Rapid spontaneous resolution of acute subdural hematoma occurs by redistribution--Two case reports.
(25/230)
Coronal magnetic resonance imaging provided evidence of redistribution during the rapid spontaneous resolution of acute subdural hematoma (ASDH) in two patients. A 79-year-old female was transferred to our hospital after a traffic accident. Computed tomography (CT) on admission demonstrated an ASDH in the right frontal cerebral cortex. CT 12 hours after the accident revealed spontaneous resolution of the ASDH. Coronal magnetic resonance (MR) imaging 3 days after the accident clearly detected a very thin, sharply demarcated layer diffusely covering the cerebral convexity and the middle cranial fossa. A 41-year-old female fell and sustained head trauma with the loss of consciousness. CT on admission demonstrated an ASDH in the left frontal cerebral cortex. CT 12 hours after the accident revealed spontaneous resolution of the ASDH. Coronal MR imaging 3 days after the insult clearly demonstrated the redistribution and dispersal of the hematoma. Although CT showed the disappearance of the hematoma, MR imaging demonstrated redistribution rather than disappearance of the blood in both cases. These cases indicate that spontaneous resolution of ASDH occurs by redistribution and dispersal of the hematoma. (+info)
Studies of vehicular padding materials.
(26/230)
The Federal Motor Vehicle Safety Standard 571.201 discusses occupant protection with interior impacts of vehicles. Rule making by the National Highway Traffic Safety Administration (NHTSA) has identified padding for potential injury reduction in vehicles. In these studies, head injury mitigation with padding on vehicular roll bars and brush bars was evaluated. Studies were conducted with free falling Hybrid 50% male head form drops on the forehead and side of the head and a 5% female head. Marked reductions in angular acceleration, as well as Head Injury Criterions (HIC), were observed when compared to unpadded roll bars and brush bars. (+info)
Airbag effectiveness on brain trauma in frontal crashes.
(27/230)
The purpose of this study was to evaluate the effectiveness of frontal restraint systems in reducing the potential for head injuries, specifically brain injuries and skull fractures. The US DOT NASS database files from 1991-1998 were evaluated for drivers and right front seat occupants in frontal crashes. Of the total driver and right front seat occupants in this data set, 3.83% sustained a brain injury without skull fracture, 0.05% sustained a skull fracture without a brain injury, and 0.16% sustained both brain injury and skull fracture. The incidence of head injury was lowest among occupants who were restrained by belt alone (2.76%) and by both airbag and belt systems (3.51%). The unrestrained population had a 10.39% incidence of at least one type of head injury. In general, for maximum AIS > or = 2 head injuries, airbag effectiveness was greatest between 16-45 kph crash delta V. For the more severe maximum AIS > or = 3 head injuries, the airbag restraint had its greatest effect up to 35 kph. It can be concluded that brain injury in frontal crashes is substantially reduced with the presence of a restraint system and the use of both airbag and belt restraint offers the greatest protection across all delta V categories. Restraint system effectiveness for the non-head-injured occupant is variable but, generally, the belted occupant sustained the lowest percentage of injuries. Skull fractures in frontal impact were relatively rare and the incidence appeared to be unaffected by the presence of a restraint system. (+info)
The neurobehavioural rating scale-revised: sensitivity and validity in closed head injury assessment.
(28/230)
OBJECTIVES: To investigate the factor structure and psychometric properties of the neurobehavioural rating scale-revised (NRS-R) and to determine its usefulness in clinical trials. METHODS: A consecutive series of patients sustaining severe closed head injury were evacuated to one of 11 large regional North American trauma centres and entered into a randomised, phase III, multicentre clinical trial investigating the therapeutic use of moderate hypothermia. Acute care personnel were blinded to outcome and outcome personnel were blinded to treatment condition. The Glasgow outcome scale (GOS) was the primary outcome measure. Secondary outcome measures included the disability rating scale (DRS) and the NRS-R. RESULTS: Exploratory factor analysis of NRS-R data collected at 6 months after injury (n=210) resulted in a five factor model including: (1) executive/cognition, (2) positive symptoms, (3) negative symptoms, (4) mood/affect, and (5) oral/motor. These factors showed acceptable internal consistency (0.62 to 0.88), low to moderate interfactor correlations (0.19 to 0.61), and discriminated well between GOS defined groups. Factor validity was demonstrated by significant correlations with specific neuropsychological domains. Significant change was measured from 3 to 6 months after injury for the total score (sum of all 29 item ratings) and all factor scores except mood/affect and positive symptoms. The total score and all factor scores correlated significantly with concurrent GOS and DRS scores. CONCLUSIONS: The NRS-R is well suited as a secondary outcome measure for clinical trials as its completion rate exceeds that of neuropsychological assessment and it provides important neurobehavioural information complementary to that provided by global outcome and neuropsychological measures. (+info)
Tight Sylvian cisterns associated with hyperdense areas mimicking subarachnoid hemorrhage on computed tomography--four case reports.
(29/230)
Four patients with supratentorial mass lesions (two chronic subdural hematomas, one acute epidural hematoma, and one acute subdural hematoma) showed hyperdense sylvian cisterns on computed tomography (CT). Association of subarachnoid hemorrhage was suspected initially, but was excluded by intraoperative observation or postoperative lumbar puncture. CT showed disappearance of the hyperdense areas just after evacuation of the mass lesions. The hyperdense areas are probably a result of the partial volume phenomenon or concentrations of calcium deposits rather than abnormally high hematocrit levels, which were not found in these patients. (+info)
dl-3-n-butylphthalide reduces brain damage in mice with closed head injury.
(30/230)
OBJECTIVE: To investigate the protective effect of dl-3-n-butylphthalide (NBP) as an anti-cerebral ischemic drug on brain damage 24 h after closed head injury in mice. METHODS: Closed head injury was induced by dropping a 50-g weight from a height of 18 cm on a metal impounder resting on the parietal bone in mice. RESULTS: The neurotraumatic model induced impairment of memory function, significant cerebral edema, and disruption of the blood-brain barrier. dl-3-n-butylphthalide (50 mg.kg-1) given intraperitoneally 5 minutes and 60 minutes after the onset of closed head injury was found to attenuate the impairment of memory function (P < 0.05), alleviate brain edema in the injured cerebral cortex (P < 0.05), and reduce extravasation of plasma protein bound to Evans blue dye by 63.5% (P < 0.01). NBP was also shown to increase the activity of choline acetyltransferase in the injured cortex to 0.83 +/- 0.21 ng.min-1.mg-1 (P < 0.01, compared with 0.48 +/- 0.14 ng.min-1.mg-1 of vehicle group). CONCLUSION: NBP provides therapeutic response in experimental closed head injury. (+info)
Repetitive mild brain trauma accelerates Abeta deposition, lipid peroxidation, and cognitive impairment in a transgenic mouse model of Alzheimer amyloidosis.
(31/230)
Traumatic brain injury (TBI) increases susceptibility to Alzheimer's disease (AD), but it is not known how TBI contributes to the onset or progression of this common late life dementia. To address this question, we studied neuropathological and behavioral consequences of single versus repetitive mild TBI (mTBI) in transgenic (Tg) mice (Tg2576) that express mutant human Abeta precursor protein, and we demonstrate elevated brain Abeta levels and increased Abeta deposition. Nine-month-old Tg2576 and wild-type mice were subjected to single (n = 15) or repetitive (n = 39) mTBI or sham treatment (n = 37). At 2 d and 9 and 16 weeks after treatment, we assessed brain Abeta deposits and levels in addition to brain and urine isoprostanes generated by lipid peroxidation in these mice. A subset of mice also was studied behaviorally at 16 weeks after injury. Repetitive but not single mTBI increased Abeta deposition as well as levels of Abeta and isoprostanes only in Tg mice, and repetitive mTBI alone induced cognitive impairments but no motor deficits in these mice. This is the first experimental evidence linking TBI to mechanisms of AD by showing that repetitive TBI accelerates brain Abeta accumulation and oxidative stress, which we suggest could work synergistically to promote the onset or drive the progression of AD. Additional insights into the role of TBI in mechanisms of AD pathobiology could lead to strategies for reducing the risk of AD associated with previous episodes of brain trauma and for preventing progressive brain amyloidosis in AD patients. (+info)
Increases in GABA concentrations during cerebral ischaemia: a microdialysis study of extracellular amino acids.
(32/230)
OBJECTIVES: Increases in the extracellular concentration of the excitatory amino acids glutamate and aspartate during cerebral ischaemia in patients are well recognised. Less emphasis has been placed on the concentrations of the inhibitory amino acid neurotransmitters, notably gamma-amino-butyric acid (GABA), despite evidence from animal studies that GABA may act as a neuroprotectant in models of ischaemia. The objective of this study was to investigate the concentrations of various excitatory, inhibitory and non-transmitter amino acids under basal conditions and during periods of cerebral ischaemia in patients with head injury or a subarachnoid haemorrhage. METHODS: Cerebral microdialysis was established in 12 patients with head injury (n=7) or subarachnoid haemorrhage (n=5). Analysis was performed using high performance liquid chromatography for a total of 19 (excitatory, inhibitory and non-transmitter) amino acids. Patients were monitored in neurointensive care or during aneurysm clipping. RESULTS: During stable periods of monitoring the concentrations of amino acids were relatively constant enabling basal values to be established. In six patients, cerebral ischaemia was associated with increases (up to 1350 fold) in the concentration of GABA, in addition to the glutamate and aspartate. Parallel increases in the concentration of glutamate and GABA were found (r=0.71, p<0.005). CONCLUSIONS: The results suggest that, in the human brain, acute cerebral ischaemia is not accompanied by an imbalance between excitatory and inhibitory amino acids, but by an increase in all neurotransmitter amino acids. These findings concur with the animal models of ischaemia and raise the possibility of an endogenous GABA mediated neuroprotective mechanism in humans. (+info)