Acta neurochirurgica. Supplement
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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.
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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
Randomized Controlled Trial Multicenter StudyDevelopment of nicardipine prolonged-release implants after clipping for preventing cerebral vasospasm: from laboratory to clinical trial.
We have developed a drug delivery system using a vasodilating drug that can be implanted intracranially at the time of surgery for aneurysm clipping, without systemic side effects or side effects associated with long-term intrathecal drug administration. We started our project on 1994 for making a slowly releasing drug delivery system in vitro because cerebral vasospasm occurs 4-14 days following subarachnoid hemorrhage (SAH). A rod-shaped pellet containing 1 mg of nicardipine for animal study was prepared by heat compression. ⋯ Vasospasm was completely prevented in the arteries by placing NPRIs adjacent to the arteries during surgery. No complications were experienced. We have performed three studies (a single-center study with consecutive patients; a single-center, randomized, double-blind trial; and a multicenter cooperative study) and have proved that implantation of NPRIs reduces the incidence of cerebral vasospasm and DINDs and improves clinical outcome after SAH.