122 research outputs found
The Young Male Syndrome—An Analysis of Sex, Age, Risk Taking and Mortality in Patients With Severe Traumatic Brain Injuries
Higher risk taking is particularly characteristic for males between 15 and 35 years, the age when intrasexual competition is the strongest. This fitness-maximizing strategy, however, also has negative consequences; previous data revealed that males have a significantly higher tendency to die in accidents. This retrospective study aimed to assess whether age-related risk taking, often associated with the reproductive competition between males, and referred to as the Young Male Syndrome (YMS), may play a role in the high incidence of severe traumatic brain injury (sTBI) in young males. Derived from the available evidence and the main assumptions of the YMS, we expected that men, especially when they are in the age when their reproductive potential peaks, are more likely to suffer sTBI from highly risky behaviors that also lead to higher mortality. It was also expected that alcohol intoxication makes the demographic pattern of sTBI even more similar to what previous research on the YMS implies. We analyzed demographic data of patients with sTBI (N = 365) registered in a clinical database. To this end, we built Generalized Linear Mixed Models (GLMM) to reveal which of the demographic characteristics are the best predictors for risky behaviors leading to sTBI and death as a consequence of the injury. The data suggest that younger people acquired sTBI from riskier behaviors compared to members of older age groups, irrespective of their sex. Moreover, being male and being alcohol intoxicated also contributed significantly to risk-taking behavior. Mortality rate after the injury, however, increased with the age of the patient and did not depend on the riskiness of the behavior. The results indicate that the demographic distribution of the specific patient population in our focus cannot be simply explained by the YMS. However, higher incidence rates of males among the patients are in line with the core assumptions of the YMS. These data indicate that epidemiological studies should also take into consideration evolutionary theories and highlight the importance of age and sex specific prevention strategies
Traumatic axonal injury in the spinal cord evoked by traumatic brain injury
Although it is well known that traumatic brain injury (TBI) evokes traumatic axonal injury (TAI)
within the brain, TBI-induced axonal damage in the spinal cord (SC) has been less extensively investigated.
Detection of such axonal injury in the spinal cord would further the complexity of TBI
while also challenging some functional neurobehavioral endpoints frequently used to assess recovery
in various models of TBI. To assess TAI in the spinal cord associated with TBI, we analyzed
the craniocervical junction (CCJ), cervico-thoracic (CT), and thoraco-lumber (ThL) spinal cord in
a rodent model of impact acceleration of TBI of varying severities. Rats were transcardially fixed
with aldehydes at 2, 6, and 24 h post-injury (n � 36); each group included on sham-injured rodent.
Semi-serial vibratome sections were reacted with antibodies targeting TAI via alteration in cytoskeletal
integrity or impaired axonal transport. Consistent with previous observations in this
model, the CCJ contained numerous injured axons. Immunoreactive, damaged axonal profiles were
also detected as caudal, as the ThL spinal cord displayed morphological characteristics entirely consistent
with those described in the brainstem and the CCJ. Quantitative analyses demonstrated that
the occurrence and extent of TAI is positively associated with the impact/energy of injury and negatively
with the distance from the brainstem. These observations show that TBI can evoke TAI in
regions remote from the injury site, including the spinal cord itself. This finding is relevant to shaken
baby syndrome as well as during the analysis of data in functional recovery in various models of
TBI
Traumatic brain injury-induced autoregulatory dysfunction and spreading depression-related neurovascular uncoupling: pathomechanism and therapeutic implications.
Vibrational spectroscopy for the triage of traumatic brain injury CT priority and hospital admissions
Molecular Pathomechanisms of Impaired Flow-Induced Constriction of Cerebral Arteries Following Traumatic Brain Injury: A Potential Impact on Cerebral Autoregulation
(1) Background: Traumatic brain injury (TBI) frequently occurs worldwide, resulting in high morbidity and mortality. Here, we hypothesized that TBI impairs an autoregulatory mechanism, namely the flow-induced constriction of isolated rat middle cerebral arteries (MCAs). (2) Methods: TBI was induced in anaesthetized rats by weight drop model, and then MCAs were isolated and transferred into a pressure-flow chamber. The internal diameter was measured by a video-microscopy. (3) Results: In MCAs from intact rats, increases in flow and pressure + flow elicited constrictions (−26 ± 1.9 µm and −52 ± 2.8 µm, p < 0.05), which were significantly reduced after TBI or in the presence of thromboxane-prostanoid (TP receptor) antagonist SQ 29,548. Flow-induced constrictions were significantly reduced by HET0016, inhibitor of cytochrome P450 4A (CYP450 4A). Arachidonic acid, (AA, 10(−7) M), and CYP-450 4A metabolite 20-hydroxyeicosatetraenoic acid (20-HETE) elicited constrictions of intact MCA (−26 ± 2.3% and −31 ± 3.6%), which were significantly reduced after TBI (to 11 ± 1.3% and −16 ±2.5%). The TP receptor agonist U46619 (10(−7) M) elicited substantial constrictions of MCA from intact rats (−21 ± 3.3%), which were also significantly reduced, after TBI (to −16 ± 2.4%). (4) Conclusions: Flow-induced constrictor response of MCA is impaired by traumatic brain injury, likely due to the reduced ability of cytochrome P450 4A to convert arachidonic acid to constrictor prostaglandins and the mitigated sensitivity of thromboxane-prostanoid receptors
Neuronal and glial markers are differently associated with computed tomography findings and outcome in patients with severe traumatic brain injury: a case control study
Súlyos koponya-agy sérülés vizsgálata diffúziós tenzor és funkcionális MR-képalkotással alacsony térerőn. Esetismertetés
Single Mild Traumatic Brain Injury Induces Persistent Disruption of the Blood-Brain Barrier, Neuroinflammation and Cognitive Decline in Hypertensive Rats
Traumatic brain injury (TBI) induces blood-brain barrier (BBB) disruption, which contributes to secondary injury of brain tissue and development of chronic cognitive decline. However, single mild (m)TBI, the most frequent form of brain trauma disrupts the BBB only transiently. We hypothesized, that co-morbid conditions exacerbate persistent BBB disruption after mTBI leading to long term cognitive dysfunction. Since hypertension is the most important cerebrovascular risk factor in populations prone to mild brain trauma, we induced mTBI in normotensive Wistar and spontaneously hypertensive rats (SHR) and we assessed BBB permeability, extravasation of blood-borne substances, neuroinflammation and cognitive function two weeks after trauma. We found that mTBI induced a significant BBB disruption two weeks after trauma in SHRs but not in normotensive Wistar rats, which was associated with a significant accumulation of fibrin and increased neuronal expression of inflammatory cytokines TNFα, IL-1β and IL-6 in the cortex and hippocampus. SHRs showed impaired learning and memory two weeks after mild TBI, whereas cognitive function of normotensive Wistar rats remained intact. Future studies should establish the mechanisms through which hypertension and mild TBI interact to promote persistent BBB disruption, neuroinflammation and cognitive decline to provide neuroprotection and improve cognitive function in patients with mTBI
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