Although IBD had been known to be a feature in some cases, previous studies had logged its presence but not undertaken a systematic study to establish its amount, patterns and hence possible causation. The initial studies identified IBD in 91% of 138 cases.

From the pattern of IBD it seemed likely that much of it occurred shortly after injury and in large measure was due to a reduction in cerebral perfusion pressure. This was confirmed by statistically significant associations between IBD and an episode of hypoxia (hypoxaemia or hypotension) and raised intracranial pressure.

When cerebral blood flow began to be measured in the 1970s there was a lack of evidence of clinical ischaemia which seemed to contradict the neuropathological findings and their possible pathophysiology. These discrepancies have been clarified by more recent techniques with sufficient resolution to detect impairments.

P MACPHERSON AND D I GRAHAM

"We have also found for the first time a statistically significant correlation between intracranial haematoma, either singly or in combination with asospasm, and ischaemic brain damage particularly in the distribution of arterial territories."

Mapping of cerebral blood flow and perfusion by single photon emission computed tomography with radioisotopes, xenon-enhanced computed tomography, positron emission tomography and more recently magnetic resonance imaging have shown that dense zones of ischaemia are associated with cerebral contusions and intracranial clots.

Neuroscience research in Glasgow in the latter part of the 20th century was led by key international figures - Graham Teasdale, professor of neurosurgery, David Graham, professor of neuropathology and Jim McCulloch, professor of experimental neuroscience. Their research on brain injury and neuroprotection was widely acclaimed.