Furthermore, additional information regarding the role of LGI1 in the development of temporal lobe epilepsy was elucidated, and a potential relationship was established between cortical neuronal migration dysfunction and autosomal dominant partial epilepsy with auditory features.
Continuous video-EEG recordings were acquired in four patients with anti-LGI1 encephalitis: each had frequent motor spasms/FBDS as well as frequent subclinical temporal lobe seizures (an independent indicator of anti-LGI1 encephalitis).
None of these polymorphisms showed a significant association with IPEAF, whereas a tendency towards association with the prodynorphin low expression (L) alleles was found in the small group of ADLTE index cases, in agreement with previous studies suggesting that this polymorphism is a susceptibility factor in familial forms of temporal lobe epilepsy.
The authors performed a clinical and molecular analysis on 75 pedigrees comprising 54 with a variety of familial epilepsies associated with TLE and 21 sporadic TLE cases.All were studied for mutations in LGI1.
We show that the expression pattern of mouse Lgi1 is predominantly neuronal and is consistent with the anatomic regions involved in temporal lobe epilepsy.