008 – Surrogate markers of central nervous system inflammation in cerebrospinal fluid in autoimmune encephalitis and psychosis
Jocelyn X Jiang (1, 2, 4) – Nicole Fewings (5) – Suat Dervish (5) – Alessandro F Fois (3, 4) – Stephen R. Duma (3, 4) – Matthew Silsby (3, 4) – Sudarshini Ramanathan (3, 4, 6) – Bryne John (7) – Andrew Bleasel (3, 4) – Ming-Wei Lin (1, 2, 4) – Anthony Harris (4, 8, 9) – David Brown (1, 2, 4*)
Department of Immunopathology, New South Wales Health Pathology-ICPMR, Westmead Hospital, Westmead NSW Australia (1) – Department Clinical Immunology Westmead Hospital, Westmead NSW Australia (2) – Sydney Medical School, University of Sydney, Sydney NSW Australia (4)
Background: Autoimmune encephalitis is an important cause of encephalopathy, refractory epilepsy and unexplained movement disorders in adults. Whilst there is an increasing identification of associated antibodies, there remains a group of patients with high clinical probability of autoimmune encephalitis but no associated characterised autoantibody. Furthermore, a significant proportion of these patients present with treatment resistant psychosis as part of their clinical phenotype and this has led to new interest in the role of autoimmunity in psychiatric disease and the diagnosis of autoimmune encephalitis in the psychiatric cohort. We reviewed current diagnostic investigations of serum and cerebrospinal fluid (CSF) in a previous study of patients with high probability of autoimmune encephalitis to identify surrogate biomarkers indicative of neuroinflammation including two novel markers: CSF light chains and CSF cytokines. These results were compared with a cohort of patients with treatment resistant psychiatric disease. Methods: Adult patients with treatment resistant psychiatric disease (TRPD) were recruited. Serum and CSF were examined with standard investigations for encephalitis and novel markers (CSF cytokines; CSF light chains). These results were compared with an established cohort of patients with autoimmune encephalitis, viral encephalitis and non-inflammatory neurological disease (NIND). Results: 19 patients with TRPD were recruited (11 psychosis and 8 with mood disorder). These patients were compared to a cohort of 32 patients with autoimmune encephalitis (9 with antibody-positive autoimmune encephalitis; 23 with high clinical probability of autoimmune encephalitis at time of lumbar puncture,)21 viral and 13 NIND samples. There were an increased proportion of TRPD patients with CSF monocytosis and oligoclonal bands compared to normal controls however these are not specific for autoimmune disease. Elevations of CSF cytokines in the TRPD group overlapped with cytokine signatures in both the autoimmune and viral control groups which may suggest role of neuroinflammation in these patients. These results need to be confirmed with further study.