[The leading edge of epilepsy research]

For diagnosis of seizure type and epilepsy syndrome, we always take all the three aspects of 1) history and symptoms (symptomatology), 2) EEG (clinical neurophysiology) and 3) neuroimaging into account, and thus an appropriate treatment approach based on both short- and long-term concerns is individualized. Recent advances in clinical epileptology on the three aspects (i, ii, iii) and on genetic analysis (iv, v) are briefly introduced as follows. i) Wide-band EEG analysis Clinical EEG provides us with diagnostic information of epileptogenicity by epileptiform discharges, i.e., spikes, sharp waves, which reflects the paroxysmal depolarization shifts (PDS) in the epileptic neurons. Currently advanced technology has enabled us to record wide-band EEG: direct current (DC) shifts (Ikeda et al., 1996) and high frequency oscillation (HFO) (Bragin et al., 1999). The both conditions occurred together as early as electrodecremental pattern occurred or earlier than conventional ECoG changes, and that ictal DC shifts happened earlier than HFO on some occasions, that may suggest more active role of glia (Imamura et al., 2011). ii) Amygdalar enlargement in patients with temporal lobe epilepsy (TLE). With absence of hippocampal atrophy (HA), some patients with TLE clearly showed amygdalar enlargement on focus side; they had older onset age and better seizure control than HA. It may be a subtype of TLE (Mitsueda-Ono et al., 2011). iii) Focal epilepsy syndrome as antibody-mediated gray matter disease? Recently delineated antibodies to cell surface antigens such as anti-VGKC antibody, anti-GAD antibody or anti-NMDA receptor antibody could develop chronic epileptic condition, being apart from so-called acute limbic encephalitis with ovarian teratoma. iv) Gentic abnormality in epilepsy other than channelopathy Abnormality of LGI1 gene is responsible for autosomal dominant lateral temporal lobe epilepsy (ADLTE), where synaptic transmission could be impaired. Clinically significant divergence in symptoms and the degree of abnormality within family as well as between families remains to be solved (Kawamata et al., 2010). v) Genetic polymorphism in CYP2C19 in drug choice Information of genetic polymorphism in CYP2C19 could individualize drug choice and its dose in advance (Yasuda et al., 2009).