abbreviatioNs ACA = anterior cerebral artery; BA = basilar artery; BP = blood pressure; CBF = cerebral blood flow; CCT = cranial computed tomography; CVS = cerebral vasospasm; DIND = delayed ischemic neurological deficit; DSA = digital subtraction angiography; GCS = Glasgow Coma Scale; HES = hydroxyethyl starch; HH = Hunt and Hess; ICA = internal carotid artery; ICP = intracranial pressure; MAP = mean arterial blood pressure; MCA = middle cerebral artery; mNIHSS = modified National Institutes of Health Stroke Scale; mRS = modified Rankin Scale; MTG = molsidomine treatment group; NO = nitric oxide; SAH = subarachnoid hemorrhage; STG = standard therapy group; TCD = transcranial Doppler; VA = vertebral artery. submitted May 5, 2013. accepted December 29, 2014. iNclude wheN citiNg Published online July 10, 2015; DOI: 10.3171/2014.12.JNS13846. disclosures The authors report no conflict of interest concerning the materials or methods used in this study or the findings specified in this paper. obJective Delayed ischemic neurological deficits (DINDs) and cerebral vasospasm (CVS) are responsible for a poor outcome in patients with aneurysmal subarachnoid hemorrhage (SAH), most likely because of a decreased availability of nitric oxide (NO) in the cerebral microcirculation. In this study, the authors examined the effects of treatment with the NO donor molsidomine with regard to decreasing the incidence of spasm-related delayed brain infarctions and improving clinical outcome in patients with SAH. methods Seventy-four patients with spontaneous aneurysmal SAH were included in this post hoc analysis. Twentynine patients with SAH and proven CVS received molsidomine in addition to oral or intravenous nimodipine. Control groups consisted of 25 SAH patients with proven vasospasm and 20 SAH patients without. These patients received nimodipine therapy alone. Cranial computed tomography (CCT) before and after treatment was analyzed for CVS-related infarcts. A modified National Institutes of Health Stroke Scale (mNIHSS) and the modified Rankin Scale (mRS) were used to assess outcomes at a 3-month clinical follow-up. results Four of the 29 (13.8%) patients receiving molsidomine plus nimodipine and 22 of the 45 (48%) patients receiving nimodipine therapy alone developed vasospasm-associated brain infarcts (p < 0.01). Follow-up revealed a median mNIHSS score of 3.0 and a median mRS score of 2.5 in the molsidomine group compared with scores of 11.5 and 5.0, respectively, in the nimodipine group with CVS (p < 0.001). One patient in the molsidomine treatment group died, and 12 patients in the standard care group died (p < 0.01). coNclusioNs In this post hoc analysis, patients with CVS who were treated with intravenous molsidomine had a significant improvement in clinical outcome and less cerebral infarction. Molsidomine offers a promising therapeutic option in patients with severe SAH and CVS and should be assessed in a prospective study. Molsidomine for the prevention of vasospasm-related

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Research using rats sometimes requires long-term placement of catheters in the subarachnoid space, the cavity between the arachnoid mater and the pia mater in the brain. These catheters can be used to experimentally induce subarachnoid bleeding by injecting blood or to locally administer drugs or other substances. To date, published techniques for penetrating the subarachnoid space of small experimental animals require the use of inflexible or relatively inflexible catheters. These catheters typically consist of metal or stiff plastic and are used to access the occipital or frontal cranial cavity or to directly access the cisterna magna via the atlantooccipital membrane. However, inflexible catheters are not ideal for long-term placement in the subarachnoid space. In this paper, the authors describe a reliable procedure for long-term catheterization of the subarachnoid cavity of the rat. For this method, personnel insert the catheter and keep it in place in the rat's middle cranial cavity, in the vicinity of the cerebral arterial circle. This new approach allows personnel to repeatedly use the catheter for a period of at least 2 weeks. The catheter, which is well-tolerated by rats, can be used for administering saline solutions and for injecting blood that has not been treated with heparin into the subarachnoid space.

Background: Patients with aneurysmal subarachnoid hemorrhage (aSAH) require close treatment in neuro intensive care units (NICUs). The treatments available to counteract secondary deterioration and delayed ischemic events remain restricted; moreover, available neuro-monitoring of comatose patients is undependable. In comatose patients, clinical signs are hidden, and timing interventions to prevent the evolution of a perfusion disorder in response to fixed ischemic brain damage remain a challenge for NICU teams. Consequently, comatose patients often suffer secondary brain infarctions. The outcomes for long-term intubated patients w/wo pupil dilatation are the worst, with only 10% surviving. We previously added two nitroxide (NO) donors to the standard treatment: continuous intravenous administration of Molsidomine in patients with mild-to-moderate aSAH and, if required as a supplement, intraventricular boluses of sodium nitroprusside (SNP) in high-risk patients to overcome the so-called NO-sink effect, which leads to vasospasm and perfusion disorders. NO boluses were guided by clinical status and promptly reversed recurrent episodes of delayed ischemic neurological deficit. In this study, we tried to translate this concept, the initiation of intraventricular NO application on top of continuous Molsidomine infusion, from awake to comatose patients who lack neurological-clinical monitoring but are primarily monitored using frequently applied transcranial Doppler (TCD). Methods: In this observational, retrospective, nonrandomized feasibility study, 18 consecutive aSAH comatose/intubated patients (Hunt and Hess IV/V with/without pupil dilatation) whose poor clinical status precluded clinical monitoring received standard neuro-intensive care, frequent TCD monitoring, continuous intravenous Molsidomine plus intraventricular SNP boluses after TCD-confirmed macrospasm during the daytime and on a fixed nighttime schedule. Results: Very likely associated with the application of SNP, which is a matter of further investigation, vasospasmrelated TCD findings promptly and reliably reversed or substantially weakened (p < 0.0001) afterward. Delayed cerebral ischemia (DCI) occurred only during loose, low-dose or interrupted treatment (17% vs. an estimated 65% with secondary infarctions) in 17 responders. However, despite their worse initial condition, 29.4% of the responders survived (expected 10%) and four achieved Glasgow Outcome Scale Extended (GOSE) 8-6, modified Rankin Scale (mRS) 0-1 or National Institutes of Health Stroke Scale (NIHSS) 0-2.