13 research outputs found

    Reversible cerebral vasoconstriction syndrome with concurrent bilateral carotid artery dissection

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    Background: The pathophysiological basis of reversible cerebral vasoconstriction syndrome is poorly understood but carotid artery dissection has been discussed as a rare possible cause. So far, only single cases of unilateral carotid artery dissection and reversible cerebral vasoconstriction syndrome have been reported. Case: Here, we describe the case of a 54-year old patient presenting to the emergency department with right hemiparesis, hypaesthesia and dysarthria. Furthermore, he reported two episodes of thunderclap headache after autosexual activity. Cerebral imaging showed ischaemic infarcts, slight cortical subarachnoid haemorrhage, bilateral carotid artery dissection and fluctuating intracranial vessel irregularities, compatible with reversible cerebral vasoconstriction syndrome. An extensive diagnostic work-up was normal. No typical trigger factors of reversible cerebral vasoconstriction syndrome could be found. The patient received intravenous heparin and the calcium channel blocker nimodipine. Follow-up imaging revealed no vessel irregularities, the left internal carotid artery was still occluded. Conclusion: This case supports the assumption that carotid artery dissection should be considered as a potential trigger of reversible cerebral vasoconstriction syndrome, possibly by altering sympathetic vascular tone

    Expansive arterial remodeling of the carotid arteries and its effect on atherosclerotic plaque composition and vulnerability: an in-vivo black-blood 3T CMR study in symptomatic stroke patients

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    Background: Based on intravascular ultrasound of the coronary arteries expansive arterial remodeling is supposed to be a feature of the vulnerable atheroslerotic plaque. However, till now little is known regarding the clinical impact of expansive remodeling of carotid lesions. Therefore, we sought to evaluate the correlation of expansive arterial remodeling of the carotid arteries with atherosclerotic plaque composition and vulnerability using in-vivo Cardiovascular Magnetic Resonance (CMR). Methods: One hundred eleven symptomatic patients (74 male/71.8 +/- 10.3y) with acute unilateral ischemic stroke and carotid plaques of at least 2 mm thickness were included. All patients received a dedicated multi-sequence black-blood carotid CMR (3Tesla) of the proximal internal carotid arteries (ICA). Measurements of lumen, wall, outer wall, hemorrhage, calcification and necrotic core were determined. Each vessel-segment was classified according to American Heart Association (AHA) criteria for vulnerable plaque. A modified remodeling index (mRI) was established by dividing the average outer vessel area of the ICA segments by the lumen area measured on TOF images in a not affected reference segment at the distal ipsilateral ICA. Correlations of mRI and clinical symptoms as well as plaque morphology/vessel dimensions were evaluated. Results: Seventy-eight percent (157/202) of all internal carotid arteries showed atherosclerotic disease with AHA Lesion-Type (LT) III or higher. The mRI of the ICA was significantly different in normal artery segments (AHA LT I;mRI 1.9) compared to atherosclerotic segments (AHA LT III-VII;mRI 2.5;p < 0.0001). Between AHA LT III-VII there was no significant difference of mRI. Significant correlations (p < 0.05) of the mRI with lumen-area (LA), wall-area (WA), vessel-area (VA) and wall-thickness (WT), necrotic-core area (NC), and ulcer-area were observed. With respect to clinical presentation (symptomatic/asymptomatic side) and luminal narrowing (stenotic/non-stenotic) no relevant correlations or significant differences regarding the mRI were found. Conclusion: Expansive arterial remodeling exists in the ICA. However, no significant association between expansive arterial remodeling, stroke symptoms, complicated AHA VI plaque, and luminal stenosis could be established. Hence, results of our study suggest that expansive arterial remodeling is not a very practical marker for plaque vulnerability in the carotid arteries

    The carotid plaque imaging in acute stroke (CAPIAS) study:

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    Background: In up to 30% of patients with ischemic stroke no definite etiology can be established. A significant proportion of cryptogenic stroke cases may be due to non-stenosing atherosclerotic plaques or low grade carotid artery stenosis not fulfilling common criteria for atherothrombotic stroke. The aim of the CAPIAS study is to determine the frequency, characteristics, clinical and radiological long-term consequences of ipsilateral complicated American Heart Association lesion type VI (AHA-LT VI) carotid artery plaques in patients with cryptogenic stroke. Methods/Design: 300 patients (age > 49 years) with unilateral DWI-positive lesions in the anterior circulation and non- or moderately stenosing (<70% NASCET) internal carotid artery plaques will be enrolled in the prospective multicenter study CAPIAS. Carotid plaque characteristics will be determined by high-resolution black-blood carotid MRI at baseline and 12 month follow up. Primary outcome is the prevalence of complicated AHA-LT VI plaques in cryptogenic stroke patients ipsilateral to the ischemic stroke compared to the contralateral side and to patients with defined stroke etiology. Secondary outcomes include the association of AHA-LT VI plaques with the recurrence rates of ischemic events up to 36 months, rates of new ischemic lesions on cerebral MRI (including clinically silent lesions) after 12 months and the influence of specific AHA-LT VI plaque features on the progression of atherosclerotic disease burden, on specific infarct patterns, biomarkers and aortic arch plaques. Discussion: CAPIAS will provide important insights into the role of non-stenosing carotid artery plaques in cryptogenic stroke. The results might have implications for our understanding of stroke mechanism, offer new diagnostic options and provide the basis for the planning of targeted interventional studies

    Erratum: Location of crossings in the Floquet spectrum of a driven two-level system (vol B 67, art no 165301, 2003)

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    Background: The purpose of this prospective study was to perform a head-to-head comparison of the two methods most frequently used for evaluation of carotid plaque characteristics: Multi-detector Computed Tomography Angiography (MDCTA) and black-blood 3 T-cardiovascular magnetic resonance (bb-CMR) with respect to their ability to identify symptomatic carotid plaques. Methods: 22 stroke unit patients with unilateral symptomatic carotid disease and > 50% stenosis by duplex ultrasound underwent MDCTA and bb-CMR (TOF, pre- and post-contrast fsT1w-, and fsT2w-sequences) within 15 days of symptom onset. Both symptomatic and contralateral asymptomatic sides were evaluated. By bb-CMR, plaque morphology, composition and prevalence of complicated AHA type VI lesions (AHA-LT6) were evaluated. By MDCTA, plaque type (non-calcified, mixed, calcified), plaque density in HU and presence of ulceration and/or thrombus were evaluated. Sensitivity (SE), specificity (SP), positive and negative predictive value (PPV, NPV) were calculated using a 2-by-2-table. Results: To distinguish between symptomatic and asymptomatic plaques AHA-LT6 was the best CMR variable and presence/absence of plaque ulceration was the best CT variable, resulting in a SE, SP, PPV and NPV of 80%, 80%, 80% and 80% for AHA-LT6 as assessed by bb-CMR and 40%, 95%, 89% and 61% for plaque ulceration as assessed by MDCTA. The combined SE, SP, PPV and NPV of bb-CMR and MDCTA was 85%, 75%, 77% and 83%, respectively. Conclusions: Bb-CMR is superior to MDCTA at identifying symptomatic carotid plaques, while MDCTA offers high specificity at the cost of low sensitivity. Results were only slightly improved over bb-CMR alone when combining both techniques

    Reversible cerebral vasoconstriction syndrome with concurrent bilateral carotid artery dissection

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    Background: The pathophysiological basis of reversible cerebral vasoconstriction syndrome is poorly understood but carotid artery dissection has been discussed as a rare possible cause. So far, only single cases of unilateral carotid artery dissection and reversible cerebral vasoconstriction syndrome have been reported. Case: Here, we describe the case of a 54-year old patient presenting to the emergency department with right hemiparesis, hypaesthesia and dysarthria. Furthermore, he reported two episodes of thunderclap headache after autosexual activity. Cerebral imaging showed ischaemic infarcts, slight cortical subarachnoid haemorrhage, bilateral carotid artery dissection and fluctuating intracranial vessel irregularities, compatible with reversible cerebral vasoconstriction syndrome. An extensive diagnostic work-up was normal. No typical trigger factors of reversible cerebral vasoconstriction syndrome could be found. The patient received intravenous heparin and the calcium channel blocker nimodipine. Follow-up imaging revealed no vessel irregularities, the left internal carotid artery was still occluded. Conclusion: This case supports the assumption that carotid artery dissection should be considered as a potential trigger of reversible cerebral vasoconstriction syndrome, possibly by altering sympathetic vascular tone

    Peripheral glucose levels and cognitive outcome after ischemic stroke : Results from the Munich Stroke Cohort

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    Introduction: The relationship between glucose metabolism and stroke outcome is likely to be complex. We examined whether there is a linear or non-linear relationship between glucose measures in the acute phase of stroke and post-stroke cognition, and whether altered glucose metabolism at different time intervals (long- and short-term before stroke, acute phase) is associated with cognitive outcome. Patients and methods: In all, 664 consecutively recruited patients with acute ischemic stroke and without pre-stroke dementia were included in this prospective observational study. Blood samples were taken at admission and fasting on the first morning after stroke. Duration of diabetes was assessed by interview. Cognitive outcome was assessed by the Telephone Interview for Cognitive Status 3 months post-stroke. Dose-response analyses were used to investigate non-linearity. Regression analyses were stratified by diabetes status and adjusted for relevant confounders. Results: Cognitive status was testable in 422 patients (81 with diabetes). There was a non-linear relationship between both admission and fasting glucose levels and cognitive outcome. Lower glucose values were significantly associated with lower Telephone Interview for Cognitive Status scores 3 months post-stroke in patients without diabetes with a similar trend in diabetic patients. There was an inverse association between duration of diabetes and Telephone Interview for Cognitive Status scores (linear regression: −0.10 (95% confidence interval: −0.17 to −0.02) per year increase of diabetes duration), whereas HbA1c was not related to cognitive outcome. Results were supported by sensitivity analyses accounting for attrition. Conclusion: Lower glucose levels in the acute phase of stroke are associated with worse cognitive outcome but the relationship is non-linear. Long-term abnormalities in glucose metabolism are also related to poor outcome but this is not the case for shorter term abnormalities. Altered glucose levels at different stages of stroke may affect stroke outcome through different pathways

    Peripheral glucose levels and cognitive outcome after ischemic stroke : Results from the Munich Stroke Cohort

    No full text
    Introduction: The relationship between glucose metabolism and stroke outcome is likely to be complex. We examined whether there is a linear or non-linear relationship between glucose measures in the acute phase of stroke and post-stroke cognition, and whether altered glucose metabolism at different time intervals (long- and short-term before stroke, acute phase) is associated with cognitive outcome. Patients and methods: In all, 664 consecutively recruited patients with acute ischemic stroke and without pre-stroke dementia were included in this prospective observational study. Blood samples were taken at admission and fasting on the first morning after stroke. Duration of diabetes was assessed by interview. Cognitive outcome was assessed by the Telephone Interview for Cognitive Status 3 months post-stroke. Dose-response analyses were used to investigate non-linearity. Regression analyses were stratified by diabetes status and adjusted for relevant confounders. Results: Cognitive status was testable in 422 patients (81 with diabetes). There was a non-linear relationship between both admission and fasting glucose levels and cognitive outcome. Lower glucose values were significantly associated with lower Telephone Interview for Cognitive Status scores 3 months post-stroke in patients without diabetes with a similar trend in diabetic patients. There was an inverse association between duration of diabetes and Telephone Interview for Cognitive Status scores (linear regression: −0.10 (95% confidence interval: −0.17 to −0.02) per year increase of diabetes duration), whereas HbA1c was not related to cognitive outcome. Results were supported by sensitivity analyses accounting for attrition. Conclusion: Lower glucose levels in the acute phase of stroke are associated with worse cognitive outcome but the relationship is non-linear. Long-term abnormalities in glucose metabolism are also related to poor outcome but this is not the case for shorter term abnormalities. Altered glucose levels at different stages of stroke may affect stroke outcome through different pathways
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