LAUSR

DOI:10.1097/WCO.0000000000000442 Most neurologists would agree that the characterization of central nervous system (CNS) disorders associated with antibodies against synaptic receptors represents one of the major advances in clinical neurology in the last 10 years with practical implications in the management and treatment of patients with encephalitis, epilepsy, and other neurological syndromes [1]. Since the initial characterization of the encephalitis associated with N-Methyl-D-aspartate (NMDA) receptor (NMDAR) antibodies, more than 10 CNS syndromes and antibodies against different synaptic receptors or other neuronal surface antigens have been identified [2]. The study of these syndromes indicates that the pathophysiological mechanism of brain damage is not homogeneous albeit most of them are probably antibody-mediated. In addition, the knowledge generated goes beyond the field of autoimmune neurology and redefines our understanding of particular psychiatric syndromes and how cancer or viral CNS infections interplay with the immune system to lastly induce an autoimmune attack to the brain. In the current section of Current Opinion of Neurology, leading experts in the field of autoimmune neurology update our knowledge in these issues, confirming these are exciting times for the research that is expanding the spectrum of inflammatory CNS disorders. Although we did not pretend to include in this section inflammatory disorders mainly targeting the white matter, we considered it pertinent to include a review, done by Markus Reindl et al., (pp. 295–301) on the clinical use of myelin oligodendrocyte glycoprotein (MOG) antibodies. In our opinion, the inclusion of this topic is relevant for two reasons: MOG antibodies are reported in more than 50% of children with acute demyelinating encephalomyelitis (ADEM) [3]. Patients with ADEM are frequently considered in the differential diagnosis of autoimmune encephalitis and that associated with GABAa receptor antibodies may show similar MRI findings than those seen in ADEM [4]. Second, the spectrum of neurological syndromes associated with MOG antibodies is expanding as demonstrated by the recent description of patients with unilateral cortical encephalitis presenting with epilepsy [5].