In 2007, serum IgG autoantibodies to the NMDAR (NMDAR-Ab) were identified in subjects with an autoimmune encephalopathy responsive to immunotherapy; two thirds of whom present with psychiatric symptoms (Dalmau et al., 2007, Irani et al., 2010 and Titulaer et al., 2013). There is increasing evidence for NMDAR-hypofunction and neuroinflammation in the pathophysiology of first episode schizophrenia (Kahn and Sommer, 2014). Whilst many patients with NMDAR-ab develop a widespread encephalopathy, restricted phenotypes, including isolated psychosis, epilepsy, or movement disorders have also been described (Irani et al., 2010, Zandi et al., 2011, Brenner et al., 2013, Titulaer et al., 2013 and Hacohen et al., 2014). We reported in 2010 for the first time IgG NMDAR, and voltage gated potassium channel-complex (VGKC), antibodies in 3 of 46 (6.5%) patients with a first episode psychosis without other neurological symptoms (Zandi et al., 2011). Pollak and colleagues, found IgG NMDAR-ab in 1.46% (95% CI 0.94–2.23) cases of psychosis and schizophrenia from 7 studies, compared to (5/1598) 0.3% controls, but a variety of assays including fixed assays were compared (Pollak et al., 2013). In their analysis, rates of IgA and IgM antibodies were higher in both cases (7.1%) and controls (10.2%), though IgA and IgM antibodies are of unlikely pathogenic relevance. Dalmau and colleagues found isolated psychotic episodes in 23/571 (4%) patients with NMDAR-Ab encephalitis either in presentation (5) or at relapse (18) (Kayser et al., 2013). One test of clinical relevance of autoantibodies is the immunotherapy response. Here we describe 18 cases of acute psychosis with NMDAR-ab measured by live cell based assay without clear clinical ‘neurological’ involvement, 9 of whom we treated with immunotherapy.