Abstract
Introduction Autoimmune encephalitis (AE) is an acute neuroinflammatory disease that has high prevalence of chronic (>3 months post-acute illness) morbidity characterized by cognitive and functional impairment. It remains unclear if this morbidity is residual injury from the acute event or driven by ongoing neurodegeneration.
Objective Evaluate NfL and GFAP in serum and CSF in AE across subtypes, timepoints and outcomes.
Methods Patients with AE were recruited through the Australian Autoimmune Encephalitis Consortium and serum and CSF was analysed for GFAP and neurofilament light chain (NfL) using the Quanterix Simoa system. Subtypes included LGI-1, NMDAR and seronegative (SN) and timepoints included acute and chronic (>3 months). Timepoints and serum/CSF samples were paired where possible. Relationship to cognition and functional status (mRS) were also evaluated.
Results We recruited 26 patients with acute AE, 33 patients SN AE, 19 LGI-1 AE, 15 NMDAR AE, 10 patients with non-inflammatory neurological diseases (NIND) and 28 healthy controls. Compared with controls the acute AE cohort had higher serum NfL (30.59 pg/ml vs 8.89 pg/ml, p < 0.01) and GFAP (614.2 pg/mL vs 104.3 pg/Ml, p < 0.05). CSF GFAP was not significantly altered in AE compared with NIND. AE patients with severe cognitive dysfunction demonstrated higher serum NfL and GFAP (p<0.05).
Conclusion Whilst markers of neurodegeneration in AE are highest during the acute disease, higher levels persist in patients with ongoing severely impaired cognition despite treatment. Further evaluation of NfL and GFAP may provide biomarkers of prognosis and impetus for ongoing therapy after the acute illness.
