Barber, P Alan PhD, FRACP; Hach, Sylvia MSc; Tippett, Lynette J. PhD; Ross, Linda et al
Cerebral Ischemic Lesions on Diffusion-Weighted Imaging Are Associated With Neurocognitive Decline After Cardiac Surgery
Stroke. Publish Ahead of Print, published online before print, 6 March 2008
Abstract
Background and Purpose-: Improvements in cardiac surgery mortality and morbidity have focused interest on the neurological injury such as stroke and cognitive decline that may accompany an otherwise successful operation. We aimed to investigate (1) the rate of stroke, new ischemic change on MRI, and cognitive impairment after cardiac valve surgery; and (2) the controversial relationship between perioperative cerebral ischemia and cognitive decline.Methods-: Forty patients (26 men; mean [SD] age 62.1 [13.7] years) undergoing intracardiac surgery (7 also with coronary artery bypass grafting) were studied. Neurological, neuropsychological, and MRI examinations were performed 24 hours before surgery and 5 days (MRI and neurology) and 6 weeks (neuropsychology and neurology) after surgery. Cognitive decline from baseline was determined using the Reliable Change Index.Results-: Two of 40 (5%) patients had perioperative strokes and 22 of 35 (63%) tested had cognitive decline in at least one measure (range, 1 to 4). Sixteen of 37 participants (43%) with postoperative imaging had new ischemic lesions (range, 1 to 17 lesions) with appearances consistent with cerebral embolization. Cognitive decline was seen in all patients with, and 35% of those without, postoperative ischemic lesions (P<0.001),>
Tsivgoulis, Georgios MD; Alexandrov, Andrei MD;
Ultrasound-Enhanced Thrombolysis: From Bedside to Bench. [Editorial]
Stroke. Publish Ahead of Print, published online before print, 13 March 2008
Alexandrov, Andrei V. MD; Mikulik, Robert MD; Ribo, Marc MD; Sharma, Vijay K. et al
A Pilot Randomized Clinical Safety Study of Sonothrombolysis Augmentation With Ultrasound-Activated Perflutren-Lipid Microspheres for Acute Ischemic Stroke
Stroke. Publish Ahead of Print, published online before print, 20 March 2008
Abstract
Background and Purpose-: Ultrasound transiently expands perflutren-lipid microspheres ([mu]S), transmitting energy momentum to surrounding fluids. We report a pilot safety/feasibility study of ultrasound-activated [mu]S with systemic tissue plasminogen activator (tPA).Methods-: Stroke subjects treated within 3 hours had abnormal Thrombolysis in Brain Ischemia (TIBI) residual flow grades 0 to 3 before tPA on transcranial Doppler (TCD). Randomization included Controls (tPA+TCD) or Target (tPA+TCD+2.8 mL [mu]S). The primary safety end point was symptomatic intracranial hemorrhage (sICH) with worsening by >=4 NIHSS points within 72 hours.Results-: Fifteen subjects were randomized 3:1 to Target, n=12 or Control, n=3. After treatment, asymptomatic ICH occurred in 3 Target and 1 Control, and sICH was not seen in any study subject. [mu]S reached MCA occlusions in all Target subjects at velocities higher than surrounding residual red blood cell flow: 39.8+/-11.3 vs 28.8+/-13.8 cm/s, P<0.001. p="0.028." p="0.003," p="0.456.Conclusions-:">
Stroke. Publish Ahead of Print, published online before print, 20 March 2008
Abstract
Background and Purpose-: Ultrasound transiently expands perflutren-lipid microspheres ([mu]S), transmitting energy momentum to surrounding fluids. We report a pilot safety/feasibility study of ultrasound-activated [mu]S with systemic tissue plasminogen activator (tPA).Methods-: Stroke subjects treated within 3 hours had abnormal Thrombolysis in Brain Ischemia (TIBI) residual flow grades 0 to 3 before tPA on transcranial Doppler (TCD). Randomization included Controls (tPA+TCD) or Target (tPA+TCD+2.8 mL [mu]S). The primary safety end point was symptomatic intracranial hemorrhage (sICH) with worsening by >=4 NIHSS points within 72 hours.Results-: Fifteen subjects were randomized 3:1 to Target, n=12 or Control, n=3. After treatment, asymptomatic ICH occurred in 3 Target and 1 Control, and sICH was not seen in any study subject. [mu]S reached MCA occlusions in all Target subjects at velocities higher than surrounding residual red blood cell flow: 39.8+/-11.3 vs 28.8+/-13.8 cm/s, P<0.001. p="0.028." p="0.003," p="0.456.Conclusions-:">
Shah, Rajiv R. MD; Haghpanah, Sepideh MD; Elovic, Elie P. MD; Flanagan, Steven R. et al
MRI Findings in the Painful Poststroke Shoulder
Stroke. Publish Ahead of Print, published online before print, 3 April 2008
Abstract
Background and Purpose-: We describe the structural abnormalities in the painful shoulder of stroke survivors and their relationships to clinical characteristics.Method-: Eighty-nine chronic stroke survivors with poststroke shoulder pain underwent T1- and T2-weighted multiplanar, multisequence MRI of the painful paretic shoulder. All scans were reviewed by one radiologist for the following abnormalities: rotator cuff, biceps and deltoid tears, tendinopathies and atrophy, subacromial bursa fluid, labral ligamentous complex abnormalities, and acromioclavicular capsular hypertrophy. Clinical variables included subject demographics, stroke characteristics, and the Brief Pain Inventory Questions 12. The relationship between MRI findings and clinical characteristics was assessed through logistic regression.Results-: Thirty-five percent of subjects exhibited a tear of at least one rotator cuff, biceps or deltoid muscle. Fifty-three percent of subjects exhibited tendinopathy of at least one rotator cuff, bicep or deltoid muscle. The prevalence of rotator cuff tears increased with age. However, rotator cuff tears and rotator cuff and deltoid tendinopathies were not related to severity of poststroke shoulder pain. In approximately 20% of cases, rotator cuff and deltoid muscles exhibited evidence of atrophy. Atrophy was associated with reduced motor strength and reduced severity of shoulder pain.Conclusions-: Rotator cuff tears and rotator cuff and deltoid tendinopathies are highly prevalent in poststroke shoulder pain. However, their relationship to shoulder pain is uncertain. Atrophy is less common but is associated with less severe shoulder pain.
MRI Findings in the Painful Poststroke Shoulder
Stroke. Publish Ahead of Print, published online before print, 3 April 2008
Abstract
Background and Purpose-: We describe the structural abnormalities in the painful shoulder of stroke survivors and their relationships to clinical characteristics.Method-: Eighty-nine chronic stroke survivors with poststroke shoulder pain underwent T1- and T2-weighted multiplanar, multisequence MRI of the painful paretic shoulder. All scans were reviewed by one radiologist for the following abnormalities: rotator cuff, biceps and deltoid tears, tendinopathies and atrophy, subacromial bursa fluid, labral ligamentous complex abnormalities, and acromioclavicular capsular hypertrophy. Clinical variables included subject demographics, stroke characteristics, and the Brief Pain Inventory Questions 12. The relationship between MRI findings and clinical characteristics was assessed through logistic regression.Results-: Thirty-five percent of subjects exhibited a tear of at least one rotator cuff, biceps or deltoid muscle. Fifty-three percent of subjects exhibited tendinopathy of at least one rotator cuff, bicep or deltoid muscle. The prevalence of rotator cuff tears increased with age. However, rotator cuff tears and rotator cuff and deltoid tendinopathies were not related to severity of poststroke shoulder pain. In approximately 20% of cases, rotator cuff and deltoid muscles exhibited evidence of atrophy. Atrophy was associated with reduced motor strength and reduced severity of shoulder pain.Conclusions-: Rotator cuff tears and rotator cuff and deltoid tendinopathies are highly prevalent in poststroke shoulder pain. However, their relationship to shoulder pain is uncertain. Atrophy is less common but is associated with less severe shoulder pain.
Wintermark, Max MD; Albers, Gregory W. MD; Alexandrov, Andrei V. MD; Alger, Jeffry R. et al Acute Stroke Imaging Research Roadmap. [Report]
Stroke. Publish Ahead of Print, published online before print, 10 April 2008
Abstract
mdash;: The recent "Advanced Neuroimaging for Acute Stroke Treatment" meeting on September 7 and 8, 2007 in Washington DC, brought together stroke neurologists, neuroradiologists, emergency physicians, neuroimaging research scientists, members of the National Institute of Neurological Disorders and Stroke (NINDS), the National Institute of Biomedical Imaging and Bioengineering (NIBIB), industry representatives, and members of the US Food and Drug Administration (FDA) to discuss the role of advanced neuroimaging in acute stroke treatment. The goals of the meeting were to assess state-of-the-art practice in terms of acute stroke imaging research and to propose specific recommendations regarding: (1) the standardization of perfusion and penumbral imaging techniques, (2) the validation of the accuracy and clinical utility of imaging markers of the ischemic penumbra, (3) the validation of imaging biomarkers relevant to clinical outcomes, and (4) the creation of a central repository to achieve these goals. The present article summarizes these recommendations and examines practical steps to achieve them.(C) 2008 American Heart Association, Inc.
Stroke. Publish Ahead of Print, published online before print, 10 April 2008
Abstract
mdash;: The recent "Advanced Neuroimaging for Acute Stroke Treatment" meeting on September 7 and 8, 2007 in Washington DC, brought together stroke neurologists, neuroradiologists, emergency physicians, neuroimaging research scientists, members of the National Institute of Neurological Disorders and Stroke (NINDS), the National Institute of Biomedical Imaging and Bioengineering (NIBIB), industry representatives, and members of the US Food and Drug Administration (FDA) to discuss the role of advanced neuroimaging in acute stroke treatment. The goals of the meeting were to assess state-of-the-art practice in terms of acute stroke imaging research and to propose specific recommendations regarding: (1) the standardization of perfusion and penumbral imaging techniques, (2) the validation of the accuracy and clinical utility of imaging markers of the ischemic penumbra, (3) the validation of imaging biomarkers relevant to clinical outcomes, and (4) the creation of a central repository to achieve these goals. The present article summarizes these recommendations and examines practical steps to achieve them.(C) 2008 American Heart Association, Inc.
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