Acta neurochirurgica. Supplement
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Acta Neurochir. Suppl. · Jan 2008
ReviewVasospasm after aneurysmal subarachnoid hemorrhage: need for further study.
Cerebral vasospasm is the classic cause of delayed neurological deterioration leading to cerebral ischemia and infarction, and thus, poor outcome and occasionally death, after aneurysmal subarachnoid hemorrhage (SAH). Advances in diagnosis and treatment, principally nimodipine, intensive care management, hemodynamic manipulations, and endovascular neuroradiology procedures, have improved the prospects for these patients, but outcomes remain disappointing. A phase 2b clinical trial (CONSCIOUS-1) demonstrated marked prevention of vasospasm with the endothelin antagonist, clazosentan, yet patient outcome was not improved. ⋯ Clazosentan reduced angiographic vasospasm in a dose-dependent manner in patients with aneurysmal SAH following coiling or clipping of the aneurysm. Reducing the incidence of vasospasm should have an important effect on clinical outcome. A phase 3 clinical trial (CONSCIOUS-2) will focus on quantifying this outcome in patients undergoing aneurysm clipping receiving placebo or 5 mg/h of clazosentan.
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Acta Neurochir. Suppl. · Jan 2008
ReviewDysfunction of nitric oxide synthases as a cause and therapeutic target in delayed cerebral vasospasm after SAH.
Nitric oxide (NO), also known as endothelium-derived relaxing factor, is produced by endothelial nitric oxide synthase (eNOS) in the intima and by neuronal nitric oxide synthase (nNOS) in the adventitia of cerebral vessels. It dilates the arteries in response to shear stress, metabolic demands, pterygopalatine ganglion stimulation, and chemoregulation. Subarachnoid haemorrhage (SAH) interrupts this regulation of cerebral blood flow. ⋯ CSF ADMA levels are closely associated with the degree and time-course of vasospasm; when CSF ADMA levels decrease, vasospasm resolves. Thus, the exogenous delivery of NO, inhibiting the L-arginine-methylating enzyme (IPRMT3) or stimulating DDAH II, may provide new therapeutic modalities to prevent and treat vasospasm. This paper will present results of preclinical studies supporting the NO-based hypothesis of delayed cerebral vasospasm development and its prevention by increased NO availability.
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Acta Neurochir. Suppl. · Jan 2008
Clinical TrialEffect of hyperbaric oxygen on patients with traumatic brain injury.
Hyperbaric oxygen therapy (HBOT) is the medical therapeutic use of oxygen at a higher atmospheric pressure. The United States Food and Drug Administration have approved several clinical applications for HBOT, but HBOT in traumatic brain injury (TBI) patients has still remained in controversial. The purpose of our study is to evaluate the benefit of HBOT on the prognosis of subacute TBI patients. ⋯ The GCS of the HBOT group was improved from 11.1 to 13.5 in average, and from 10.4 to 11.5 (p < 0.05) for control group. Among those patients with GOS = 4 before the HBOT, significant GOS improvement was observed in the HBOT group 6 months after HBOT. Based on this study, HBOT can provide some benefits for the subacute TBI patients with minimal adverse side effects.
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Acta Neurochir. Suppl. · Jan 2008
ReviewNovel treatments for cerebral vasospasm following aneurysmal subarachnoid hemorrhage.
Cerebral vasospasm is a major cause of cerebral ischemia and poor outcomes in the setting of aneurysmal subarachnoid hemorrhage (SAH). Despite advances in diagnosis and treatment of SAH, the pathophysiology of vasospasm is still poorly understood and outcomes remain disappointing. Recent advances in understanding the role of hemoglobin in initiating an inflammatory cascade in the subarachnoid space open new avenues for therapy. Preliminary experimental and clinical evidence indicate that targets in the inflammatory and oxidative cascades hold promise in reducing the incidence and impact of cerebral vasospasm.
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Acta Neurochir. Suppl. · Jan 2008
Clinical TrialVentriculostomy for control of raised ICP in acute traumatic brain injury.
The aim of this study was to evaluate the effect of ventriculostomy on intracranial pressure (ICP), and related parameters, including cerebrospinal compensation, cerebral oxygenation (PbtO2) and metabolism (microdialysis) in patients with traumatic brain injury (TBI). ⋯ Ventriculostomy is a useful ICP-lowering manoeuvre, with sustained ICP reduction and related physiological improvements achieved in > 50% of patients.