Before the description of the vegetative state there were occasional reports of the structural damage in the brains of patients whom we would now probably call vegetative, and there have been a few since then. Reports up to 1994 were reviewed by Kinney and Samuels (1), although they included some traumatic cases who were not vegetative by the present definition. In hypoxic–ischaemic cases the damage is usually extensive necrosis in the cerebral cortex, almost always associated with thalamic damage. This is because of the selective vulnerability to hypoxia of the grey matter in the cerebral hemispheres. Occasionally, however, there is relative sparing of the cortex, with the main damage in the thalamus (2,3,4).

In traumatic cases the dominant lesion is diffuse damage to the subcortical white matter – what is now known as diffuse axonal injury (DAI). The original description of this type of brain damage was by Strich in 1956 and 1961 (5,6), when she proposed that this damage was the result of shearing forces acting on nerve fibres in the white matter of the cerebral hemispheres at the moment of injury. However, some continental European reports of these lesions in apallic patients claimed that this axonal damage was secondary to hypoxia and ischaemia related to high intracranial pressure (7,8,9).