Traumatic Brain Injury in the Elderly: Increased Mortality and Worse Functional Outcome At Discharge Despite Lower Injury Severity

Susman, Mark; DiRusso, Stephen; Sullivan, Thomas; Risucci, Donald A.; Nealon, Peter; Cuff, Sara; Haider, Adil H.; Benzil, Deborah L.

doi:10.1097/00005373-200208000-00004

Cited by 387 publications

(295 citation statements)

References 15 publications

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“…Clinical characteristics of the studied subgroups a poor prognosis. For example, the mortality rate in a study by Susman et al was 24% in a group of older patients [7], whereas in the present study only one patient (0.3%) died. However, the patients presented in that report were treated at a trauma center, whereas in the present study the patients were treated in an ED and were not preselected.…”

Section: Discussioncontrasting

confidence: 70%

Head Trauma in Elderly Patients: Mechanisms of Injuries and CT Findings

Timler¹,

Dworzyński²,

Szarpak³

et al. 2015

Adv Clin Exp Med

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Section: Discussioncontrasting

confidence: 70%

Head Trauma in Elderly Patients: Mechanisms of Injuries and CT Findings

Timler¹,

Dworzyński²,

Szarpak³

et al. 2015

Adv Clin Exp Med

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“…Confirmed factors of poor prognosis for patients with GCS 3 or 4 and older than 65 years are closed basal cisterns and midline shift > 15 mm on the first CT (Brazinova et al, 2010). The worse outcomes in elderly human subjects occur despite what appears to be less severe TBI, as measured by a higher GCS upon admission (Livingston et al, 2005;Susman et al, 2002). …”

Section: Discussionmentioning

confidence: 97%

“…Unfortunately, increasing age is strongly associated with a poor prognosis both in experimental trauma models and following TBI in humans (Livingston et al, 2005;Onyszchuk et al, 2008;Rothweiler et al, 1998;Sendroy-Terrill et al, 2010;Susman et al, 2002). Confirmed factors of poor prognosis for patients with GCS 3 or 4 and older than 65 years are closed basal cisterns and midline shift > 15 mm on the first CT (Brazinova et al, 2010).…”

Section: Discussionmentioning

confidence: 99%

The Cerebral Extracellular Release of Glycerol, Glutamate, and FGF2 Is Increased in Older Patients following Severe Traumatic Brain Injury

Mellergård

Sjögren

Hillman

2012

Journal of Neurotrauma

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Old age is associated with a poor recovery from traumatic brain injury (TBI). In a retrospective study we investigated if the biochemical response following TBI is age dependent. Extracellular fluids were continuously sampled by microdialysis in 69 patients admitted to our NSICU following severe TBI. The concentrations of glycerol, glutamate, lactate, pyruvate, and eight different cytokines (IL-1b, IL-6, IL-10, IL-8, MIP-1b, RANTES, FGF2, and VEGF) were determined by fluorescence multiplex bead technology. Patients in the oldest age group ( ‡ 65 years) had significantly higher microdialysate concentrations of glycerol and glutamate compared to younger patients: the mean microdialysate concentration of glycerol increased from 55.9 lmol/L (25-44 year) to 252 lmol/L ( ‡ 65 years; p < 0.0001); similarly glutamate increased from 15.8 mmol/L to 92.2 mmol/L ( p < 0.0001). The lactate-pyruvate ratio was also significantly higher in the patients ‡ 65 years of age (63.9) compared with all the other age groups. The patterns of cytokine responses varied. For some cytokines (IL-1b, IL-10, and IL-8) there were no differences between age groups, while for others (MIP-1b, RANTES, VEGF, and IL-6) some differences were observed, but with no clear correlation with increasing age. For FGF2 the mean microdialysate concentration was 43 pg/mL in patients ‡ 65 years old, significantly higher compared to all other age groups ( p < 0.0001). Increased concentrations of glycerol and glutamate would indicate more extensive damaging processes in the elderly. An increase in concentration of FGF2 could serve a protective function, but could also be related to a dysregulation of the timing in the cellular response in elderly patients.

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“…Taking a lead from the physical model of ageing, characterized by frailty, it is a common sense assertion that age brings vulnerability also in the domain of cellular physiology. Indeed, using the traumatic brain injury as an experimental model in rodents, it has been long demonstrated that age is associated with a significantly increased mortality and, for smaller levels of injury, with a greater level of acute neurological deficits (Hamm et al 1991), with comparable equivalent results in human studies (Susman et al 2002). However, the issue is fraught with some difficulties of interpretation and assessment, since there is a certain developmentally controlled maturation of vulnerability to excitotoxic insults.…”

Section: Functional Consequencesmentioning

confidence: 99%

Normal brain ageing: models and mechanisms

Toescu

2005

Phil. Trans. R. Soc. B

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Normal ageing is associated with a degree of decline in a number of cognitive functions. Apart from the issues raised by the current attempts to expand the lifespan, understanding the mechanisms and the detailed metabolic interactions involved in the process of normal neuronal ageing continues to be a challenge. One model, supported by a significant amount of experimental evidence, views the cellular ageing as a metabolic state characterized by an altered function of the metabolic triad: mitochondria-reactive oxygen species (ROS)-intracellular Ca 2C . The perturbation in the relationship between the members of this metabolic triad generate a state of decreased homeostatic reserve, in which the aged neurons could maintain adequate function during normal activity, as demonstrated by the fact that normal ageing is not associated with widespread neuronal loss, but become increasingly vulnerable to the effects of excessive metabolic loads, usually associated with trauma, ischaemia or neurodegenerative processes. This review will concentrate on some of the evidence showing altered mitochondrial function with ageing and also discuss some of the functional consequences that would result from such events, such as alterations in mitochondrial Ca 2C homeostasis, ATP production and generation of ROS.

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Traumatic Brain Injury in the Elderly: Increased Mortality and Worse Functional Outcome At Discharge Despite Lower Injury Severity

Abstract: Elderly traumatic brain injury patients have a worse mortality and functional outcome than nonelderly patients who present with head injury even though their head injury and overall injuries are seemingly less severe.

Cited by 387 publications

References 15 publications

Head Trauma in Elderly Patients: Mechanisms of Injuries and CT Findings

Head Trauma in Elderly Patients: Mechanisms of Injuries and CT Findings

The Cerebral Extracellular Release of Glycerol, Glutamate, and FGF2 Is Increased in Older Patients following Severe Traumatic Brain Injury

Normal brain ageing: models and mechanisms

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