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Diffuse axonal injury and traumatic coma in the primate
- T. Gennarelli, L. Thibault, J. Adams, D. Graham, Carson J. Thompson, R. Marcincin
- Medicine, BiologyAnnals of neurology
- 1 December 1982
It is concluded that axonal damage produced by coronal head acceleration is a major cause of prolonged traumatic coma and its sequelae and is identical to that seen in severe head injury in humans.
Diffuse axonal injury in head injury: Definition, diagnosis and grading
- J. Adams, D. Doyle, I. Ford, T. Gennarelli, D. Graham, D. Mclellan
- Medicine, BiologyHistopathology
- 1 July 1989
Diffuse axonal injury was identified in 122 of a series of 434 fatal non‐missile head injuries–‐10 grade 1, 29 grade 2 and 83 grade 3; in 24 of these cases the diagnosis could not have been made without microscope examination, while in a further 31 microscopical examination was required to establish its severity.
Lateral fluid percussion brain injury: a 15-year review and evaluation.
It is concluded that the LFP brain injury model is an appropriate tool to study the cellular and mechanistic aspects of human TBI that cannot be addressed in the clinical setting, as well as for the development and characterization of novel therapeutic interventions.
Diffuse axonal injury due to nonmissile head injury in humans: An analysis of 45 cases
The available evidence indicates that DAI in human beings occurs at the time of head injury and is not due to complicating factors such as hypoxia, brain swelling, or raised intracranial pressure.
Focal Cerebral Ischaemia in the Rat: 1. Description of Technique and Early Neuropathological Consequences following Middle Cerebral Artery Occlusion
- A. Tamura, D. Graham, J. Mcculloch, G. Teasdale
- Biology, MedicineJournal of cerebral blood flow and metabolism…
- 1 March 1981
The ability to produce a consistent focal ischaemic lesion in the rodent brain provides a technical approach that is sufficiently reproducible to enable investigation of the pathophysiology of ischaemia using recently developed autoradiographic and neurochemical methods.
Multiple proteins implicated in neurodegenerative diseases accumulate in axons after brain trauma in humans
Recent Advances in Neurotrauma
- D. Graham, T. Mcintosh, W. Maxwell, J. Nicoll
- BiologyJournal of neuropathology and experimental…
- 1 August 2000
TBI in humans is heterogeneous, reflecting various pathologies in differing proportions in patients whose genetic background (APOE gene polymorphisms) contributes to the outcome at 6 months, although considerable progress has been made in the understanding of TBI.
Beta amyloid protein deposition in the brain after severe head injury: implications for the pathogenesis of Alzheimer's disease.
- G. Roberts, S. Gentleman, A. Lynch, L. Murray, M. Landon, D. Graham
- Biology, MedicineJournal of neurology, neurosurgery, and…
- 1 April 1994
The data from this study support proposals that increased expression of beta APP is part of an acute phase response to neuronal injury in the human brain, that extensive overexpression ofbeta APP can lead to deposition of beta AP and the initiation of an Alzheimer disease-type process within days, and that head injury may be an important aetiological factor in Alzheimer's disease.
Neuropathological sequelae of traumatic brain injury: relationship to neurochemical and biomechanical mechanisms.
- T. Mcintosh, D. Smith, D. Meaney, M. Kotapka, T. Gennarelli, D. Graham
- Biology, MedicineLaboratory investigation; a journal of technical…
- 1 February 1996
The laboratory investigations linking experimental models of brain injury to clinical diagnosis and treatment are reviewed and the role of neurochemical alterations in contributing to the development of secondary or delayed cellular death and damage is studied.
Apoptosis after traumatic brain injury.
The regional and temporal patterns of apoptosis following TBI and the possible mechanisms underlying trauma-induced apoptosis are reviewed, and whether apoptosis may serve a protective role in the injured brain is considered.