Serial Contrast-Enhanced MR in Patients with Multiple Sclerosis and Varying Levels of Disability

Filippi, Massimo; Rossi, Pasqualino; Campi, A.; Colombo, Bruno S.; Pereira, Célia da Costa; Comi, G.

doi:10.1097/00041327-199906000-00030

Cited by 22 publications

(25 citation statements)

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“…The fact that patients with enhancing lesions and cytokine dysregulation showed significant decrease in FA within the CC supports an association between progressive brain damage and inflammatory disease activity. This concurs with the conclusion reached in many articles, though not all [5], that a higher level of MR enhancing activity is associated with a greater degree of disease progression [26,27].…”

Section: Discussionsupporting

confidence: 92%

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Progressive decline in fractional anisotropy on serial DTI examinations of the corpus callosum: a putative marker of disease activity and progression in SPMS

et al. 2011

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Section: Discussionsupporting

confidence: 92%

“…Some studies report that the frequency of gadolinium enhancing lesions are markedly decreased in SPMS as compared with RRMS despite continued and even accelerated accumulation of neurological disability [5]. Furthermore, the speed of progression varies widely among individuals.…”

Section: Introductionmentioning

confidence: 99%

Progressive decline in fractional anisotropy on serial DTI examinations of the corpus callosum: a putative marker of disease activity and progression in SPMS

et al. 2011

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“…It is not clear whether this represents a degree of autonomous tissue inflammation less dependent on recruitment of immune cells from the circulation. Consistent with this possibility are reports that Gdþ lesions are less frequently seen in progressive disease (Thompson et al, 1991;Filippi et al, 1997). Perivascular cuffs of mononuclear cells are also less apparent (Prineas et al, 2001).…”

Section: The Development Of Progressive Diseasementioning

confidence: 54%

Current concepts of the cellular and molecular pathophysiology of multiple sclerosis

Greenstein

2007

Developmental Neurobiology

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Multiple sclerosis (MS) is the most common demyelinating disease. It poses many challenges both clinically and scientifically. Progress made in understanding the genetics, immunology, and neurobiology of MS to date has positioned the field for further breakthroughs both in understanding the etiology and pathogenesis as well as the development of rationally based therapeutics. This review will cover fundamental aspects of the clinical and pathologic features of MS. Identified genetic markers will be considered as well as the evolving understanding of immunologic and neurobiological aspects of the disease. The development of immune therapy based on this knowledge is already apparent and it is likely that neuroprotective therapies will evolve to complement immune modulation in treating the disease.

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“…These active lesions contain large numbers of macrophages containing myelin debris as well as significant complement and immunoglobulin deposition (13). While early RRMS inflammatory lesions generally correlate with gadolinium-enhancing MRI lesions, the inflammation in progressive disease generally does not (14). In the progressive stage of MS, disease is characterized by gradual lesion expansion with myelin-laden macrophages typically restricted to the edge of the plaque, diffuse abnormal inflammation of the normal appearing white matter, and extensive axonal injury and transection associated with demyelinated lesions (15)(16)(17)(18).…”

Section: Immunopathologymentioning

confidence: 99%

Multiple sclerosis

Nylander¹,

Hafler²

2012

J. Clin. Invest.

462

359

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Multiple sclerosis (MS) is a multifocal demyelinating disease with progressive neurodegeneration caused by an autoimmune response to self-antigens in a genetically susceptible individual. While the formation and persistence of meningeal lymphoid follicles suggest persistence of antigens to drive the continuing inflammatory and humoral response, the identity of an antigen or infectious agent leading to the oligoclonal expansion of B and T cells is unknown. In this review we examine new paradigms for understanding the immunopathology of MS, present recent data defining the common genetic variants underlying disease susceptibility, and explore how improved understanding of immune pathway disruption can inform MS prognosis and treatment decisions. IntroductionMS is a multifocal demyelinating disease with progressive neurodegeneration caused by an autoimmune response to self-antigens in a genetically susceptible individual. Clinical symptoms vary based on the site of neurologic lesions and often correlate with invasion of inflammatory cells across the blood-brain barrier with resulting demyelination and edema (1). Patients often exhibit an initial clinically isolated syndrome, followed by a series of subacute clinical events that spontaneously abate, referred to as relapsing remitting MS (RRMS). While patients generally return to near normal neurologic function at the cessation of each episode, over a variable period of time there can be irreversible progression of clinical disability termed secondary progressive MS (SPMS), although early therapeutic intervention may delay time to progression (2, 3). However, 10%-15% of MS patients will instead experience primary progressive MS, characterized by clinical progression from the initiation of disease without preceding relapses and remissions (4).The diagnosis is made primarily on the basis of the medical history and physical exam, which was formalized as the McDonald criteria and updated to reflect the increased reliance on imaging for lesion identification (5-7). These criteria indicate that the neurologic lesions should be disseminated in both space and time to distinguish them from monophasic self-limiting diseases such as acute disseminated encephalomyelitis, and additionally they should reflect a pattern of neurological inflammation typical of MS in the absence of a more appropriate diagnosis. A diagnosis of MS reflects clinical evaluation of episodes of intermittent neurological impairment and may take into account laboratory data, such as the characteristic oligoclonal bands in the cerebrospinal fluid (CSF), which indicate intrathecal immunoglobulin production, or abnormal visual evoked responses in the absence of optic neuritis. Over the past two decades, the diagnosis has come to include the more sensitive and specific spatial identification of white matter lesions via evaluation of T2-hyperintense lesions and gadolinium-enhancing T1 lesions on MRI (8). Gadolinium enhancement serves as a marker of focal inflammation when the dye leaks through vessels due to the ...

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Serial Contrast-Enhanced MR in Patients with Multiple Sclerosis and Varying Levels of Disability

Cited by 22 publications

References 0 publications

Progressive decline in fractional anisotropy on serial DTI examinations of the corpus callosum: a putative marker of disease activity and progression in SPMS

Progressive decline in fractional anisotropy on serial DTI examinations of the corpus callosum: a putative marker of disease activity and progression in SPMS

Current concepts of the cellular and molecular pathophysiology of multiple sclerosis

Multiple sclerosis

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