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Anti–N-methyl-D-aspartate-glutamic-receptor encephalitis presenting as paroxysmal exercise-induced foot weakness

Authors

  • Angelo Labate MD,

    1. Institute of Neurology University Magna Graecia, Italy
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  • Aldo Quattrone MD,

    1. Institute of Neurology University Magna Graecia, Italy
    2. Institute of Neurological Sciences, National Research Council, Italy
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  • Josep Dalmau MD, PhD,

    1. Institució Catalana de Recerca i Estudis Avançats (ICREA), Universitat de Barcelona and Institut d'Investigació Biomèdica August Pi i Sunyer (IDIBAPS), Hospital Clinic, University of Barcelona, Spain
    2. Department of Neurology, University of Pennsylvania, Philadelphia, Pennsylvania
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  • Antonio Gambardella MD

    Corresponding author
    1. Institute of Neurology University Magna Graecia, Italy
    2. Institute of Neurological Sciences, National Research Council, Italy
    • Correspondence to: Dr. Antonio Gambardella, Cattedra ed U.O. di Neurologia, Università degli Studi “Magna Graecia”, Campus Universitario Germaneto, Viale Europa, 88100 Catanzaro, Italy; a.gambardella@unicz.it

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  • Funding agencies: Supported in part by the National Institutes of Health (RO1NS077851, RO1MH094741 to J.D.), the National Cancer Institute (RO1CA089054 to J.D.), Fondo de Investigaciones Sanitarias (FIS) (11/01780 to J.D.), and Fundació la Marató de TV3 (to J.D.).

  • Relevant conflicts of interest/financial disclosures: J.D. has a research grant from Euroimmun, and receives royalties from patents for the use of Ma2 and NMDAR as autoantibody tests.

  • Full financial disclosures and author roles may be found in the online version of this article.

ABSTRACT

Background

Patients with anti-N-methyl-D-aspartate-glutamic-receptors (NMDAR) encephalitis often develop complex abnormal movements that may manifest early in the course of illness.

Methods/Results

A 17-year-old boy developed paroxysmal exercise-induced right foot weakness, without behavioral change. Two weeks later, he had hyperthermia and convulsive status epilepticus. Intravenous valproate resolved the status, but the paroxysmal episodes of right foot weakness persisted. They recurred any time he began running, without any refractory period or other triggering factors. Neurological examination between attacks was normal. Ictal video-polygraphy showed transient loss of lower limb muscle activity without any EEG changes. Results of brain MRI and extensive laboratory tests were normal. NMDAR antibodies were present in liquor and serum. No tumor was found. He was treated with intravenous methylprednisolone plus immunoglobulins with resolution of his symptoms that have not recurred at 8-month follow-up.

Conclusions

Our case enlarges the spectrum of abnormal movements as presentation of oligosymptomatic anti-NMDAR encephalitis. © 2013 Movement Disorder Society

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