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Nilufer Kale, MD; Sean J. Pittock, MD; Vanda A. Lennon, MD; Kristine Thomsen; Shanu Roemer, MD; Andrew McKeon, MD; Claudia F. Lucchinetti, MD

Arch Neurol. 2009;66(10):1298-1299.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

The pathogenic relationship between neuromyelitis optica (NMO) and multiple sclerosis (MS) continues to be debated despite mounting evidence that these are distinct entities.^1-3 The NMO-IgG, which targets the water channel protein aquaporin-4 (AQP4), is the first confirmed serum biomarker for any form of central nervous system inflammatory demyelinating disease and reliably distinguishes NMO from MS and other neurological diseases. Four immunopathological patterns (IP I-IV) have been described in early active MS lesions.⁴ Some investigators have interpreted humoral MS IP II as having an immunopathogenic link with NMO because both share complement and immunoglobulin deposition and have a greater likelihood than other forms of MS to respond favorably to plasma exchange therapy.^4-5 Here, we describe the NMO-IgG status of a cohort of patients with biopsy-proven early active lesions . . . [Full Text of this Article]

Methods


Results
Clinical Characteristics of Biopsy Cohort

NMO-IgG Status Of Biopsy MS Cohort

Comment

AUTHOR INFORMATION


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