Quantitative EEG in patients with alcohol-related seizures.

BACKGROUND: To investigate whether quantitative electroencephalography (QEEG) recorded within a few days after a generalized seizure can improve the discrimination between alcohol-related seizures (ARSs), seizures in epilepsy and other seizures. In addition, we wanted to evaluate the influence of various external factors on QEEG, e.g., drug use, time from seizure occurrence, and alcohol intake. METHODS: An ARS was defined by (i) scores ≥8 in the Alcohol Use Disorders Identification Test (AUDIT) and (ii) no history of epilepsy. Twenty-two ARS patients, 21 epileptic patients with seizures (ES), 30 AUDIT-negative patients with seizures (OS), and 37 well-controlled epileptic outpatients (EPO) were included. EEG from 79 sciatica patients (SC) served as an additional control group. EEG was recorded in relaxed wakefulness with eyes closed. Spectral analysis of ongoing resting EEG activity was performed. For the main analysis, spectral band amplitudes were averaged across 14 electrodes. RESULTS: Major quantitative EEG abnormalities were mainly seen in the ES group. AUDIT score correlated negatively with QEEG band amplitudes in patients with seizures unrelated to alcohol, but not in the ARS group. Recent alcohol intake correlated negatively with delta and theta amplitude. We could not confirm that beta activity is increased in ARS subjects. CONCLUSIONS: A QEEG with slightly reduced alpha amplitude supports a clinical diagnosis of ARS. An abnormally slow QEEG profile and asymmetry in the temporal regions indicates ES. QEEG predicted the clinical diagnosis better than standard EEG.

Speech-induced aphasic seizures in epilepsy caused by LGI1 mutation.

PURPOSE: Patients with autosomal dominant lateral temporal lobe epilepsy (ADTLE) may have seizures precipitated by sound or speech. We have examined a patient with speech-induced seizures caused by an LGI1 mutation (C46R). METHODS: A clinical study and a video-EEG recording using interrogative speech as the activation procedure was performed in a 23-year-old man. RESULTS: He had experienced short episodes of sensory aphasia in situations in which he was suddenly verbally addressed. Voices became distorted, and he could not comprehend despite hearing words. The day after a late party, his girlfriend unexpectedly spoke to him. Her speech became unintelligible to him. He did not reply and had a generalized tonic-clonic (GTC) seizure. During an EEG, he was suddenly asked for the names of his siblings. He answered, but lost understanding of the further conversation and described how syllables floated together with an echoing character. With a versive movement to the right, another GTC occurred. In the EEG, rhythmic 6-Hz activity built up in the frontotemporal areas starting on the left side with bilateral and posterior spreading. Postictal slowing was symmetrical, and no aphasia was noted on awakening. CONCLUSIONS: To our knowledge, this is the first video-EEG recorded seizure in LGI1-caused ADTLE. This peculiar seizure semiology and precipitating effect of speech may serve as a marker for identifying further individuals with this particular phenotype and genotype and may indicate that the LGI1 gene may have a physiologic function connected to the human capacity for speech and language.