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Biomedical subjects

David S Liebeskind

Publications and source records attributed to David S Liebeskind.

At least 19 recordsLinked to original sources
PubMed2006

Evidence of publication bias in reporting acute stroke clinical trials.

OBJECTIVE: To ascertain the extent of publication bias in the reporting of acute stroke clinical trials. METHODS: We identified controlled acute ischemic stroke clinical trials reported in English over a 45-year period from 1955 to 1999 through systematic search of MEDLINE, the Cochrane Controlled Stroke Trials Register, and additional databases. We analyzed trial methodology, quality, outcome, study sponsorship, and timing of publication to identify various forms of publication bias, including nonpublication bias, abbreviated publication bias, and time-lag bias. RESULTS: One hundred seventy-eight acute ischemic stroke trials, enrolling 73,949 subjects, evaluated 75 agents or nonpharmacologic interventions. A greater proportion of harmful outcomes in unpublished studies (n = 4) compared with published trials (0.75 vs 0.06, p < 0.0001) and underreporting of smaller, nonbeneficial studies in acute stroke suggest nonpublication bias. Although a definite time-lag bias was not evident, nonbeneficial studies were slower to proceed from enrollment completion to publication (2.3 vs 2.0 years, p = 0.207), with an even longer delay for nonbeneficial corporate pharmaceutical sponsored trials (2.8 vs 2.1 years, p = 0.086), despite superior trial report quality scores for corporate-sponsored studies when compared with nonprofit/governmental studies (mean 69.2 +/- 95% CI 3.9 vs 53.4 +/- 95% CI 9.2, p < 0.005). CONCLUSION: Publication bias is evident in the acute stroke research literature, supporting the need for prospective trial registration.

Chi-Square Distribution↗
PubMed2006

Leukoaraiosis is a risk factor for symptomatic intracerebral hemorrhage after thrombolysis for acute stroke.

BACKGROUND AND PURPOSE: The aim of the study was to evaluate whether leukoaraiosis (LA) is a risk factor for symptomatic intracerebral hemorrhage (sICH) in patients treated with thrombolysis for acute stroke. METHODS: In this retrospective, multicenter analysis, we evaluated data from acute anterior circulation stroke patients (n=449; <6 hours after symptom onset) treated with thrombolysis. All patients had received standard magnetic resonance imaging evaluation before thrombolysis, including a high-quality T2-weighted sequence. For the analysis, LA in the deep white matter was dichotomized into absent or mild versus moderate or severe (corresponding to Fazekas scores of 0 to 1 versus 2 to 3). RESULTS: The rate of sICH was significantly more frequent in patients with moderate to severe LA of the deep white matter (n=12 of 114; 10.5%) than in patients without relevant LA (n=13 of 335; 3.8%), corresponding to an odds ratio of 2.9 (95% CI, 1.29 to 6.59; P=0.015). In a logistic-regression analysis (including age, National Institutes of Health Stroke Scale score at presentation, and type of thrombolytic treatment), LA remained a significant independent risk factor (odds ratio, 2.9; P=0.03). CONCLUSIONS: LA of the deep white matter is an independent risk factor for sICH after thrombolytic treatment for acute stroke.

Aged↗
PubMed2006

Predictors of cerebral microbleeds in acute ischemic stroke and TIA patients.

BACKGROUND: Cerebral microbleeds (CMB) detected on gradient-echo T2*-weighted MRI have been associated with cognitive impairment and the potential for increased risk of intracranial hemorrhage. We evaluated risk factors for these microangiopathic lesions in a cohort of stroke and transient ischemic attack patients. METHODS: Presence and number of CMB in consecutive acute stroke patients admitted to a university hospital stroke service over an 18-month period were rated. Multivariate models were generated to determine the contribution of 21 demographic and clinical variables to the frequency and number of CMB. RESULTS: Of 164 patients (mean age 71 years, 52% female), 57 (35%) had CMB evident on gradient-echo T2*-weighted MRI. CMB were more commonly noted among patients with small vessel disease ischemic stroke mechanism (47%) than large vessel atherothromboembolic (12%) or cardioembolic (18%, p = 0.0001). In univariate analysis, patients with CMB were older, (p = 0.008), more likely to have been on >1 antihypertensive prior to admission (p = 0.024) than those without CMB. In multivariate logistic regression analyses, presumed small vessel stroke subtype, history of atrial fibrillation, being on >1 antihypertensive prior to admission, and smoking were independent factors increasing the risk of CMB. Logistic regression analysis by number of CMB showed almost similar findings. CONCLUSIONS: CMB are more frequently noted in hospitalized stroke and transient ischemic attack patients with small vessel ischemia, as well as those with important modifiable vascular risk factors like atrial fibrillation and smoking.

Adult↗
PubMed2006

Achieving target cholesterol goals after stroke: is in-hospital statin initiation the key?

BACKGROUND: National advisories recommend statin therapy as an element of secondary prevention for patients with ischemic stroke or transient ischemic attack of atherosclerotic origin. Statins are of proven benefit in persons at high risk of vascular disease. OBJECTIVES: To evaluate the effects of in-hospital initiation of statins on 3-month treatment adherence rates and achievement of national guideline target cholesterol goals. METHODS: Data were collected in consecutively encountered patients with ischemic stroke or transient ischemic attack admitted to a university hospital stroke service beginning September 1, 2002. Patients were included in the study if they were not receiving a statin before admission and had an indication for statin therapy. Adherence to statin treatment and achievement of national guideline target cholesterol goals were assessed 3 months after discharge. RESULTS: From September 1, 2002, through April 30, 2005, 92 (17%) of 552 individuals met the study criteria. Hospital initiation of statin therapy yielded high rates of adherence (93% [86/92]), lowered mean low-density lipoprotein cholesterol levels from 120 to 78 mg/dL (3.1 to 2.0 mmol/L; P<.001), and increased the proportion of patients with low-density lipoprotein cholesterol levels lower than 100 mg/dL (2.6 mmol/L) from 36% to 88% (P<.001) at 3 months. CONCLUSIONS: Statin initiation during hospitalization for an ischemic cerebrovascular event is associated with high rates of adherence to treatment, lowering of low-density lipoprotein cholesterol levels, and higher rates of achieving national cholesterol guidelines.

Adult↗
PubMed2006

Stroke associated with Barth syndrome.

Barth syndrome is an inherited disorder characterized by dilated cardiomyopathy, neutropenia, growth retardation, and skeletal myopathy. We describe a case of acute stroke owing to Barth syndrome that required intra-arterial thrombolysis. This case suggests that cardiovascular complications can be observed in patients with Barth syndrome. Stroke prevention measures, including the use of antithrombotic agents, might be warranted.

Adolescent↗
PubMed2005

Altered hemodynamics and regional cerebral blood flow in patients with hemodynamically significant stenoses.

BACKGROUND AND PURPOSE: Blood oxygen level-dependent (BOLD) contrast largely depends on changes in cerebral blood flow (CBF). Because cerebrovascular disease may result in altered CBF, we assessed the temporal dynamics and magnitude of the BOLD response in patients with major arterial stenoses. METHODS: Seven patients with hemodynamically significant stenoses affecting the anterior circulation (primarily left internal carotid and middle cerebral arteries) were compared with 7 neurologically healthy subjects. Continuous arterial spin-labeled perfusion MRI was used to measure resting CBF globally and within various vascular distributions. The BOLD response was acquired during a visually guided bilateral handball squeeze task while motor performance was recorded by a pressure transducer. RESULTS: Baseline CBF was reduced in bilateral middle cerebral artery and left anterior cerebral artery territories in patients. A prolonged BOLD hemodynamic response was observed in patients in bilateral primary motor cortices but not visual cortex. Patients also exhibited a larger early negative BOLD response, or "initial dip," in left primary motor cortex. There were no differences in motor performance between groups, suggesting behavioral differences were not primarily responsible for the characteristics of the BOLD response. CONCLUSIONS: An initial deoxygenation followed by a delayed hyperemic BOLD response was observed in patients, although resting flow values were not within an ischemic range. A simple visuomotor BOLD activation paradigm can reflect alterations in the hemodynamic response in patients with hemodynamically significant stenoses.

Adult↗
PubMed2005

Treatment-responsive limbic encephalitis identified by neuropil antibodies: MRI and PET correlates.

We report seven patients, six from a single institution, who developed subacute limbic encephalitis initially considered of uncertain aetiology. Four patients presented with symptoms of hippocampal dysfunction (i.e. severe short-term memory loss) and three with extensive limbic dysfunction (i.e. confusion, seizures and suspected psychosis). Brain MRI and [(18)F]fluorodeoxyglucose (FDG)-PET complemented each other but did not overlap in 50% of the patients. Combining both tests, all patients had temporal lobe abnormalities, five with additional areas involved. In one patient, FDG hyperactivity in the brainstem that was normal on MRI correlated with central hypoventilation; in another case, hyperactivity in the cerebellum anticipated ataxia. All patients had abnormal CSF: six pleocytosis, six had increased protein concentration, and three of five examined had oligoclonal bands. A tumour was identified and removed in four patients (mediastinal teratoma, thymoma, thymic carcinoma and thyroid cancer) and not treated in one (ovarian teratoma). An immunohistochemical technique that facilitates the detection of antibodies to cell surface or synaptic proteins demonstrated that six patients had antibodies to the neuropil of hippocampus or cerebellum, and one to intraneuronal antigens. Only one of the neuropil antibodies corresponded to voltage-gated potassium channel (VGKC) antibodies; the other five (two with identical specificity) reacted with antigens concentrated in areas of high dendritic density or synaptic-enriched regions of the hippocampus or cerebellum. Preliminary characterization of these antigens indicates that they are diverse and expressed on the neuronal cell membrane and dendrites; they do not co-localize with VGKCs, but partially co-localize with spinophilin. A target autoantigen in one of the patients co-localizes with a cell surface protein involved in hippocampal dendritic development. All patients except the one with antibodies to intracellular antigens had dramatic clinical and neuroimaging responses to immunotherapy or tumour resection; two patients had neurological relapse and improved with immunotherapy. Overall, the phenotype associated with the novel neuropil antibodies includes dominant behavioural and psychiatric symptoms and seizures that often interfere with the evaluation of cognition and memory, and brain MRI or FDG-PET abnormalities less frequently restricted to the medial temporal lobes than in patients with classical paraneoplastic or VGKC antibodies. When compared with patients with VGKC antibodies, patients with these novel antibodies are more likely to have CSF inflammatory abnormalities and systemic tumours (teratoma and thymoma), and they do not develop SIADH-like hyponatraemia. Although most autoantigens await characterization, all share intense expression by the neuropil of hippocampus, with patterns of immunolabelling characteristic enough to suggest the diagnosis of these disorders and predict response to treatment.

Adult↗
PubMed2005

Hyperacute imaging of ischemic stroke: role in therapeutic management.

Ischemic stroke remains a significant cause of morbidity and mortality. Current therapeutic options for acute ischemic stroke include intravenous thrombolysis and endovascular approaches for recanalization of proximal arterial occlusion. The rapid identification of underlying stroke etiology or mechanism may facilitate selection criteria for emergent therapy. Hyperacute imaging plays an integral role in the delineation of stroke pathophysiology and the formulation of rational stroke therapy. Hyperacute imaging of ischemic stroke may demonstrate proximal vascular occlusion, compensatory collateral circulation, residual or collateral tissue perfusion, and the differentiation of ischemic core from penumbral regions. Characterization of the ischemic field, including core and penumbra, with various mismatch models on multimodal computed tomography or MRI may refine current therapeutic strategies for cerebral ischemia. The diagnostic and therapeutic role of hyperacute imaging has emerged as a pivotal component in the evaluation and management of ischemic stroke.

Brain↗
PubMed2005

Advanced MR imaging of acute stroke: the University of California at Los Angeles endovascular therapy experience.

Rapid implementation of multimodal MR imaging, including diffusion-perfusion imaging before and following endovascular therapies for treatment of acute ischemic stroke, has yielded novel observations and expanded contemporary knowledge of acute stroke pathophysiology. For more than a decade at the University of California at Los Angeles, an intensive imaging strategy has been used to establish stroke diagnosis, delineate early patterns of cerebral ischemia, and monitor response to various reperfusion techniques. Angiographic findings before thrombolysis have substantiated stroke subtype, and documentation of concomitant recanalization has provided considerable insight regarding the vascular and imaging correlates of intra-arterial therapies. MR imaging studies have progressively characterized the complex pathophysiology of acute ischemic stroke, providing imaging strategies and models that may be used to optimize acute stroke care. The ensuing review emphasizes salient aspects of these neuroimaging studies, addressing numerous facets of acute stroke pathophysiology.

Acute Disease↗
PubMed2005

Collaterals in acute stroke: beyond the clot.

Collateral circulation is a fundamental determinant of stroke pathophysiology. Distal arterial embolism and hypoperfusion resulting from severe proximal arterial stenosis may be offset by collateral flow. Collaterals influence whether or not infarction results. The detection and characterization of arterial deoxygenation and other consequences of collateral perfusion depend on neuroimaging techniques. Imaging advances will further the understanding of clinical correlates, including collateral sustenance and collateral failure, and possibly promote the development of collateral therapeutics. Refinements of perfusion imaging protocols may quantify the delay and dispersion of collateral flow more accurately. This review explores the role of collateral flow in acute ischemic stroke and describes the imaging modalities used to investigate phenomena "beyond the clot."

Blood Coagulation↗
PubMed2005

Neuroimaging advances and the transformation of acute stroke care.

Neuroimaging techniques have transformed the delivery of stroke care. Multimodal computed tomography and magnetic resonance imaging rapidly illustrate the vascular and parenchymal correlates in acute ischemic and hemorrhagic stroke. Optimal selection of thrombolytic candidates and the characterization of ischemic sequelae may be achieved with imaging. The nature and topography of intracerebral hemorrhage may also be defined. Increasing use of multimodal imaging in acute stroke has expanded our current understanding of stroke pathophysiology and streamlined the care of stroke patients from the hyperacute to chronic phases. The integration of neuroimaging techniques in research studies has elucidated pitfalls in the translation of novel therapy into clinical practice. This review explores the impact of neuroimaging advances in stroke and emphasizes the critical role of these modalities in the care of patients with ischemic and hemorrhagic events.

Brain Ischemia↗
PubMed2005

Cerebral gumma mimicking glioblastoma multiforme.

This article reports an unusual case of a syphilitic gumma with a clinical and radiographical presentation initially suggestive of glioblastoma multiforme. Pathological evaluation was essential in establishing the diagnosis of neurosyphilis and in excluding neoplastic involvement. Cerebral gumma should be considered as part of the differential diagnosis of a midline intracranial lesion observed on magnetic resonance imaging.

Adult↗
PubMed2005

Neuroprotection from the collateral perspective.

Neuroprotection for acute ischemic stroke has undergone intense research for more than half a century, but has yielded no therapeutic application and remains an elusive goal. Detailed studies of the ischemic cascade conducted to date appear to have ignored the fundamental role of collateral circulation in the pathophysiology of ischemic stroke. Vascular aspects of neuroprotection and collateral dependence are becoming increasingly apparent following the refinement of multimodal imaging and improvements in the options for revascularization. Collateral perfusion demarcates the ischemic penumbra, influences drug delivery and alters clinical outcome. As outlined in this review, combined revascularization and neuroprotection that take into consideration the collateral perspective may ultimately determine the fate of neuroprotection in acute ischemic stroke.

Animals↗
PubMed2005

Age and sex variability and normal reference values for the V(MCA)/V(ICA) index.

BACKGROUND AND PURPOSE: The index of mean blood flow velocity (V) in the middle cerebral artery (MCA) divided by respective velocity in the ipsilateral internal carotid artery (ICA), or V(MCA)/V(ICA) index, is commonly used as a marker of vasospasm, although reference values are not established. We sought to provide reference data for these velocities and index. METHODS: Transcranial color-coded duplex and carotid duplex sonography was performed in 335 healthy volunteers (211 women, 124 men; mean age +/- SD, 42 +/- 18 years; range, 18-86 years). Age analyses were based on three groups: I, <40; II, 40-60; and III, >60 years. The V(MCA)/V(ICA) index was calculated based on angle-corrected blood flow velocities determined in the MCA and extracranial ICA. RESULTS: Mean flow velocities in the MCA and ICA diminished with increasing age, most pronounced in those subjects >40 years. The V(MCA)/V(ICA) index increased significantly (1.67 + 0.005 [age]; P < .05) with age in women, but not in men. In women, reference values and ranges for the V(MCA)/V(ICA) index were as follows, by group: I, 1.82 (range, 0.88-2.68); II, 1.91 (range, 0.94-2.88); and III, 2.06 (range, 0.59-3.53). Respective values for men were as follows, by group: I, 2.10 (range, 0.96-3.24); II, 2.04 (range, 0.71-3.37); and III, 1.78 (range, 0.81-2.75). In subjects <40 years, the V(MCA)/V(ICA) index was significantly higher in men than in women. CONCLUSION: The V(MCA)/V(ICA) index significantly varies with age and sex. Sonographic diagnosis of cerebral vasospasm should be based on age- and sex-adjusted reference values of the V(MCA)/V(ICA) index.

Adolescent↗