). In several clinical studies, the development of PTH has been correlated with negative outcome in patients after TBI (Sazbon and Groswasser, 1990;Heindl and Laub, 1996;Behr et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

Development of Posttraumatic Hyperthermia after Traumatic Brain Injury in Rats is Associated with Increased Periventricular Inflammation

Thompson

Hoover

Tkacs

et al. 2005

J Cereb Blood Flow Metab

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Posttraumatic hyperthermia (PTH) is a noninfectious elevation in body temperature that negatively influences outcome after traumatic brain injury (TBI). We sought to (1) characterize a clinically relevant model and (2) investigate potential cellular mechanisms of PTH. In study I, body temperature patterns were analyzed for 1 week in male rats after severe lateral fluid percussion (FP) brain injury (n ¼ 75) or sham injury (n ¼ 17). After injury, 27% of surviving animals experienced PTH, while 69% experienced acute hypothermia with a slow return to baseline. A profound blunting or loss of circadian rhythmicity (CR) that persisted up to 5 days after injury was experienced by 75% of brain-injured animals. At 2 and 7 days after injury, patterns of cell loss and inflammation were assessed in selected brain thermoregulatory and circadian centers. Significant cell loss was not observed, but PTH was associated with inflammatory changes in the hypothalamic paraventricular nucleus (PVN) by one week after injury. In brain-injured animals with altered CR, reactive astrocytes were bilaterally localized in the suprachiasmatic nucleus (SCN) and the PVN. Occasional IL-1b þ / ED-1 þ macrophages/microglia were observed in the PVN and SCN exclusively in brain-injured animals developing PTH. In animals with PTH there was a significant positive correlation (r ¼ 0.788, Po0.01) between the degree of postinjury hyperthermia and the total number of cells positive for inflammatory markers within selected thermoregulatory and circadian nuclei. In study II, a separate group of animals underwent the same injury and temperature monitoring paradigm as in study I, but had additional physiologic data obtained, including vital signs, arterial blood gases, white blood cell counts, and C-reactive protein levels. All parameters remained within normal ranges after injury. These data suggest that PTH and the alteration in CR of temperature may be due, in part, to acute reactive astrocytosis and inflammation in hypothalamic centers responsible for both thermoregulation and CR.

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Early and Longtime Modifications of Temperature Regulation after Severe Head Injury

Cited by 14 publications

References 22 publications

Dissemination of brain inflammation in traumatic brain injury

Dissemination of brain inflammation in traumatic brain injury

Hydration and thermal strain during tennis in the heat

Development of Posttraumatic Hyperthermia after Traumatic Brain Injury in Rats is Associated with Increased Periventricular Inflammation

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