The neuropathology of the vegetative state after head injury.

The technologies of resuscitation and intensive care have reduced mortality after acute brain damage, but some of those rescued are left with permanent brain damage, the most severely aVected being in a vegetative state. This was first defined by Jennett and Plum in 1972 and consists of continuing unconsciousness with no evidence of awareness or cognitive responsiveness although there are periods of wakefulness with the eyes open. The patients breathe spontaneously and have a range of reflex activity but require tube feeding. Clinically, the condition is considered to be one in which the cerebral cortex seems no longer to be functioning but with the brain stem relatively intact. Some 40–50% of patients who are vegetative after an acute brain damage have sustained a head injury, the rest having mostly suVered hypoxic-ischaemic brain damage (reviewed by Jennett). Some 6–14% of patients admitted with a severe head injury are in a vegetative state one month later. Analysis by the Multi-Society Task Force (1994) of over 700 published cases of patients in a vegetative state one month after an acute insult found that some of these patients recovered consciousness over the next few months, this being more common after traumatic than non-traumatic damage. It concluded that the vegetative state should not be declared permanent until 12 months after a head injury, a view endorsed by the Royal College of Physicians. The neuropathology of the vegetative state has been reviewed by Kinney and Samuel, but there have been many fewer detailed reports of the lesions after traumatic than after nontraumatic insults. We report here the findings in a series of 35 cases considered vegetative until the time of their deaths a month or more after head injury. They are drawn from a database of over 1300 cases of fatal blunt head injury covering the period 1968–1998 held in the department of neuropathology in the Institute of Neurological Sciences, Southern General Hospital, Glasgow and used in many of our previous publications. In a preliminary study of 18 patients surviving at least 30 days in vegetative state after head injury, McLellan et al identified diVuse axonal injury, extensive hypoxic damage in the neocortex, and secondary damage to the brain stem as the principal neuropathological bases of the vegetative state. A particular problem facing forensic pathologists, however, is the frequency with which there may be minimal or even absent macroscopic abnormalities in the brain, including even classic surface contusions, in a patient who has remained in the vegetative state after a head injury. The present study of 35 patients includes the 18 reported earlier: 32 were male and three female, with an age range of 7 to 75 years (median 38 years; 95% confidence interval (CI) 31 to 45 years); the cause of injury in 17 was a road traYc accident, in nine an assault, in six a fall, and in three it was not known. Survival was less than three months in 11, between three and 12 months in 11, and longer than 12 months in 13. It is possible that some of the cases studied who survived for less than a year might have shown a degree of recovery had they survived longer. The clinical records were assessed with particular reference to deterioration in the conscious level after a lucid interval, to determine whether or not the patient had talked after injury; if the patient had talked but had not been completely rational the lucid interval was defined as having been partial. All brains were fixed in 10% formal saline for a minimum of three weeks before dissection, after which a full macroscopic and microscopic examination was undertaken in each case. Contusions were assessed semiquantitatively using the total contusion index. This index takes into account the depth and extent of surface contusions in various parts of the brain: zero means that there were no contusions, a contusion index in the twenties indicates moderately severe contusions, while one of more than 37 indicates severe contusions. DiVuse axonal injury was graded as described previously, 11 and in this series was always of the more severe grades—either grade 2 with a focal lesion in the corpus callosum or grade 3 with a similar lesion also in the dorsolateral sector of the rostral brainstem. The focal lesions that are not apparent macroscopically are not diYcult to identify on microscopic examination, although it may be necessary to examine several levels of the corpus callosum. Shortly after the injury, the focal lesions are typically rarefied and may be haemorrhagic. By a month after injury the lesions are intensely cellular as a result of astrocytosis and microglial hyperplasia, often with the formation of lipid containing phagocytes. They are also well J Clin Pathol 1999;52:804–806 804