77 research outputs found

    MIRIAD--Public release of a multiple time point Alzheimer's MR imaging dataset

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    The Minimal Interval Resonance Imaging in Alzheimer's Disease (MIRIAD) dataset is a series of longitudinal volumetric T1 MRI scans of 46 mild-moderate Alzheimer's subjects and 23 controls. It consists of 708 scans conducted by the same radiographer with the same scanner and sequences at intervals of 2, 6, 14, 26, 38 and 52 weeks, 18 and 24 months from baseline, with accompanying information on gender, age and Mini Mental State Examination (MMSE) scores. Details of the cohort and imaging results have been described in peer-reviewed publications, and the data are here made publicly available as a common resource for researchers to develop, validate and compare techniques, particularly for measurement of longitudinal volume change in serially acquired MR

    Long-term effects of delayed-release dimethyl fumarate in multiple sclerosis: Interim analysis of ENDORSE, a randomized extension study

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    BACKGROUND: Delayed-release dimethyl fumarate (DMF) demonstrated strong efficacy and a favorable benefit-risk profile for patients with relapsing-remitting multiple sclerosis (RRMS) in phase 3 DEFINE/CONFIRM studies. ENDORSE is an ongoing long-term extension of DEFINE/CONFIRM. OBJECTIVE: We report efficacy and safety results of a 5-year interim analysis of ENDORSE (2 years DEFINE/CONFIRM; minimum 3 years ENDORSE). METHODS: In ENDORSE, patients randomized to DMF 240 mg twice (BID) or thrice daily (TID) in DEFINE/CONFIRM continued this dosage, and those initially randomized to placebo (PBO) or glatiramer acetate (GA) were re-randomized to DMF 240 mg BID or TID. RESULTS: For patients continuing DMF BID (BID/BID), annualized relapse rates were 0.202, 0.163, 0.139, 0.143, and 0.138 (years 1-5, respectively) and 63%, 73%, and 88% were free of new or enlarging T2 hyperintense lesions, new T1 hypointense lesions, and gadolinium-enhanced lesions, respectively, at year 5. Adverse events (AEs; serious adverse events (SAEs)) were reported in 91% (22%; BID/BID), 95% (24%; PBO/BID), and 88% (16%; GA/BID) of the patients. One case of progressive multifocal leukoencephalopathy was reported in the setting of severe, prolonged lymphopenia. CONCLUSION: Treatment with DMF was associated with continuously low clinical and magnetic resonance imaging (MRI) disease activity in patients with RRMS. These interim data demonstrate a sustained treatment benefit and an acceptable safety profile with DMF

    Optimisation of unenhanced MRI for detection of lesions in multiple sclerosis: a comparison of five pulse sequences with variable slice thickness

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    We used five MRI sequences in six patients with multiple sclerosis (MS): conventional spin-echo (CSE) with 5-mm slices; 2D fast spin-echo (FSE) with 2-mm slices; multishot T2*-weighted echo-planar imaging (EPI) with 5-mm slices; fast fluid-attenuated inversion recovery (fFLAIR) with 2-mm slices; and 3D fast spin-echo with 1.5mm-thick slices. A total of 225 lesions were detected on CSE, 274 on 2D FSE, 137 on EPI, 385 on fFLAIR and 320 on 3D FSE. The EPI sequence was clearly the least sensitive and susceptibility artefact was a problem, particularly in the brain stem and temporal lobes. Fast FLAIR displayed a much higher number of supratentorial lesions (380) than 3D FSE (297), 2D FSE (264) or CSE (211). However, in the posterior cranial fossa 3D FSE was the most sensitive sequence (23 lesions), followed by CSE (14) and 2D FSE (10), while fFLAIR (5) was extremely insensitive

    Trigeminal neuralgia in patients with multiple sclerosis: Lesion localization with magnetic resonance imaging

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    We performed conventional T2-weighted brain MRI examinations in six patients with multiple sclerosis (MS) and trigeminal neuralgia. In all patients brainstem lesions in positions expected to involve trigeminal fibers, particularly the entry zone of sensory fibers, were demonstrated. Compression of the trigeminal nerve by ectatic vessels, a recognized cause of idiopathic trigeminal neuralgia, was not observed. We conclude that in MS trigeminal neuralgia is usually caused by demyelinating lesions affecting pontine trigeminal pathways
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