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Delayed cerebral ischaemia: the pathological substrate

Neil-Dwyer, G., Lang, D.A., Doshi, B., Gerber, Ch. J. and Smith, P.W.F. (1994) Delayed cerebral ischaemia: the pathological substrate Acta Neurochirurgica. Supplement: Intracranial Pressure & Brain Biochemical Monitoring, 131, (1-2), pp. 137-145. (doi:10.1007/BF01401464).

Record type: Article


Ischaemic complications both at the level of the cortex and the hypothalamus are well recognised after an aneurysmal subarachnoid haemorrhage. We have studied histological changes in the cortex (53 patients) and hypothalamus (48 patients) in patients who died after an aneurysmal subarachnoid haemorrhage.
Cortical ischaemic lesions were demonstrated in 41 of the 53 patients studied. These changes were more common in patients who had impaired control of systemic blood pressure (p=0.0004) and in patients who died gradually (p=0.0003). Hypothalamic lesions were found in 24 of 48 patients studied; 23 of these patients had widespread associated changes in the cerebral cortex. Patients with moderate/severe cortical changes tended to have hypothalamic lesions and it was uncommon for patients with no cortical lesions to have changes in the hypothalamus (p=0.0007).
We believe that these histological changes are due to a diffuse microangiopathy which develops slowly after a subarachnoid haemorrhage and affects the cortex and hypothalamus. Because the cortical lesions are widespread we postulate that they may be implicated in the aetiology of the well described psychosocial or cognitive problems in patients who survive a subarachnoid haemorrhage.

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Published date: 1994
Keywords: autoregulation, blood pressure control, cerebral cortex, delayed cerebral ischaemia, hypothalamus, subarachnoid haemorrhage


Local EPrints ID: 34754
ISSN: 0001-6268
PURE UUID: 16bb3e96-0eac-4f9e-af1b-1a310b6383c6
ORCID for P.W.F. Smith: ORCID iD

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Date deposited: 08 May 2007
Last modified: 17 Jul 2017 15:49

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Author: G. Neil-Dwyer
Author: D.A. Lang
Author: B. Doshi
Author: Ch. J. Gerber
Author: P.W.F. Smith ORCID iD

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