J H Adams

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.

Axonal injury: a universal consequence of fatal closed head injury?

Abstractβ-Amyloid precursor protein immunostaining has recently been shown to be a reliable method for detecting the damage to axons associated with fatal head injury. In an attempt to compare the efficacy of this technique with conventional histological detection of axonal damage, we have reanalysed sections from a large well-characterised series of head-injured and control patients. The results indicate that the frequency of axonal injury has been vastly underestimated using conventional silver techniques, and that axonal injury may in fact be an almost universal consequence of fatal head injury.

Head Injury in Man and Experimental Animals: Neuropathology

All of the principal types of brain damage that occur in man as a result of a non-missile head injury, viz. cerebral contusions, intracranial haematoma, raised intracranial pressure, diffuse axonal injury, diffuse hypoxic damage, and diffuse swelling have been produced in subhuman primates subjected to inertial, i.e. non-impact, controlled angular acceleration of the head through 60 degrees in the sagittal, oblique and lateral planes.

THE CONTUSION INDEX: A REAPPRAISAL IN HUMAN AND EXPERIMENTAL NON-MISSILE HEAD INJURY

Adams J. H., Doyle D., Graham D. I., Lawrence A. E., McLellan D. R., Gennarelli T. A., Pastuszko M. & Sakamoto T. (1985) Neuropathology and Applied Neurobiology 11, 299–308

The neuropathology of the vegetative state after head injury.

A detailed neuropathological study of patients identified clinically after head injury as either severely disabled (SD, n = 30) or vegetative (VS, n = 35) has been carried out to determine the nature and frequency of the various pathologies that form the basis of these clinical states. Patients who were SD were older (SD median 49.5 yrs vs. VS median 38 yrs, p = .04), more likely to have a lucid interval (SD 31% vs. VS 9%, p = .03), and to have had an acute intracranial haematoma (SD 70% vs. VS 26%, p < .001). SD patients less often had severe, Grades (2 or 3) of traumatic diffuse axonal injury (SD 30% vs. VS 71%, p = .001) and less often had thalamic damage (SD 37% vs. VS 80%, p < .001). Similar features of both focal and diffuse damage were present in some SD and VS cases with both groups having considerable damage to white matter and to the thalamus. It is concluded that the principal structural basis of both SD and VS is diffuse traumatic axonal injury (DAI) with widespread damage to white matter and changes in the thalami. However, both ischaemic brain damage and the vascular complications of raised intracranial pressure contributed to the clinical signs and symptoms.

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.

Analysis of abnormalities in pituitary gland in non-missile head injury: study of 100 consecutive cases.

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.

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.

Computerised tomography after recent severe head injury in patients without acute intracranial haematoma.

Sixty patients with severe head injury who did not have an acute intracranial haematoma on CAT scanning are reviewed. The scans are correlated with the level of consciousness at the time of scanning and with the outcome six months after injury. The initial scan was interpreted as being normal in 38% of the cases. In the remainder the most common abnormalities were small ventricles and areas of mixed increased and decreased density interpreted as contusions. All the patients with small ventricles were under 20 years of age. Postmortem examinations were undertaken on 15 of the 19 fatal cases. There was evidence of a high intracranial pressure in 12, cerebral contusions were absent or minimal in 10, there was diffuse immediate impact damage to white matter in six, and there was moderate or severe hypoxic damage in four.

Brain Damage in Non-Missile Head Injury Secondary to High Intracranial Pressure

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.