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Abstract Details

Two Cases with Acute Tumefactive non enhancing Demyelinating lesions; The Significance of Gadolinium Contrast enhancement in MRI
Multiple Sclerosis
P13 - Poster Session 13 (5:30 PM-6:30 PM)
9-013

Most of the acute tumefactive demyelinating lesions(TDLs) are enhancing with gadolinium on MRI. Here we report two unique cases of acute symptomatic non-enhancing TDLs.

Tumefactive multiple sclerosis is a rare form of demyelination, typically presenting as large lesions (>2cm) with associated vasogenic edema that can mimic tumors.

First case is a 34 year-old female admitted with right sided weakness and numbness for two days. She had mild transient left sided weakness two months prior to admission that resolved spontaneously. MRI showed diffusion restriction in the left parietal region and increased FLAIR signal in the right frontal and occipital regions. Workup revealed elevated CSF oligoclonal bands(OCB) and myelin basic protein(MBP) in addition to abnormal right eye visual evoked potential.

Second case is a 22 year-old female admitted with three days of progressive right sided weakness. MRI showed large right frontoparietal lesion, abnormal diffusion and no gadolinium enhancement. Workup showed elevated CSF MBP and OCB.

The two patients had a similar clinical course, and their symptoms improved rapidly with 5 days of intravenous steroids. Repeat MRI showed resolution of the mass effect; however, both patients’ symptoms recurred in one month, and plasmapharesis was initiated after which MRI improved with no recurrence of symptoms.

TDLs biospy shows typical demyelination as in Multiple sclerosis lesions but they have unique hypercellularity, astrocytic pleomorphism and mitotic figure. Acute demyelinating lesions typically enhance due to blood brain barrier breakdown resulting in leakage of gadolinium contrast into the lesion; however, no enhancement seen in our cases. We hypothesize that lack of enhancement with abnormal diffusion restriction is associated with less inflammation, more vasogenic edema causing the presenting symptoms that usually improve rapidly with steroids, good response to plasmapharesis and maybe lower risk to develop MS. The significance of this finding remains uncertain and requires further study.
Authors/Disclosures
Faisal A. Ibrahim, MD (Cleveland Clinic Foundation)
PRESENTER
Dr. Ibrahim has nothing to disclose.
Syed Rizvi, MD (Neurology Foundation) Dr. Rizvi has received personal compensation in the range of $500-$4,999 for serving as a Consultant for Serono Roche Bristol Myers . Dr. Rizvi has received personal compensation in the range of $5,000-$9,999 for serving as an Expert Witness for Na.
No disclosure on file
Joshua Battley, MD (UT Southwestern Medical Center) Dr. Battley has nothing to disclose.
Arooj Kohli, MD (University of Chicago) Dr. Kohli has nothing to disclose.
James M. Gilchrist, MD, FÂé¶¹´«Ã½Ó³»­ (Southern Illinois University School of Medicine) Dr. Gilchrist has received publishing royalties from a publication relating to health care.