Acta neurochirurgica. Supplement
-
Acta Neurochir. Suppl. · Jan 2012
Pressure reactivity index correlates with metabolic dysfunction in a porcine model of intracerebral hemorrhage.
We correlated oxygen, flow, and pressure indices of cerebrovascular reactivity (CR) with extracellular cerebral metabolite concentrations in a porcine model of intracerebral hemorrhage (ICH). ⋯ We found evidence for impaired CR in a porcine model of ICH. The findings suggest that, among other parameters of CR, positive PRx coefficients have the highest significance and could be associated with microdialysis alterations during hypoxic events.
-
Acta Neurochir. Suppl. · Jan 2012
Spontaneous cortical spreading depression and intracranial pressure following acute subdural hematoma in a rat.
Acute subdural hemorrhage (ASDH) is a frequent and devastating consequence of traumatic brain injury. Tissue damage develops rapidly and makes treatment even more difficult. Management of increased intracranial pressure (ICP) due to extravasated blood volume and brain swelling is often insufficient to control all adverse effects of ASDH. ⋯ Tissue impedance increased by around 203% of baseline during subdural infusion of 300 μl of autologous, venous blood and dropped back to baseline within 22 min. Fifty-six minutes after the start of ASDH a cluster of four short-lasting (3-3.5 min; 140-160% of baseline) IMP increases started that reflected spontaneous CSDs. This pattern presumes that CSD occurs early after ASDH and therefore may contribute to the rapid lesion development in this disease.
-
Acta Neurochir. Suppl. · Jan 2012
Development of an experimental model to study the pathophysiology of cerebral salt wasting following subarachnoid hemorrhage.
Hyponatremia is frequent following cranial -neurosurgery or acute brain injury like subarachnoid hemorrhage (SAH), and increases mortality by 30%. The patho-physiology is not understood nor does a causal therapy exist. Since clinical trials are potentially dangerous in this very ill population, we examined whether an established rat model allows studying cerebral salt wasting (CSW) following SAH. ⋯ Neither SAH(mild) (100 μL), the injection of hemolyzed blood (100 μL) or hypertonic saline (200 μL) replicated the effect. The immediate release of ADH (32.23 ± 34.87 pg/mL) following SAH(severe) normalized over the next few days. We conclude that first, the rat model of SAH is suitable for studying CSW, second the increase in intracranial pressure generates the delayed hyponatremia, and third, the ADH release does not mediate natriuresis.
-
Acta Neurochir. Suppl. · Jan 2011
Review Randomized Controlled TrialIntravenous magnesium sulfate after aneurysmal subarachnoid hemorrhage: current status.
Delayed ischemic neurological deficit or clinical vasospasm remained a major cause for delayed neurological morbidity and mortality for patients with aneurysmal subarachnoid hemorrhage (SAH). Magnesium is a cerebral vasodilator. In experimental model of drug or SAH-induced vasospasm, magnesium blocks voltage-dependent calcium channels and reverses cerebral vasoconstriction. ⋯ Using random effects model (Mantel-Haenszel, Robins-Breslow-Greenland), the pooled odds ratio for symptomatic vasospasm or delayed cerebral ischemia is, 0.620, 95% CI 0.389-0.987, statistically significant. Similarly, the pooled odds ratio for favorable outcome is 1.598, 95% CI 1.074-2.377, statistically significant. There are two multi-center phase III studies (IMASH and MASH2) being carried out to assess the clinical effects, in which IMASH has finished data collection on 30th June 2009.
-
Acta Neurochir. Suppl. · Jan 2011
Randomized Controlled Trial Multicenter StudyClazosentan: prevention of cerebral vasospasm and the potential to overcome infarction.
Cerebral vasospasm is a common complication occurring after aneurysmal subarachnoid hemorrhage (SAH). It is recognized as a leading preventable cause of morbidity and mortality in this patient group, but its management is challenging, and new treatments are needed. Clazosentan is an endothelin receptor antagonist designed to prevent endothelin-mediated cerebral vasospasm. ⋯ Clazosentan reduced angiographic vasospasm dose-dependently relative to placebo with a maximum risk reduction of 65% with the highest dose. Despite this, there was no benefit of clazosentan on the secondary protocol-defined morbidity/mortality endpoint; however, additional post-hoc and modified endpoint analyses provided some evidence for a potential clinical benefit. Two additional large-scale studies (CONSCIOUS-2 and CONSCIOUS-3) are now underway to further investigate the potential of clazosentan to improve long-term clinical outcome.