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The discovery by Dalmau and colleagues1 less than 10 years ago that antibodies targeting the N-methyl-d-aspartate receptor (NMDAR) cause autoimmune encephalitis has had serious implications. That discovery showed us a new type of disorder, which has led to the identification of more than 10 new antibodies, each associated with a specific type of encephalitis. The finding allowed us to recognize the less strict distinction between neurology and psychiatry since most patients with anti-NMDAR encephalitis develop both neurologic and psychiatric symptoms, and both disciplines should be involved in treatment. In addition, recognition of this disorder fueled old hypotheses regarding the role of different neurotransmitters in the origin of diseases, for example, the role of the NMDAR in schizophrenia. Finally, and not the least important, anti-NMDAR encephalitis is treatable and, even in patients who are severely affected, a good outcome is often possible. Approximately 80% of patients with anti-NMDAR encephalitis achieve a good outcome,2,3 although the level remains largely unexplored, especially with respect to cognitive function.4 The focus of recent research has shifted toward determining the prognosis early in the disease and finding ways to improve the levels of good outcomes and reduce the 20% incidence of poor results.
Titulaer MJ. The Association Between Atrophy and the Prognosis of Anti-N-Methyl-d-Aspartate Receptor Encephalitis. JAMA Neurol. 2016;73(6):643–644. doi:10.1001/jamaneurol.2016.0530
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