Published in

Oxford University Press, Brain Communications, 3(5), 2023

DOI: 10.1093/braincomms/fcad133

Links

Tools

Export citation

Search in Google Scholar

Perfusion gradients promote delayed perihaematomal oedema in intracerebral haemorrhage

This paper is made freely available by the publisher.
This paper is made freely available by the publisher.

Full text: Download

Green circle
Preprint: archiving allowed
Green circle
Postprint: archiving allowed
Green circle
Published version: archiving allowed
Data provided by SHERPA/RoMEO

Abstract

Abstract Perihaematomal oedema is a potential therapeutic target to improve outcome of patients with intracerebral haemorrhage, but its pathophysiology remains poorly elucidated. We investigated the longitudinal changes of cerebral perfusion and their influence on perihaematomal oedema development in 150 patients with intracerebral haemorrhage who underwent computed tomography perfusion within 6 h from onset, at 24 h and at 7 days. Perfusion parameters were measured in haemorrhagic core, perihaematomal rim, surrounding normal appearing and contralateral brain tissue. Computed tomography perfusion parameters gradually improved from the core to the periphery in each time interval with an early increase at 24 h followed by a delayed decline at 7 days compared with admission values (P < 0.001). Multivariable linear regression analysis showed that haematoma volume and cerebral blood flow gradient between normal appearing and perihaematomal rim were independently associated with absolute perihaematomal oedema volume in the different time points (within 6 h, B = 0.128, P = 0.032; at 24 h, B = 0.133, P = 0.016; at 7 days, B = 0.218, P < 0.001). In a secondary analysis with relative perihaematomal oedema as the outcome of interest, cerebral blood flow gradient between normal appearing and perihaematomal rim was an independent predictor of perihaematomal oedema only at 7 days (B = 0.239, P = 0.002). Our findings raise the intriguing hypothesis that perfusion gradients promote perihaematomal oedema development in the subacute phase after intracerebral haemorrhage.