Brain damage in non-missile head injury secondary to a high ICP
ABSTRACT A comprehensive neuropathological analysis was undertaken on 434 patients who died as a result of a non-missile head injury in order to determine the frequency and extent of brain damage secondary to high intracranial pressure (ICP) in head injury. Using the criterion of pressure necrosis in the parahippocampal gyrus as evidence of high ICP due to a supratentorial expanding lesion, it was established that the ICP had been high in 324 cases. In 42 of these there was no other brain damage attributable to a high ICP. There was evidence of secondary brain stem damage in 221 cases and in 44 of these the damage could be seen only microscopically. In 54 cases there was a contralateral peduncular lesion. Other abnormalities were infarction in the territories of various arteries and in the anterior lobe of the pituitary. There was a supracallosal hernia in 80 cases and haemorrhage in the oculomotor nerves in 48 cases. These results further emphasise the frequency and range of brain damage due to secondary vascular factors brought about by high ICP in a patient who has sustained a head injury.
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- "Brain oedema and shift can compromise blood supply and lead to secondary infarction in the corpus callosum and deep grey matter, and elevated intracranial pressure (ICP) can cause damage to the brainstem in TBI (Graham et al., 1987). And although the diagnosis of DAI can only be clearly confirmed by microscopic examination, it may be inferred from specific neuroimaging findings such as haemorrhages in the corpus callosum or areas of rostral brainstem (Geddes, 1997; Geddes et al., 1997). "
ABSTRACT: Traumatic brain injury (TBI) is a serious public health problem. Even injuries classified as mild, the most common, can result in persistent neurobehavioural impairment. Diffuse axonal injury is a common finding after TBI, and is presumed to contribute to outcomes, but may not always be apparent using standard neuroimaging. Diffusion tensor imaging (DTI) is a more recent method of assessing axonal integrity in vivo. The primary objective of the current investigation was to characterize white matter integrity utilizing DTI across the spectrum of chronic TBI of all severities. A secondary objective was to examine the relationship between white matter integrity and cognition. Twenty mild, 17 moderate to severe TBI and 18 controls underwent DTI and neuropsychological testing. Fractional anisotropy, axial diffusivity and radial diffusivity were calculated from the DTI data. Fractional anisotropy was the primary measure of white matter integrity. Region of interest analysis included anterior and posterior corona radiata, cortico-spinal tracts, cingulum fibre bundles, external capsule, forceps minor and major, genu, body and splenium of the corpus callosum, inferior fronto-occipital fasciculus, superior longitudinal fasciculus and sagittal stratum. Cognitive domain scores were calculated from executive, attention and memory testing. Decreased fractional anisotropy was found in all 13 regions of interest for the moderate to severe TBI group, but only in the cortico-spinal tract, sagittal stratum and superior longitudinal fasciculus for the mild TBI group. White Matter Load (a measure of the total number of regions with reduced FA) was negatively correlated with all cognitive domains. Analysis of radial and axial diffusivity values suggested that all severities of TBI can result in a degree of axonal damage, while irreversible myelin damage was only apparent for moderate to severe TBI. The present data emphasize that white matter changes exist on a spectrum, including mild TBI. An index of global white matter neuropathology (White Matter Load) was related to cognitive function, such that greater white matter pathology predicted greater cognitive deficits. Mechanistically, mild TBI white matter changes may be primarily due to axonal damage as opposed to myelin damage. The more severe injuries impact both. DTI provides an objective means for determining the relationship of cognitive deficits to TBI, even in cases where the injury was sustained years prior to the evaluation.Brain 11/2007; 130(Pt 10):2508-19. DOI:10.1093/brain/awm216 · 10.23 Impact Factor