Tumefactive Multiple Sclerosis Research Articles

Population-based incidence and clinico-radiological characteristics of tumefactive demyelination in Olmsted County, Minnesota, United States.

Tumefactive demyelination (TD) presents with large inflammatory lesions mimicking tumors or other space-occupying lesions. Limited epidemiological, clinical and radiological data exist for TD. We aimed to report the incidence rate, and clinical and radiological features of TD in Olmsted County, Minnesota. We retrospectively reviewed patients with central nervous system inflammatory demyelination-related diagnostic codes (January 1, 1998 to December 31, 2018) in the Rochester Epidemiology Project database, and adjusted incidence rates by age and sex to the 2010 US total population. We used the Expanded Disability Status Scale (EDSS) to assess outcomes (index attack and last follow-up). Of 792 multiple sclerosis (MS) patients, 15 (eight males, seven females) had tumefactive MS, representing 1.9% of the MS population. The median (range) age at attack onset was 34.2(2-61) years. Tumefactive lesion was the first clinical MS attack in 8/16 patients. Cerebrospinal fluid oligoclonal bands (OCBs) were present in 8/12 patients and 11/16 patients met the Barkhof criteria for dissemination in space. Most patients remained fully ambulatory (EDSS score ≤4 in 13/16 patients [81%]) after a median (range) follow-up duration of 10.5(1-20.5) years. Age-adjusted annual incidence rates were 0.46/100,000 (95% confidence interval [CI] 0.12-0.81) for female patients, 0.66/100,000 (95% CI 0.23-1.02) for male patients, and 0.56/100,000 [95% CI 0.28-0.83] overall. When age- and sex-adjusted to the 2010 US total population, the overall annual incidence rate was 0.57 (95% CI 0.28-0.84). Despite aggressive clinical presentation at disease onset, most patients remained fully ambulatory (EDSS score ≤4 in 13/16 patients) with a relapsing-remitting course. Although incidence is rare, TD should be suspected in patients presenting with subacutely progressive neurological deficits associated with magnetic resonance imaging findings of ring enhancement, apparent diffusion coefficient restriction, and OCB on spinal fluid analysis.

Anti‐myelin oligodendrocyte glycoprotein antibody‐associated disease presenting tumefactive demyelinating lesions and bilateral optic neuritis with chiasmatic lesion

AbstractA 15‐year‐old girl presented with a headache accompanied by bilateral visual impairment. Brain magnetic resonance imaging showed tumefactive lesions in the white matter of the right occipital lobe on fluid‐attenuated inversion recovery images accompanied by open‐ring gadolinium enhancement and high‐intensity lesions in the bilateral optic nerve, including chiasma. Since anti‐myelin oligodendrocyte glycoprotein (MOG) antibody was detected by blood examination, the patient was diagnosed with anti‐MOG antibody‐associated disease (MOGAD) exhibiting overlapping characteristics with tumefactive multiple sclerosis (MS) and neuromyelitis optica spectrum disorders (NMOSDs). Steroid pulse therapy and plasma exchange therapy completely improved her symptoms, and oral prednisolone therapy prevented relapse of the disease for at least 2 years. Since MOGAD exhibits overlapping characteristics with MS and NMOSD, it is important to screen anti‐MOG antibodies in patients with atypical MS and seronegative NMOSD.

Long-term clinical, MRI, and cognitive follow-up in a large cohort of pathologically confirmed, predominantly tumefactive multiple sclerosis

Background: Limited studies have described long-term outcomes in pathology confirmed multiple sclerosis (MS). Objectives: To describe long-term clinical–radiographic–cognitive outcomes in a prospectively followed cohort of patients with pathologically confirmed CNS demyelinating disease, consistent with MS. Methods: Subjects underwent clinical assessment, standardized 3T-MRI brain, and cognitive battery. Results: Seventy-five patients were included. Biopsied lesion size was ⩾ 2 cm in 62/75. At follow-up, median duration since biopsy was 11 years. Median EDSS was 3 and lesion burden was large (median 10 cm3). At follow-up, 57/75 met MS criteria, 17/75 had clinically isolated syndrome, and 1 radiographic changes only. Disability scores were comparable to a prevalence cohort in Olmsted County (p < 0.001, n = 218). Cognitive outcomes below age-normed standards included psychomotor, attention, working memory, and executive function domains. Total lesion volume and index lesion-related severity correlated with EDSS and cognitive performance. Volumetric cortical/subcortical GM correlated less than lesion metrics to cognitive outcomes. Conclusion: Despite early aggressive course in pathologically confirmed MS, its long-term course was comparable to typical MS in our study. Cognitive impairment in this group seemed to correlate strongest to index lesion severity and total lesion volume. It remains to be established how the aggressive nature of the lesion, biopsy, and treatment affect clinical/cognitive outcomes.

A case of recurrent tumefactive demyelination or tumefactive multiple sclerosis

The Journal is the primary organ of Continuing Paediatric Medical Education in Sri Lanka. The journal also has a website. Free full text access is available for all readers.The Sri Lanka Journal of Child Health is now indexed in SciVerse Scopus (Source Record ID 19900193609), Index Medicus for South-East Asia Region (IMSEAR), CABI (Centre for Agriculture and Bioscience International Global Health Database), DOAJ and is available in Google, as well as Google Scholar.The policies of the journal are modelled on the Committee on Publication Ethics (COPE) Guidelines on Principles of Transparency and Best Practice in Scholarly Publishing. Sri Lanka Journal of Child Health is recognised by the International Committee of Medical Journal Editors (ICMJE) as a publication following the ICMJE Recommendations.

Tumefactive multiple sclerosis versus high-grade glioma: A diagnostic dilemma.

Background: Tumefactive demyelinating lesions (TDLs) share similar clinical features and MRI characteristics with high-grade glioma (HGG). This study develops an approach to navigating this diagnostic dilemma, with significant treatment implications as the management of both entities is drastically different.Methods: A retrospective analysis of 41 TDLs and 91 HGG with respect to demographics, presentation, and classical MRI characteristics was performed. A diagnostic pathway was then developed to help diagnose TDLs based on whole neuraxis MRI and cerebrospinal fluid (CSF) examination.Results: The diagnosis of TDL is more likely than HGG in younger females who present with subacute or chronic symptoms. MRI characteristics favoring TDL over HGG include smaller size, open rim enhancement, little or no associated edema or mass effect, and the presence of a T2 hypointense rim. MRI of the whole neuraxis for detection of other lesions typical of multiple sclerosis (MS), in combination with a lumbar puncture (LP) showing positive CSF-specific oligoclonal bands (OCB), was positive in 90% of the TDL cohort.Conclusion: The diagnostic pathway, proposed on the basis of specific clinicoradiological features, should be followed in patients with suspected TDL. If MRI demonstrates other lesions typical of MS and LP demonstrates positive CSF-specific OCBs, then patients should undergo a short course of IV steroids to look for clinical improvement. Patients who continue to deteriorate, do not demonstrate other lesions on MRI or where the LP is negative for CSF-specific OCB, should be considered for biopsy if safe to do so. This pathway will give the patients the best chance at neurological preservation.

A false-positive case on brain 18F-Choline PET/MR due to tumefactive multiple sclerosis. A case report

A false-positive case on brain 18F-Choline PET/MR due to tumefactive multiple sclerosis. A case report

Imaging Mimics: A Case of Nearly Mistaken Identity with Tumefactive Multiple Sclerosis and X-linked Adrenoleukodystrophy (5135)

Imaging Mimics: A Case of Nearly Mistaken Identity with Tumefactive Multiple Sclerosis and X-linked Adrenoleukodystrophy (5135)

Abstract PO-023: Differentiation of tumefactive multiple sclerosis and glioblastoma using radiomics features extracted from magnetic resonance imaging and machine learning

Abstract Introduction Tumefactive multiple sclerosis (MS) and glioblastoma (GBM) can be difficult to differentiate. Clinical presentations are nonspecific and may occur in patients with both diseases. Magnetic resonance imaging (MRI) scans are routinely used to generate an initial differential diagnosis. Although imaging features can help distinguish these entities, there are no pathognomonic signs, neither on traditional nor advanced MRI. Moreover, the ability to differentiate these entities depends on the radiologists’ experience. Ensuring the correct diagnosis has important therapeutic and prognostic implications, as the management of these diseases is very different. To date, a brain biopsy often represents the only option to obtain a diagnosis, but it may be inconclusive and could add unnecessary morbidity. We hypothesize that a machine-learning tool based on routinely performed MRI scans could guarantee a more reliable, fast, and reproducible diagnosis. Methods Only patients with a histological diagnosis were included in the study. Patients that underwent any form of radiation therapy before the surgery were excluded to avoid confounding factors due to treatment-related effects. A total of 99 MS and 257 GBMs were included, and preoperative T2-weighted images were collected. For each patient, the lesions' segmentation was performed, including both the contrast-enhancing and non-enhancing areas of the lesions. The segmentation masks were used to extract radiomic features from the T2-weighted sequences. All MRI images were standardized to the same mean and standard deviation before feature extraction and resampled to a voxel size of 1.0 × 1.0 × 1.0 mm. Features extraction was performed using Pyradiomics (v. 3.0.1) and included first order, shape, and texture features, totaling 100 features. The classifier consisted of a support vector machine (SVM) model. Patients were randomly assigned to the training and test sets with an 80-20% proportion for each class. To select the best hyperparameters for the SVM classifier, a grid-search analysis was performed on the training set using a nested cross-validation scheme (k=5). All experiments were performed using Python (v. 3.5) and the Scikit-learn library (v. 0.23.1). Results The mean accuracy and area under the ROC curve for the best set of hyperparameters on the validation set were 0.83 and 0.86, respectively. The weighted-average precision, recall, and F1 scores on the test set were 0.78, 0.76, and 0.77, respectively. Conclusions Radiomic features extracted from a routinely acquired MRI sequence showed promising results in differentiating tumefactive multiple sclerosis from glioblastoma, opening the possibility to obtain a reliable diagnosis without the need for a brain biopsy. Future experiments Future experiments will focus on using post-contrast T1-weighted images for the radiomic features extractions, testing multiple machine learning models and features selection algorithms, and including more diagnostic classes (i.e., metastasis, lymphomas). Citation Format: Gian Marco Conte, Jeanette E. Eckel-Passow, W. Oliver Tobin, Paul Decker, Daniel H. Lachance, Robert B. Jenkins, Bradley J. Erickson. Differentiation of tumefactive multiple sclerosis and glioblastoma using radiomics features extracted from magnetic resonance imaging and machine learning [abstract]. In: Proceedings of the AACR Virtual Special Conference on Artificial Intelligence, Diagnosis, and Imaging; 2021 Jan 13-14. Philadelphia (PA): AACR; Clin Cancer Res 2021;27(5_Suppl):Abstract nr PO-023.

Defining the course of tumefactive multiple sclerosis: A large retrospective multicentre study.

Tumefactive multiple sclerosis (TuMS) (i.e., MS onset presenting with tumefactive demyelinating lesions [TDLs]) is a diagnostic and therapeutic challenge. We performed a multicentre retrospective study to describe the clinical characteristics and the prognostic factors of TuMS. One hundred two TuMS patients were included in this retrospective study. Demographic, clinical, magnetic resonance imaging (MRI), laboratory data and treatment choices were collected. TuMS was found to affect women more than men (female:male: 2.4), with a young adulthood onset (median age: 29.5years, range: 11-68 years, interquartile range [IQR]: 38 years). At onset, 52% of TuMS patients presented with the involvement of more than one functional system and 24.5% of them with multiple TDLs. TDLs most frequently presented with an infiltrative MRI pattern (38.7%). Cerebrospinal fluid immunoglobulin G oligoclonal bands were often demonstrated (76.6%). In 25.3% of the cases, more than one acute-phase treatment was administered, and almost one-half of the patients (46.6%) were treated with high-efficacy treatments. After a median follow-up of 2.3years (range: 0.1-10.7 years, IQR: 3.4 years), the median Expanded Disability Status Scale (EDSS) score was 1.5 (range: 0-7, IQR: 2). Independent risk factors for reaching an EDSS score ≥3 were a higher age at onset (odds ratio [OR]: 1.08, 95% confidence interval [CI]: 1.03-1.14, p<0.01), a higher number of TDLs (OR: 1.67, 95% CI: 1.02-2.74, p<0.05) and the presence of infiltrative TDLs (OR: 3.34, 95% CI: 1.18-9.5, p<0.001) at baseline. The management of TuMS might be challenging because of its peculiar characteristics. Large prospective studies could help to define the clinical characteristics and the best treatment algorithms for people with TuMS.

Oral Cladribine is Effective in the Treatment of Tumefactive Demyelination in Relapsing Remitting Multiple Sclerosis – A Case Report

This case report describes a 32-year old Emirati patient with tumefactive multiple sclerosis (TMS) treated with a short course of cladribine tablets. The patient presented initially with acute onset of progressive gait unsteadiness, lower limb weakness, associated with numbness of four days duration. Neurological examination of right arms and both legs weakness with sensory level at T10. Contrast-enhanced magnetic resonance imaging (MRI) of the brain showed a large tumefactive demyelination with multiple demyelinating lesions in the brain, consistent with a diagnosis of multiple sclerosis. MRI of the spine cervical and dorsal revealed multiple enhancing lesions as well. Cerebrospinal fluid oligoclonal bands were positive, and IgG index was high. Magnetic resonance spectroscopy showed elevation of lactate on short echo time (TE) and elevation of choline on long TE. The patient was treated with pulse steroid followed by oral cladribine as immune reconstitution therapy in the acute phase. The patient showed significant improvement clinically and radiologically to the treatment. The patient was followed up for 2 years and showed excellent resolution of the tumefactive lesion with no new lesions. Immune reconstitution therapy can be an option for treatment of tumefactive demyelination in multiple sclerosis in the acute setting. To our knowledge, there are no reports of the use of immune reconstitution therapies for the treatment of tumefactive lesions in multiple sclerosis.

Tumefactive multiple sclerosis (TMS): A case series of this challenging variant of MS

BackgroundTumefactive MS is a rare variant of multiple sclerosis that poses a diagnostic and a therapeutic challenge due to its close resemblance to central nervous neoplasms on MRI. TMS is defined as acute large >2 cm, tumour like demyelinating lesion in the CNS that may occur with surrounding edema, mass effect and ring enhancement. Some of the known mimickers are CNS lymphoma, metastasis, primary brain tumour such as glioblastoma, brain abscesses. The prevalence of TMS is estimated to be 1-3/1000 cases. There are also reported cases of drug induced TMS cases especially with fingolimod and natalizumab therapy. We report the occurrence of tumefactive MS at our institution. MethodsWe retrospectively reviewed the chart of the patients with multiple sclerosis including initial visits, hospitalizations, clinic follow up notes and collected data on demographic, ethnicity, presenting signs and symptoms, imaging modalities, cerebrospinal fluid analysis results, disease progression. After reviewing the charts, we isolated the patients with tumefactive multiple sclerosis from the group and summarized the cases. Four of these patients were managed with Glatiramer acetate, 2 on dimethyl fumarate and 1 on beta interferon with 0-2 clinical flare ups on subsequent years. ResultsOut of 323 patients reviewed with multiple sclerosis or possible multiple sclerosis, 7 carried a diagnosis of tumefactive MS. The age range of these patients were 19 to 62 years old with 4 females and 3 males. Five patients were Caucasian and 2 were Hispanic. Out of seven patients, 6 were newly diagnosed MS following biopsy of the lesion. The histological findings in 3 patients who underwent biopsy demonstrated include reactive gliosis and inflammatory cells predominantly macrophages and lymphocytes while 1 patient showed hypercellular brain tissue with perineuronal satellosis. ConclusionTumefactive MS remains a challenging disease to diagnosis and often times requires a biopsy for definitive diagnosis or to exclude neoplasms, other inflammatory conditions such as neurosarcoidosis. The demographic of the patients in this case series is no different than patients with relapsing remitting multiple sclerosis (RRMS). However, based on our experience, the patients with TMS do respond to disease modifying agents such as Glatiramer acetate and Dimethyl fumarate with similar progression as of RRMS.

Cyclophosphamide in treatment of tumefactive multiple sclerosis

Objective. To review the Mayo clinic experience of cyclophosphamide in the treatment of tumefactive Multiple Sclerosis (TMS). Methods. Retrospective chart review was performed to identify patients with TMS who did not respond to corticosteroid and plasma exchange and were treated with cyclophosphamide. Demographic, clinical, treatment, and outcome parameters were collected. Results. We identified 12 patients with TMS who were treated with cyclophosphamide. Median follow-up was 17 (range 1-72) months after cyclophosphamide administration. The tumefactive attack was the first clinical symptom in 5/12 patients. The median age at index attack onset was 36 (range 22-57). The median age at the first demyelinating attack was 29.3 (range 20-55). The most common clinical presentation at the index attack was the visual disturbance, followed by motor symptoms. The index attack was accompanied by headache in 5/12 patients. Median attack related Expanded Disability Status Scale (EDSS) score was 6 (range 3-9.5), which improved to 5.25 (range 1-10) after treatment with cyclophosphamide. All patients were treated with corticosteroids and plasma exchange prior to treatment with cyclophosphamide. EDSS score improved in 8/12 patients and targeted neurological deficits improved to a moderate or marked degree in 9/12 patients after cyclophosphamide administration. The number of gadolinium enhancing lesions decreased in 10/12 and 8/12 patients had lack of disease activity (no new T2 or GAD lesions) in a median (range) time of 11 months (1-16) after the last dose of cyclophosphamide. Conclusion. Cyclophosphamide could be an effective option for the treatment of TMS, refractory to corticosteroids and plasmapheresis, and is associated with improvement of clinical and radiological disease activity.

Case Report: A Case of Severe Clinical Deterioration in a Patient With Multiple Sclerosis.

Tumefactive multiple sclerosis (MS) is a rare variant of MS that may lead to a rapidly progressive clinical deterioration requiring a multidisciplinary diagnostic workup. Our report describes the diagnostic and therapeutic approach of a rare and extremely severe course of MS. A 51-year-old man with an 8-year history of relapsing-remitting MS (RRMS) was admitted with a subacute progressive left lower limb weakness and deterioration of walking ability. After extensive investigations including repeated MRI, microbiological, serological, cerebrospinal fluid (CSF) studies, and finally brain biopsy, the diagnosis of a tumefactive MS lesion was confirmed. Despite repeated intravenous (IV) steroids as well as plasma exchanges and IV foscarnet and ganciclovir owing to low copy numbers of human herpesvirus 6 (HHV-6) DNA in polymerase chain reaction (PCR) analysis, the patient did not recover. The clinical presentation of tumefactive MS is rare and variable. Brain biopsy for histopathological workup should be considered in immunocompromised patients with rapidly progressive clinical deterioration with brain lesions of uncertain cause.

TSPO PET With 18F-GE-180 to Differentiate Variants of Multiple Sclerosis: Relapsing-Remitting Multiple Sclerosis, Tumefactive Demyelination, and Baló's Concentric Sclerosis.

PET targeting the translocator protein (TSPO) expression is an interesting approach to detect neuroinflammation, as TSPO is upregulated in activated macrophages and microglia. Considering the variable pathophysiology of multiple sclerosis (MS) variants, we compare TSPO PET using F-GE-180 in 3 different demyelinating diseases of the central nervous system: relapsing-remitting MS, tumefactive MS, and Baló's concentric sclerosis. Visualization of neuroinflammation and its PET patterns in addition to MRI may contribute to accurate distinction and monitoring of central nervous system demyelination.

Tumefactive multiple sclerosis in association with fingolimod initiation and discontinuation

Background: Tumefactive multiple sclerosis (TMS) is a rare multiple sclerosis (MS) form that usually manifests as the initial presentation or in the early stages of MS. Objective: The aim of this study is to evaluate reports of TMS associated with fingolimod use. Methods: The Food and Drug Administration (FDA) Adverse Event Reporting System (FAERS) database and the medical literature were searched for cases of TMS occurring during or after fingolimod treatment. Results: We identified 29 TMS cases, 19 following fingolimod initiation and 10 following fingolimod discontinuation. In these cases, a TMS diagnosis occurred at a median of 7 years after MS diagnosis, and a median of 7 and 3 months following initiation and discontinuation of fingolimod, respectively. Twenty-two cases were assessed as possible and seven as probable from a causal association perspective. A much larger crude number of TMS reports was observed for fingolimod compared to other disease-modifying therapies. Conclusion: TMS should be considered when a severe or atypical MS relapse occurs shortly after fingolimod initiation or discontinuation, and should prompt imaging evaluation and appropriate treatment initiation. Prescribers’ awareness of the association between TMS and fingolimod may avoid unnecessary diagnostic procedures. In light of our findings, fingolimod (Gilenya) prescribing information was amended to include TMS in the Warnings and Precautions section.

Natural Course of Relapsing Tumefactive Multiple Sclerosis and Tumefactive Demyelinating Lesions (4193)

Natural Course of Relapsing Tumefactive Multiple Sclerosis and Tumefactive Demyelinating Lesions (4193)

Tumefactive multiple sclerosis: Emerging role of MR spectroscopy

Tumefactive multiple sclerosis (TMS) is a rare variant of multiple sclerosis (MS) comprising of large demyelinating lesions that frequently mimic intracranial neoplasm or abscess. MR Spectroscopy (MRS) is an exciting new tool to differentiate radiologically. We present three cases with TMS who were diagnosed with MRS brain. A 24-years-old male presented with sensory symptoms that resolved after steroid pulse therapy. MRI spine and brain showed lesions consistent with MS and CSF showed Oligoclonal bands. Despite disease modifying therapy, he developed new symptoms. A repeat MRI brain was static and MRS showed evidence of elevated peaks of Choline and lactate with mild reduction of NAA consistent with demyelination. A 32-years-old male came for lower limb weakness and numbness with progressive gait impairment. He had history of urinary symptoms, imbalance, dizziness, ataxia and excessive fatigue. CSF analysis was normal. MRI brain revealed multiple lesions consistent with MS along with a left frontal lesion with perilesional edema and faint rim enhancement. MRS showed elevation of lactate and choline consistent with TMS. NAA was reduced. He was started on Cladribine with good response. A 37-years-old female known to have MS, on Fingolimod, developed a new relapse. MRI brain showed a left parietal cystic lesion with no contrast enhancement along with other lesions consistent with MS. MRS of the cystic lesion shows low NAA and high Choline. She was switched to Natalizumab. MR spectroscopy may serve as a helpful diagnostic tool to differentiate TMS from other counterparts.

Usefulness of Histogram-Profile Analysis in Ring-Enhancing Intracranial Lesions

Several intracranial pathologies present as a ring-enhancing lesion on conventional magnetic resonance imaging (MRI), creating diagnostic difficulty. We studied the characteristics of the anatomical border of gadolinium enhancement on T1-weighted imaging (WI) and hypointensity on T2WI to employ a simple technique of histogram-profile analysis of MRI for differentiation of various ring-enhancing intracranial lesions. After approval from the institutional review board, preoperative MRI (T2WI, postcontrast T1WI) scans were analyzed retrospectively in 18 patients with histologically confirmed brain abscess, 66 glioblastomas, 46 brain-metastases, and 16 tumefactive multiple sclerosis (MS). T2WI and postcontrast T1WI were overlapped, and histogram-profile analysis was performed with in-house image-fusion software. The pattern of differential-peaks in histogram-profile was assessed visually. Kaplan-Meier survival analysis incorporating histogram-profile patterns was performed in patients with glioblastoma. The histogram-profile study revealed 4 distinct patterns. Pattern 1 showed no differential T2-hypointensity trough, pattern 2 had T2-hypointensity trough inside, whereas pattern 3 had T2-hypointensity trough overlapping the enhanced margin. Pattern 4 had T2-hypointensity trough immediately external to the enhanced margin. Pattern 1 was specific for tumefactive MS (93.3%), whereas pattern 4 was specific for glioblastoma (40.7%). Pattern 4 glioblastoma was subdivided into rim (T2-hypointensity ≥50% of circumference of contrast-enhanced tumor) and arc (T2-hypointensity <50% of circumference of contrast-enhanced tumor). Pattern 4 glioblastoma was further subdivided into group A (edema: T2-hyperintensity ≥50% of circumference of contrast-enhanced tumor) and group B (less edema: T2-hyperintensity <50% of circumference of contrast-enhanced tumor). Patients with pattern 3 glioblastoma (37.6%) had better survival compared with others (P= 0.0341) and pattern 4B had decreased survival compared with pattern 4A (P= 0.0001) and others (P= 0.0003). Tumefactive MS and a subset of glioblastomas show specific patterns in histogram-profile analysis. The difference in anatomical border also determines difference in survival in glioblastoma. Histogram-profile analysis is a simple and efficient technique to differentiate these pathologies.

Dominant hemisphere and upper cervical cord tumefactive multiple sclerosis in a Nigerian teenager initially misdiagnosed and managed

A 13-year old right handed Nigerian girl presented with eleven weeks history of progressive visual loss, three weeks right hemi-body weakness which progressed to quadriparesis, dysphasia, severe headache, tonic-clonic seizures, neck pain, vomiting and fever.Examination revealed Glasgow Coma Score (E4M6V2), expressive dysphasia and depressed mood. Visual Acuity was counting finger bilaterally. Neck was supple. She had global hypotonia, grade 3 hyper-reflexia and extensor Babinski bilaterally. Power was 0/5 in the right upper limb and right lower limb, 2/5 in the left lower limb and 4/5 in the left upper limb. Other examinations were unremarkable.Contrast enhanced brain MRI revealed three cystic ring enhancing masses at left fronto-parieto-occipital region, associated oedema, midline shift and C2-C4 intramedullary mass with cord oedema. The ring enhancement was incomplete towards the cortex.Following initial suspicions of cystic brain tumour with spinal cord metastasis, she had decompression biopsy. Histology was inflammatory lesion, clinically assumed to be from brain abscess. Failure of antibiotic treatment and the deteriorating neurology prompted mini-craniectomy and biopsy of the cyst wall. Final diagnosis was tumefactive multiple sclerosis. She was successfully managed with methylprednisolone. Follow-up clinical condition has been satisfactory.Keywords: TMS, cranial masses, multiple sclerosis, visual loss

The utility of proton MR spectroscopy in diagnosing B cell lymphoma.

e13536 Background: Diffuse Large B Cell Lymphoma (DLBCL) is the most common and increasingly prevalent subtype of Non-Hodgkin lymphoma in both immunocompromised and immunocompetent patients. Its pathogenesis is thought to represent rearrangements, translocations, and transformations of both the immunoglobulin heavy and light chain genes along with somatic mutations of the variable regions of these same genes. A 66-year old Caucasian male with a past medical history of smoking presented to the hospital due to concerns of mental status change, flat affect, and fronto-orbital headache for one-week duration. The patient denied any drug or substance abuse. Physical exam was diffusely normal with the exception of flat affect. Methods: Magnetic resonance spectroscopy is a noninvasive, non-ionizing diagnostic analytical technique that has been used to measure metabolic changes in brain lesions. Results: Lhermitte’s sign was negative and NIH stroke scale was calculated to be 0. CT demonstrated a 17mm frontal lobe lesion. Follow up with MRI showed three bilateral enhancing brain lesions, but no metastasis or primary tumor was seen via CT of chest, abdomen, and pelvis. Initial differential diagnosis included: Tumefactive Multiple Sclerosis, Acute Demyelinating Encephalomyelitis or CNS lymphoma. EEG did not highlight any focal or epileptiform abnormalities and lumbar puncture was negative for Creutzfeld Jacob Disease and Multiple Sclerosis. The patient was discharged with a course of intravenous steroids only to present a few weeks later with no improvement of symptoms. The patient then had proton magnetic resonance spectroscopy (MRS). MRS pattern spikes and chemical profile suggested lymphoma, which was confirmed by a brain biopsy. The patient was subsequently transferred to the University of Pennsylvania for treatment and further management. Conclusions: This case illustrates the beneficial use of MRS, as data patterns it provides compliments the clinician’s knowledge to proceed with appropriate treatment.