Abstract
Background: The prevalence of neural autoantibodies in epilepsy of unknown etiology varies among studies. We aimed to conduct a systematic review and meta-analysis to determine the pooled global prevalence and the prevalence for each antibody. Methods: A systematic search was conducted for studies that included prospectively patients ≥16 years old with epilepsy of unknown etiology and systematically determined neural autoantibodies. A meta-analysis was undertaken to estimate pooled prevalence in total patients with a positive result for at least one neural autoantibody in serum and/or cerebrospinal fluid (CSF) and for each autoantibody. Results: Ten of the eleven studies that met the inclusion criteria and a total of 1302 patients with epilepsy of unknown etiology were included in themeta-analysis. The global pooled prevalence (IC95%) was 7.6% (4.6–11.2) in a total of 82 patients with a positive result for any neural autoantibody. None of the controls available in the studies had a positive result. Individual pooled prevalence for each autoantibody was: glycine receptor (GlyR) (3.2%), glutamic acid decarboxylase (GAD) (1.9%), N-methyl-d-aspartate receptor (NMDAR) (1.8%), leucine-rich glioma inactivated-1 protein (LGI1) (1.1%), contactin-2-associated protein (CASPR2) (0.6%) and onconeuronal (0.2%). Conclusions: The pooled prevalence of neural autoantibodies in patients with epilepsy of unknown etiology is small but not irrelevant. None of the controls had a positive result. There was high heterogeneity among studies. In the future, a homogeneous protocol for testing neural autoantibodies is recommended.
Highlights
Epileptic seizures are one of the most frequent clinical presentations of autoimmune encephalitis [1], and in some cases, it may be the only symptom [2]
We attempted to estimate the pooled prevalence of neural autoantibodies in patients 16 years or older with epilepsy of unknown etiology through a systematic review of the literature and a meta-analysis
Our results show a pooled prevalence of 7.6% (IC95, 4.6–11.2%) in patients with epilepsy of unknown etiology
Summary
Epileptic seizures are one of the most frequent clinical presentations of autoimmune encephalitis [1], and in some cases, it may be the only symptom [2]. Many experts have considered that not all seizures triggered by immune damage to the brain should be considered as immune epilepsy [2] since epilepsy is understood as a chronic process [5] With this in mind, they suggest two different concepts [6]: “acute symptomatic seizures secondary to autoimmune encephalitis” and “autoimmune-associated epilepsy”. They suggest two different concepts [6]: “acute symptomatic seizures secondary to autoimmune encephalitis” and “autoimmune-associated epilepsy” The former consider cases in which immune encephalitis with positive neural surface antibodies presents with symptomatic seizures but reaches long-term seizure freedom with immune-targeted therapy [7]; the latter would account for those with antibodies targeting intracellular antigens such as glutamic acid decarboxylase (GAD) and onconeural protein antibodies, in which immunotherapy is frequently ineffective as a result of neural death and permanent brain damage [8]. A homogeneous protocol for testing neural autoantibodies is recommended
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