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Case Report

Diagnostic Dilemma: An Atypical Case of Astrocytoma in a Patient with Relapsing–Remitting Multiple Sclerosis

1
Saskatoon Multiple Sclerosis Clinic, Saskatchewan Health Authority, Saskatoon, SK S7K 0M7, Canada
2
Office of the Saskatchewan Multiple Sclerosis Clinical Research Chair, College of Medicine, University of Saskatchewan, Saskatoon, SK S7K 0M7, Canada
3
Department of Medicine, Neurology Division, College of Medicine, University of Saskatchewan, Saskatoon, SK S7N 0X8, Canada
4
Department of Anatomy, Physiology and Pharmacology, College of Medicine, University of Saskatchewan, Saskatoon, SK S7N 5E5, Canada
*
Author to whom correspondence should be addressed.
Submission received: 26 April 2021 / Revised: 18 May 2021 / Accepted: 20 May 2021 / Published: 3 June 2021

Abstract

:
Distinguishing between tumefactive demyelinating lesions (TDLs) and brain tumors in multiple sclerosis (MS) can be challenging. A progressive course is highly common with brain tumors in MS and no single neuroimaging technique is foolproof when distinguishing between the two. We report a case of a 41-year-old female with relapsing–remitting multiple sclerosis, who had a suspicious lesion within the left frontal hemisphere, without a progressive course. The patient experienced paresthesias primarily to her right hand but remained stable without any functional decline and new neurological symptoms over the four years she was followed. The lesion was followed with brain magnetic resonance imaging (MRI) scans, positron emission tomography–computed tomography scans, and magnetic resonance spectroscopy. Together, these scans favored the diagnosis of a TDL, but a low-grade tumor was difficult to rule out. Examination of serial brain MRI scans showed an enlarging lesion in the left middle frontal gyrus involving the deep white matter. Neurosurgery was consulted and an elective left frontal awake craniotomy was performed. Histopathology revealed a grade II astrocytoma. This case emphasizes the importance of thorough and continuous evaluation of atypical MRI lesions in MS and contributes important features to the literature for timely diagnosis and treatment of similar cases.

1. Introduction

The concurrence of glioma and relapsing–remitting multiple sclerosis (RRMS) is uncommon. Multiple sclerosis (MS) is diagnosed by clinical and radiological criteria meeting the 2017 McDonald’s Criteria [1]. In patients with tumefactive MS (an atypical variant of MS with large isolated demyelinated plaque), differentiating between tumefactive demyelinating lesions (TDLs) and glioma can be complicated [2]. For instance, some atypical TDLs may resemble gliomas and conversely, early-stage gliomas may mimic MS. This diagnostic dilemma may lead to a delay in diagnosis and could potentially affect the long-term clinical outcomes in such patients. TDLs are usually defined as large (>2 cm) demyelinating lesions with/without mass effect, perilesional edema, or gadolinium enhancement, which could mimic brain tumors radiologically and clinically [2]. Brain magnetic resonance imaging (MRI) is a sensitive technique for depicting demyelinating lesions in MS patients, but when used alone it fails to provide an accurate diagnosis in many cases of atypical TDLs that mimic a tumor. The definitive diagnosis is often made only after a surgical biopsy or resection of the lesion. Clinical suspicion of a brain tumor in MS usually arises if a patient experiences a steady progression of symptoms or neurological deficits in the presence of a TDL. We report a patient without a progressive course, who met clinical and MRI criteria for the diagnosis of relapsing–remitting multiple sclerosis (RRMS), with one of the lesions initially described as tumefactive (a TDL was deemed more likely than a neoplasm based on brain MRI imaging), which was later found to be a primary diffuse astrocytoma (WHO grade II). The patient provided informed consent for the publication of this case report.

2. Case Presentation

The 41-year-old female (non-smoker with a history of ulcerative colitis and celiac disease) had the onset of her MS 14 years ago, characterized by sensory symptoms of the lateral three fingers of the right hand, which resolved completely over several months. Seven years later, she experienced a second relapse characterized by paresthesias to her right hand, which spread to the medial aspect of her right arm, torso, leg, and toes. Following the second attack, she was diagnosed with RRMS based on MRI and clinical criteria. The initial MRI showed a large lesion (hypointense, non-enhancing on T1; hyperintense on fluid-attenuated inversion recovery (FLAIR) imaging) within the left frontal hemisphere involving the cortex and adjacent white matter (Figure 1, top row, “lesion”). Multiple white matter lesions were seen in both cerebral hemispheres compatible with MS (Figure 1, top row, “MS”). Focal hyperintensity was also observed in the right dorsal column of the cervical spinal cord at the C5–6 vertebral body level. Further evaluation by fluorodeoxyglucose positron emission tomography-computed tomography (FDG PET-CT) showed that the lesion was hypometabolic (Figure 1, middle row, “PET”). Magnetic resonance spectroscopy (MRS) revealed decreased N-acetylaspartate (NAA) with an NAA/creatine (Cr) ratio of 1.1 (Figure 1, middle row, “MRS”). The choline (Cho) was elevated, the Chol/Cr ratio was high at 1.59, and the Cho/NAA was 1.44. A significant lactate peak was not demonstrated. Neurosurgical and neuroradiological consultation suggested that the lesion in the left frontal hemisphere was consistent with a TDL in MS. Glatiramer acetate was initiated and the patient remained stable for the next four years without relapse or MRI activity. The patient had an expanded disability status scale (EDSS) of 1.0 since her diagnosis, without any evidence of confirmed disability progression or functional decline. The left frontal hemispheric lesion was followed over four years with serial MRI scans, which showed that the lesion increased in size with a mild mass effect involving the left middle frontal gyrus and underlying white matter (Figure 1, bottom row, “lesion”). There was interval stability of demyelinating plaques in the brain and cervical spinal cord. Neurosurgery was reconsulted and an elective left frontal awake craniotomy with the total resection of the lesion was carried out. Tissue diagnosis revealed primary left frontal diffuse astrocytoma (WHO grade II), 1p19q non-co-deleted, O6-methylguanine-DNA-methyltransferase (MGMT) methylated (46.5%), isocitrate dehydrogenase 1 (IDH1) R132H mutation, and loss of ATRX (alpha-thalassemia/mental retardation X-linked) expression. Post-operatively the patient experienced mild expressive dysphasia and was discharged on a tapering dose of dexamethasone. Following surgery, the patient received radiotherapy (54 Gray in 30 fractions) followed by temozolomide (6-cycle regime) for six months as an adjuvant treatment. She experienced a seizure, which was successfully treated with levetiracetam (750 mg) orally twice daily. She was on glatiramer acetate (20 mg) subcutaneously once daily throughout her course, and her MS remained stable by clinical and MRI criteria. Follow-up MRIs showed no recurrence of the glioma (Figure 1, bottom row, “post-op”) and stable white matter, ovoid, and periventricular lesions consistent with MS.

3. Discussion

Differentiating between TDLs and brain tumors is challenging, particularly in the early stages of brain cancer. In this patient, diagnostic delay likely occurred because she was clinically stable, the lesion occurred in the setting of MS diagnosis (early in disease) and multiple imaging techniques could not adequately distinguish between TDL and early glioma. In addition to standard brain MRI imaging, the patient underwent FDG-PET-CT, which was hypometabolic (favoring TDL), and MRS, which was equivocal (Cho/NAA ratio = 1.44; >1.72 highly correlates with high-grade glioma [3]). The co-occurrence of glioma and MS in the same patient is uncommon, and most of the previously reported cases had high-grade astrocytic tumors that developed after MS diagnosis [4].
TDLs and brain tumors may share several characteristics, including size (>2 cm), gadolinium enhancement pattern, and a predilection for the frontal and parietal lobes. Importantly, several studies have attempted to distinguish between TDLs and brain tumors. For example, a study by Abdoli and Freedman [2] found that in contrast to TDLs, brain tumors in MS more commonly occurred in late or established MS, evolved over a few months, showed symptoms consistent with space-occupying lesions (cortical symptoms, raised intracranial pressure), had mostly a progressive course, and the lesion typically had more mass effect, necrosis, and perilesional edema and contained calcification or hemorrhage. Remarkably, the patient presented in this report had none of these findings.
Considering that there has been no recent review on this topic, we conducted an up-to-date topical review of the cases of gliomas in persons living with MS. A literature search was done on MEDLINE/PubMed, Scopus (Elsevier), and Google (internet search) using the following search terms: multiple sclerosis, glioma, tumefactive lesion, brain tumor, astrocytoma, ependymomas, and oligodendroglioma. Case reports or case series reporting gliomas in an individual with MS and published in the English language since 2012 were included. We found 14 articles published in the last eight years (2012–2020) (Table 1). There were 16 patients (seven females, nine males), of which 13 had RRMS and 3 had SPMS. Table 2 presents a brief summary and classification of the glioma cases identified in people living with MS. Fourteen tumors were located in the frontal and parietal lobes. The most commonly reported gliomas were glioblastomas/astrocytomas, followed by oligodendrogliomas. Importantly, in contrast to the patient presented in this report, the vast majority of the cases presented with a progressive course or new neurological symptoms. Unfavorable clinical outcomes were mostly observed in elderly patients with high-grade gliomas who were either in palliative care or had refused interventional procedures. Tumor recurrence was observed in two cases.
Low-grade glioma in an MS patient may pose a diagnostic dilemma as the MRI findings of low-grade gliomas may be similar to those of TDLs [11]. Table 3 highlights the characteristic features for the differential diagnosis of MS, TDLs, and brain tumors in MS. A high level of clinical suspicion in atypical TDLs is required to differentiate glioma from MS [12]. A stereotactic biopsy and histopathological examination of the lesion aids in making a definitive diagnosis in equivocal cases [19]. It is a reliable procedure and has a diagnostic accuracy of 82–99% [20]. Total resection of the tumor without inflicting additional neurological deficits typically offers better patient outcomes for long-term survival [21].

4. Conclusions

This case report highlights that slow-growing suspicious TDLs in MS patients with a non-progressive course should be carefully monitored by MRI over time to exclude low-grade gliomas. An elective craniotomy (with a total resection of the lesion) followed by radiation and chemotherapy may provide favorable outcomes in patients with concurrent RRMS and low-grade diffuse astrocytoma.

Author Contributions

M.C.L. and C.K. were involved in the clinical management of the patient, the preparation of all the images, and the manuscript writing, review, and editing. A.S. was involved in the manuscript writing, literature review, and editing. All authors have read and agreed to the published version of the manuscript.

Funding

We have received no external funding. This work is based, in part, on work supported by the Saskatchewan MS Clinic and the office of the Saskatchewan MS Clinical Research Chair, College of Medicine, University of Saskatchewan, SK, Canada.

Institutional Review Board Statement

Not applicable.

Informed Consent Statement

The patient provided written informed consent for the publication of this case report.

Data Availability Statement

The data used to support the findings of this case report are available within the article.

Patient’s Perspective on the Treatment

From her initial diagnosis, they had found a rather large “MS lesion” in her left fronto-temporal region. A local neurologist determined that it was a large tumefactive lesion and referred her to the MS clinic for a second opinion. It was on her initial visit to the MS clinic in September 2017 that she heard the news that it might not be an MS lesion, but a low-grade glioma. The team at the clinic activated a referral process that ended with her having a craniotomy to remove the tumor. She is profoundly grateful to the team at the Saskatchewan MS Clinic for how they expedited her care. This team, she can say with wholehearted confidence, saved her life. She is also indebted to her neurosurgeons. Today she is optimistic about her prognosis and the progression of her disease.

Acknowledgments

We are extremely grateful to the individual living with MS described in this case report for providing her perspective on the treatment she received. We are also grateful to our clinical team at the Saskatchewan MS Clinic, College of Medicine, University of Saskatchewan, SK, Canada.

Conflicts of Interest

The authors declare no conflict of interest.

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Figure 1. Work-up and progression of the left frontal lobe lesion. The top row shows the large, non-enhancing lesion distinct from MS lesions (left to right: T1 following gadolinium administration (T1 + GAD) and fluid attenuated inversion recovery (FLAIR) showing the lesion; FLAIR showing MS lesions). The middle row shows hypometabolism of the lesion using fluorodeoxyglucose positron emission tomography–computed tomography imaging and results of magnetic resonance spectroscopy (MRS). MRS values are as follows: N-acetylaspartate (NAA)/creatine (Cr) 1.10, NAA/Cr(h) 0.99, choline (Cho)/Cr 1.59, Cho/Cr(h) 1.44, NAA/Cho 0.70, NAA/Cho(h) 0.69, Cho/NAA 1.44, and Cho/NAA(h) 1.45. The bottom row shows that the lesion increased in size compared to the original MRI (“pre-op”) and successful resection of the lesion (“post-op”). Abbreviations: MS: multiple sclerosis; PET: positron emission tomography; MRS: magnetic resonance spectroscopy; Pre-op: pre-operative; Post-op: post-operative.
Figure 1. Work-up and progression of the left frontal lobe lesion. The top row shows the large, non-enhancing lesion distinct from MS lesions (left to right: T1 following gadolinium administration (T1 + GAD) and fluid attenuated inversion recovery (FLAIR) showing the lesion; FLAIR showing MS lesions). The middle row shows hypometabolism of the lesion using fluorodeoxyglucose positron emission tomography–computed tomography imaging and results of magnetic resonance spectroscopy (MRS). MRS values are as follows: N-acetylaspartate (NAA)/creatine (Cr) 1.10, NAA/Cr(h) 0.99, choline (Cho)/Cr 1.59, Cho/Cr(h) 1.44, NAA/Cho 0.70, NAA/Cho(h) 0.69, Cho/NAA 1.44, and Cho/NAA(h) 1.45. The bottom row shows that the lesion increased in size compared to the original MRI (“pre-op”) and successful resection of the lesion (“post-op”). Abbreviations: MS: multiple sclerosis; PET: positron emission tomography; MRS: magnetic resonance spectroscopy; Pre-op: pre-operative; Post-op: post-operative.
Neurolint 13 00025 g001
Table 1. Topical review of recently reported cases of gliomas in MS patients.
Table 1. Topical review of recently reported cases of gliomas in MS patients.
Author, YearAge/SexAge at MS DiagnosisAge at Tumor DiagnosisMS PhenotypeTumor LocationProgressive Course or New Neurological Symptoms (Yes/No)MRI FindingsHistopathologyClinical Outcomes
Index Case (This Report)41 y/F34 y41 yRRMSLeft FrontalNoLarge, Non-Enhancing Lesion, T1 Hypointense, FLAIR HyperintensePrimary Diffuse Astrocytoma (WHO grade II)Post-Operative Mild Expressive Dysphasia and a Seizure. MS Remained Stable by Clinical and MRI Criteria
Turatti et al. [5], 201343 y/FN.A.43 yRRMSSplenium of corpus callosum and the optic radiationsYes (progressive visual field restriction)Large tumefactive lesion (>3 cm) that involved the spleniumof corpus callosum and the optic radiations, with moderate perilesional edema and without gadolinium enhancement High-grade astrocytomaFully ambulatory, hyperreflexia with impaired vibration sensation and pain in the left leg, main disability: blindness caused by radiotherapy
Neil et al. [6], 201479 y/M45 y79 ySPMSRight parieto-occipital regionYes (rapidly progressive cognitive decline)Extensive, infiltrative mass which extended from the right parieto-occipital region across a significantly expanded corpus callosumAnaplastic gliomaFamily declined any further intervention and patient died in hospice
Carvalho et al. [7], 201443 y/M23 y37 yRRMSLeft frontal lobeYes (progressive right hemiparesis)Extensive subcortical and deep white matter lesion in the left frontal lobe (non-contrast-enhancing) on routine brain MRIGrade II oligodendroglioma At 3-year follow-up: stable MRI lesions with minor right hemiparesis and dysarthria
Mantero et al. [8], 201560 y/M42 y60 ySPMSBrainstemYes (rapidly progressing deterioration with tetraparesis, dysphagia, and dysarthria)T2 hyperintense lesion in the brainstem, which increased in size on repeat MRI; thick enhancement surrounding a cyst-like cavity with involvement of left middle cerebellar peduncle GlioblastomaPatient died before the procedure (open brain biopsy); diagnosis was confirmed on autopsy
Morales et al. [9], 2017 Case 167 y/F42 yN.ARRMSRight frontoparietal lobeYes (had aggressive tumor and died 13 weeks after symptom onset)Contrast-enhancing lesions in the right frontoparietal area which expanded in size and number over timeGlioblastoma multiforme with areas of necrosis and endothelial proliferation Patient and family abstained from diagnostic work-up and patient died in hospice
Case 226 y/M22 y25 yRRMSRight superior frontal lobeNo (lesion was discovered in the routine surveillance MRI)Right superior frontal lobe mass at the cortical surface Diffuse astrocytoma,IDH-mutant, WHO grade IIDeveloped focal seizures after surgery (treated with levetiracetam); treated with natalizumab, stable for 5 years
Same patient as above22 y26 yRRMSRight frontal lobeYes (developed new left-sided weakness)Recurrence of the right frontal lobe lesion was observed on subsequent brain MRIGlioblastoma multiforme with primary neuroectodermal tumor (PNET)-like component, IDH-mutant, WHO grade IVShowed no evidence of tumor recurrence; continued monthly natalizumab and daily levetiracetam treatment for seizure prophylaxis
Kantorova et al. [10], 201727 y/F19 y28 yRRMSRight frontal lobeYes (progression of expanded disability status scale (EDSS) from 2.0 to 5.0 and development of new symptoms)Atypical hyperintense tumefactive demyelinating lesion Anaplastic astrocytomaRemained unstable (frequent epileptic seizures) and died during status epilepticus before starting oncological treatment
Abrishamchi et al. [11], 201741 y/F26 yN.A.RRMSLeft frontal lobe involving corpus callosumYes (progressive ataxia and dizziness)High signal lesions in the left frontal lobe involving corpus callosum on FLAIRGrade II astrocytomaImpaired tandem gait, Romberg sign, bilateral Babinski signs, quadriparesis
Myserlis et al. [12], 201737 y/M23 y37 yRRMSFrontoparietal Yes (gradual loss sensory and motor symptoms with cognitive decline)A 5 cm circular, ring-enhancing lesionGlioblastoma multiforme (grade IV)Recurrence of the tumor with gradual loss of motor and sensory functions, ataxia, speech difficulties, cognitive decline and EDSS = 9
Preziosa et al. [13], 2017Case 159 y/M43 y59 ySPMSRight post-rolandic regionsYes (gradual progression of spastic hypertonia, hyposthenia and EDSS)T2-hyperintense and T1-hypointense pseudotumoral lesion in the right post-rolandic region with irregular and poorly defined marginsGlioblastoma with leptomeningeal infiltration (grade IV)Deterioration of locomotor functions and inability to walk (possible consequences of radiotherapy). Patient refused diagnostic procedure
Case 255 y/M38 y53 yRRMSLeft supero-anterior parietal regionsYes (subtle difficulty in reading and fatigue)Heterogeneous T2-hyperintense and T1-hypointense lesion in the left superior anterior parietal regions with internal cystic areas and irregular enhancement Grade IV glioblastomaDeterioration of cognitive function, fatigue, reading difficulty and acalculia (only radiotherapy and temozolomide were used; no surgical removal of lesion)
Shirani et al. [14], 201844 y/M44 y9 months after MS dsRRMSRight frontal lobeNot evident (only the initial presentation of sudden onset right-sided optic neuritis was described)Multiple FLAIR white matter lesions in periventricular, juxtacortical and subcortical areasGrade II oligodendroglioma An early postoperative brain MRI revealed a new demyelinating lesion in the right posterior periventricular white matter and the patient remained on glatiramer acetate at the time of the report.
Sinclair et al. [15], 201941 y/FN.A.30 yRRMSLeft frontal lobeYes (gradually developed the clinical signs of mass-effect)Suspected glioma in the left frontal lobe and multiple supratentorial MS-like lesions in both hemispheresOligodendroglioma; WHO grade 2–3During the next 5 years after microsurgery, patient underwent systemic treatment due to a series of tumor- or MS-like relapses (signs of focal recurrence on postoperative MRI, scattered MS-suspected lesions, right-sided hemiparesis)
Same patient as aboveN.A.39 yRRMSLeft frontal lobeYes (right-sided hemiparesis)Tumor regrowth was observed next to surgical site (deemed unsuitable for microsurgery)Anaplastic astrocytomaPatient suffered from right foot palsy from the second surgical resection and fatigue (due to chemotherapy)
Sirko et al. [16], 202030 y/M31 y32 yRRMSRight temporal lobeYes (a negative trend in the neurological examination)T2 hyperintense lesion in the right temporal lobe and insula with irregular edges and blurred outlines involving both gray and white matterAnaplastic oligoastrocytomaPatient was waiting for surgery and was under the active supervision of a neurologist and a neurosurgeon
Algahtani et al. [17], 202023 y/F23 y23 yRRMSLeft superior and part of the middle frontal gyriYes (gradually progressive walking difficulty and imbalance)5.6 cm cortical-based tumor which originated from the left superior and part of the middle frontal gyri (surrounded by vasogenic edema)Anaplastic oligodendroglioma (WHO grade III)Six months post-surgery, new white matter demyelinating lesions consistent with MS were detected and diagnosis of RRMS was confirmed. Targeted sequencing revealed a mutation in the GBA2 gene consistent with the diagnosis of autosomal-recessive cerebellar ataxia with spasticity (positive family history)
London et al. [18], 202055 y/F26 y55 yRRMSLeft frontal lobeYes (developed mild gait ataxia, right hypoesthesia, and nystagmus)Closed-ring contrast-enhancing lesion in the left frontal lobe with surrounding edemaGlioblastoma (WHO grade IV)Follow-up MRI 3 months post-operation showed tumor progression. Despite treatment, the patient worsened and she died 5 months after diagnosis
Abbreviations: M: male; F: female; N.A.: not available; y: year; MS: multiple sclerosis; RRMS: relapsing–remitting MS; SPMS: secondary progressive MS; IDH: isocitrate dehydrogenase; WHO: World Health Organization; MRI: magnetic resonance imaging; EDSS: expanded disability status scale; FLAIR: fluid attenuated inversion recovery.
Table 2. Summary and classification of the identified glioma cases in patients with MS.
Table 2. Summary and classification of the identified glioma cases in patients with MS.
ClassificationAge (years)SexMS PhenotypeTumor Type
[Case Reference]
Tumor Site
Glioblastoma/Astrocytoma
(n = 10)
  • Mean age = 47 years
  • 5 M, 5 F
  • Mostly in frontal or parietal lobes
  • RRMS or SPMS
43FRRMSAstrocytoma [5]Splenium of corpus callosum and the optic radiations
26MRRMSDiffuse astrocytoma [9]
Glioblastoma multiforme [9]
Right superior frontal
Right frontal
27FRRMSAnaplastic astrocytoma [10]Right frontal
41FRRMSAstrocytoma [11]Left frontal lobe involving corpus callosum
60MSPMSGlioblastoma [8]Brainstem
67FRRMSGlioblastoma multiforme [9]Right frontoparietal
37MRRMSGlioblastoma multiforme [12]Frontoparietal
59MSPMSGlioblastoma [13]Right post-rolandic
55MRMMSGlioblastoma [13]Left supero-anterior parietal
55FRRMSGlioblastoma [18]Left frontal
Oligodendroglioma
(n = 5)
  • Mean age = 36.2 years
  • 3 M, 2 F
  • Frontal lobe
  • RRMS
43MRRMSOligodendroglioma [7]Left frontal
44MOligodendroglioma [14]Right frontal
41FOligodendroglioma [15]
Anaplastic astrocytoma [15]
Left frontal
Left frontal
30MAnaplastic oligodendroglioma [16]Left superior and part of the middle frontal gyri
23FAnaplastic oligodendroglioma [17]Left superior and part of the middle frontal gyri
Undifferentiated
(n = 1)
79MSPMSAnaplastic glioma [6]Right parieto-occipital
Abbreviations: M: male; F: female; MS: multiple sclerosis; RRMS: relapsing–remitting MS; SPMS: secondary progressive MS.
Table 3. Differential diagnosis of MS, TDLs, and brain tumors in MS.
Table 3. Differential diagnosis of MS, TDLs, and brain tumors in MS.
MSTDLsBrain Tumors in MS
Demographic featuresFemales > males; can occur at any age (usually between 20 and 40 years); relatively subacute onset [22]Females > males; usually in young adults (middle age); relatively slow onset [23]Brain tumors are more likely in males (this may vary with type of tumor); usually in older adults; gradual onset [24]
Clinical presentationVariable, but typical syndromes include monocular loss of vision, double vision, ataxia, sensory loss, or limb weakness [25]Polysymptomatic (usually sensory, motor, and cognitive symptoms), but may include focal neurological deficits, seizure, or aphasia [23] Atypical manifestations may include (but are not limited to) headaches, tumor location-specific symptoms, or behavioral changes [26]
Clinical courseRelapsing–remitting (most common), secondary progressive, primary progressive Could be monophasic or recurrent [23]Usually progressive
Size and site of lesion(s)3–5 mm or larger, typical white matter lesions in MS are periventricular, juxtacortical, and callososeptal, or at cerebellar peduncles in the infratentorial region [27]>2 cm, often found in the supratentorial region (mostly in the frontal and parietal lobes) [28]Large and variable size, usual distribution at frontal and temporal lobes [29]
MRITypical white matter lesions are round to ovoid in shape, should be at least 3 mm in size (long axis), and appear hyperintense on T2 and FLAIR sequences [30]Large lesion (>2 cm) but with relatively little mass effect or surrounding edema, incomplete (open-ring pattern) contrast enhancement [28]Mass effect, perilesional edema, necrosis, and continued enlargement of lesion [10]
H-MRSAcute MS lesions: increased Cho, reduced NAA, and presence of lipids in acute MS lesions Chronic MS lesions: reduced NAA levels [31]Increased Cho and lactate are supportive, but non-specific Typically demonstrates increased Cho/NAA ratio, reduced NAA/Cr ratio, and increased Cho/Cr ratio [23,32,33]Persistently elevated Cho is more suggestive of tumor, could exhibit decreased NAA/Cr ratio, increased Cho/Cr ratio, and variable lactate and lipid peaks [13]
Abbreviations: MS: multiple sclerosis; TDLs: tumefactive demyelinating lesions; H-MRS: proton-magnetic resonance spectroscopy; mm: millimeter; cm: centimeter; Cho: choline; NAA: N-acetylaspartate; Cr: creatine; FLAIR: fluid-attenuated inversion recovery.
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Kahovec, C.; Saini, A.; Levin, M.C. Diagnostic Dilemma: An Atypical Case of Astrocytoma in a Patient with Relapsing–Remitting Multiple Sclerosis. Neurol. Int. 2021, 13, 240-251. https://0-doi-org.brum.beds.ac.uk/10.3390/neurolint13020025

AMA Style

Kahovec C, Saini A, Levin MC. Diagnostic Dilemma: An Atypical Case of Astrocytoma in a Patient with Relapsing–Remitting Multiple Sclerosis. Neurology International. 2021; 13(2):240-251. https://0-doi-org.brum.beds.ac.uk/10.3390/neurolint13020025

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Kahovec, Chantal, Aman Saini, and Michael C. Levin. 2021. "Diagnostic Dilemma: An Atypical Case of Astrocytoma in a Patient with Relapsing–Remitting Multiple Sclerosis" Neurology International 13, no. 2: 240-251. https://0-doi-org.brum.beds.ac.uk/10.3390/neurolint13020025

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