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Research Letter
July 2018

Novel Glial Targets and Recurrent Longitudinally Extensive Transverse Myelitis

Author Affiliations
  • 1Department of Neurology, Mayo Clinic, Rochester, Minnesota
  • 2Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, Minnesota
  • 3Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, Minnesota
JAMA Neurol. 2018;75(7):892-895. doi:10.1001/jamaneurol.2018.0805

A 2014 study1 reported that autoimmune aquaporin 4 (AQP4) channelopathy was the most common cause of immune-mediated recurrent longitudinally extensive transverse myelitis (rLETM), with seropositivity in 42 of 47 cases (89%). Autoimmune myelin oligodendrocyte glycoproteinopathy (MOG-opathy) with serum antibodies targeting MOG (MOG-IgG) has recently been reported in AQP4-IgG seronegative longitudinally extensive transverse myelitis (LETM).2 Another autoimmune astrocytopathy with glial fibrillary acidic protein (GFAP-IgG) as a biomarker may include myelitis sometimes longitudinally extensive as a component of a meningoencephalomyelitis.3 We present additional serological data with regard to 2 novel glial targets (MOG and GFAP) in patients with rLETM.

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