University of Glasgow, Glasgow, Scotland, United Kingdom

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Publications (6)29.46 Total impact

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    ABSTRACT: We investigated how the occurrence and severity of the main neuropathological types of traumatic brain injury (TBI) influenced the severity of disability after a head injury. Eighty-five victims, each of whom had lived at least a month after a head injury but then died, were studied. Judged by the Glasgow Outcome Scale (GOS), before death 35 were vegetative, 30 were severely and 20 were moderately disabled. Neuropathological assessment showed that 71 (84%) victims had sustained cerebral contusions, 49 (58%) had diffuse axonal injury (DAI), 57 (67%), had ischemic brain damage (IBD), 58 (68%) had symmetrical ventricular enlargement, and in 47 (55%) intracranial pressure (ICP) had been increased. Thirty-five (41%) had undergone evacuation of an intracranial hematoma. Brainstem damage was seen in only 11 (13%). Analysis (χ(2) test for trends) of the relationship between these features and outcome showed that findings of DAI, raised ICP, thalamic damage, or ventricular enlargement (all p<0.005), and IBD (p=0.04) were associated with an increasingly worse outcome. Conversely, moderate or severe contusions (p=0.001) were increasingly associated with better outcomes, and evacuation of a hematoma was associated (p=0.001) with outcomes likely to be better than vegetative. We conclude that diffuse or multifocal neuropathological patterns of TBI from primary axonal injury or secondary ischemic damage are most likely to be associated with the most severely impaired outcomes after a head injury.
    Journal of neurotrauma 03/2011; 28(5):701-9. · 4.25 Impact Factor
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    ABSTRACT: The relationship between ventricular fluid pressure and the neuropathology of raised intracranial pressureThe brains from 56 patients whose ventricular fluid pressure had been continuously monitored during life have been subjected to a neuropathological analysis. This has shown that the morphological criterion of a significantly high intracranial pressure during life is pressure necrosis in one or both parahippocampal gyri. In patients known to have had a high ventricular fluid pressure, there is also a high incidence of pressure necrosis in the cingulate gyrus and infarction in the medial occipital cortex (‘calcarine infarction’), but these changes do not occur in the absence of pressure necrosis in the parahippocampal gyri. Conventional maeroscopic tentorial and supracallosal herniae may occur without the intracranial pressure having been high. There was no correlation between pressure necrosis in the parahippocampal gyri and hypoxic necrosis in the hippocampus: this suggests that a high intracranial pressure is not an important factor in the pathogenesis of such hypoxic necrosis. It is concluded that the neuropathologist can state with a high degree of accuracy post mortem if intracranial pressure has been significantly high, i. e. an increase associated with a pressure differential between the supratentorial and infratentorial compartments, even when it has not been monitored clinically.
    Neuropathology and Applied Neurobiology 05/2008; 2(4):323 - 332. · 4.84 Impact Factor
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    ABSTRACT: A detailed neuropathological study was undertaken of the brains of patients who had been assessed clinically as vegetative after blunt head injury. There were 35 cases, (33 male; median age 38 years) with a survival of 6.5-19 months (median 9): 17 were injured in a road traffic accident, 9 after assault and 6 after a fall; 3 were recorded as having had a lucid interval. There was an intracranial hematoma in 9 and the median contusion index was 4; raised intracranial pressure was identified in 25, grades 2 and 3 diffuse traumatic axonal injury was present in 25, ischemic damage in 15 and hydrocephalus in 27. Thalamic and hippocampal damage was present in 28 and stereological studies revealed a differential loss of neurons in three principal nuclei of the thalamus and in different sectors of the hippocampus. Immunohistochemistry provided evidence of an inflammatory reaction and in situ DNA fragmentation, features that are strongly indicative of a continuing neuronal loss in subcortical gray matter. These findings provide evidence for the importance of diffuse brain damage to white matter as the structural basis of the vegetative state after blunt head injury with contributions from neuronal loss in the thalami and the hippocampus. Although amyloid plaques and tau inclusions were identified in some, their contribution did not seem important in the ultimate clinical outcome.
    Progress in brain research 02/2005; 150:445-55. · 5.10 Impact Factor
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    ABSTRACT: Traumatically induced subtotal hippocampal neuronal loss traditionally has been considered a consequence of intracranial hypertension and impaired cerebral perfusion. We have examined the frequency and distribution of hippocampal lesions in an acceleration model of brain injury in 54 anesthetized nonhuman primates undergoing physiologic monitoring and subjected postinjury to comprehensive neuropathologic examination. Hippocampal lesions occurred in 32/54 animals (59%). These lesions always involved the CA-1 hippocampal subfield and were bilateral in 24 animals. Hippocampal involvement was not associated with marked elevation of intracranial pressure or depression of cerebral perfusion pressure. These lesions occurred in the absence of involvement of other brain regions considered selectively vulnerable to hypoxic insults. Hippocampal damage occurred in 46% of animals with mild injury characterized by brief periods of unconsciousness and no residual neurologic deficit. Ninety-four percent of animals with severe injuries and prolonged posttraumatic coma had hippocampal involvement. Traumatically induced selective neuronal necrosis of the hippocampus is a specific lesion not explained by the conventional mechanistic theories of head injury. An alternative hypothesis, such as excitotoxicity involving glutamate or other neurotransmitters, may account for the lesions demonstrated in this study.
    Journal of Neurotrauma 02/1991; 8(4):247-58. · 3.97 Impact Factor
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    ABSTRACT: In a variety of brain injury models, both reactive axonal change and microvascular abnormalities occur. Development of a stretch injury model in the guinea pig optic nerve has allowed for the characterization of the early axonal response to injury. In this same model, we have now attempted to characterize those morphologic changes occurring in the visual system microvasculature after injury. Thirty adult guinea pigs were subjected to axonal stretch injury and killed at posttraumatic survival periods ranging from 10 minutes to 14 days. Twenty animals were examined by scanning electron microscopy (SEM) for the detection of posttraumatic changes in the surface morphology of the microvasculature, and 10 animals were processed for transmission electron microscopy (TEM) analysis. Through this approach, increased pit vesicle activity and formation of endothelial microvilli were recognized within 10 minutes of injury. Pit vesicle activity returned to control levels by 2 hours. The formation of endothelial microvilli was widespread, affecting the microvessels in both the stretched and unstretched optic nerves and in the chiasm. The greatest response developed most slowly in the stretched nerve, and it was faster but less marked in the unstretched nerve and chiasm. Microvilli were more numerous in larger vessels. Related astrocytic swelling/lucency was not apparent until 6 hours after injury. The astrocyte response was less marked than that documented after brain injury. The results of this investigation demonstrate a widespread microvascular response to stretch injury of the guinea pig optic nerve. Comparison with the documented responses to traumatic brain injury indicates different rates of response to different types of insult.
    Journal of Neurotrauma 02/1991; 8(4):271-9. · 3.97 Impact Factor
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    ABSTRACT: There is increasing evidence that there is a direct response of the cerebral microvasculature to head injury. We have investigated using SEM and TEM the response of microvessels within the white matter of the baboon brain to lateral head acceleration. There is rapid endothelial disruption and swelling of perivascular astrocytes near the sites of petechial haemorrhage. The formation of microvilli in all vessels reaches a peak at 6 h and extends at least 5 mm from the site of haemorrhage. The astrocyte response suggests a partial recovery by 6 h. The endothelial response is most marked in arterioles and venules and is maintained for 6 days after injury. We suggest there is a biphasic cerebrovascular response to brain injury. First there is rapid astrocytic swelling possibly correlated with transient disruption of the blood-brain barrier. This is followed by morphological changes in the endothelium of all vessels which are most marked in arterioles and venules and extend considerable distances throughout the neuropile. This response is discussed in the light of disruption of the blood–brain barrier.
    The Journal of Pathology 07/1988; 155(4):327 - 335. · 7.33 Impact Factor