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Physiopathologie des lésions cérébrales précoces et retardées dans l’hémorragie sous-arachnoïdienne : avancées récentes

Pathophysiology of acute and delayed brain injury after subarachnoid hemorrhage: an update

  • Enseignement Supérieur en Réanimation
  • Médecin
  • Published:
Réanimation

Résumé

L’hémorragie sous-arachnoïdienne (HSA) par rupture anévrismale est toujours compliquée actuellement d’une mortalité et d’une morbidité importante, qui peuvent être attribuées en grande partie à la survenue de lésions ischémiques précoces ou retardées. Le vasospasme des artères cérébrales est un des facteurs associés aux lésions ischémiques, mais il apparaît avec un certain retard. Les travaux expérimentaux récents s’intéressent aux lésions cérébrales précoces survenant après l’HSA. Plusieurs mécanismes étiologiques sont proposés : facteurs mécaniques, atteinte de la microcirculation et vasospasme non détectable angiographiquement, perturbation de l’homéostasie ionique, induction de l’apoptose, stress oxydatif… La quantité de sang présente dans les espaces sous-arachnoïdiens déclenche par ailleurs une riposte inflammatoire qui fait intervenir des éléments cellulaires, mais également des facteurs moléculaires (cytokines, endothéline, oxyde nitrique [NO]…). Elle est probablement largement responsable des lésions ischémiques retardées dans un contexte de vasospasme. Une meilleure connaissance des mécanismes physiopathologiques impliqués à la phase aiguë devrait permettre de proposer de nouvelles cibles thérapeutiques.

Abstract

Aneurysmal subarachnoid hemorrhage (SAH) is still further complicated by a high mortality and morbidity rate related to early or delayed ischemic brain injury. Cerebral vasospasm is one of the factors associated with ischemic injury, but it usually appears with some delay. Recent experimental data are focusing on early brain injury after SAH. Several etiological factors have been suggested: changes in intracranial pressure and cerebral blood flow, microvascular vasospasm and platelet aggregation, cortical spreading depolarization, induction of apoptosis, oxidative stress, etc. The amount of blood present in the subarachnoid space causes an intense inflammatory response that involves both cellular and molecular factors (cytokines, endothelin, nitric oxide) and triggers vasospasm and delayed ischemic neurologic deficit. A better understanding of the pathophysiology of the early brain injury after SAH can lead to a more targeted therapy.

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  1. Département des soins intensifs, cliniques Saint-Luc, université catholique de Louvain, avenue Hippocrate, 10, B-1200, Bruxelles, Belgique

    P. Hantson

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Correspondence to P. Hantson.

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Cet article correspond à la conférence faite par l’auteur au congrès de la SRLF 2012 dans la session : Pathologies cérébrales vasculaires graves : actualités.

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Hantson, P. Physiopathologie des lésions cérébrales précoces et retardées dans l’hémorragie sous-arachnoïdienne : avancées récentes. Réanimation 21 (Suppl 2), 475–481 (2012). https://doi.org/10.1007/s13546-011-0418-9

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  • DOI: https://doi.org/10.1007/s13546-011-0418-9

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