Fatal Non-missile Head Injuries Research Articles

Ischemic brain damage is still common in fatal nonmissile head injury

Ischemic brain damage is still common in fatal nonmissile head injury

Ischaemic brain damage is still common in fatal non-missile head injury.

A detailed neuropathological examination has been undertaken on a consecutive series of head injuries dying in the Institute of Neurological Sciences, Glasgow, between 1968-72 (151 cases) and 1981-82 (112 cases) in order to determine the frequency and distribution of any ischaemic brain damage. Ischaemic damage was found in the brains of 92% of the 1968-72 cases and in 88% of the 1981-82 cases: there was no statistical difference in the amount of moderately severe and severe ischaemic damage in the two groups, 55% and 54% respectively. There was evidence, however, that an increased number of patients with severe ischaemic brain damage was admitted in 1981-82 as a result of a changed admission policy of the Department of Neurosurgery that resulted in an increased detection of intracranial haematomas. It is concluded that ischaemic brain damage is still common after severe head injury, and it seems likely that it remains an important cause of mortality and morbidity.

Brain damage in fatal non-missile head injury in relation to age and type of injury.

Brain damage in a series of 635 fatal non-missile head injuries has been analysed with particular reference to the age of the patient and the type of injury. The differences in the type of brain damage in relation to age were less than we had anticipated, lending further support to the contention that the aged brain has a reduced potential for recovery. The analysis confirms the relationship between road traffic accidents, diffuse axonal injury, gliding contusions and 'basal ganglia' haematomas, and the importance of diffuse brain swelling resulting from a head injury in children.

Brain damage in fatal non-missile head injury without high intracranial pressure.

As part of a comprehensive study of brain damage in 635 fatal non-missile head injuries, the type and prevalence of brain damage occurring in the absence of high intracranial pressure were analysed. Of 71 such cases, 53 sustained their injury as a result of a road traffic accident; only 25 experienced a lucid interval. Thirty eight had a fractured skull, a mean total contusion index of 12.9 and diffuse axonal injury in 29: severe to moderate ischaemic damage was present in the cerebral cortex in 25, brain swelling in 13, and acute bacterial meningitis in nine. The prevalence and range of brain damage that may occur in the absence of high intracranial pressure are important to forensic pathologists in the medicolegal interpretation of cases of fatal head injury.

The autopsy in fatal non-missile head injuries.

The identification and interpretation of brain damage resulting from a non-missile head injury is often not easy — if only because the most obvious structural damage identified post mortem may not be the most important. There must be many occasions when death is certified as being due to fracture of the skull and cerebral contusions when neither may have even been the reason for the patient having been unconscious. Patients with a fracture and quite severe contusions can make an uneventful and complete recovery from their injury if no other types of brain damage are present (cf. Figs. 7 and 9). The aim of this chapter therefore is to advise on a pragmatic approach to the autopsy, to define clearly the various types of brain damage that may occur, and to remind the pathologist that he must know what he is looking for. This is particularly important when there is no evidence of severe cerebral contusions or of a large intracranial haematoma. A patient may die as a result of a non-missile head injury without either of these being present. Thus a systematic approach is required, and the pathologist must be aware of the more subtle — and often most important — types of brain damage that can occur in a patient who sustains a non-missile head injury. Frequently the damage can be identified only microscopically.

Deep intracerebral (basal ganglia) haematomas in fatal non-missile head injury in man.

Deep intracerebral (basal ganglia) haematomas were found post mortem in 63 of 635 fatal non-missile head injuries. In patients with a basal ganglia haematoma, contusions were more severe, there was a reduced incidence of a lucid interval, and there was an increased incidence of road traffic accidents, gliding contusions and diffuse axonal injury than in patients without this type of haematoma. Intracranial haematoma is usually thought to be a secondary event, that is a complication of the original injury, but these results suggest that a deep intracerebral haematoma is a primary event. If a deep intracerebral haematoma is identified on an early CT scan it is likely that the patient has sustained severe diffuse brain damage at the time of injury. In the majority of head injuries damage to blood vessels or axons predominates. In patients with a traumatic deep intracerebral haematoma, it would appear that the deceleration/acceleration forces are such that both axons and blood vessels within the brain are damaged at the time of injury.

Diffuse axonal injury in head injuries caused by a fall.

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.

Acceleration induced head injury in the monkey. II. Neuropathology.

A comprehensive neuropathological study has been undertaken in 53 adult subhuman primates subjected to a single sagittal plane angular acceleration impulse. The types of injury produced correlated well with the input force and were very similar to those seen in fatal nonmissile head injuries in man. There was a fracture of the skull in 14 animals. Subdural haematoma occurred in 33 animals, contusions in the frontal and temporal regions of the brain in 39, and discrete intracerebral haematoma in 4. Brain shift and tentorial herniation were also seen. There was evidence of hypoxic brain damage in 22 animals, and central chromatolysis in Betz cells and in the motor nuclei of the brain stem in 16.

Brain damage in fatal non-missile head injury.

Brain damage in fatal non-missile head injury.

Ischaemic brain damage in fatal non-missile head injuries

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.

Diffuse brain damage of immediate impact type. Its relationship to 'primary brain-stem damage' in head injury.

In a neuropathological analysis of 151 fatal non-missile head injuries, there were 19 cases with focal lesions in the dorsolateral quadrant of the brain-stem in the corpus callosum, and histological evidence of diffuse damage to white matter. Eight of these cases had not experienced a high intracranial pressure during life. All 19 cases had been rendered unconscious at the moment of impact and had remained so or in the persistent vegetative state until death. It is therefore concluded that diffuse damage to white matter may occur as a primary event at the moment of impact, that is, it is one type of immediate impact damage to the brain. It is also concluded that this type of damage is the pathological basis of 'primary brain-stem injury' since in no patient thought clinically to have sustained 'primary brain-stem injury' were abnormalities confined to the brain-stem. Since no patient with this type of brain damage recovered consciousness after injury, it is probable that diffuse damage to white matter is the most important single factor governing the outcome in a patient who sustains a non-missile head injury.