Neurological Autoantibody Prevalence in Epilepsy of Unknown Etiology

Abstract

IMPORTANCE Autoimmune epilepsy is an underrecognized condition, and its true incidence is unknown. Identifying patients with an underlying autoimmune origin is critical because these patients' condition may remain refractory to conventional antiseizure medications but may respond to immunotherapy.OBJECTIVE To determine the prevalence of neurological autoantibodies (Abs) among adult patients with epilepsy of unknown etiology. DESIGN, SETTING, AND PARTICIPANTSConsecutive patients presenting to neurology services with new-onset epilepsy or established epilepsy of unknown etiology were identified. Serum samples were tested for autoimmune encephalitis Abs as well as thyroperoxidase (TPO) and glutamic acid decarboxylase 65 (GAD65) Abs. An antibody prevalence in epilepsy (APE) score based on clinical characteristics was assigned prospectively. Data were collected from June 1, 2015, to June 1, 2016. MAIN OUTCOMES AND MEASURESPresence of neurological Abs. A score based on clinical characteristics was assigned to estimate the probability of seropositivity prior to antibody test results. Good seizure outcome was estimated on the basis of significant reduction of seizure frequency at the first follow-up or seizure freedom. RESULTSOf the 127 patients (68 males and 59 females) enrolled in the study, 15 were subsequently excluded after identification of an alternative diagnosis. Serum Abs suggesting a potential autoimmune etiology were detected in 39 (34.8%) cases. More than 1 Ab was detected in 7 patients (6.3%): 3 (2.7%) had TPO-Ab and voltage-gated potassium channel complex (VGKCc) Ab, 2 (1.

Neuronal antibodies in adult patients with new‐onset seizures: A prospective study

“…Our findings are in agreement with recent reports from unselected children with new‐onset seizures, in which 1.9% had unspecific voltage‐gated potassium channel (VGKC)‐complex reactivity and 3.9% had reactivity to mouse neuropil (Garcia‐Tarodo et al, ). Our findings contrast somewhat to those in another adult cohort, in which 13 of 35 (37%) of patients with new‐onset epilepsy of unknown etiology were antibody‐positive (Dubey, Alqallaf, et al, ). Importantly, we included patients with new‐onset single seizures in our cohort, which may explain part of the difference.…”

Familial mesial temporal lobe epilepsy and the borderland of déjà vu

“…The identification of suspicious d ej a vu may also reflect the presence of a continuum between physiological d ej a vu and epileptic d ej a vu. In cohorts comprising new onset and established epilepsies, 15 to 22% of individuals with focal epilepsy of unknown cause had detectable serum neurological autoantibodies 35,36 ; whether these cases have a true autoimmune etiology remains uncertain. 33 The minor disturbance of function responsible for d ej a vu in the healthy brain may possibly propagate further and with greater intensity in the brain of some relatives of patients with MTLE, leading to suspicious d ej a vu, and even more so in the epileptic brain, resulting in epileptic d ej a vu.…”

Complement system biomarkers in epilepsy

“…Currently, primary immunemediated epilepsies are recognised as neural autoantibody disorders affecting both cellsurface expressed proteins such as LGI1 and N-methyl-D-aspartate (NMDA) receptor, and intacellular proteins such as GAD [11]. A study of neural auto-antibodies in epilepsies of apparent unknown aetiology suggested that immune activation may explain up to 20% of nonparaneoplastic cases [12].…”