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Brain, Vol. 123, No. 7, 1327-1338, July 2000
© 2000 Oxford University Press

The neuropathology of the vegetative state after an acute brain insult

J. Hume Adams1, D. I. Graham1 and Bryan Jennett2

1 University Departments of Neuropathology and 2 Neurosurgery, Institute of Neurological Sciences, South Glasgow University Hospitals NHS Trust, Glasgow, UK

Correspondence to: J. Hume Adams, University Department of Neuropathology, Institute of Neurological Sciences, Southern General Hospital, South Glasgow University Hospitals NHS Trust, 1345 Govan Road, Glasgow G51 4TF, UK

The vegetative state is often described clinically as loss of function of the cortex while the function of the brainstem is preserved. In an attempt to define the structural basis of the vegetative state we have undertaken a detailed neuropathological study of the brains of 49 patients who remained vegetative until death, 1 month to 8 years after an acute brain insult. Of these, 35 had sustained a blunt head injury and 14 some type of acute non-traumatic brain damage. In the traumatic cases the commonest structural abnormalities identified were grades 2 and 3 diffuse axonal injury (25 cases, 71%). The thalamus was abnormal in 28 cases (80%), and in 96% of the cases who survived for more than 3 months. Other abnormalities included ischaemic damage in the neocortex (13 cases, 37%) and intracranial haematoma (nine cases, 26%). In the non-traumatic cases there was diffuse ischaemic damage in the neocortex in nine cases (64%) and focal damage in four (29%); the thalamus was abnormal in every case. There were cases in both groups where the cerebral cortex, the cerebellum and the brainstem were of structurally normal appearance. In every case, however, there was profound damage to the subcortical white matter or to the major relay nuclei of the thalamus, or both. These lesions render any structurally intact cortex unable to function because connections between different cortical areas via the thalamic nuclei are no longer functional, and there is also extensive damage to afferent and efferent cerebral connections.


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