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. 2023 Apr;29(4-5):637-641.
doi: 10.1177/13524585221149886. Epub 2023 Jan 26.

Should trigeminal neuralgia be considered a clinically isolated syndrome?

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Should trigeminal neuralgia be considered a clinically isolated syndrome?

Sarasa Tohyama et al. Mult Scler. 2023 Apr.

Abstract

The association between trigeminal neuralgia (TN) and multiple sclerosis (MS) is well established. Many MS patients with TN have magnetic resonance imaging (MRI) evidence of a symptomatic demyelinating lesion. Although infratentorial presentations are included in the diagnostic criteria for MS, there remains confusion in clinical practice as to whether TN should be considered a clinically isolated syndrome for the application of McDonald criteria. In this case series, we discuss this diagnostic quandary in patients presenting with TN and additional MRI findings suggestive of MS and highlight the unmet need for data in such patients to optimally guide their care.

Keywords: MRI; Trigeminal neuralgia; clinically isolated syndrome; diagnosis; diagnostic criteria; lesion; multiple sclerosis.

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Conflict of interest statement

The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: A.J.S.: Consulting or Advisory Boards: EMD Serono, Genentech, Biogen, Alexion, Celgene, Greenwich Biosciences, TG Therapeutics, Octave Bioscience. Non-Promotional Speaking: EMD Serono. Research Funding: Bristol Myers Squibb and Biogen. Contracted Research: Sanofi, Biogen, Novartis, Actelion, Genentech/Roche. Medicolegal consultations including expert witness testimony. J.O.: Consulting or speaking from Biogen-Idec, BMS, EMD Serono, Novartis, Roche, Sanofi-Genzyme, and Alexion. Research funding: Biogen-Idec, Roche, and EMD-Serono. S.T., M.T., J..C.C., A.H., D.J.M., M.H.: No COI to declare.

Figures

Figure 1.
Figure 1.
Magnetic resonance imaging sequences demonstrating demyelinating lesions characteristic of MS. Left column: axial T2-FLAIR MRI demonstrating periventricular lesions (a, b) and axial T1-weighted FSPGR MRI demonstrating a left-sided pontine lesion presumed responsible for TN (c) in Case 1. Middle column: axial T2-FLAIR MRI demonstrating periventricular lesions (d, e) and axial T1-weighted FSPGR MRI demonstrating infratentorial lesions (f, g), with the left-sided lesion (g) presumed responsible for TN in Case 2. Right column: axial T2-weighted and sagittal T1-FLAIR MRI demonstrating periventricular lesions (h, i), axial T1-weighted FSPGR MRI demonstrating a juxtacortical lesion (j), and axial T2-weighted MRI demonstrating the pontine lesion presumed responsible for TN (k) and spinal cord (l) lesions in Case 3. FLAIR: fluid-attenuated inversion recovery; FSPGR: fast spoiled gradient-echo.

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