A giant MS plaque mimicking PML during natalizumab treatment

Twyman, Cary; Berger, Joseph R.

doi:10.1016/j.jns.2010.01.001

Cited by 13 publications

(7 citation statements)

References 12 publications

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“…However, recently, reports of patients receiving natalizumab for MS have been identified with PML. 5 Similar to the clinical presentation in our case, the sudden onset of marked cognitive impairment has been associated with the development of PML and rapidly progressing MS. 5 Contrast enhancement in PML is considered unusual, however, nearly 10% of patients with PML will have some contrast enhancement. 5 These features can make the differential between MS and PML difficult.…”

Section: Discussionsupporting

confidence: 82%

The Development of Primary Central Nervous System B-Cell Lymphoma in Multiple Sclerosis

Lyons

Boucher

Birch

et al. 2011

The Neurohospitalist

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When coupled with classical clinical signs and symptoms, magnetic resonance imaging can significantly aid in the diagnosis of multiple sclerosis (MS). However, the differential diagnosis of multiple sclerosis is large and, in the absence of pathognomonic clinical features, can be challenging to diagnose initially. Some conditions, such as primary central nervous system lymphoma (PCNSL) and progressive multifocal leukoencephalopathy (PML), can mimic clinically some of the symptoms prominent in multiple sclerosis. Early treatment with corticosteroids can dramatically improve patient symptoms in MS and PCNSL. We report a case of a man diagnosed with histologically confirmed relapsing remitting multiple sclerosis who subsequently developed histologically confirmed primary central nervous system lymphoma. Immunosuppressant therapy in the treatment of multiple sclerosis may be a potential catalyst in the development of central nervous system lymphoma. The course of his disease and treatment are presented and the current literature reviewed.

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Section: Discussionsupporting

confidence: 82%

The Development of Primary Central Nervous System B-Cell Lymphoma in Multiple Sclerosis

Lyons

Boucher

Birch

et al. 2011

The Neurohospitalist

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“…On the other hand, TDLs have been frequently reported in patients with MS and NMO undergoing treatment with Natalizumab or more commonly after withdrawal of it, which justifies more cautious usage of Natalizumab in TDLs (Barnett et al, 2012;Berger, 2008;Beume et al, 2014;Borriello et al, 2011;Fox et al, 2014;Grimaldi et al, 2012;Jokubaitis et al, 2014;O'Connor et al, 2011;Twyman and Berger, 2010;Vellinga et al, 2008). There is also the additional concern that a TDL arising in an individual taking Natalizumab, and now Fingolimod and dimethyl fumarate as well, could indicate the presence of PML -a clear indication for the rapid discontinuation of that MS treatment.…”

Section: Disease Modifying Therapymentioning

confidence: 99%

Neuro-oncology dilemma: Tumour or tumefactive demyelinating lesion

Abdoli

Freedman

2015

Multiple Sclerosis and Related Disorders

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Tumefactive demyelinating lesions (TDLs) are not an uncommon manifestation of demyelinating disease but can pose diagnostic challenges in patients without a pre-existing diagnosis of multiple sclerosis (MS) as well as in known MS patients. Brain tumours can also arise in MS patients and can be seen in chronic MS patients as co-morbidities. Delayed diagnosis or unnecessary intervention or treatment will affect the ultimate prognosis of these patients. In this article, we will review some typical cases illustrating the dilemma and review the information that helps to differentiate the two conditions. The intention is not to present an extensive differential diagnosis of both entities, but to examine some typical examples when the decision arises to decide between the two. We take a somewhat different approach, by presenting the cases in "real time", allowing the readers to consider in their own minds which diagnosis they favour, discussing in detail some of the pertinent literature, then revealing later the actual diagnosis. We would urge readers to consider re-visiting their first thoughts about each case after reading the discussion, before reading the follow-up of each case. The overall objective is to highlight the real possibility of being forced to decide between these two entities in clinical practise, present a reasonable approach to help differentiate them and especially to focus on the possibility of TDLs in order to avoid unnecessary biopsy.

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“…[6][7][8][9] There are limited cases describing the presence of large demyelinating lesions with an aggressive clinical presentation during natalizumab therapy that were not progressive multifocal leukoencephalopathy (PML). [8][9][10] Moreover, various pathological entities such as atypical MS variants (Marburg's type, Balo's concentric sclerosis, Schilder's disease, and acute disseminated encephalomyelitis) have been shown to present with tumefactive lesions, with overlapping clinical presentation, and distinct immunological signatures. [11][12][13] Nevertheless, it is still controversial whether tumefactive CNS lesions represent a variant of MS or a unique form of an idiopathic isolated demyelinating disease.…”

Section: Introductionmentioning

confidence: 99%

Clinico-radiologic features and therapeutic strategies in tumefactive demyelination: a retrospective analysis of 50 consecutive cases

Vakrakou

Tzanetakos

Evangelopoulos

et al. 2021

Ther Adv Neurol Disord

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Aims: Our goal was to expand the spectrum of clinico-radiologic characteristics and the possible therapeutic choices in patients with tumefactive demyelinating lesions (TDLs). Methods: A retrospective analysis of 50 patients with at least one TDL was performed at an academic neurology center (2008–2020). Results: Our cohort comprised mostly women (33/50) with a mean age of 38 years at TDL onset. The mean follow-up time was 76 months. The mean Expanded Disability Status Scale score at TDL onset and at the latest neurological evaluation was 3.7 and 2.3, respectively. We subcategorized the patients into seven groups based mainly on the clinical/radiological findings and disease course. Group A included patients presenting with a Marburg-like TDL ( n = 4). Groups B and C comprised patients presenting with monophasic ( n = 7) and recurrent TDLs ( n = 12), respectively. Multiple sclerosis (MS) patients who subsequently developed TDL ( n = 16) during the disease course were categorized as Group D. Group E comprised patients who initially presented with TDL and subsequently developed a classical relapsing–remitting MS without further evidence of TDL ( n = 5). Groups F ( n = 2) and G ( n = 4) involved MS patients who developed TDL during drug initiation (natalizumab, fingolimod) and cessation (interferon, fingolimod), respectively. Regarding long-term treatments applied after corticosteroid administration in the acute phase, B-cell-directed therapies were shown to be highly effective especially in cases with recurrent TDLs. Cyclophosphamide was spared for more aggressive disease indicated by a poor response to corticosteroids and plasma exchange failure. Conclusion: Tumefactive central nervous system demyelination is an heterogenous disease; its stratification into distinct groups according to different phenotypes can establish more efficient treatment strategies, thus improving clinical outcomes in the future.

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A giant MS plaque mimicking PML during natalizumab treatment

Cited by 13 publications

References 12 publications

The Development of Primary Central Nervous System B-Cell Lymphoma in Multiple Sclerosis

The Development of Primary Central Nervous System B-Cell Lymphoma in Multiple Sclerosis

Neuro-oncology dilemma: Tumour or tumefactive demyelinating lesion

Clinico-radiologic features and therapeutic strategies in tumefactive demyelination: a retrospective analysis of 50 consecutive cases

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