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BackgroundAdvances in diagnostic imaging of stroke include multimodal techniques such as noninvasive angiography and perfusion imaging. We aimed to characterize trends in neuroimaging utilization among acute stroke patients. Utilization of multimodal imaging for acute stroke in the community has remained largely uncharacterized despite its increased adoption at academic medical centers.MethodsWe quantified neuroimaging utilization in the emergency department (ED) for 1,700 hyperacute stroke patients presenting

The recent culmination of imaging-endowed endovascular stroke trials has decisively proven the utility of clinically relevant neuroimaging in improving the outcome of patients with potentially debilitating neurological disorders. These large multicenter trials conducted across several continents notably utilized a variety of multimodal CT/MRI modalities to rapidly identify a favorable collateral profile that presages clinically beneficial revascularization. The modern clinical neuroimager may accelerate complex decision-making through the rational use of a variety of imaging modalities and an active feedback loop of imaging at the bedside. The modern clinical neuroimager is often the initial care provider for a wide range or type of stroke patients from hemorrhage to ischemia, armed with the incredibly important aspects of clinical history and examination findings and best poised to utilize imaging to guide therapy from acute stroke to recovery and prevention. The next generation in stroke should not exclusively focus on whether to order a CT or MRI counting minutes at the bedside, but actively and efficiently integrate the vast wealth of information available when imaging is used in the proper clinical context. The novel endovascular era in stroke provides an ideal venue for the synergistic goals of translating research advances, improving patient outcomes and ongoing education as a modern neuroimager.

Ischemic stroke remains a leading cause of death and disability worldwide. Various endovascular trials have addressed clinical outcomes without elucidating the impact of imaging studies in patient selection. The success of recent endovascular trials was bolstered by the use of advanced imaging techniques for optimal selection of reperfusion candidates. This seminal juncture in the history of stroke trials warrants further consideration on the use of imaging to guide future refinements in the treatment of acute stroke. In this article, we systematically review the imaging methodology and key facets used in all published endovascular stroke trials to date, discuss the success of recent trials using latest advanced imaging techniques and focus on the importance of imaging studies for future patient selection.

Background and purposeFractional flow may identify hemodynamic effects and ischemic risk beyond percent stenosis of an artery. We hypothesized that diminished TOF-MRA signal intensity distal to an intracranial stenosis predicts stroke risk.MethodsTOF-MRA was acquired prospectively in the SONIA-WASID trials. The distal/proximal signal intensity ratio (SIR) was calculated from 3 mm regions of interest, blinded to outcome. Univariate and multivariate analyses included clinical variables, SIR, and invasive angiography measures to identify predictors for risk of stroke in the territory.Results189 patients with 50-99% symptomatic intracranial stenosis in SONIA-WASID had TOF-MRA available. In univariate analysis, the hazard ratio (HR) for stroke in the territory of the symptomatic artery with SIR < .9 was 5.2 (1.8, 15.3; P < .001) as compared to SIR ≥ .9. Multivariate analysis correcting for baseline systolic blood pressure, LDL, centrally measured percent stenosis, recency of symptoms, TICI and downstream collaterals, the HR for SIR < .9 was 10.9 (2.0, 58.9; P < .001). In those with

To authenticate to the full-text of this article, please visit this link: http://dx.doi.org/10.1111/j.1552-6569.2008.00295.x Byline: David S. Liebeskind (1), Doojin Kim (1), Sidney Starkman (1), Kelly Changizi (1), Arbi G. Ohanian (1), Reza Jahan (1), Fernando Vinuela (1) Keywords: Collaterals; MRI; angiography Abstract: ABSTRACT BACKGROUND AND PURPOSE Collaterals may compensate for reduced blood flow in acute ischemic stroke, yet endurance and quality of collateral perfusion may vary. Collateral sustenance of penumbra may falter after initial recruitment, resulting in progressive ischemia and clinical deficits. Delayed collateral failure may extend the time window for revascularization, even after failed intravenous thrombolysis. CASE DESCRIPTION A 76-year-old woman returned to normal from National Institutes of Health Stroke Scale (NIHSS) score of 18 following intravenous thrombolysis, despite persistent occlusion of the left middle cerebral artery. Subsequent deterioration was successfully reversed with mechanical thrombectomy almost 14 hours after symptom onset. CONCLUSIONS Early clinical improvement or deterioration may reflect collateral perfusion, not necessarily recanalization or reocclusion. The definition of collateral failure must incorporate the expected role and endurance of collaterals. Further investigation of collateral pathophysiology may reveal predictive clinical or imaging features and disclose collateral therapeutic approaches to augment revascularization. J Neuroimaging 2010;20:78-82. Author Affiliation: (1)Department of Neurology, UCLA Stroke Center, Los Angeles, California (DSL, DK, SS, KC, AGO); and Department of Radioloy, UCLA Stroke Center, Los Angeles, California (RJ, FV) Article History: Acceptance: Received April 12, 2008, and in revised form June 3, 2008. Accepted for publication July 22, 2008. Article note: Correspondence: Address correspondence to David S. Liebeskind, MD, UCLA Stroke Center and Department of Neurology, 710 Westwood Plaza, Los Angeles, CA 90095. E-mail: davidliebeskind@yahoo.com

To authenticate to the full-text of this article, please visit this link: http://dx.doi.org/10.1111/j.1552-6569.2008.00303.x Byline: Oh Young Bang (1), David S. Liebeskind (1), Brian H. Buck (1), Sa Rah Yoon (1), Jeffry R. Alger (1), Bruce Ovbiagele (1), Jeffrey L. Saver (1) Keywords: Stroke; ischemic; perfusion; thrombolysis; diffusion-weighted imaging; magnetic resonance imaging Abstract: ABSTRACT BACKGROUND Reperfusion of penumbral tissue is a promising strategy for treatment of acute cerebral ischemia more than 3 hours from symptom onset. However, there has been only sparse direct evidence that reperfusion after 3 hours prevents infarct growth. METHODS We analyzed clinical and serial magnetic resonance imaging (MRI) data on patients who received endovascular recanalization therapy 3-12 hours after last known well time. Multimodal MRIs were acquired pretreatment, early (1-20 hours), and late (2-7 days) after treatment. Degree of recanalization was assessed on end of procedure catheter angiogram, degree of reperfusion on early posttreatment perfusion MRI, and infarct growth by analysis of diffusion lesion volumes on pretreatment and late MRIs. RESULTS Twenty-seven (12 men, 15 women) underwent endovascular recanalization procedures at 6.0 [+ or -] 2.1 hours (range, 3.0-11.5 hours) after last known well time. Immediate posttreatment perfusion lesion (Tmax [greater than or equal to]4 seconds) volume correlated strongly with infarct growth (r= .951, P < .001), exceeding the correlations of vessel recanalization score (r=-.198, P= .446) and pretreatment diffusion-perfusion mismatch volume (r= .518, P= .033). Without reperfusion, enlargement of DWI lesion volume was observed in all patients, and extent of enlargement depended on volume of immediate posttreatment perfusion defects. CONCLUSION Our data indicate that posttreatment reperfusion is the major determinant of threatened tissue outcome, and suggest reperfusion even after 3 hours of symptom onset can alter tissue fate over a wide range of mismatch volumes. Author Affiliation: (1)From the Department of Neurology, University of California, Los Angeles, CA (OYB, DSL, JRA, BO, JLS); Department of Neurology, Samsung Medical Center, Sungkyunkwan University, Seoul, South Korea (OYB); Division of Neurology, Department of Medicine, University of Alberta, Edmonton, Canada (BHB); Department of Radiology, University of California, Los Angeles, CA (SRY).[Correction added after online publication 14-September-2009: Received date has been corrected.] Article History: Acceptance: Received August 3, 2007, and in revised form December 16, 2007. Accepted for publication January 11, 2008. Article note: Correspondence: Address correspondence to Jeffrey L. Saver, MD, UCLA Stroke Center, 710 Westwood Plaza, Los Angeles, CA 90095. E-mail: jsaver@ucla.edu.

To purchase or authenticate to the full-text of this article, please visit this link: http://dx.doi.org/10.1111/j.1552-6569.2007.00167.x Byline: Sindhu Ramchandren (1), David S. Liebeskind (1) Keywords: Hypoxia; ischemia; demyelination; neurogenic bladder; Wallerian degeneration Abstract: ABSTRACT BACKGROUND AND PURPOSE Hypoxia is commonly known to target neuronal cell bodies. Although myelin is a non-infrequent target, posthypoxic demyelination is a rarely described entity. We describe the case of a man who developed neurogenic bladder following a motor vehicle accident. CASE REPORT Following a severe motor-vehicle accident involving massive blood loss, a 46-year-old man developed urinary urgency requiring catheterization, with hyperactive reflexes and bilateral Babinski signs on exam. RESULTS Magnetic resonance imaging of the brain and cervical cord revealed diffuse, isolated white matter signal abnormality in a symmetric, confluent distribution, extending inferiorly into the spinal cord, with changes consistent with bilateral Wallerian degeneration. Serologic and CSF evaluations were normal. CONCLUSIONS Unlike previous reports of hypoxic-ischemic demyelination, our patient lacked any cortical abnormalities, presumably due to isolated white matter changes. This report alerts physicians to the possibility of hypoxic-ischemic demyelination due to global hypoxia-ischemia as an etiologic factor for neurogenic bladder. Author Affiliation: (1)University of Michigan Health System, Neurology, Ann Arbor, MI (SR); and UCLA Stroke Center-University of California, Los Angeles, CA (DSL). Article History: Acceptance: Received October 6, 2006, and in revised form May 24, 2007. Accepted for publication June 18, 2007. Article note: Correspondence: Address correspondence to Sindhu Ramchandren, MD, Department of Neurology, University of Michigan at Ann Arbor, 300 North Ingalls St, #3D06, Ann Arbor, MI 48109. E-mail: sindhur@med.umich.edu.

Background and Purpose: It is unknown whether intracranial atherosclerotic disease (ICAD), in addition to causing stenosis, also associates with abnormal arterial enlargement, a condition known as intracranial dolichoectasia (IDE). Across symptomatic ICAD patients, we aim to determine IDE prevalence and IDE impact on cerebral hemodynamics and recurrent cerebral ischemia. Methods: We analyzed 98 participants (mean age 63.8 ± 11.9 years, 56.1% men) of the prospective observational study MYRIAD. Participants were enrolled within 21 days of an ischemic stroke or transient ischemic attack caused by moderate‐to‐severe ICAD. Semi‐automatic vessel segmentation was used to determine diameters, length, and tortuosity‐index of proximal intracranial arteries. Either ectasia (increased diameter) or dolichosis (increased length or TI) defined IDE. We assessed IDE association with new infarcts during 12‐month follow‐up, and IDE correlation with cerebral hemodynamics determined by quantitative MR‐angiography (QMRA), MR‐perfusion weighted‐imaging, and transcranial Doppler breath‐holding index. Results: IDE was present in 35.7% of patients and 10.2% of symptomatic arteries. Basilar stenosis was associated with higher IDE prevalence (27.8% vs. 8.8%, p = 0.04), whereas other symptomatic arteries showed no association with IDE. Symptomatic arteries with IDE had lower hypoperfusion prevalence on MR‐PWI (11.1% vs. 28.4%, p = 0.03). Increased diameter (r = 0.33, p<0.01) and tortuosity‐index (r = 0.29, p = 0.01) showed positive correlation with QMRA flow rate. IDE was not associated with new infarcts during follow‐up. Conclusions: IDE was common among symptomatic ICAD patients. IDE was not associated with stroke recurrence. Instead, increased diameter and tortuosity correlated with improved blood flow across the stenotic artery, suggesting that IDE may originate as an adaptive mechanism in ICAD. [ABSTRACT FROM AUTHOR]

Background and Purpose: Acetazolamide reactivity on 123 I-IMP SPECT is used to detect misery perfusion due to intracranial atherosclerosis. Noninvasive fractional flow assessed by signal intensity ratio (SIR) on time of flight-magnetic resonance angiography (TOF-MRA) might offer a feasible alternative to identify high-risk intracranial stenosis.Methods: Data from consecutive patients with unilateral middle cerebral artery (MCA) stenosis who underwent both TOF-MRA and acetazolamide reactivity on 123 I-IMP SPECT were retrospectively analyzed. Signal intensity was measured in the background and on the MCA proximal and distal to the stenotic lesion on TOF-MRA. Mean cerebral blood flow (CBF) at rest and cerebrovascular reactivity were measured in the target MCA territory. CBF patterns of the MCA were divided into three groups (Powers' stage 0-II).Results: A total of 56 sets of diagnostic imaging in 33 patients were assessed. Four CBF patterns were stage II in four MCA territories, stage I in 31, and stage 0 in 21. Median SIR of the MCA was .53 (interquartile range .46-.69) for stage II, .78 (.63-.90) for stage I, and .91 (.85-.95) for stage 0. The optimal cutoff for SIR obtained from receiver operating characteristic curve analysis to predict stage II was < .56.Conclusions: In patients with unilateral MCA stenosis, decreased SIR was correlated with misery perfusion, providing a simpler, widely available predictor of high-risk intracranial stenosis. [ABSTRACT FROM AUTHOR]

Background and Purpose: Impaired distal perfusion predicts neurological deterioration in large artery atherosclerosis. We aim to determine the optimal threshold of Tmax delay on perfusion imaging that is associated with neurological deterioration in patients with symptomatic proximal anterior circulation large artery stenosis.Methods: Data were abstracted from a prospective ischemic stroke database of consecutively enrolled patients with symptomatic proximal intracranial stenosis (internal carotid artery or M1 segment of the middle cerebral artery) who underwent magnetic resonance perfusion imaging within 24 hours of symptom onset during a 15-month period. Tissue volumes of perfusion delay Tmax 0-4 seconds, Tmax > 4 seconds, Tmax > 6 seconds, and Tmax > 8 seconds were calculated using an automated approach. A target mismatch (penumbra-core) was defined as ≥15mL of brain tissue using each of the Tmax threshold categories. The outcome was neurological deterioration at 30 days defined as new or worsening neurological deficits that are not attributed to a nonvascular etiology.Results: Among 52 patients with symptomatic intracranial stenosis, 26 patients met inclusion criteria. Neurological deterioration was associated with target mismatch profile defined according to Tmax > 6 seconds (66.7% [6/9] vs. 5.9% [1/17], P < .01) and Tmax >8 seconds (57.1% [4/7] vs. 15.8% [3/19], P = .05] but not according to Tmax > 4 seconds (27.3% [6/17] vs. 11.1% [1/9], P = .35].Conclusions: A target mismatch profile using Tmax > 6 seconds may define tissue at risk in patients with acute symptomatic proximal anterior circulation intracranial stenosis. More studies are needed to confirm our findings. [ABSTRACT FROM AUTHOR]

BACKGROUND Reperfusion of penumbral tissue is a promising strategy for treatment of acute cerebral ischemia more than 3 hours from symptom onset. However, there has been only sparse direct evidence that reperfusion after 3 hours prevents infarct growth. METHODS We analyzed clinical and serial magnetic resonance imaging (MRI) data on patients who received endovascular recanalization therapy 3-12 hours after last known well time. Multimodal MRIs were acquired pretreatment, early (1-20 hours), and late (2-7 days) after treatment. Degree of recanalization was assessed on end of procedure catheter angiogram, degree of reperfusion on early posttreatment perfusion MRI, and infarct growth by analysis of diffusion lesion volumes on pretreatment and late MRIs. RESULTS Twenty-seven (12 men, 15 women) underwent endovascular recanalization procedures at 6.0 ± 2.1 hours (range, 3.0-11.5 hours) after last known well time. Immediate posttreatment perfusion lesion (Tmax ≥4 seconds) volume correlated strongly with infarct growth ( r= .951, P < .001), exceeding the correlations of vessel recanalization score ( r=−.198, P= .446) and pretreatment diffusion-perfusion mismatch volume ( r= .518, P= .033). Without reperfusion, enlargement of DWI lesion volume was observed in all patients, and extent of enlargement depended on volume of immediate posttreatment perfusion defects. CONCLUSION Our data indicate that posttreatment reperfusion is the major determinant of threatened tissue outcome, and suggest reperfusion even after 3 hours of symptom onset can alter tissue fate over a wide range of mismatch volumes. [ABSTRACT FROM AUTHOR]