Delayed Cerebral Ischaemia: the Pathological Substrate

Overview

Journal Acta Neurochir (Wien)

Specialty Neurosurgery

Date 1994 Jan 1

PMID 7709776

Citations 32

Authors

G Neil-Dwyer

D A LANG

B Doshi

C J Gerber

P W Smith

Affiliations

Soon will be listed here.

Abstract

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 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.

Citing Articles

All Three Supersystems-Nervous, Vascular, and Immune-Contribute to the Cortical Infarcts After Subarachnoid Hemorrhage.

Dreier J, Joerk A, Uchikawa H, Horst V, Lemale C, Radbruch H Transl Stroke Res. 2024; 16(1):96-118.

PMID: 38689162 PMC: 11772491. DOI: 10.1007/s12975-024-01242-z.

Dreier J, Lemale C, Horst V, Major S, Kola V, Schoknecht K Transl Stroke Res. 2024; 16(1):147-168.

PMID: 38396252 PMC: 11772537. DOI: 10.1007/s12975-024-01237-w.

Spreading depolarization and angiographic spasm are separate mediators of delayed infarcts.

Horst V, Kola V, Lemale C, Major S, Winkler M, Hecht N Brain Commun. 2023; 5(2):fcad080.

PMID: 37038498 PMC: 10082345. DOI: 10.1093/braincomms/fcad080.

White Matter Injury: An Emerging Potential Target for Treatment after Subarachnoid Hemorrhage.

Liu Y, He Y, Zhang J, Wang X, Zhang A, Yu Q Oxid Med Cell Longev. 2023; 2023:3842493.

PMID: 36798684 PMC: 9928519. DOI: 10.1155/2023/3842493.

Angiotensin-(1-7) as a Potential Therapeutic Strategy for Delayed Cerebral Ischemia in Subarachnoid Hemorrhage.

Annoni F, Moro F, Caruso E, Zoerle T, Taccone F, Zanier E Front Immunol. 2022; 13:841692.

PMID: 35355989 PMC: 8959484. DOI: 10.3389/fimmu.2022.841692.

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