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REVIEW ARTICLE
Year : 2021  |  Volume : 69  |  Issue : 6  |  Page : 1539-1546

Multiple Sclerosis-Minimizing Errors in Radiological Diagnosis


1 Dr. Gulati Imaging at National Heart Institute, New Delhi, India
2 Nalanda Medical College, Patna, Bihar, India
3 Dr. Gulati Imaging Institute, New Delhi, India

Date of Submission03-May-2020
Date of Decision08-Aug-2020
Date of Acceptance15-May-2021
Date of Web Publication23-Dec-2021

Correspondence Address:
Dr. Parveen Gulati
Dr. Gulati Imaging Institute, J-16, Hauz Khas Enclave, New Delhi
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.333497

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 » Abstract 


Background: Multiple sclerosis is a chronic demyelinating disorder with a myriad of imaging and clinical features that overlap with number of other neurological conditions. Incorrect diagnosis poses a significant risk to patients, it may lead to delays in management, increased morbidity, and also adds to the financial cost.
Objective: The aim of this study was to highlight strategies for the efficient differentiation of multiple sclerosis from other diseases which may masquerade as MS clinico-radiologically.
Material and Methods: A systematic literature review was conducted through online databases including PubMed and Medline. Relevant publications on radiological aspects of multiple sclerosis, white matter diseases and mimickers of Multiple sclerosis were included in the analysis.
Results: Common mimickers of MS include small vessel disease, acute disseminated encephalomyelitis, neuromyelitis optica, anti-MOG encephalomyelitis, vasculitis, and CADASIL. Contrast-enhanced MRI study performed using MS protocol on high strength MRI system evaluated following a structured protocol along with clinical correlation is effective in differentiating MS from its mimickers.
Conclusions: Contrast-enhanced MRI performed on a high strength scanner using MS protocol with structured protocol for evaluation along, with a better collaboration between radiologists and clinicians may help in minimizing errors in diagnosis of multiple sclerosis.


Keywords: 2017 revisions of McDonald's criteria, MS mimics, MS-typical lesions, multiple sclerosis
Key Message: Several diseases may mimic MS clinically as well as on imaging making minimization of diagnostic errors crucial for proper management. Good communication with the clinician, keeping updated with the constantly evolving diagnostic criteria for MS and other MS-mimicking conditions is imperative.


How to cite this article:
Boski N, Gulati V, Raj R, Gulati P. Multiple Sclerosis-Minimizing Errors in Radiological Diagnosis. Neurol India 2021;69:1539-46

How to cite this URL:
Boski N, Gulati V, Raj R, Gulati P. Multiple Sclerosis-Minimizing Errors in Radiological Diagnosis. Neurol India [serial online] 2021 [cited 2022 Jan 19];69:1539-46. Available from: https://www.neurologyindia.com/text.asp?2021/69/6/1539/333497




Multiple sclerosis (MS) is a chronic demyelinating disorder with variable symptoms, fluctuating course, and severity. Symptoms range from minimally interfering fatigue to chronically disabling weakness, bladder-bowel disturbances, blindness, and cognitive decline. Just like its symptomatic spectrum, its imaging spectrum also varies widely and overlaps with other neurological conditions to an extent that distinguishing it from mimicking conditions becomes difficult. A constantly evolving knowledge base and recent developments in imaging techniques have led to the refinement of the diagnostic criteria over time, this has helped in diagnosing MS with more specificity and sensitivity than ever before. Exclusion of other possibilities is of paramount importance, not only for diagnosis but also for adequate and timely management. The purpose of this review is to present radiological perspectives in diagnosing MS and excluding other possibilities based on imaging and relevant background clinical data.

For simplicity, the review is divided into five basic sections. In section one, the prerequisites for minimizing errors in MS diagnosis and follow-up are discussed. Section two covers the latest diagnostic criteria for MS from an imaging point of view. In section three, the characteristic imaging features of MS lesions are outlined. In the next section, the role of newer magnetic resonance (MR) imaging sequences and higher MR magnet strength in difficult-to-diagnose lesions are highlighted. Lastly, we provide a brief insight into MS-mimicking lesions from the viewpoint of the latest developments in their diagnostic criteria, associated relevant history, and lab findings.

Section 1- Prerequisites for minimizing errors in the diagnosis of MS

The foremost requirement for diagnosing MS is having better collaboration between radiologists and clinicians in the decision-making process. A functional clinico-radiological meet should be encouraged for discussing and deciding the next best step for diagnosis, excluding other possibilities and management.[1],[2]

Magnetic resonance imaging plays a pivotal role in MS diagnosis and excluding other mimicking lesions.[3] Knowledge of characteristic MS-typical lesions on MRI and the latest diagnostic criteria with adherence to fix imaging protocol can save a lot of time and toil. Appropriate use of newer imaging sequences and higher strength magnet can be a problem-solving tool in difficult cases.

MR imaging and clinical criteria for MS-mimicking entities like neuromyelitis optica (NMO),[4] anti-myelin oligodendrocyte glycoprotein (MOG) encephalomyelitis[5] are also constantly evolving. Being aware of relevant history and characteristic MR imaging features of such entities can help prevent errors in diagnosis and management.

For cases that present a persistent diagnostic dilemma, discussion with the clinician for a decision on the next best step[2] should be promoted. This may include further probing into history, family history, demographics, disease course from onset to progression, cerebrospinal fluid (CSF) analysis, antibody panel for encephalomyelitis, and brain biopsy.[6]

In centers with high volume MS cases, it is important to have a picture archiving and communication system (PACS)-based image archive for comparison with previous imaging and follow-up in diagnosed cases. The integration of a computer-aided diagnosis toolkit or imaging software for comparison with past scans can also be useful in such centers.[7],[8]

Good quality images and consistent MR protocols are invaluable for diagnosis and follow-up. In the revised guidelines of the Consortium of MS Centers, various imaging protocols have been discussed and advised for the diagnosis of MS.[9] Adopting these guidelines will yield a relatively uniform image quality for comparison, both within and outside the center.

Another important requisite is developing a structured template for reporting, for both screening and follow-up of MS. This will ensure that important points are not missed, and all relevant checklists are included.[10] The white matter lesions should be evaluated for symmetry/asymmetry, whether lesions are focal or confluent, location of lesions, involvement of the U fibers or gray matter, enhancement patterns, leptomeningeal enhancement, evidence of cord lesions – and if present, their size, shape, and enhancement patterns. Artificial intelligence software can help in calculating the lesions overload which can help in the follow-up of these patients as well as in assessing the newer therapies.

Section 2- Latest diagnostic criteria

The initial diagnostic criteria of MS were given by Professor Ian McDonald.[11] These have frequently been revisited and revised for minimizing errors in diagnosis and to help in the early diagnosis of the condition. The latest version at the time of manuscript preparation is the 2017 revisions of McDonald's criteria [Table 1].
Table 1: 2017 McDonald Diagnostic Criteria

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Based on the set criteria, the key requirements for the diagnosis are:

  1. Exclusion of any other possible neurological diagnosis
  2. Clinical or radiological demonstration of demyelinating plaques disseminated in space and time.


Latest changes in the current criteria (with respect to 2010 McDonald's criteria) are:

  1. Addition of cortical lesions for demonstration of dissemination in space.
  2. Addition of CSF-oligoclonal bands for demonstration of dissemination in time in clinically isolated syndrome.
  3. Exclusion of optic nerve lesions from the current set of criteria.


The criteria for demonstration of demyelinating plaques disseminated in space and time on MRI are as follows:

  1. For dissemination in space, the presence of one or more MS-typical T2 lesions in two or more areas of these central nervous system locations- Periventricular, cortical or juxtacortical, infratentorial, and spinal cord.
  2. For dissemination in time, the simultaneous presence of both enhancing and non-enhancing MS-typical MRI lesions, or new T2-bright or enhancing MRI lesion compared to baseline scan.


Section 3- MR features of MS-typical lesions

In the brain, an MS lesion is a T2/proton density (PD)/FLAIR hyperintense area which measures at least 3 mm longitudinally. Based on location, various characteristic appearances have been described.[11],[12],[13],[14],[15]

Periventricular lesions tend to be triangular with their bases along the ventricle perpendicular to the calloso-septal margin – Dawson's Fingers [Figure 1]. Ependymal 'Dot Dash' sign – ependymal hyperintense irregularity on FLAIR images seen along the undersurface of corpus callosum is sensitive for early detection of MS lesion [Figure 2].
Figure 1: FLAIR sagittal images showing multiple hyperintense lesions involving the corpus callosum and calloso-septal interface. Perpendicularly oriented triangular lesions are seen with their base towards the ventricular margin – Dawson's Finger

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Figure 2: FLAIR sagittal image showing irregular linear hyperintense signal along the undersurface of the corpus callosum – Dot Dash sign

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Lesions in the deep white matter can be linear, ovoid, or round with centripetal distribution pattern and in perivenular locations. Using a higher strength magnet helps define the perivenular location of these plaques by showing the presence of a central vein also called Central vein sign with a hypointense rim (Phase-ring) on T2* and fluid-attenuated inversion recovery (FLAIR)* sequences in at least two planes. Few studies have suggested a 'Rule of 6' whereby if more than 6 white matter lesions demonstrate central vein sign it suggests MS.[16] On phase image of SWI or GRE sequence presence of increased magnetic susceptibility along the margin of plaque called as Paramagnetic rim sign may be used to differentiate MS from mimics[17],[18]

Juxtacortical lesions appear bright on T2 sequences and are differentiated from deep white matter plaques by the lack of any separation between the lesion and gray matter [Figure 3].
Figure 3: FLAIR axial image of brain showing juxtacortical plaque (red arrow) without any discernible intervening white matter between the lesion and gray matter. Note the involvement of the U fibers

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Cortical lesions are plaques within the cortex or involving cortex as well as adjacent white matter and are likely to be missed on conventional sequences. 3D FLAIR [Figure 2] and newer MR sequences like MP-RAGE (Magnetization prepared rapid acquisition with gradient echo), DIR (Double inversion recovery), and PSIR (Phase-sensitive inversion recovery) are promising in helping identify hidden cortical lesions. These lesions are generally detected in the deep gray matter rather than in the superficial cortex just beneath the pia mater.

Lesions in infratentorial location involve the brainstem, cerebellum, and cerebellar peduncles. These tend to be located near the surface [Figure 4]. Preferential areas of involvement include middle cerebellar peduncles, intra pontine portion of trigeminal tract [Figure 5], surface of pons and floor of fourth ventricle Infratentorial involvement is more common in children compared to adults, where supratentorial lesions are seen more often.
Figure 4: T2 axial image of brain through the posterior fossa showing hyperintense plaques located along the surface of pons with relative sparing of the central portion

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Figure 5: Axial T2 (a), T1 (b), DRIVE (c) and post contrast (d) images showing hyperintense signal with mild enhancement suggestive of demyelination along the pontine portion of the trigeminal nerve in a 35 years old female followup case of multiple sclerosis

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On T1 weighted images the plaques are iso or hypointense, black holes, due to inflammatory edema in fresh and axonal loss in chronic plaques. Chronic black holes burden has been found to be one factor which correlates with neurological disability.

On diffusion weighted imaging (DWI) the plaques usually show normal or increased diffusivity, restricted diffusion in a plaque suggests activity but is not a reliable biomarker.

On post-gadolinium sequences, various enhancement patterns have been described for MS plaques including horseshoe or open ring, punctate, nodular, linear, rim, and leptomeningeal patterns. Of these, the horseshoe or open ring enhancement pattern is considered specific for large tumefactive demyelinating plaques. The ring is open towards gray matter and the enhancing part represents active demyelination. For tumefactive lesions, other characteristic features are disproportionately less edema or mass effect compared to the actual size of the lesion [Figure 6]a,[Figure 6]b,[Figure 6]c, presence of a central vein within the mass, and increased diffusivity. Response to steroid treatment has been described as another important marker. MR spectroscopy may not be able to differentiate between tumefactive demyelination and malignancy as the elevation of choline, reduction of N-acetylaspartate with respect to creatinine, and elevation of lactate are noted in both.[19],[20] However, perfusion scans can help in differentiating the two as malignant lesion will show hyperperfusion against the hypoperfusion in demyelination.
Figure 6: Axial FLAIR (a), contrast T1 (b), and DWI (c) images showing a large solitary lesion with open ring enhancement. On the FLAIR image (a), the lesion shows mildly hyperintense signal with peripheral open ring showing more intense signal. The ring shows contrast enhancement (b) with restricted diffusion (c). As compared to the size of the lesion, there is mild perilesional edema

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In the spinal cord, typical MS plaques should be demonstrated in two sequences (T2 and STIR/PD or any other sequence) or in two planes on T2 sequence. The most frequently involved part is the cervical spinal cord [Figure 7] followed by dorsal. The plaque is typically located in peripheral white matter, is cigar shaped and involves two or fewer vertebral segments in the longitudinal dimension and less than half the area of the cord in the cross-sectional dimension.
Figure 7: Sagittal T2 weighted images of cervical spine showing multiple focal oval/cigar shaped lesions. None of the lesion is extending beyond two vertebral segments

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Additional concerns in the diagnosis/follow-up of MS –

To avoid confusion with other disease entities or wrongly assigning a lesion as a relapse, we should be aware of the following entities:

  1. Progressive multifocal leukoencephalopathy (PML) and immune reconstitution inflammatory syndrome (IRIS)-PML are known complications of long-term immunosuppressant treatment (Natalizumab) in MS. Awareness of the condition and application of a specialized MR imaging protocol is necessary to differentiate it from MS-relapse. Typical PML lesions are multifocal, bilateral, and asymmetric subcortical lesions with a well-defined margin towards the gray matter and an ill-defined border towards the white matter on T2-weighted images [Figure 8]a, [Figure 8]b. Diffusion-weighted imaging demonstrates increased diffusivity without obeying vascular territory. Whereas, in PML-IRIS lesions, contrast enhancement at the margin of the lesion and presence of edema and mass effect could be seen, which are not seen with typical PML lesions.[21]
  2. Gadolinium-based contrast should be used judiciously in follow-up cases in view of gadolinium deposition disease. On unenhanced, T1-weighted sequence, increased signal intensity may be observed in the dentate nucleus, globus pallidus, and thalamus in this condition. It is related to the cumulative contrast dose in a lifetime and is observed more frequently with linear compared to macrocyclic gadolinium contrast agents.[22],[23],[24]
Figure 8: Axial T2 (a) and coronal FLAIR (b) images showing multiple asymmetrical hyperintense white matter lesions with sharper margin on gray matter side. Involvement of the U fibers is seen – Progressive multifocal leukoencephalopathy

Click here to view


Section 4- Higher magnet strength and special sequences for difficult-to-diagnose lesions

As already discussed in section 2 & 3, certain lesions may not be adequately characterized on basic MR imaging sequences. For problem-solving in such cases, a higher strength MR scanner[25],[26] and additional sequences should be used.

Sequences like MP-RAGE, DIR, and PSIR are helpful in identifying hidden cortical lesions.[14],[15] Central vein sign, Paramagnetic rim sign may help in differentiating MS from other entities.

White matter lesions are likely to create confusion, especially in patients over 40 years of age, with other pre-existing conditions like hypertension, diabetes, etc. Using an MR scanner of higher strength can help differentiate among these conditions by demonstrating a Phase-ring in MS plaques on T2*/FLAIR* sequences.

Similarly, in tumefactive lesions, the use of diffusion-weighted imaging, perfusion, and susceptibility imaging sequences can be handy as described earlier.

Magnetization Transfer Imaging (MTI) provides a unique imaging marker of myelin. Magnetization transfer ratio (MTR) correlates well with level of myelin content and axonal density. White matter has higher MTR than gray matter. Areas of demyelination show low MTR. It can be helpful parameter in follow up – increase in MTR during follow up indicates remyelination while progressive reduction in MTR points to worsening and precedes new lesions. Can also be used to differentiate MS from inflammatory as well as vascular lesions as MS lesions have lower MTR.[27]

Section 5- Exclusion of other diagnoses (through history, characteristic lab, and imaging findings)

The exclusion of other possible diagnoses is an essential criterion under the 2017 revisions of McDonald criteria. One of the most important steps in excluding other neurological diagnoses is promoting clinico-radiological meets in the department and discussing radiological findings in view of the relevant history and laboratory findings. Maintaining an image archive where patient's images could be saved for comparison and follow up is also very important as already discussed.

Excluding other diagnoses is vital, not doing so could prove to be deleterious to the patient's health in several cases. Disease-modifying drugs like interferon-beta and natalizumab which are used in MS may exacerbate NMO.[28],[29] Another important instance is in relapse versus PML cases, where the former is treated with immunosuppressants while the latter requires immediate cessation of ongoing MS treatment.[30]

There are a number of pathologies which may mimic MS, some of the important differentials to be familiar with include:

  1. Small Vessel Disease (SVD): White matter lesions due to small vessel disease are common mimickers of the lesions of MS and can pose a diagnostic dilemma, especially in the middle-age group. These are subcortical, non-specific, white matter lesions and lacunar infarcts. The SVD lesions don't involve U fibers [Figure 9] which, in contrast, are preferentially involved in MS. Another other useful differentiating feature is the sparing of the temporal lobe and corpus callosum in SVD. Additionally, the brain stem involvement in SVD is central, whereas it is peripheral in MS. Similarly, microbleeds seen on GRE or SWI sequences go in favor of SVD.
  2. Acute disseminated encephalomyelitis (ADEM): It is a monophasic disorder common in children and usually follows a viral infection or vaccination. Typical lesions are bilateral, symmetrical, round, and flocculent (cotton balls), and these are typically located in the white matter, basal ganglia and posterior fossa [Figure 10]. The periventricular region is usually spared with contrast scans showing all lesions to be enhancing simultaneously. The enhancement patterns may be variable – punctate, nodular, complete, or incomplete ring enhancement, however, no enhancement does not rule out ADEM. Spinal involvement is frequent with the thoracic segment getting involved most frequently. The size of the lesions is variable, at least one large lesion of 1-2 cm will usually be seen. This is one of the greatest mimickers of MS in children and it may be difficult at times to differentiate between the two in the absence of encephalopathy and a preceding viral infection. Follow up scans may be of help in such cases.
  3. Neuromyelitis optica (NMO): Typical imaging findings include longitudinally extensive transverse myelitis involving three or more segments, optic neuritis, and permanent or evanescent demyelinating lesions in the brain [Figure 11] and [Figure 12] in areas with high aquaporin-4 (AQP4) expression (circumventricular organs). AQP4-Immunoglobulin G may or may not be positive.[31]
  4. Anti-MOG encephalomyelitis: Presentation may include acute optic neuritis, acute myelitis, brainstem encephalitis, and encephalitis. MR findings include longitudinally extensive optic neuritis primarily involving the anterior segment, longitudinally extensive spinal cord lesions with signal alteration more around the central lesions (mostly in the conus medullaris) [Figure 13], and large confluent T2 lesions in the brain. Patients are often misdiagnosed as MS, ADEM, or NMO and present with flare-ups after steroid treatment. A careful history and anti-MOG-IgG antibody positivity can aid in its diagnosis.[5]
  5. Susac syndrome: It is an autoimmune microangiopathy comprising a triad of encephalopathy, branch retinal artery occlusion, and sensorineural hearing loss. It involves the gray and white matter of both infra-and supratentorial brain parenchyma. It involves the central corpus callosum, in contrast to MS where peripheral involvement of corpus callosum is seen.[12]
  6. Vasculitis: MRI findings are variable and will depend upon the underlying etiology. T2/FLAIR hyperintense lesions, foci of microhemorrhages, calcifications in gray-white matter junction, basal ganglia, and meningeal involvement along with clinical profile may help in reaching a conclusion. Evaluation with vessel wall imaging may demonstrate thickening and enhancement of vessel wall and help in making a diagnosis.[12]
  7. Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL): MR imaging demonstrates the presence of bilateral, confluent white matter hyperintensities with subcortical lacunar infarcts and microbleeds. The preferred sites of involvement are the anterior temporal lobes with involvement of U fibers and the external capsules [Figure 14]a,[Figure 14]b,[Figure 14]c,[Figure 14]d. A positive family history of recurrent strokes in the young is very helpful in reaching a diagnosis. Mutation in the Notch3 gene has been implicated as its cause.[32]
  8. Cerebral autosomal recessive arteriopathy with subcortical infarcts and leukoencephalopathy (CARASIL): The imaging findings are like CADASIL. However, gait disturbance, back pain, and presence of adolescent alopecia are its distinguishing features. In advanced cases, the Arc sign has been described, referring to a signal abnormality extending from the pons to the middle cerebellar peduncles.[33]
  9. Glioblastoma multiforme/metastasis/abscess can be confused with tumefactive MS. The presence of incomplete rim enhancement can differentiate tumefactive MS from a mitotic lesion. Perfusion is increased in masses but not in tumefactive MS.[19],[34]
  10. Other miscellaneous conditions may also be confused with MS. Characteristic imaging features, clinical history and in some cases, brain biopsy may be required to reach conclusive diagnosis. These include Lyme disease (commonly shows cranial nerve involvement[35]), sarcoidosis (leptomeningeal enhancement is often seen[36]), and intravascular lymphomas (imaging findings including-infarct-like/mass-like lesions, non-specific white matter changes, meningeal enhancement, and T2 hyperintensity in pons have been described[37]).
Figure 9: Multiple axial FLAIR (a-d) images showing multiple small focal hyperintense signal areas bilaterally in sub cortical white matter with sparing of the corpus callosum and U fibres in a diabetic 55 years old female suggestive of small vessel disease

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Figure 10: Multiple Axial T2 weighted images showing multiple hyperintense focal lesions involving brain stem, right cerebellum, right ganglio thalamic region as well as frontal, parietal and parieto occipital white matter in a 12 years old male following a viral fever

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Figure 11: Axial T2 W (a) and coronal FLAIR (b) images in a 19 years old female with positive NMO antibodies showing hyperintense signal in the pontomedullary region, medulla, left cerebellum, around frontal horns with few small lesions in the supratentorial white matter

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Figure 12: 38 years old female with history and laboratory findings of NMO showing thickening with enhancement of the right optic nerve – note involvement of the posterior portion (a and b) in post contrast FATSAT images through orbit. Sagittal (c) T2 weighted image of cervical spine showing heterogenous areas of hyperintense signal. Image Courtesy: Suyash Mohan, UPEN, USA

Click here to view
Figure 13: Sagittal T2 weighted images of dorsolumbar spine (a) showing focal areas of hyperintense signal in the conus, axial FLAIR images (b and c) showing white matter hyperintense signal and Coronal T2 (c) through orbit showing hyperintense signal in the left optic nerve in a 23 year-old female with MOG associated demyelination. Image Courtesy: Suyash Mohan, UPEN, USA

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Figure 14: Axial T2 (a and b), coronal FLAIR (c), and axial GRE (d) images of a 32-year-old, non-diabetic, non-hypertensive male, showing multiple asymmetrical hyperintense lesions of varying sizes on T2 and FLAIR images. The lesions involve the external capsule bilaterally (a-c) and the left temporal lobe (b). Multiple microhemorrhages can be seen as low-intense signal on GRE images (d) – CADASIL

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 » Summary Top


Correct and timely diagnosis of MS is essential for management. Awareness of the latest diagnostic criteria, imaging protocols, and MR imaging sequences can help in minimizing diagnostic error. Importance of clinic-radiological meets, proper history taking, correlating laboratory findings and follow-up imaging cannot be overemphasized in differentiating various other conditions which may mimic MS. Use of proper MS protocol with high strength MRI scanner and proper evaluation of white matter lesions is essential Judicious use of contrast and awareness of long-term side effects of drug modifying therapy in MS is vital to prevent misdiagnosis in follow-up cases of MS.

Financial support and sponsorship

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Conflicts of interest

There are no conflicts of interest.



 
 » References Top

1.
Gallien P, Gich J, Sánchez-Dalmau BF, Feneberg W. Multidisciplinary management of multiple sclerosis symptoms. Eur Neurol 2014;72(Suppl 1):20-5.  Back to cited text no. 1
    
2.
Ghasemi N, Razavi S, Nikzad E. Multiple sclerosis: Pathogenesis, symptoms, diagnoses and cell-based therapy. Cell J 2017;19:1-10.  Back to cited text no. 2
    
3.
Ge Y. Multiple sclerosis: The role of MR imaging. Am J Neuroradiol 2006;27:1165-76.  Back to cited text no. 3
    
4.
McCreary M, Mealy MA, Wingerchuk DM, Levy M, DeSena A, Greenberg BM. Updated diagnostic criteria for neuromyelitis optica spectrum disorder: Similar outcomes of previously separate cohorts. Mult Scler J Exp Transl Clin 2018;4:2055217318815925.  Back to cited text no. 4
    
5.
Jarius S, Paul F, Aktas O, Asgari N, Dale RC, de Seze J, et al. MOG encephalomyelitis: International recommendations on diagnosis and antibody testing. J Neuroinflammation 2018;15:134.  Back to cited text no. 5
    
6.
Yamada S, Yamada SM, Nakaguchi H, Murakami M, Hoya K, Matsuno A, et al. Tumefactive multiple sclerosis requiring emergent biopsy and histological investigation to confirm the diagnosis: A case report. J Med Case Rep 2012;6:104.  Back to cited text no. 6
    
7.
Dahan A, Pereira R, Malpas CB, Kalincik T, Gaillard F. PACS integration of semiautomated imaging software improves day-to-day MS disease activity detection. AJNR Am J Neuroradiol 2019;40:1624-9.  Back to cited text no. 7
    
8.
Le AH, Liu B, Huang HK. Integration of computer-aided diagnosis/detection (CAD) results in a PACS environment using CAD-PACS toolkit and DICOM SR. Int J Comput Assist Radiol Surg 2009;4:317-29.  Back to cited text no. 8
    
9.
Traboulsee A, Simon JH, Stone L, Fisher E, Jones DE, Malhotra A, et al. Revised recommendations of the consortium of MS Centers Task Force for a standardized MRI protocol and clinical guidelines for the diagnosis and follow-up of multiple sclerosis. AJNR Am J Neuroradiol 2016;37:394-401.  Back to cited text no. 9
    
10.
Mamlouk MD, Chang PC, Saket RR. Contextual radiology reporting: A new approach to neuroradiology structured templates. Am J Neuroradiol 2018;39:1406-14.  Back to cited text no. 10
    
11.
Thompson AJ, Banwell BL, Barkhof F, Carroll WM, Coetzee T, Comi G, et al. Diagnosis of multiple sclerosis: 2017 revisions of the McDonald criteria. Lancet Neurol 2018;17:162-73.  Back to cited text no. 11
    
12.
Osborn AG, Hedlund GL, Salzman KL. Demyelinating and inflammatory diseases. In: Osborn's Brain. Elsevier Health Sciences; 2017. p. 449-93.  Back to cited text no. 12
    
13.
Filippi M, Rocca MA. MR Imaging of multiple sclerosis. Radiology 2011;259:659-81.  Back to cited text no. 13
    
14.
Nelson F, Poonawalla A, Hou P, Wolinsky JS, Narayana PA. 3D MPRAGE improves classification of cortical lesions in multiple sclerosis. Mult Scler 2008;14:1214-9.  Back to cited text no. 14
    
15.
Nelson F, Poonawalla AH, Hou P, Huang F, Wolinsky JS, Narayana PA. Improved identification of intracortical lesions in multiple sclerosis with phase-sensitive inversion recovery in combination with fast double inversion recovery MR imaging. Am J Neuroradiol 2007;28:1645-9.  Back to cited text no. 15
    
16.
Suthiphosuwan S, Sati P, Guenette M, Montalban X, Reich DS, Bharatha A, et al. The central vein sign in radiologically isolated syndrome. Am J Neuroradiol 2019;40:776-83.  Back to cited text no. 16
    
17.
Absinta M, Sati P, Fechner A, Schindler MK, Nair G, Reich DS. Identification of chronic active multiple sclerosis lesions on 3T MRI. AJNR Am J Neuroradiol 2018;39:1233-8.  Back to cited text no. 17
    
18.
Suthiphosuwan S, Sati P, Absinta M, Guenette M, Reich DS, Bharatha A, et al. Paramagnetic rim sign in radiologically isolated syndrome. JAMA Neurol 2020;77:653-5.  Back to cited text no. 18
    
19.
Given C, Stevens B, Lee C. The MRI appearance of tumefactive demyelinating lesions. AJR Am J Roentgenol 2004;182:195-9.  Back to cited text no. 19
    
20.
Masdeu JC, Moreira J, Trasi S, Visintainer P, Cavaliere R, Grundman M. The open ring a new imaging sign in demyelinating disease. J Neuroimaging 1996;6:104-7.  Back to cited text no. 20
    
21.
Yousry TA, Pelletier D, Cadavid D, Gass A, Richert ND, Radue EW, et al. Magnetic resonance imaging pattern in natalizumab-associated progressive multifocal leukoencephalopathy. Ann Neurol 2012;72:779-87.  Back to cited text no. 21
    
22.
Forslin Y, Shams S, Hashim F, Aspelin P, Bergendal G, Martola J, et al. Retention of gadolinium-based contrast agents in multiple sclerosis: Retrospective analysis of an 18-year longitudinal study. AJNR Am J Neuroradiol 2017;38:1311-6.  Back to cited text no. 22
    
23.
Kanda T. The new restrictions on the use of linear gadolinium-based contrast agents in Japan. Magn Reson Med Sci 2019;18:1-3.  Back to cited text no. 23
    
24.
Zivadinov R, Bergsland N, Hagemeier J, Ramasamy DP, Dwyer MG, Schweser F, et al. Cumulative gadodiamide administration leads to brain gadolinium deposition in early MS. Neurology 2019;93:e611-23.  Back to cited text no. 24
    
25.
Filippi M, Evangelou N, Kangarlu A, Inglese M, Mainero C, Horsfield MA, et al. Ultra-high-field MR imaging in multiple sclerosis. J Neurol Neurosurg Psychiatry 2014;85:60-6.  Back to cited text no. 25
    
26.
Schindler MK, Sati P, Reich DS. Insights from ultrahigh field imaging in multiple sclerosis. Neuroimaging Clin N Am 2017;27:357-66.  Back to cited text no. 26
    
27.
Goodkin DE, Rooney WD, Sloan R, Bacchetti P, Gee L, Vermathen M, et al. A serial study of new MS lesions and the white matter from which they arise. Neurology 1998;51:1689-97.  Back to cited text no. 27
    
28.
Barnett Y, Sutton IJ, Ghadiri M, Masters L, Zivadinov R, Barnett MH. Conventional and advanced imaging in neuromyelitis optica. Am J Neuroradiol 2014;35:1458-66.  Back to cited text no. 28
    
29.
Palace J, Leite MI, Nairne A, Vincent A. Interferon Beta treatment in neuromyelitis optica: Increase in relapses and aquaporin 4 antibody titers. Arch Neurol 2010;67:1016-7.  Back to cited text no. 29
    
30.
Williamson EM, Berger JR. Diagnosis and treatment of progressive multifocal leukoencephalopathy associated with multiple sclerosis therapies. Neurotherapeutics 2017;14:961-73.  Back to cited text no. 30
    
31.
Wingerchuk DM, Banwell B, Bennett JL, Cabre P, Carroll W, Chitnis T, et al. International consensus diagnostic criteria for neuromyelitis optica spectrum disorders. Neurology 2015;85:177-89.  Back to cited text no. 31
    
32.
Stojanov D, Vojinovic S, Aracki-Trenkic A, Tasic A, Benedeto-Stojanov D, Ljubisavljevic S, et al. Imaging characteristics of cerebral autosomal dominant arteriopathy with subcortical infarcts and leucoencephalopathy (CADASIL). Bosn J Basic Med Sci 2015;15:1-8.  Back to cited text no. 32
    
33.
Nozaki H, Sekine Y, Fukutake T, Nishimoto Y, Shimoe Y, Shirata A, et al. Characteristic features and progression of abnormalities on MRI for CARASIL. Neurology 2015;85:459-63.  Back to cited text no. 33
    
34.
Puri V, Chaudhry N, Gulati P, Tatke M, Singh D. Recurrent tumefactive demyelination in a child. J Clin Neurosci 2005;12:495-500.  Back to cited text no. 34
    
35.
Chaturvedi A, Baker K, Jeanmonod D, Jeanmonod R. Lyme disease presenting with multiple cranial nerve deficits: Report of a case. Case Rep Emerg Med 2016;2016:7218906.  Back to cited text no. 35
    
36.
Shah R, Roberson GH, Curé JK. Correlation of MR imaging findings and clinical manifestations in neurosarcoidosis. Am J Neuroradiol 2009;30:953-61.  Back to cited text no. 36
    
37.
Yamamoto A, Kikuchi Y, Homma K, O'Uchi T, Furui S. Characteristics of intravascular large B-cell lymphoma on cerebral MR imaging. AJNR Am J Neuroradiol 2012;33:292-6.  Back to cited text no. 37
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9], [Figure 10], [Figure 11], [Figure 12], [Figure 13], [Figure 14]
 
 
    Tables

  [Table 1]



 

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