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NEUROLOGY 2005;64:1290-1293
© 2005 American Academy of Neurology
Brief Communications

Sequential antibodies to potassium channels and glutamic acid decarboxylase in neuromyotonia

C. Antozzi, MD*, C. Frassoni, PhD*, A. Vincent, FRCPath, M. C. Regondi, PhD, F. Andreetta, PhD, P. Bernasconi, PhD, C. Ciano, MD, T. Chang, MD, F. Cornelio, MD, R. Spreafico, MD and R. Mantegazza, MD

From the Neurology Department IV (Drs. Antozzi, Andreetta, Bernasconi, Cornelio, and Mantegazza), Immunology and Muscular Pathology Unit, Experimental Neurophysiology Unit (Drs. Frassoni, Regondi, and Spreafico), and Clinical Neurophysiology Unit (Dr. Ciano), National Neurological Institute "Carlo Besta," Milan, Italy; and Neurosciences Group (Drs. Vincent and Chang), Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, Oxford, UK.

Address correspondence and reprint requests to Dr. C. Antozzi, Neurology Department IV, Immunology and Muscular Pathology Unit, National Neurologic Institute "Carlo Besta," Via Celoria 11, 20133, Milan, Italy; e-mail: antozzi{at}istituto-besta.it

A patient with thymoma-associated neuromyotonia and voltage-gated potassium channel (Kv1.2 and Kv1.6) antibodies by immunoprecipitation and rat brain immunolabeling was treated successfully with immunoadsorption and cyclophosphamide. Curiously, glutamic acid decarboxylase antibodies, absent at onset, appeared later. Stiff-person syndrome was absent, but fast blink reflex recovery suggested enhanced brainstem excitability. The range of antibodies produced in thymoma-associated neuromyotonia is richer, and the timing of antibody appearance more complex, than previously suspected.

*These authors contributed equally to this work.

Supported in part by MURST (project no. 2003068749).

Received June 30, 2004. Accepted in final form December 27, 2004.




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