Search

To identify novel technologies pertinent to the prevention, diagnosis, treatment, and rehabilitation of ischemic stroke, and recommend the technologies that show the most promise in advancing ischemic stroke care. A systematic literature search on PubMed and Medscape was performed. Articles were assessed based on pre-determined criteria. Included journal articles were evaluated for specific characteristics and reviewed according to a structured paradigm. A search on www.clinicaltrials.gov was performed to identify pre-clinical ischemic stroke technological interventions. All clinical trial results were included. An additional search on PubMed was conducted to identify studies on robotic neuroendovascular procedures. Thirty journal articles and five clinical trials were analyzed. Articles were categorized as follows: six studies pertinent to pre-morbidity and prevention of ischemic stroke, three studies relevant to the diagnosis of ischemic stroke, 16 studies about post-ischemic stroke rehabilitation, and five studies on robotic neuroendovascular interventions. Novel technologies across the spectrum of ischemic stroke care were identified, and the ones that appear to have the most clinical utility are recommended. Future investigation of the feasibility and long-term efficacy of the recommended technologies in clinical settings is warranted.

Preclinical and clinical studies have suggested a potential benefit from COX-2 inhibition on secondary injury activation after spontaneous intracerebral hemorrhage (ICH). The aim of this study was to investigate the effect of pre-admission NSAID use on functional recovery in spontaneous ICH patients. Consecutive adult ICH patients enrolled in the Intracerebral Hemorrhage Outcomes Project (2009–2018) with available 90-day follow-up data were included. Patients were categorized as NSAID (daily COX inhibitor use ≤ 7 days prior to ICH) and non-NSAID users (no daily COX inhibitor use ≤ 7 days prior to ICH). Primary outcome was the ordinal 90-day modified Rankin Scale (mRS) score. Outcomes were compared between cohorts using multivariable regression and propensity score-matched analyses. A secondary analysis excluding aspirin users was performed. The NSAID and non-NSAID cohorts comprised 228 and 361 patients, respectively. After 1:1 matching, the matched cohorts each comprised 140 patients. The 90-day mRS were comparable between the NSAID and non-NSAID cohorts in both the unmatched (aOR = 0.914 [0.626–1.336], p = 0.644) and matched (aOR = 0.650 [0.392–1.080], p = 0.097) analyses. The likelihood of recurrent ICH at 90 days was also comparable between the NSAID and non-NSAID cohorts in both the unmatched (aOR = 0.845 [0.359–1.992], p = 0.701) and matched analyses (aOR = 0.732 [0.241–2.220], p = 0.581). In the secondary analysis, the non-aspirin NSAID and non-NSAID cohorts comprised 38 and 361 patients, respectively. After 1:1 matching, the matched cohorts each comprised 38 patients. The 90-day mRS were comparable between the non-aspirin NSAID and non-NSAID cohorts in both the unmatched (aOR = 0.615 [0.343–1.101], p = 0.102) and matched (aOR = 0.525 [0.219–1.254], p = 0.147) analyses. The likelihood of recurrent ICH at 90 days was also comparable between the non-aspirin NSAID and non-NSAID cohorts in both the unmatched (aOR = 2.644 [0.258–27.091], p = 0.413) and matched (aOR = 2.586 [0.228–29.309], p = 0.443) analyses. After the exclusion of patients with DNR or withdrawal of care status, NSAID use was associated with lower mRS at 90 days (aOR = 0.379 [0.212–0.679], p = 0.001), lower mRS at hospital discharge (aOR = 0.505 [0.278–0.919], p = 0.025) and lower 90-day mortality rates (aOR = 0.309 [0.108–0.877], p = 0.027). History of nonselective COX inhibition may affect functional outcomes in ICH patients. Pre-admission NSAID use did not appear to worsen the severity of presenting ICH or increase the risk of recurrent ICH. Additional clinical studies may be warranted to investigate the effects of pre-admission NSAID use on ICH outcomes.

BACKGROUND/PURPOSE: Blood type has become an increasingly recognized risk factor for coagulopathy. We explored the association between blood type and hematoma expansion (HE) after intracerebral hemorrhage (ICH). METHODS: Spontaneous ICH patients prospectively enrolled in an ongoing ICH cohort study at Columbia University Irving Medical Center from 2009 to 2016 were evaluated. Primary ICH patients with admission blood type testing were evaluated for HE differences, defined as > 33% relative HE. The association of blood type with radiographic HE outcomes was assessed using multivariable logistic regression models. The association of blood type and poor clinical outcomes using modified Rankin Scale (mRS 4–6) was additionally explored. RESULTS: Of 272 ICH patients with blood type data and neuroimaging available to determine HE, there were 146 (54%) type-O, 82 (30%) type-A, 34 (13%) type-B, and 10 (3%) type-AB patients. No significant baseline demographic, clinical, or radiographic differences were noted between blood types. Type-B blood was associated with more HE compared to other blood types (OR 2.82; 95% CI 1.23–6.45) after adjusting for known covariates of HE (anticoagulant use, time to admission computed tomography scan, and baseline hematoma volume). No associations with blood type and poor 3 month mRS were identified, but these analyses were limited secondary to our smaller cohort. CONCLUSIONS: There may be differences in HE after ICH in patients with different blood types. Further work is required to replicate these findings and identify the pathophysiologic mechanisms behind coagulopathy between blood types after ICH.

Carotid endarterectomy (CEA) is associated with perioperative stroke and mortality in a minority of cases. The aim of this systematic review and meta-analysis was to investigate the effect of pre-operative statins on perioperative outcomes in patients undergoing CEA for internal carotid artery (ICA) stenosis. A systematic review of PubMed, Medline, and the Cochrane Database of Systematic Reviews was performed. Studies were included which reported perioperative stroke and/or survival outcomes following CEA for ICA stenosis and compared patients who were and were not taking pre-operative statins. Relevant data were extracted and pooled using meta-analysis. Seven studies met the inclusion criteria, comprising 21,387 patients. A total of 68.9% (14,976) were administered statins and 31.1% (6657) were statin-free. Pre-operative statin use was higher in patients with a history of cardiac disease (12.2 vs. 23.6% in the statin-free group), diabetes (31.6 vs. 25.1% in the statin-free group), and hypertension (83.5 vs. 72.2% in the statin-free group), while a greater proportion of statin-free patients had symptomatic disease (44.9 vs. 55.5% in the statin-free group). Statins were associated with reduced perioperative stroke in all patients (OR 0.57; 95% CI 0.34–0.95; p = 0.03) and in symptomatic patients (OR 0.57; 95% CI 0.35–0.93; p = 0.03). A trend towards lower perioperative mortality (OR 0.54; 95% CI 0.29, 1.03; p = 0.06) and significantly improved overall survival was observed in the statin group (HR 0.69; 95% CI 0.59–0.81; p

Despite recent advances in the understanding of the pathophysiology of cerebral ischemia, current approaches attempting to prevent ischemic brain damage after an acute stroke remain quite inadequate. Today, ischemic stroke remains the third leading cause of death in industrialized nations, and the leading cause of disability requiring long term institutional care in the U.S and other industrialized nations. While one treatment, tissue plasminogen activator, has shown efficacy in clinical trials, safety concerns limit its role in clinical practice to a narrow time window of use. Acute cerebral ischemia has been shown to evoke a profound and deleterious upregulation of the inflammatory response, initiated within the cerebral microvasculature. Recently, research efforts have focused on targeting individual components of the inflammatory cascade, such as leukocyte activation and adhesion, in an attempt to develop potential neuroprotective agents. While these strategies have shown promise preclinically, clinical trials have yet to show clear benefit. Here, we review the current understanding of the pathophysiologic consequences of acute cerebral ischemic injury. Additionally, we discuss the role of the inflammatory cascade, with specific attention given to the deleterious role played by leukocyte activation and adhesion in stroke. Finally, relevant efforts to translate these basic science observations into clinical efficacy in acute stroke trials are critically reviewed.

¶Background. Safety, feasibility, and efficacy trials in non-human primate stroke models are essential to the evaluation of experimental therapies and their translation to humans. Although Laser Doppler Flowmetry has been successfully employed in rodent stroke to continuously monitor cerebral blood flow, it has not been applied in primate studies. This investigation examined the utility of Laser Doppler Flowmetry in refining an existing baboon model of cerebral ischemia/reperfusion. Method. Continuous Laser Doppler Flowmetry monitoring was used, in non-human primates, to document local cerebral blood flow before, during, and after middle cerebral artery territory occlusion. In each baboon (n = 7) a single Doppler probe was placed into the left frontal cortex through a precoronal burr hole. Correlations between Laser Doppler Flowmetry values and latencies to Motor Evoked Potential dropout were compared using a linear regression model. Findings. Placement of the Laser Doppler probe was easily accomplished in all animals. Laser Doppler Flowmetry tracings accurately documented blood flow changes that occurred with each technical manipulation during the procedure. Laser Doppler confirmed decreased perfusion that coincided both regionally and temporally with vessel occlusion. Depth of ischemia as measured by Laser Doppler Flowmetry was associated with Motor Evoked Potential dropout latencies for individual animals. Conclusions. Continuous, single probe Laser Doppler Flowmetry is a reliable method of documenting perfusion changes following middle cerebral artery territory occlusion in a baboon model of reperfused stroke. This advanced intraoperative monitoring technique may lead to more accurate evaluation of acute stroke therapies in pre-clinical trials.

This study intends to develop a physiologic thumbprint for nonconvulsive seizures (NCSz) after acute brain injury. Abnormal electrographic brain activity including NCSz is common after acute brain injury and is associated with poor outcome. Mechanisms underlying this phenomenon are poorly understood but in animals periods of inadequate perfusion during seizures have been documented. In the present study we hope to gain better understanding of the relationship between abnormal electrographic patterns and brain homeostasis in patients with subarachnoid hemorrhage (SAH).

Active smokers comprise 35–55% of patients admitted with acute spontaneous subarachnoid hemorrhage (SAH). Transdermal nicotine replacement is sometimes prescribed to these patients to prevent a withdrawal syndrome, but the safety of exogenous nicotine during the acute period after SAH is unknown.