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Traumatic Axonal Injury (traumatic axonal + injury)

Distribution by Scientific Domains
Medical Sciences100%

Selected Abstracts

Traumatic axonal injury: practical issues for diagnosis in medicolegal cases

NEUROPATHOLOGY & APPLIED NEUROBIOLOGY, Issue 2 2000
J. F. Geddes
In the 25 years or so after the first clinicopathological descriptions of diffuse axonal injury (DAI), the criterion for diagnosing recent traumatic white matter damage was the identification of swollen axons (,bulbs') on routine or silver stains, in the appropriate clinical setting. In the last decade, however, experimental work has given us greater understanding of the cellular events initiated by trauma to axons, and this in turn has led to the adoption of immunocytochemical methods to detect markers of axonal damage in both routine and experimental work. These methods have shown that traumatic axonal injury (TAI) is much more common than previously realized, and that what was originally described as DAI occupies only the most severe end of a spectrum of diffuse trauma-induced brain injury. They have also revealed a whole field of previously unrecognized white matter pathology, in which axons are diffusely damaged by processes other than head injury; this in turn has led to some terminological confusion in the literature. Neuropathologists are often asked to assess head injuries in a forensic setting: the diagnostic challenge is to sort out whether the axonal damage detected in a brain is indeed traumatic, and if so, to decide what , if anything , can be inferred from it. The lack of correlation between well-documented histories and neuropathological findings means that in the interpretation of assault cases at least, a diagnosis of ,TAI' or ,DAI' is likely to be of limited use for medicolegal purposes [source]

There is no evidence of an association in children and teenagers between the apolipoprotein E ,4 allele and post-traumatic brain swelling

NEUROPATHOLOGY & APPLIED NEUROBIOLOGY, Issue 6 2004
T. J. Quinn
Traumatic brain injury (TBI) is an important cause of mortality and disability in children and teenagers. A particular feature of the neuropathology at post-mortem is brain swelling. The cause of the swelling in some cases is not known, while in others it is associated with traumatic axonal injury or hypoxia. Apolipoprotein E (APOE) ,4 allele is known to be an important genetic determinant of outcome in children after TBI. We hypothesized a relationship between possession of APOE,4 and diffuse traumatic brain swelling. A total of 165 cases aged between 2 and 19 years were identified from the department's tissue archive. APOE genotype was determined by polymerase chain reaction (PCR) in 106 cases. Bilateral swelling was present in 44 cases (11 with APOE,4), unilateral swelling in 25 cases (7 with APOE,4) and in 36 cases (9 with APOE,4) there was no evidence of brain swelling. There was no significant relationship between possession of APOE,4 and the presence of cerebral swelling (,2 = 0.09, df = 2, P = 0.96). The 95% confidence interval for difference in proportions with swelling, in, those, with, and, without, the,APOE,,4, is,,19%, to 22%. Thus, a significant relationship was not found between diffuse brain swelling and possession of APOE,4, and in this cohort of patients there was an identifying cause of the brain swelling in all cases. [source]

Traumatic axonal injury: practical issues for diagnosis in medicolegal cases

NEUROPATHOLOGY & APPLIED NEUROBIOLOGY, Issue 2 2000
J. F. Geddes
In the 25 years or so after the first clinicopathological descriptions of diffuse axonal injury (DAI), the criterion for diagnosing recent traumatic white matter damage was the identification of swollen axons (,bulbs') on routine or silver stains, in the appropriate clinical setting. In the last decade, however, experimental work has given us greater understanding of the cellular events initiated by trauma to axons, and this in turn has led to the adoption of immunocytochemical methods to detect markers of axonal damage in both routine and experimental work. These methods have shown that traumatic axonal injury (TAI) is much more common than previously realized, and that what was originally described as DAI occupies only the most severe end of a spectrum of diffuse trauma-induced brain injury. They have also revealed a whole field of previously unrecognized white matter pathology, in which axons are diffusely damaged by processes other than head injury; this in turn has led to some terminological confusion in the literature. Neuropathologists are often asked to assess head injuries in a forensic setting: the diagnostic challenge is to sort out whether the axonal damage detected in a brain is indeed traumatic, and if so, to decide what , if anything , can be inferred from it. The lack of correlation between well-documented histories and neuropathological findings means that in the interpretation of assault cases at least, a diagnosis of ,TAI' or ,DAI' is likely to be of limited use for medicolegal purposes [source]

Cell Death Mechanisms Following Traumatic Brain Injury

BRAIN PATHOLOGY, Issue 2 2004
Ramesh Raghupathi PhD
Neuronal and glial cell death and traumatic axonal injury contribute to the overall pathology of traumatic brain injury (TBI) in both humans and animals. In both head-injured humans and following experimental brain injury, dying neural cells exhibit either an apoptotic or a necrotic morphology. Apoptotic and necrotic neurons have been identified within contusions in the acute post-traumatic period, and in regions remote from the site of impact in the days and weeks after trauma, while degenerating oligodendrocytes and astrocytes have been observed within injured white matter tracts. We review and compare the regional and temporal patterns of apoptotic and necrotic cell death following TBI and the possible mechanisms underlying trauma-induced cell death. While excitatory amino acids, increases in intracellular calcium and free radicals can all cause cells to undergo apoptosis, in vitro studies have determined that neural cells can undergo apoptosis via many other pathways. It is generally accepted that a shift in the balance between pro- and anti-apoptotic protein factors towards the expression of proteins that promote death may be one mechanism underlying apoptotic cell death. The effect of TBI on cellular expression of survival promoting-proteins such as Bcl-2, Bcl-xL, and extracellular signal-regulated kinases, and death-inducing proteins such as Bax, c-Jun N-terminal kinase, tumor-suppressor gene, p53, and the calpain and caspase families of proteases are reviewed. In light of pharmacologic strategies that have been devised to reduce the extent of apoptotic cell death in animal models of TBI, our review also considers whether apoptosis may serve a protective role in the injured brain. Together, these observations suggest that cell death mechanisms may be representative of a continuum between apoptotic and necrotic pathways. [source]