Abstract
Introduction: Our goal was to investigate whether biomarkers of cerebral damage are found in autoimmune-mediated epilepsy (AIE) and whether these can differentiate AIE from other seizure disorders.Methods: We retrospectively searched our cerebrospinal fluid (CSF) database for patients with definite AIE, hippocampal sclerosis due to other causes (HS), genetic generalized epilepsy (GGE), and psychogenic, non-epileptic seizures (PNES). We measured serum and CSF tau, neurofilament 1 (NFL), glial fibrillary acid protein (GFAP), and ubiquitin-carboxy-terminal hydrolase L1 with a single-molecule array.Results: We identified suitable samples from patients with AIE (n = 13) with different antibodies and compared them to HS (n = 13), GGE (n = 7), and PNES (n = 8). The NFL levels were significantly elevated in the serum (p = 0.0009) and CSF (p < 0.0019) of AIE patients. The AIE group was significantly older, while the disease duration was significantly shorter than in the control groups. NFL correlated significantly with age in all groups, and the NFL levels of AIE patients were hardly higher than those of healthy elderly people published elsewhere.Conclusions: Our data indicate that the elevated NFL levels in AIE patients are most likely due to the higher age in this group and not due to the underlying inflammation. Unless larger prospective studies with intra-individual, longitudinal analyses and treatment responses would contradict our findings, NFL in serum might yet become a biomarker for disease activity and differential diagnosis.
Highlights
Our goal was to investigate whether biomarkers of cerebral damage are found in autoimmune-mediated epilepsy (AIE) and whether these can differentiate AIE from other seizure disorders
Patients with AIE were significantly older than temporal lobe epilepsy (TLE) or genetic generalized epilepsy (GGE) patients (p = 0.0014), and their disease duration before their lumbar puncture (LP) was significantly shorter (p < 0.0001)
hippocampal sclerosis (HS) and AIE patients had higher rates of cognitive alterations such as memory, executive, or other mental status disturbances PNES and GGE patients (p < 0.0001), while emotional alterations such as depression and anxiety were found in all four groups
Summary
Our goal was to investigate whether biomarkers of cerebral damage are found in autoimmune-mediated epilepsy (AIE) and whether these can differentiate AIE from other seizure disorders. In the past two decades, a subset of epilepsies, temporal lobe epilepsy (TLE), has been recognized as an antibody-mediated autoimmune disorder. The most common phenotypes are non-paraneoplastic and paraneoplastic limbic encephalitis [1]. The diagnostic criteria [2] include subacute onset seizures, neurocognitive changes, cerebral magnetic resonance imaging changes suggestive of encephalitis with FLAIR hyperintensities of the temporal lobes and/or other cortical areas, and cerebrospinal fluid (CSF) pleocytosis. Antibody testing is important in cases that do Cerebral Damage Biomarkers Autoimmune Epilepsy not meet all criteria in order to define the clinical syndrome and to plan the appropriate short- and long-term treatments [2]. The histopathological correlates in brain biopsies reach from mostly lymphocyte-driven inflammation of limbic structures to hippocampal sclerosis (HS) [3]
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