11 results match your criteria: "10 Center Drive MSC 1400[Affiliation]"

Diagnosis of multiple sclerosis through the lens of ultra-high-field MRI.

J Magn Reson

June 2018

Translational Neuroradiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, 10 Center Drive MSC 1400, Building 10 Room 5C103, Bethesda, MD 20852, USA. Electronic address:

The long-standing relationship between ultra-high-field (7 T) MRI and multiple sclerosis (MS) has brought new insights to our understanding of lesion evolution and its associated pathology. With the recent FDA approval of a commercially available scanner, 7 T MRI is finally entering the clinic with great expectations about its potential added value. By looking through the prism of MS diagnosis, this perspective article discusses current limitations and prospects of 7 T MRI techniques relevant to helping clinicians diagnose patients encountered in daily practice.

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The central vein sign and its clinical evaluation for the diagnosis of multiple sclerosis: a consensus statement from the North American Imaging in Multiple Sclerosis Cooperative.

Nat Rev Neurol

December 2016

Translational Neuroradiology Section, National Institute of Neurological Disorders and Stroke, NIH, 10 Center Drive MSC 1400, Building 10 Room 5C103, Bethesda, Maryland, USA.

Over the past few years, MRI has become an indispensable tool for diagnosing multiple sclerosis (MS). However, the current MRI criteria for MS diagnosis have imperfect sensitivity and specificity. The central vein sign (CVS) has recently been proposed as a novel MRI biomarker to improve the accuracy and speed of MS diagnosis.

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Advanced MRI and staging of multiple sclerosis lesions.

Nat Rev Neurol

June 2016

Translational Neuroradiology Unit, National Institute of Neurological Disorders and Stroke, National Institutes of Health, 10 Center Drive MSC 1400, Building 10 Room 5C103, Bethesda, Maryland 20852, USA.

Over the past few decades, MRI-based visualization of demyelinated CNS lesions has become pivotal to the diagnosis and monitoring of multiple sclerosis (MS). In this Review, we outline current efforts to correlate imaging findings with the pathology of lesion development in MS, and the pitfalls that are being encountered in this research. Multimodal imaging at high and ultra-high magnetic field strengths is yielding biologically relevant insights into the pathophysiology of blood-brain barrier dynamics and both active and chronic inflammation, as well as mechanisms of lesion healing and remyelination.

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Custom fit 3D-printed brain holders for comparison of histology with MRI in marmosets.

J Neurosci Methods

January 2016

Division of Neuroimmunology and Neurovirology, National Institute of Neurologic Disorders and Stroke, 10 Center Drive MSC 1400, Building 10 Room 5C103, Bethesda, MD 20892, United States. Electronic address:

Background: MRI has the advantage of sampling large areas of tissue and locating areas of interest in 3D space in both living and ex vivo systems, whereas histology has the ability to examine thin slices of ex vivo tissue with high detail and specificity. Although both are valuable tools, it is currently difficult to make high-precision comparisons between MRI and histology due to large differences inherent to the techniques. A method combining the advantages would be an asset to understanding the pathological correlates of MRI.

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Quantification of multiple-sclerosis-related brain atrophy in two heterogeneous MRI datasets using mixed-effects modeling.

Neuroimage Clin

November 2013

Translational Neuroradiology Unit, National Institute of Neurological Disorders and Stroke, NIH, 10 Center Drive MSC 1400, Building 10 Room 5C103, Bethesda, MD 20892, USA ; Case Western Reserve University School of Medicine, 10900 Euclid Ave., Cleveland, OH 44106, USA.

Brain atrophy, measured by MRI, has been proposed as a useful surrogate marker for disease progression in multiple sclerosis (MS). However, it is conventionally assumed that the accurate quantification of brain atrophy is made difficult, if not impossible, by changes in the parameters of the MRI acquisition, which are almost inevitable over the course of a longitudinal study since MRI technology changes rapidly. This state of affairs can negatively affect clinical trial design and limit the use of historical data.

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Limited success with antigen-specific immunotherapies has led to the identification of novel approaches which consider the degeneracy of the T cell response, i.e. their ability to respond to multiple antigenic peptides.

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Evolution of T1 black holes in patients with multiple sclerosis imaged monthly for 4 years.

Brain

August 2003

Neuroimmunology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Building 10, Room 5B16, 10 Center Drive MSC 1400, Bethesda, MD 20892-1400, USA.

T1 black holes (BHs) on MRIs may represent either areas of oedema or axonal loss in patients with multiple sclerosis. BHs begin as contrast enhancing lesions (CELs) and evolve differently from patient to patient, and within the same patient over time. We analysed BHs formation over a 4-year period.

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The role of nonconventional magnetic resonance imaging techniques in demyelinating disorders.

Curr Neurol Neurosci Rep

May 2003

Neuroimmunology Branch, National Institutes for Neurological Disease and Stroke, National Institutes of Health, Building 10, Room 5B16, 10 Center Drive MSC 1400, Bethesda, MD 20892-1400, USA.

The use of nonconventional magnetic resonance imaging techniques (eg, magnetization transfer, magnetic resonance spectroscopy, and diffusion weighted imaging) allows for an accurate characterization of lesions as compared with conventional or standard approaches in demyelinating diseases. Magnetization transfer, magnetic resonance spectroscopy, and diffusion weighted imaging have revolutionized our understanding of demyelinating diseases because these techniques have been used to identify pathologic changes of normal-appearing brain tissue and characterize the differences in lesions. Metrics derived from these methods correlate with clinical disability and provide more accurate tools for monitoring disease activity and treatment effect over time.

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Immunopathogenesis of the multiple sclerosis lesion.

Curr Neurol Neurosci Rep

May 2001

Neuroimmunology Branch, National Institute for Neurological Diseases and Stroke, National Institutes of Health, Building 10, Room 5B-16, 10 Center Drive MSC 1400, Bethesda, MD 20892-1400, USA.

Multiple sclerosis (MS) is thought to be an autoimmune disease with a chronic inflammatory response directed against central nervous system (CNS) myelin antigens. Immunologic studies indicate that autoreactive CD4+ lymphocytes migrate into the CNS causing blood brain barrier (BBB) disruption, an initial event in the evolution of the MS lesion. Subsequent antigen recognition within the CNS initiates inflammatory responses that, through the multiple effector mechanisms, lead to demyelination.

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Neuroimmunology of multiple sclerosis and experimental allergic encephalomyelitis.

Neuroimaging Clin N Am

November 2000

Cellular Immunology Section, Neuroimmunology Branch, National Institute of Neurological Disease and Stroke/NIH, 10 Center Drive MSC 1400, Bethesda, MD 20892, USA.

The potential causes, immunopathology, and treatment of multiple sclerosis (MS) are summarized in this article. Findings from a well-examined animal model for MS, experimental allergic encephalomyelitis (EAE), are described and used to illustrate the paths of research in MS. Data from a recent clinical trial with a modified myelin peptide provide support for concepts deduced from EAE.

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Multiple Sclerosis: Immunotherapy.

Curr Treat Options Neurol

July 1999

Cellular Immunology Section, Neuroimmunology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Building 10, Room 5B-16, 10 Center Drive MSC 1400, Bethesda, MD 20892, USA.

Given our current knowledge, there is a need for the early institution of immunomodulatory therapy, especially for patients with poor prognostic factors (motor and cerebellar symptoms, frequent disease exacerbations, and a high level of activity on magnetic resonance imaging ). Patients who progress despite immunomodulatory therapy should be reevaluated in terms of diagnosis, development of neutralizing antibodies, or compliance. If a patient has a partial response to immunomodulatory therapy but his or her disease, as assessed by clinical and MRI criteria, remains very active, every effort should be made to modify disease progression by searching for an immunosuppressive therapy regimen before irreversible and considerable disability has accumulated.

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