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Background and Purpose: The current self-initiated approach by which hospitals acquire Primary Stroke Center (PSC) certification provides insufficient coverage for large areas of the United States. An alternative, directed, algorithmic approach to determine near optimal locations of PSCs would be justified if it significantly improves coverage., Methods: Using geographic location-allocation modeling techniques, we developed a universal web-based calculator for selecting near optimal PSC locations designed to maximize the population coverage in any state. We analyzed the current PSC network population coverage in Iowa and compared it with the coverage that would exist if a maximal coverage model had instead been used to place those centers. We then estimated the expected gains in population coverage if additional PSCs follow the current self-initiated model and compared it against the more efficient coverage expected by use of a maximal coverage model to select additional locations., Results: The existing 12 self-initiated PSCs in Iowa cover 37% of the population, assuming a time-distance radius of 30 minutes. The current population coverage would have been 47.5% if those 12 PSCs had been located using a maximal coverage model. With the current self-initiated approach, 54 additional PSCs on average will be needed to improve coverage to 75% of the population. Conversely, only 31 additional PSCs would be needed to achieve the same degree of population coverage if a maximal coverage model is used., Conclusions: Given the substantial gain in population access to adequate acute stroke care, it appears justified to direct the location of additional PSCs or recombinant tissue-type plasminogen activator-capable hospitals through a maximal coverage model algorithmic approach.

Background: The influence of lesion size and laterality on each component of the National Institutes of Health Stroke Scale has not been delineated. The objective of this study was to use perfusion-weighted imaging to characterize the association of ischaemic volume and laterality on each component item and the total score of the  10 s. Ordinal regression was used to clarify the relationship between ischaemic volume, laterality, and

Background: Early disruption of the blood-brain barrier (BBB) due to severe ischemia can be detected by MRI T2* permeability imaging. In middle cerebral artery (MCA) infarction, pretreatment T2* permeability derangements have been found in 22% of patients and are powerful predictors of hemorrhagic transformation after revascularization therapy. The frequency, clinical correlates, and relation to hemorrhagic transformation of permeability derangements in posterior circulation have not been previously explored, and may differ as ischemia volume and collateral status are different between vertebrobasilar and MCA infarcts., Methods: We analyzed clinical and pretreatment MRI data on consecutive patients undergoing recanalization therapy for acute vertebrobasilar ischemia at a medical center November 2001 through September 2009. Pretreatment MRI permeability images were derived from perfusion source imaging acquisitions. Permeability abnormality was detected as persisting increased signal intensity at later time points in perfusion MRI acquisition, indicating local accumulation of contrast caused by BBB leakage., Results: Among the 14 patients meeting study entry criteria, mean age was 71.1 years and median pretreatment NIHSS was 20.5. Permeability imaging abnormality was present in 1 of the 14 patients (7%). Among 14 patients, post-treatment parenchymal hematoma occurred in one and more minor degrees of hemorrhagic transformation in four. The one patient with pretreatment permeability abnormality was the patient to develop post-treatment parenchymal hematoma (Fisher's exact test, P=0.07)., Conclusion: Pretreatment permeability abnormality, an indicator of BBB derangements, is an infrequent finding in acute posterior circulation ischemic stroke and may be associated with an increased risk of parenchymal hematoma development undergoing recanalization therapy., (Copyright © 2011 Elsevier B.V. All rights reserved.)

Vasospasm after subarachnoid hemorrhage (SAH) is attributable to inflammation and oxidative stress associated with extracellular hemoglobin (Hb). Haptoglobin (Hp) binds free Hb and the Hp-Hb complex is cleared by macrophages, and the Hp-2 isoform of Hp is associated with more oxidative stress and more severe vasospasm. We hypothesized that treatment with an anti-oxidant, the glutathione peroxidase mimetic SYI-2074, would reduce vasospasm after SAH in Hp-2 mice. We found that SAH induced significant vasospasm in Hp-2 mice (lumen patency reduced to 65.9%), but no vasospasm was seen in mice that received SYI-2074 after SAH (lumen patency of 98.7%). We conclude that vasospasm after SAH in Hp-2 mice can be prevented with SYI-2074, suggesting that oxidative stress contributes significantly to vasospasm., (Copyright 2010 Elsevier Ltd. All rights reserved.)

Background: Perimesencephalic subarachnoid hemorrhage (P-SAH) is a benign subset of subarachnoid hemorrhage with a favorable prognosis and low rate of re-bleeding. Risk factors may include hypertension and tobacco use, but it has not previously been reported during pregnancy., Methods: We report two cases of P-SAH in pregnant women, a 40-year-old female, 8-weeks pregnant and a 37-year-old female at 35 weeks gestational age., Results: CT scan confirmed P-SAH in both cases. CT angiography in one case and cerebral angiogram in the other did not reveal aneurysm or other potential bleeding source. The patients underwent transcranial Doppler ultrasound monitoring without evidence of vasospasm., Conclusion: P-SAH hemorrhage may occur during early or late pregnancy. We do not propose an increased risk of P-SAH during pregnancy. The clinical course appears favorable and CT angiography alone may be considered the preferred diagnostic test to assess for aneurysm in first trimester pregnancy.

Therapeutic hypothermia is a proven part of cardio-cerebral resuscitation after cardiac arrest as it improves neurologic outcomes after hypoxic brain injury. This article reviews the mechanisms of hypothermic neuroprotection, the clinical trials that support its use after cardiac arrest, as well as the impact of hypothermia on patient management and prognosis. In caring for patients suffering hypoxic brain injury after cardiac arrest, the role of the neurologist is no longer limited to prognosis but is now to become actively involved in clinical management which includes the use of therapeutic hypothermia.

We recorded neuronal activity in monkey medial superior temporal (MST) cortex during movement on a motorized sled. Most neurons showed a preferred heading direction, but some responded only when that heading was part of a particular path. Others responded only when the animal was at a certain place in the room, regardless of its path to that place. Video simulations of the self-movement scene evoked path, but not place, responses. Stationary positioning in the room revealed location preferences that matched place preferences recorded during movement. We conclude that MST encodes heading, path, and place information to support visuospatial orientation.