Acta neurochirurgica. Supplement
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Acta Neurochir. Suppl. · Jan 2015
Risk factors for vasospasm-induced cerebral infarct when both clipping and coiling are equally available.
Vasospasm-induced cerebral infarct is still a significant cause of poor outcome after aneurysmal subarachnoid hemorrhage (SAH). ⋯ New treatment strategies for vasospasm-induced cerebral infarct are needed, especially for ruptured middle cerebral artery aneurysm cases associated with massive SAH.
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Acta Neurochir. Suppl. · Jan 2015
Detection of delayed cerebral ischemia (DCI) in subarachnoid haemorrhage applying near-infrared spectroscopy: elimination of the extracerebral signal by transcutaneous and intraparenchymatous measurements in parallel.
Detection of delayed cerebral ischemia (DCI) in high-grade subarachnoid haemorrhage (SAH) is an unsolved issue. Conventional near-infrared spectroscopy (NIRS) with optodes applied over the skin is controversial because the NIRS signal is contaminated by extracerebral tissue. The objective is to quantify and subtract the contribution from extracerebral tissue from the signal by using measurements in parallel with a NIRS brain tissue probe and conventional NIRS. ⋯ Blood flow values obtained with conventional NIRS correlated significantly with absolute CBF values obtained directly within the brain tissue. Simultaneous measurements with the NeMo Probe and NeMo Patch allow quantification and subtraction of the contribution from extracerebral tissues from the signal obtained with conventional NIRS.
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Acta Neurochir. Suppl. · Jan 2015
Effects of tenascin-C on early brain injury after subarachnoid hemorrhage in rats.
We previously reported that tenascin-C (TNC), a matricellular protein, was involved in the pathogenesis of cerebral vasospasm after subarachnoid hemorrhage (SAH), but the role of TNC in early brain injury (EBI) is unknown. This study assessed whether inhibition of TNC upregulation in brain by imatinib mesylate (imatinib), an inhibitor of the tyrosine kinases of platelet-derived growth factor receptors, prevents EBI after experimental SAH. ⋯ TNC may be involved in the pathogenesis of EBI after SAH.
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Acta Neurochir. Suppl. · Jan 2015
Impaired cerebrovascular reactivity in the early phase of subarachnoid hemorrhage in good clinical grade patients does not predict vasospasm.
Subarachnoid hemorrhage (SAH) alters cerebrovascular reactivity (CVR) to carbon dioxide (CO2), which may be related to an increased risk of delayed ischemic neurological deficits (DINDs). We report the results of bedside CVR testing in the acute phase of SAH in good clinical grade patients without established vasospasm or signs of DIND. ⋯ Patients with SAH had significantly lower CVR indexes compared with healthy controls. Although impaired CVR was present in 50 % of the patients early after SAH, no correlation with later occurrence of DINDs was found.