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Regional rates of glucose utilization in the cat following concussive head injury.

Injections of [14C]-deoxyglucose ([14C]DG) were used to study rates of local cerebral glucose utilization (LCGU) in control cats and cats subjected to concussive brain injury produced by a fluid-percussion device. Studies in separate groups of animals demonstrated that the injury level selected produced transient behavioral suppression probably associated with traumatic disturbances of consciousness. LCGU was sampled near the site of fluid-percussion injury and more caudally in pontine regions. Histopathologic studies examined the possibility of hemorrhage, contusion, or breakdown of the blood-brain barrier in regions within which LCGU was calculated. These studies yielded analyses indicating that (1) the [14C]DG technique can be applied usefully to infer changes in regional levels of brain activity after concussion, (2) concussive injury produces changes in brain function that differ reliably across various regions of the central nervous system and may include both depression and focal activation of specific brain sites. Data are discussed that suggest that changes in brain activity in specific regions indicated by changes in LCGU could contribute to acute neurologic disturbances after concussion including unconsciousness.

Animals↗

Traumatic brain injury in northern Sweden. Incidence and prevalence of long-standing impairments and disabilities.

Based on a retrospective survey of hospital admissions and autopsies the incidence of traumatic brain injury (TBI) for the age range 16-60 was found to be 24.9/10,000 in the Umeå district of Northern Sweden. In male youngsters aged 16-19 the incidence was remarkably high in comparison with reports from other parts of the western hemisphere. Self-reports on the prevalence of impairments and disabilities 1 1/2-3 years after the injury were obtained by a mailed questionnaire. Among the subjects with brain concussion 1/3 reported impairments and 1/10 disabilities, most commonly leisure-disability. By factor analysis impairments and disabilities could be logically grouped into three factors. Two of these factors clearly circumscribed combinations of impairments and disabilities, one of them being dominated by instrumental ADL, the other by basic self-care ADL. The third factor incorporated the classic post-concussion triad and memory. Taken together the findings indicate that many subjects with an early diagnosis of brain concussion, hospitalized for only one day, experienced losses in pre-injury functions and abilities. It is therefore suggested that not only radiologically and/or operatively confirmed TBIs but also subjects with brain concussion should be followed after discharge in order to minimize losses in social well-being.

Activities of Daily Living↗

Marked hippocampal neuronal damage without motor deficits after mild concussive-like brain injury in apolipoprotein E-deficient mice.

Of various biological factors, only allele epsilon 4 of apolipoprotein E (apoE, protein; APOE4, gene) has been thus far suggested as a major determinant of genetic risk for sporadic and late-onset familial Alzheimer's disease (AD). Environmental influences such as lack of education, traumatic brain injury, oxidative stress, environmental toxins, hormonal imbalances, and alterations in immune or inflammatory responses may also contribute to the pathogenesis of AD. Thus genetic susceptibility and environmental risk factors may have synergistic effects on the development of AD. The purpose of present report was to assess whether the gene (APOE) and the environmental risk factor (traumatic brain injury) could interact in hippocampal neuronal degeneration. We investigated the histopathological changes of hipoccampal regions after mild concussive-like brain injury without motor deficits in apoE-deficient mice using the recently described novel weight-drop device. Control mice revealed minimal neurodegenerative changes limited to CA2 and CA3, while apoE-deficient mice showed widespread neuronal degeneration throughout hippocampal subfields and part of dentate gyrus. We also observed widespread glial fibrillary acidic protein (GFAP) immunoreactivity throughout the hippocampus, which was more intense in apoE-deficient mice. The results of this study indicate that even very mild traumatic brain injury could result in widespread hippocampal damage in apoE-deficient mice. This again supports the hypothesis that apoE might play a neurotrophic or neuroprotective function in the central nervous system.

Alzheimer Disease↗

Hearing loss after head injury.

This work reports on the hearing loss of 395 patients who were hospitalized after brain concussion. The percentage of hearing loss and vestibular disturbances appearing after fracture of the temporal bone is higher than in cases with skull fractures without fracture of the temporal bone or with brain concussion alone. Conductive deafness caused by head injury usually disappears in two months time. If conductive deafness remains, the suspicion of dislocation of the ossicular bones arises and such patients must undergo an operation. As the cases where sensorineural deafness disappeared within six months after head injury were rare, final evaluation of the hearing loss can be made one year after the head injury. In the majority of cases, vestibular disturbances and positional nystagmus disappear within six months after the head injury.

Adolescent↗

Enhanced neurofibrillary tangle formation, cerebral atrophy, and cognitive deficits induced by repetitive mild brain injury in a transgenic tauopathy mouse model.

Traumatic brain injury (TBI) is a risk factors for Alzheimer's disease (AD), and repetitive TBI (rTBI) may culminate in dementia pugilistica (DP), a syndrome characterized by progressive dementia, parkinsonism, and the hallmark brain lesions of AD, including neurofibrillary tangles (NFTs), formed by abnormal tau filaments and senile plaques (SPs) composed of Abeta fibrils. Previous study showed that mild rTBI (mrTBI) accelerated the deposition of Abeta in the brains of transgenic (Tg) mice (Tg2576) that over-express human Abeta precursor proteins with the familial AD Swedish mutations (APP695swe) and model of AD-like amyloidosis. Here, we report studies of the effects of mrTBI on AD-like tau pathologies in Tg mice expressing the shortest human tau isoform (T44) subjected to mrTBI, causing brain concussion without structural brain damage to simulate injuries linked to DP. Twelve-month-old Tg T44 (n = 18) and wild-type (WT; n = 24) mice were subjected to mrTBI (four times a day, 1 day per week, for 4 weeks; n = 24) or sham treatment (n = 18). Histopathological analysis of mice at 9 months after mrTBI revealed that one of the Tg T44 mice showed extensive telencephalic NFT and cerebral atrophy. Although statistical analysis of neurobehavioral tests at 6 months after mrTBI did not show any significant difference in any of groups of mice, the Tg T44 mouse with extensive NFT had an exceptionally low neurobehavioral score. The reasons for the augmentation of tau pathologies in only one T44 tau Tg mouse subjected to mrTBI remain to be elucidated.

Animals↗

[Forensic medical differential diagnosis of craniocerebral trauma in children].

It is emphasized that history, complaints, a comprehensive neurological examination, craniography are not often sufficient for differentiation between brain concussion and mild brain contusion in children because of specific characteristics of craniocerebral trauma (CCT) in such patients. To make an adequate forensic medical diagnosis of CCT in children, it is necessary to take into consideration anatomophysiological peculiarities of a child, biomechanical conditions of the brain injury, to apply modern methods of neurovisualization (ultrasonography, computed and MR imaging), to follow up brain function with quantitative electroencephalography. Improvement of differential forensic-medical assessment of CCT severity in childhood should be made according to the principles of evidence-based medicine.

Child↗