Acta neurochirurgica. Supplement
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Acta Neurochir. Suppl. · Jan 2013
ReviewSpreading ischemia after aneurysmal subarachnoid hemorrhage.
Spreading depolarization (SD) is a wave of mass neuronal and glial depolarization associated with net influx of cations and water. Prolonged SDs facilitate neuronal death. SD induces tone alterations in cerebral resistance arterioles, leading to either transient hyperperfusion (physiological neurovascular coupling) in healthy tissue or hypoperfusion (inverse neurovascular coupling = spreading ischemia) in tissue at risk for progressive damage. ⋯ In animals, spreading ischemia produced widespread cortical necrosis. In patients, spreading ischemia occurred in temporal correlation with ischemic lesion development early and late after aSAH. We briefly review important features of SD and spreading ischemia following aSAH.
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Acta Neurochir. Suppl. · Jan 2013
ReviewEndovascular management of posthemorrhagic cerebral vasospasm: indications, technical nuances, and results.
Posthemorrhagic cerebral vasospasm (PHCV) is a common problem and a significant cause of mortality and permanent disability following aneurysmal subarachnoid hemorrhage. While medical therapy remains the mainstay of prevention against PHCV and the first-line treatment for symptomatic patients, endovascular options should not be delayed in medically refractory cases. Although both transluminal balloon angioplasty (TBA) and intra-arterial vasodilator therapy (IAVT) can be effective in relieving proximal symptomatic PHCV, only IAVT is a viable treatment option for distal vasospasm. ⋯ Conversely, IAVT is generally considered an effective and low-risk procedure, despite the transient nature of its therapeutic effects and the risk of intracranial hypertension associated with its use. Moreover, newer vasodilator agents appear to have a longer duration of action and a much better safety profile than papaverine, which is rarely used in current clinical practice. Although endovascular treatment of PHCV has been reported to be effective in clinical series, whether it ultimately improves patient outcomes has yet to be demonstrated in a randomized controlled trial.
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Acta Neurochir. Suppl. · Jan 2013
ReviewAngiographic vasospasm versus cerebral infarction as outcome measures after aneurysmal subarachnoid hemorrhage.
Despite a significant reduction of angiographic vasospasm, the reduction of poor functional outcome in clinical trials on aneurysmal subarachnoid hemorrhage (SAH) remains challenging. While there is general consensus that vasospasm is associated with delayed cerebral ischemia (DCI), cerebral infarction, poor functional outcome, and mortality after SAH, causal relationships are subject to discussion. Therefore, it was the aim of our study to investigate the relationship between various outcome measures and poor functional outcome in clinical trials on pharmaceutical treatment of SAH. ⋯ Future clinical trials may use cerebral infarction and functional outcome as main outcome measures to -investigate the true impact of an intervention, assuming that the intervention targets cerebral infarction and hereby improves outcome.
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Acta Neurochir. Suppl. · Jan 2013
ReviewMagnesium sulphate for aneurysmal subarachnoid hemorrhage: why, how, and current controversy.
The neuroprotective effect of magnesium sulphate infusion has been confirmed in experimental models. Pilot clinical trials using magnesium sulphate in patients with acute aneurysmal subarachnoid hemorrhage (SAH) have reported a trend toward a reduction in clinical deterioration due to delayed cerebral ischemia (DCI) and an improvement in clinical outcomes. ⋯ In post hoc analysis, data also did not support that a higher dose of magnesium sulphate infusion might improve clinical outcome. We here review the current literature, highlight these discrepancies, and explore alternatives.
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Acta Neurochir. Suppl. · Jan 2013
ReviewThe roles of early brain injury in cerebral vasospasm following subarachnoid hemorrhage: from clinical and scientific aspects.
Cerebral vasospasm research has been focused on investigating the mechanisms of prolonged delayed vasoconstriction of cerebral arteries following subarachnoid hemorrhage (SAH). However, it has been clarified that induction of significant vasodilation of such arteries does not lead to better overall outcomes in SAH patients. ⋯ It is of utmost importance to investigate whether early brain injury and delayed cerebral vasospasm correlate with each other following SAH or are independent. Recent results of cerebral vasospasm research indicates future directions, and such investigations would lead to better outcome for SAH patients.