J. Hume Adams

University of Glasgow, Glasgow, Scotland, United Kingdom

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Publications (24)234.69 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. DOI:10.1089/neu.2010.1733 · 3.71 Impact Factor
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    ABSTRACT: The relationship between ventricular fluid pressure and the neuropathology of raised intracranial pressure The 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. DOI:10.1111/j.1365-2990.1976.tb00506.x · 3.93 Impact Factor
  • D.I. Graham · W.L. Maxwell · J Hume Adams · Bryan Jennett ·
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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. DOI:10.1016/S0079-6123(05)50031-1 · 2.83 Impact Factor
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    J Hume Adams · D I Graham · B Jennett ·
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    ABSTRACT: The objective was to discover the nature of brain damage in survivors of head injury who are left with moderate disability. Macroscopic and microscopic examination was carried out on the brains of 20 persons who had died long after a head injury that had been treated in a neurosurgical unit. All had become independent but had various disabilities (moderate disability on the Glasgow outcome scale) Most deaths had been sudden, which had led to their referral from forensic pathologists. Post-traumatic epilepsy was a feature in 75%. An intracranial haematoma had been evacuated in 75%, and in 11 of the 15 with epilepsy. Diffuse axonal injury was found in six patients, five of the mildest type (grade 1) and one of grade 2. No patient had diffuse thalamic damage but one had a small focal ischaemic lesion in the thalamus. No patient had severe ischaemic brain damage, but three had moderate lesions which were bilateral in only one. No patient had severe cortical contusions. In conclusion, the dominant lesion was focal damage from an evacuated intracranial haematoma. Severe diffuse damage was not found, with diffuse axonal injury only mild and thalamic damage in only one patient.
    Journal of Neurology Neurosurgery & Psychiatry 11/2001; 71(4):521-4. DOI:10.1136/jnnp.71.4.521 · 6.81 Impact Factor
  • D.I. Graham · J. Hume Adams · J.A.R. Nicoll · W.L. Maxwell · T.A. Gennarelli ·
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    ABSTRACT: The identification and interpretation of brain damage resulting from a non-missile head injury is often not easy with the result that the most obvious structural damage identified postmortem may not be the most important in trying to establish clinicopathological correlations. For example patients with a fracture of the skull, quite severe cerebral contusions or a large intracranial haematoma that is successfully treated can make an uneventful and complete recovery if no other types of brain damage are present. However, not infrequently more subtle forms of pathology are present and ones that can only be identified microscopically. A systematic and pragmatic approach through the autopsy is therefore required and one that recognises the need for tissue to be retained in ways that are appropriate for cellular and molecular studies.
    Brain Pathology 11/1995; 5(4):397-406. DOI:10.1111/j.1750-3639.1995.tb00618.x · 3.84 Impact Factor
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    ABSTRACT: Traumatically induced hippocampal damage is a frequent sequela of fatal human head injury and is traditionally considered to be the result of decreased cerebral perfusion secondary to raised intracranial pressure (ICP). However, in previous studies employing an experimental model of acceleration head injury, hippocampal lesions have been observed in the absence of high ICP. To further elucidate the role of raised ICP in the production of posttraumatic hippocampal neuronal damage, 14 cases of fatal human nonmissile head injury, in which the measured ICP was less than 20 mm Hg, were subjected to light microscopic evaluation for the frequency and anatomic distribution of hippocampal damage. The mean maximal ICP of the 14 patients was 17.6 mm Hg. Detailed light microscopic evaluation revealed hippocampal lesions in 12 of the 14 cases studied (86%). These lesions were typically bilateral foci of selective neuronal loss in the CA1 subfield of the hippocampus. The nature and distribution of hippocampal lesions were similar to those previously reported both in fatal human head injury associated with elevated ICP and in experimental acceleration head injury without raised ICP. These results provide further evidence that the occurrence of hippocampal neuronal loss following head injury is not exclusively dependent on elevated ICP. Other mechanisms, such as pathologic excitation of neurons, may be involved.
    Journal of Neurotrauma 07/1994; 11(3):317-24. DOI:10.1089/neu.1994.11.317 · 3.71 Impact Factor
  • M J Kotapka · D I Graham · J. Hume Adams · D Doyle · T A Gennarelli ·
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    ABSTRACT: The hippocampus is known to be frequently involved in head injury. In adults, such hippocampal lesions frequently include regions of selective neuronal necrosis. The present report examines the frequency and distribution of hippocampal damage in 37 cases of fatal head injury in children. Damage to the hippocampus was noted in 27 of 37 cases (73%). Lesions were often focal areas of selective neuronal necrosis located in the CA-1 subfield. Other subfields of the hippocampus were involved to lesser degrees. The frequency and distribution of hippocampal damage in fatal childhood head injury is similar to that reported for fatal head injuries of all ages. Pathological evidence of high intracranial pressure and/or hypoxic brain damage in other anatomical locations was present in the majority of cases. Clinical seizures prior to death occurred in 22% of the cases studied. However, these factors could not account for all cases of hippocampal damage in the present report. Thus, the hippocampus is frequently damaged in fatal head injury in children. The mechanisms involved in the production of such damage may involve hypoxia, raised intracranial pressure and altered cerebral perfusion. However, other, yet to be elucidated, mechanisms may be involved.
    Neuropathology and Applied Neurobiology 05/1993; 19(2):128-33. DOI:10.1111/j.1365-2990.1993.tb00417.x · 3.93 Impact Factor
  • Douglas T. Ross · David I. Graham · J. Hume Adams ·
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    ABSTRACT: The GABAergic neurons of the thalamic reticular nucleus, or nucleus reticularis thalami (RT), have been implicated as important components in attentional processing systems. Neurons in the RT are exquisitely sensitive to degeneration following kainic and domoic acid toxicity, experimental global ischemia, human cardiac arrest, and experimental closed head injury in nonhuman primates. The present study was performed to establish whether the selective loss of human RT neurons occurred following severe head injury. Brains from 37 human nonsurvivors of head injury were examined for evidence of RT neuronal loss. RT lesions in were found in 36 of 37 cases, representing 65 of 73 (89%) of the reticular nuclei examined. The incidence of RT lesions was similar in all age groups: 13 of 14 cases (92.9%) in the pediatric (< or = 16 years) group, 33 of 37 (89.2%) in the young adult (18-45 years) group, and 19 of 22 (86.4%) in the older adult (> 45 years) group. RT lesions were characterized by loss of one fourth to three fourths of the neurons from the region of the nucleus associated with the frontal cortex and thalamic mediodorsal (MD) and ventrolateral (VL) nuclei. Sparing of RT neurons correlated highly with the presence of extensive frontal cortical lesions, suggesting that an intact corticothalamic projection was necessary for RT degeneration following head injury. A pathologic cascade with a prominent excitotoxic component is proposed. The loss of these inhibitory thalamic reticular neurons and the resultant thalamic and neocortical neuronal dysfunctions may underlie some forms of attentional deficits that persist following head injury.
    Journal of Neurotrauma 01/1993; 10(2):151-65. DOI:10.1089/neu.1993.10.151 · 3.71 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. DOI:10.1089/neu.1991.8.247 · 3.71 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. DOI:10.1089/neu.1991.8.271 · 3.71 Impact Factor
  • J. Hume Adams · D Doyle · I Ford · TA Gennarelli · D I Graham · D R McLellan ·
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    ABSTRACT: Diffuse axonal injury is one of the most important types of brain damage that can occur as a result of non-missile head injury, and it may be very difficult to diagnose post mortem unless the pathologist knows precisely what he is looking for. Increasing experience with fatal non-missile head injury in man has allowed the identification of three grades of diffuse axonal injury. In grade 1 there is histological evidence of axonal injury in the white matter of the cerebral hemispheres, the corpus callosum, the brain stem and, less commonly, the cerebellum; in grade 2 there is also a focal lesion in the corpus callosum; and in grade 3 there is in addition a focal lesion in the dorsolateral quadrant or quadrants of the rostral brain stem. The focal lesions can often only be identified microscopically. 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 microscopical examination, while in a further 31 microscopical examination was required to establish its severity.
    Histopathology 08/1989; 15(1):49-59. DOI:10.1111/j.1365-2559.1989.tb03040.x · 3.45 Impact Factor
  • P. G. E. Kennedy · J. Hume Adams · D I Graham · G B Clements ·
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    ABSTRACT: A retrospective clinical and pathological analysis has been performed of 24 cases of herpes simplex virus encephalitis (HSE) seen at the Institute of Neurological Sciences, Glasgow, between 1972 and 1985. All patients had been diagnosed on the basis of isolation of herpes simplex virus (HSV) from, and/or the demonstration of characteristic histological changes of acute necrotizing encephalitis (ANE) in brain biopsy and/or autopsy tissue. Clinical presentation on admission included a prodromal influenza-like illness (46%), sudden onset of headache and confusion (54%), meningism (38%), deep coma (42%), aphasia (54%) and focal neurological signs (79%). Seizures occurred in 46% of cases during the course of the illness. Of the 24 cases, 14 (58%) died and 10 (42%) survived. Intravenous acyclovir treatment was associated with the best prognosis. Cerebral biopsy of one temporal lobe was performed in 22 cases and in 19 of these a positive histological diagnosis of HSE could be made. HSV was isolated from 15 of the 19 (79%) biopsied cases in whom virus isolation was attempted. Only seven out of the 15 cases (47%) in which immunofluorescence assays for HSV antigens were performed were unequivocally positive. Herpes simplex virus was isolated in culture from all cases which were negative by immunofluorescence. Immunocytochemical analysis on tissue sections of five representative brain biopsies demonstrated the presence of HSV antigens in some astrocytes, neurons and macrophages especially within areas of inflammatory infiltration. In situ hybridization experiments with a cloned HSV DNA probe demonstrated viral RNA in astrocytes, neurons and macrophages in two human biopsies and mouse brains in areas broadly corresponding to the distribution of viral antigen labelling. The combined immunocytochemical and in situ hybridization procedure showed that many but not all of the cells containing viral RNA also contained HSV antigens, indicating a productive infection in these double-labelled cells.
    Neuropathology and Applied Neurobiology 10/1988; 14(5):395-415. DOI:10.1111/j.1365-2990.1988.tb01141.x · 3.93 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 08/1988; 155(4):327 - 335. DOI:10.1002/path.1711550408 · 7.43 Impact Factor
  • R A Rodda · J Hume Adams · D I Graham · D Doyle ·
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    ABSTRACT: Brain damage in fatal non-missile head injury is outlined in 100 cases with and in 100 cases without an intracranial hematoma. The patients with intracranial hematomas were significantly older, and had a higher incidence of lucid interval and of unilateral diffuse brain swelling but a lower incidence of ischemic lesions in the cerebral cortex and of bilateral diffuse brain swelling than the patients with no hematoma. Cases with unilateral hematomas and cases with unilateral diffuse brain swelling had significantly more severe ipsilateral cerebral contusions.
    Clinical neuropathology 01/1987; 6(4):179-84. · 1.53 Impact Factor
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    C G Harper · D Doyle · J. Hume Adams · D I Graham ·
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    ABSTRACT: Pituitary glands, obtained at necropsy from a consecutive series of 100 patients who had died as a result of non-missile head injuries, were examined to define the incidence and pathogenesis of abnormality.
    Journal of Clinical Pathology 08/1986; 39(7):769-73. DOI:10.1136/jcp.39.7.769 · 2.92 Impact Factor
  • J.Hume Adams · D Doyle · D.I. Graham · A E Lawrence · D.R. Mclellan ·
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    ABSTRACT: 82 cases of diffuse axonal injury were found at necropsy in 635 patients with fatal nonmissile head injuries. 13 of these injuries were attributable to falls, and in all the patients fell from a considerable height. Diffuse axonal injury was not found in those with head injuries caused by a simple fall--ie, a fall from not more than the person's own height--but there was a statistically significant association between the presence of diffuse axonal injury and falls from a considerable height. These results indicate that diffuse axonal injury rarely, if ever, occurs as a result of a fall unless the patient has fallen some distance.
    The Lancet 01/1985; 2(8417-8418):1420-2. DOI:10.1016/S0140-6736(84)91620-9 · 45.22 Impact Factor
  • J. Hume Adams · D I Graham · Lilian S. Murray · Grace Scott ·
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    ABSTRACT: Forty-five cases of diffuse axonal injury (DAI) brought about by nonmissile head injury in humans are analyzed and compared with 132 cases of fatal head injury without DAI. All cases were subjected to a comprehensive neuropathological study. In the patients with DAI a statistically significant lower incidence of lucid interval, fracture of the skull, cerebral contusions, intracranial hematoma, and evidence of high intracranial pressure were found, with a higher incidence of head injury due to road traffic accident. Brain swelling and hypoxic brain damage were not statistically different in the two groups. The features of DAI in humans are compared with the DAI that has been produced in subhuman primates by pure inertial loading brought about by angular acceleration of the head. 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.
    Annals of Neurology 12/1982; 12(6):557-63. DOI:10.1002/ana.410120610 · 9.98 Impact Factor
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    ABSTRACT: Traumatic coma was produced in 45 monkeys by accelerating the head without impact in one of three directions. The duration of coma, degree of neurological impairment, and amount of diffuse axonal injury (DAI) in the brain were directly related to the amount of coronal head motion used. Coma of less than 15 minutes (concussion) occurred in 11 of 13 animals subjected to sagittal head motion, in 2 of 6 animals with oblique head motion, and in 2 of 26 animals with full lateral head motion. All 15 concussioned animals had good recovery, and none had DAI. Conversely, coma lasting more than 6 hours occurred in one of the sagittal or oblique injury groups but was present in 20 of the laterally injured animals, all of which were severely disabled afterward. All laterally injured animals had a degree of DAI similar to that found in severe human head injury. Coma lasting 16 minutes to 6 hours occurred in 2 of 13 of the sagittal group, 4 of 6 in the oblique group, and 4 of 26 in the lateral group, these animals had less neurological disability and less DAI than when coma lasted longer than 6 hours. These experimental findings duplicate the spectrum of traumatic coma seen in human beings and include axonal damage identical to that seen in sever head injury in humans. Since the amount of DAI was directly proportional to the severity of injury (duration of coma and quality of outcome), we conclude that axonal damage produced by coronal head acceleration is a major cause of prolonged traumatic coma and its sequelae.
    Annals of Neurology 12/1982; 12(6):564-74. DOI:10.1002/ana.410120611 · 9.98 Impact Factor
  • D I Graham · J.Hume Adams · David Doyle ·
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    ABSTRACT: The incidence and distribution of ischaemic brain damage in a consecutive series of 151 patients who died as a result of a non-missile head injury in the Institute of Neurological Sciences was determined on the basis of a comprehensive neuropathological and neurohistological examination. Ischaemic damage was identified in 138 cases (91%) even after excluding cases who only had necrosis and infarction related to contusions or fat embolism, and infarction in the brain stem of the type conventionally associated with raised intracranial pressure. The ischaemic damage was assessed as severe in 37 (27%), moderately severe in 59 (43%) and mild in 42 (30%), and in the 138 cases with ischaemic brain damage it was found more frequently in the hippocampus (122 cases; 81%), and in the basal ganglia (119 cases; 79%) than in the cerebral cortex (70 cases; 46%) and in the cerebellum (67 cases; 44%). There were statistically significant correlations between ischaemic brain damage and either an episode of hypoxia or of raised intracranial pressure. From the nature of the brain damage it seems likely that much of it was due to a reduction in the cerebral perfusion pressure. This study has shown that ischaemic brain damage is common after head injury, that at least a proportion of it is probably avoidable, and that it is more important as a cause of mortality and morbidity after head injury than has been hitherto realised.
    Journal of the Neurological Sciences 01/1979; 39(2-3):213-34. DOI:10.1016/0022-510X(78)90124-7 · 2.47 Impact Factor

    Brain 01/1977; 100(3):489-502. DOI:10.1093/brain/100.3.489 · 9.20 Impact Factor