Multiple sclerosis and systemic sclerosis are two autoimmune conditions that affect different parts of the body. The diagnosis of multiple sclerosis requires the constellation of clinical findings and various investigations (see McDonald diagnostic criteria for multiple sclerosis), including 19: 1. typical history 2. Yousuf F, Kim G, Tauhid S, Glanz B, Chu R, Tummala S, Healy B, Bakshi R. 2016. The Natural History of Multiple Sclerosis: A Geographically Based Study. 2001; Dalton et al. Spinal cord lesions are part of the diagnostic criteria for dissemination in space in the International Panel guidelines (Polman et al. 2011. 2001; Bakshi et al. lesions occur at different times). Although many sequences are contributory, the 2018 Revised Guidelines of the Consortium of MS Centers MRI Protocol for the Diagnosis and Follow-up of MS plaques lists the following core sequences 25: NB: contrast is not necessary for routine asymptomatic follow-up. (Left and middle panel) White matter lesions from a 40-year-old woman with relapsing-remitting MS (RRMS), showing 3D sagittal fluid-attenuated inversion recovery (FLAIR, left panel) and 2D axial FLAIR (middle panel). With the application of directional magnetic gradients in all three planes, diffusion imaging also captures water diffusion in directions perpendicular to WM tracts (radial diffusivity). This serves as a baseline for monitoring therapy. Patients on disease modifying therapy. MS activity appears on an MRI scan as either bright or dark spots. a discussion of any symptoms. Schlaeger R, Papinutto N, Zhu AH, Lobach IV, Bevan CJ, Bucci M, Castellano A, Gelfand JM, Graves JS, Green AJ, et al. Over 90% of people with an MS diagnosis have it confirmed by an MRI scan. I. MRI scans cause a small amount of the bodys water protons to line up with their powerful magnetic field. 2015. Lin X, Tench CR, Morgan PS, Niepel G, Constantinescu CS. Brain. A: Per 2017 McDonald criteria, in order to diagnose MS, there needs to be reasonable clinical suspicion, along with supportive MRI and paraclinical evidence. 2005). Agosta F, Pagani E, Caputo D, Filippi M. 2007b. Association between thoracic spinal cord gray matter atrophy and disability in multiple sclerosis. 16. Although discussion of individual agents and therapies is well beyond the scope of this article, it is worth being aware of the main agents available and their mechanism of action 20: Prognosis is variable and depends on the pattern of disease a patient has (e.g. Routine follow up scans of spinal cord for disease monitoring purposes is recommended but can be challenging due to small anatomical area involved and physiological artifacts that commonly affect quality of the scans. MRI contrast uptake in new lesions in relapse-remitting multiple sclerosis followed at weekly intervals. You can learn more about how we ensure our content is accurate and current by reading our. Typical lesions that appear on a T-2 scan are oval in shape. T2 hyperintense lesions are more common in the cervical versus the thoracic portion (Kearney et al. Clinical disability is also significantly predicted by DTI (Agosta et al. They also tend to have more lesions in the spinal cord than people with other forms of MS. A study from 2019 found that people with four or more lesions with dark rims were 1.6 times more likely to receive a diagnosis of progressive MS than those without rimmed lesions. 2000;175(3):821-5. Schoonheim MM, Hulst HE, Brandt R, Strik M, Wink M, Uitehaag B, Barkhof F, Geurts JJ. Earlier generation self-injectables such as interferon (INF)- and glatiramer acetate (GA) reduce T2 hyperintense lesion volume by at least 30% compared with placebo measured at several months to a few years (Comi et al. Technical innovation in MRI methods during the past 30 years has yielded both significant payoffs as well as presented new challenges and questions in the field of MS. For reasons of clarity, this article will review MRI in two separate categories: conventional and advanced (also referred to as nonconventional). 2014; Kilsdonk et al. Q: Can you perform MRI in MS patients with intrathecal pumps and other implanted devices? Postmortem verification of MS cortical lesion detection with 3D DIR. If the contraindication for MRI is removed at a later time, we would recommend obtaining an MRI at that point. Accumulation of hypointense lesions (black holes) on T1 spin-echo MRI correlates with disease progression in multiple sclerosis. CIS does not always progress to another form of MS. Neema M, Stankiewicz J, Arora A, Dandamudi VSR, Batt CE, Guss ZD, Al-Sabbagh A, Bakshi R. 2007a. Patients whom we are considering switching disease modifying therapy should also obtain MRIs. MRI detection of hypointense brain lesions in patients with multiple sclerosis: T1 spin-echo vs. gradient-echo. MRI is currently considered to be the most sensitive diagnostic imaging modality for revealing demyelinating plaques, as recommended by the Consortium of Multiple Sclerosis Centers. 2009). 3. Radiology. In a study evaluating the dynamics of contrast-enhancing lesions in MS (Gaitann et al. Thalamic neurodegeneration in relapsing-remitting multiple sclerosis. Advanced MRI at higher magnetic field strengths (e.g., 3T and 7T) offers higher signal-to-noise ratios and enhanced spatial resolution as small as 100 m, but at the expense of increased artifacts, lack of standardization across institutions, and higher cost (Sinnecker et al. The effect of fingolimod on conversion of acute gadolinium-enhancing lesions to chronic T1 hypointensities in multiple sclerosis. WebTo detect MS. MRI is considered the best test to help diagnose MS. The degree of T2 hypointensity in GM has shown correlations with measures of brain atrophy and clinical status, including physical disability and cognitive impairment (Neema et al. Bakshi R, Neema M, Healy BC, Liptak Z, Betensky R, Buckle GJ, Gauthier S, Stankiewicz J, Meier D, Egorova S, et al. 2012. Other factors include subjective lesion thresholds, variable patient populations, disease subtypes, and disease durations (Sahraian et al. Ultra-high-field imaging distinguishes MS lesions from asymptomatic white matter lesions. 2007. Kirov II, Tal A, Babb JS, Herbert J, Gonen O. 2016. Davis M, Auh S, Riva M, Richert ND, Frank JA, McFarland HF, Bagnato F. 2010. 2013), as well as in the spinal cord (Sajja et al. 2005;26(8):2033-6. The most useful and frequently used measure of spinal cord atrophy is the mean cross-sectional area of the upper cervical cord (Losseff et al. Abnormal subcortical deep-gray matter susceptibility-weighted imaging filtered phase measurements in patients with multiple sclerosis. Case 12: extensive brainstem and cerebellar involvment, Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD), View Frank Gaillard's current disclosures, View Ashesh Ishwarlal Ranchod's current disclosures, see full revision history and disclosures, Schilder type (diffuse cerebral sclerosis), neuromyelitis optica spectrum disorder (Devic disease), McDonald diagnostic criteria for multiple sclerosis, progressive multifocal leukoencephalopathy (PML), acute inflammatory demyelinating polyradiculoneuropathy (AIDP), acute motor-sensory axonal neuropathy (AMSAN), chronic inflammatory demyelinating polyneuropathy (CIDP), acute disseminated encephalomyelitis (ADEM), acute hemorrhagic encephalomyelitis (AHEM), longitudinally extensive spinal cord lesion (LESCL), megalencephalic leukoencephalopathy with subcortical cysts, hypomyelination with atrophy of the basal ganglia and cerebellum (H-ABC), leukoencephalopathy with brainstem and spinal cord involvement and lactate elevation, hypomyelination with brainstem and spinal cord involvement and leg spasticity, cathepsin A-related arteriopathy with strokes and leukoencephalopathy (CARASAL), leukoencephalopathy with calcifications and cysts, pontine autosomal dominant microangiopathy with leukoencephalopathy (PADMAL), retinal vasculopathy with cerebral leukoencephalopathy and systemic manifestations (RVCL-S), adult-onset leukoencephalopathy with axonal spheroids and pigmented glia (ALSP), leukoencephalopathy due to autosomal recessive mutations in the mitochondrial alanyl-transfer RNA (tRNA) synthetase gene (AARS2-L), globoid cell leukodystrophy (Krabbe disease), adult-onset autosomal dominant leukodystrophy, cystic leukoencephalopathy without megalencephaly, classic multiple sclerosis (Charcot type), a strong association with HLA-DR15 (formerly covered by HLA-DR2)class II has been identified, patients exhibit periodic symptoms with complete recovery (early on), approximately 85% of patients with relapsing-remitting MS eventually enter a secondary progressive phase, defined by a progressive accumulation of disability for >12 months from disease onset, which can be determined prospectively or retrospectively, patients do not have remissions, with neurological deterioration being relentless, incorporates the previously described "progressive-relapsing"phenotype, defined as patients who remain functionally active for over 15 years, and thus is only a retrospective diagnosis, plaques can be homogeneously hypoattenuating, brain atrophy may be evident in long-standing chronic MS, some plaques may show contrast enhancement in the active phase, ideally performed as a 3D volumetric scan (1 mm isotropic), or, T1: 3D inversion recovery prepared gradient echo, lesions are typically iso- to hypointense (, hyperintense lesions are associated with brain atrophy and advancing disease, acute lesions often have surrounding edema, when these propagate centrifugally along the medullary venules and are arranged perpendicular to the lateral ventricles in a triangular configuration (extending radially outward - best seen on parasagittal images), they are termed, FLAIR is more sensitive than T2 in the detection of juxtacortical and periventricular plaques, while T2 is more sensitive to infratentorial lesions, enhancement is often incomplete around the periphery (, active plaques may demonstrate high or low ADC (increased or decreased diffusion), PD images are better at detecting cervical spinal cord MS lesions especially when T2W images fail to demonstrate these lesions, a sequence that suppresses both CSF and white matter signal and offers better delineation of the plaques, interferon beta: inhibition of T-lymphocyte proliferation, glatiramer acetate (Copaxone): immunomodulation, teriflunomide (Aubagio): reduces both T-cell and B-cell activation and proliferation, dimethyl fumarate (Tecfidera) and diroximel fumarate (Vumerity): immunomodulation, fingolimod (Gilenya), siponimod (Mayzent) and ozanimod (Zeposia): prevents lymphocyte migration out of lymph nodes and into CNS, natalizumab (Tysabri): inhibits binding of lymphocytes to endothelium, cladribine (Mavenclad): purine analog that targets lymphocytes, ocrelizumab (Ocrevus) and ofatumumab (Kesimpta): anti-CD20 monoclonal antibodies, alemtuzumab (Lemtrada): immunomodulation of T-cell and B-cell function, mitoxantrone (Novantrone): reduces T-cell and B-cell proliferation and reduces T-cell activation, particularly in patients treated with natalizumab with positive JC virus serology, a complication of cessation of natalizumab or treatment for natalizumab-related PML with plasma exchange or immunoabsorption, rarely lymphoma appears to arise from previously identified demyelinating lesions. 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