Abstract
Subarachnoid haemorrhage (SAH) is associated with long-term disability, serious reduction in quality of life and significant mortality. Early brain injury (EBI) refers to the pathological changes in cerebral metabolism and blood flow that happen in the first few days after ictus and may lead on to delayed cerebral ischaemia (DCI). A disruption of the nitric oxide (NO) pathway is hypothesised as a key mechanism underlying EBI. A decrease in the alpha-delta power ratio (ADR) of the electroencephalogram has been related to cerebral ischaemia. In an experimental medicine study, we tested the hypothesis that intravenous sodium nitrite, an NO donor, would lead to increases in ADR. We studied 33 patients with acute aneurysmal SAH in the EBI phase. Participants were randomised to either sodium nitrite or saline infusion for 1 h. EEG measurements were taken before the start of and during the infusion. Twenty-eight patients did not develop DCI and five patients developed DCI. In the patients who did not develop DCI, we found an increase in ADR during sodium nitrite versus saline infusion. In the five patients who developed DCI, we did not observe a consistent pattern of ADR changes. We suggest that ADR power changes in response to nitrite infusion reflect a NO-mediated reduction in cerebral ischaemia and increase in perfusion, adding further evidence to the role of the NO pathway in EBI after SAH. Our findings provide the basis for future clinical trials employing NO donors after SAH.
Highlights
Aneurysmal subarachnoid haemorrhage (SAH) is a subtype of stroke related to the accumulation of blood in the subarachnoid space, caused by a rupture of an intracranialAlexander Luettich and Edit Franko contributed to the study aneurysm [1]
early brain injury (EBI) describes the acute effects of intracranial haemorrhage and transient global cerebral ischaemia within 72 h of the bleed and includes (1) changes in physiology related to increased intracranial pressure, decreased cerebral blood flow and impaired cerebral autoregulation; (2) hydrocephalus, mechanical stress on the subarachnoid space contributing to vessel constriction; and (3) ionic, molecular and cellular changes promoting oxidative stress, inflammation, platelet aggregation, endothelial dysfunction, vessel constriction and
In order to obtain a maximally representative sample of patients, inclusion and exclusion criteria were intentionally kept to a minimum (inclusion criteria: Age range 18–80 years, aneurysm secured by intravascular coiling, all World Federation of Neurological Surgeons Subarachnoid Haemorrhage Grading (WFNS) scores, study conducted within a maximum of 5 days after the ictus; exclusion criteria: Contraindications to sodium nitrite, pre-existing aneurysmal clip)
Summary
Aneurysmal subarachnoid haemorrhage (SAH) is a subtype of stroke related to the accumulation of blood in the subarachnoid space, caused by a rupture of an intracranialAlexander Luettich and Edit Franko contributed to the study aneurysm [1]. Aneurysmal subarachnoid haemorrhage (SAH) is a subtype of stroke related to the accumulation of blood in the subarachnoid space, caused by a rupture of an intracranial. A phase of early brain injury (EBI) [4, 5] can be followed by a stage of delayed neurological deterioration often including delayed cerebral ischaemia (DCI) [6, 7]. EBI describes the acute effects of intracranial haemorrhage and transient global cerebral ischaemia within 72 h of the bleed and includes (1) changes in physiology related to increased intracranial pressure, decreased cerebral blood flow and impaired cerebral autoregulation; (2) hydrocephalus, mechanical stress on the subarachnoid space contributing to vessel constriction; and (3) ionic, molecular and cellular changes promoting oxidative stress, inflammation, platelet aggregation, endothelial dysfunction, vessel constriction and
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