Neurologic aspects of traumatic brain injury

Gottesman, Rebecca F.; Komotar, Ricardo J.; Hillis, Argye E.

doi:10.1080/09540260310001606683

Cited by 28 publications

(21 citation statements)

References 37 publications

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“…According to clinical reports, approximately half of the patients who suffer a penetrating brain injury may also develop epilepsy [25–28]. Generally, the risk of post-traumatic epilepsy increases with lesion severity; nevertheless, epileptogenesis can also be triggered by very small lesions [29]. Other severe insults with strongly epileptogenic features include cerebrovascular diseases, such as stroke [30].…”

Section: Discussionmentioning

confidence: 99%

X-ray fluorescence analysis of long-term changes in the levels and distributions of trace elements in the rat brain following mechanical injury

et al. 2010

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This paper describes the results of the application of X-ray fluorescence microscopy to the qualitative, topographic and quantitative elemental analysis of nervous tissue from rats with neocortical brain injury. The tissue samples were analyzed with a 15 μm beam defined by the size of the polycapillary focus. Raster scanning of the samples generated 2D cartographies, revealing the distributions of elements such as P, S, Cl, K, Ca, Fe, Cu, and Zn. Special emphasis was placed on the analysis of the areas neighboring the lesion site and the hippocampal formation tissue. The results obtained for rats with mechanical brain injuries were compared with those recorded for controls and animals with pilocarpine-induced seizures. There were no significant differences in the elemental compositions of gray and white matter between injured and uninjured brain hemispheres. A higher level of Ca was observed in the gray matter of both of the hemispheres in brains with neocortical injuries. A similar relation was noticed for Fe in the white matter. A comparative study of hippocampal formation tissue showed a statistically significant decrease in the mass per unit area of P in the dentate gyrus (DG) and the hilus (H) of DG for animals with brain lesions in comparison with the control group. Analogous relations were found for Cu in the DG and Zn in sector 3 of Ammon’s horn (CA3) and the DG. It is important to note that identical changes in the same areas were observed for animals with pilocarpine-induced seizures in our previous study.

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Section: Discussionmentioning

confidence: 99%

X-ray fluorescence analysis of long-term changes in the levels and distributions of trace elements in the rat brain following mechanical injury

et al. 2010

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“…Many in this group had known brain injuries (birth injuries or acquired traumatic brain injuries), and this is known to be associated with increased risk of seizures. 24,34,35 This may partly explain the increased number of "unknown" causes of death, and causes related to epilepsy, in the no-epilepsy group (see table 2). …”

Section: Discussionmentioning

confidence: 99%

Causes of death in remote symptomatic epilepsy

Day¹,

Wu²,

Strauss³

et al. 2005

Neurology

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Abstract-Objective:To determine the causes of death of individuals with developmental disabilities that occur more frequently among those with remote symptomatic epilepsy (i.e., epilepsy occurring in persons with developmental delay or identified brain lesions) than for those without. Methods: The authors compared causes of mortality in persons with (n ϭ 10,030) and without (n ϭ 96,163) history of epilepsy in a California population of persons with mild developmental disabilities, 1988 to 2002. Subjects had traumatic brain injury, cerebral palsy, Down syndrome, autism, or a developmental disability with other or unknown etiology. There were 721,759 person-years of data, with 2,397 deaths. Underlying causes of death were determined from the State of California's official mortality records. Cause-specific death rates and standardized mortality ratios (SMRs) were computed for those with and without epilepsy relative to subjects in the California general population. Comparisons were then made between SMRs of those with and without epilepsy, and CIs on the ratios of SMRs were determined. Results: Death rates for persons with epilepsy were elevated for several causes. The greatest excess was due to seizures (International Classification of Diseases-9 [ICD-9] 345; SMR 53.1, 95% CI 28.0 to 101.0) and convulsions (ICD-9 780.3; SMR 25.2, 95% CI 11.7 to 54.2). Other causes occurring more frequently in those with epilepsy included brain cancer (SMR 5.2, 95% CI 2.2 to 12.1), respiratory diseases (SMR 1.7, 95% CI 1.2 to 2.5), circulatory diseases (SMR 1.3, 95% CI 1.0 to 1.7), and accidents (SMR 2.7, 95% CI 1.9 to 3.7), especially accidental drowning (SMR 12.8, 95% CI 7.0 to 23.2). Conclusions: Remote symptomatic epilepsy is associated with an increased risk of death. Seizures, aspiration pneumonia, and accidental drowning are among the leading contributors. NEUROLOGY 2005;65:216-222 Persons with epilepsy are at increased risk of death compared with the general population.

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“…The clinical status of patients with more severe kinds of traumatic trauma injury and prolonged coma is evaluated by the Glasgow Coma Scale, which assesses eye opening and verbal and motor responses [115]. Oedema and pain (headache) occur early on after traumatic brain injury [116,117], but are probably not related to inflammatory responses.…”

Section: Ischaemic and Traumatic Brain Injurymentioning

confidence: 99%

(Peri)vascular production and action of pro-inflammatory cytokines in brain pathology

2006

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In response to tissue injury or infection, the peripheral tissue macrophage induces an inflammatory response through the release of IL-1beta (interleukin-1beta) and TNFalpha (tumour necrosis factor alpha). These cytokines stimulate macrophages and endothelial cells to express chemokines and adhesion molecules that attract leucocytes into the peripheral site of injury or infection. The aims of the present review are to (i) discuss the relevance of brain (peri)vascular cells and compartments to bacterial meningitis, HIV-1-associated dementia, multiple sclerosis, ischaemic and traumatic brain injury, and Alzheimer's disease, and (ii) to provide an overview of the production and action of pro-inflammatory cytokines by (peri)vascular cells in these pathologies of the CNS (central nervous system). The brain (peri)vascular compartments are highly relevant to pathologies affecting the CNS, as infections are almost exclusively blood-borne. Insults disrupt blood and energy flow to neurons, and active brain-to-blood transport mechanisms, which are the bottleneck in the clearance of unwanted molecules from the brain. Perivascular macrophages are the most reactive cell type and produce IL-1beta and TNFalpha after infection or injury to the CNS. The main cellular target for IL-1beta and TNFalpha produced in the brain (peri)vascular compartment is the endothelium, where these cytokines induce the expression of adhesion molecules and promote leucocyte infiltration. Whether this and other effects of IL-1 and TNF in the brain (peri)vascular compartments are detrimental or beneficial in neuropathology remains to be shown and requires a clear understanding of the role of these cytokines in both damaging and repair processes in the CNS.

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Neurologic aspects of traumatic brain injury

Cited by 28 publications

References 37 publications

X-ray fluorescence analysis of long-term changes in the levels and distributions of trace elements in the rat brain following mechanical injury

X-ray fluorescence analysis of long-term changes in the levels and distributions of trace elements in the rat brain following mechanical injury

Causes of death in remote symptomatic epilepsy

(Peri)vascular production and action of pro-inflammatory cytokines in brain pathology

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