Basal temporal language area revisited in Japanese language with a language function density map.

We revisited the anatomo-functional characteristics of the basal temporal language area (BTLA), first described by Lüders et al. (1986), using electrical cortical stimulation (ECS) in the context of Japanese language and semantic networks. We recruited 11 patients with focal epilepsy who underwent chronic subdural electrode implantation and ECS mapping with multiple language tasks for presurgical evaluation. A semiquantitative language function density map delineated the anatomo-functional characteristics of the BTLA (66 electrodes, mean 3.8 cm from the temporal tip). The ECS-induced impairment probability was higher in the following tasks, listed in a descending order: spoken-word picture matching, picture naming, Kanji word reading, paragraph reading, spoken-verbal command, and Kana word reading. The anterior fusiform gyrus (FG), adjacent anterior inferior temporal gyrus (ITG), and the anterior end where FG and ITG fuse, were characterized by stimulation-induced impairment during visual and auditory tasks requiring verbal output or not, whereas the middle FG was characterized mainly by visual input. The parahippocampal gyrus was the least impaired of the three gyri in the basal temporal area. We propose that the BTLA has a functional gradient, with the anterior part involved in amodal semantic processing and the posterior part, especially the middle FG in unimodal semantic processing.

Ictal Direct Current Shifts Preceded Much Earlier Than High Frequency Oscillations After Status: Is It the Effect of Status or Antiseizure Medication?

PURPOSE: While spikes and sharp waves are considered as markers of epilepsy in conventional electroencephalography, ictal direct current (DC) shifts and high-frequency oscillations (HFOs) appear to be useful biomarkers for epileptogenicity. We analyzed how ictal DC shifts and HFOs were affected by focal status epilepticus and antiseizure medications (ASMs). METHODS: A 20-year-old female patient who underwent long-term intracranial electrode implantation for epilepsy surgery presented with 72 habitual seizures and a focal status epilepticus episode lasting for 4 h. Ten, 3, and 10 consecutive habitual seizures were analyzed before the status, after the status, and after ASM (valproate) loading, respectively. RESULTS: Before and immediately after the status, ictal DC shifts remained the same in terms of the amplitude, duration, and slope of DC shifts. High-frequency oscillations also remained the same in terms of the duration, frequency, and power except for the power of the lower frequency band. After ASM loading, the duration, amplitude, and slope of the ictal DC shift were significantly attenuated. The duration, frequency, and power of the HFOs were significantly attenuated. Furthermore, the interval between the DC onset and HFO onset was significantly longer and the interval between the HFO onset and ictal DC shift peak was significantly shorter. CONCLUSIONS: The attenuation of ictal DC shifts and HFOs after ASM loading implies that astrocyte and neuronal activity may be both attenuated by ASMs. This finding may help with our understanding of the pathophysiology of epilepsy and can aid with the discovery of new approaches for epilepsy management.

Intracranially recorded ictal direct current shifts may precede high frequency oscillations in human epilepsy.

OBJECTIVE: We assessed the temporal-spatial characteristics of ictal direct current (DC) shifts (or infraslow activity) and high frequency oscillations (HFOs) in 16 patients with intractable focal epilepsy. METHODS: The underlying etiology consisted of cortical dysplasia, glioma, hippocampal sclerosis, and low-grade neuroepithelial tumor in nine, four, two, and one patients, respectively. The median number of analyzed seizure events was 8.0 per patient (range: 2-10). Chronic electrocorticographic recording was performed with (1) a band-pass filter of 0.016-600Hz (or 0.016-300Hz) and a sampling rate of 2000Hz (or 1000Hz). RESULTS: Ictal DC shifts and a sustained form of ictal HFOs were observed in 75.0% and 50.0% of the patients, and 71.3% and 46.3% of the analyzed seizures. Visual assessment revealed that the onset of ictal DC shifts preceded that of ictal HFOs with statistical significance in 5/7 patients. The spatial extent of ictal DC shifts or HFOs was smaller than that of the conventionally defined seizure onset zone in 9/12 patients. CONCLUSION: Both ictal DC shifts and HFOs might represent the core of tissue generating seizures. SIGNIFICANCE: The early occurrence of ictal DC shifts warrants further studies to determine the role of glia (possibly mediating ictal DC shifts) in seizure generation.

Ictal wideband ECoG: direct comparison between ictal slow shifts and high frequency oscillations.

OBJECTIVE: With advanced electroencephalography (EEG) technology, 'wideband EEG' ranging from slow shift to high frequency oscillation (HFO) is clinically available to study human epileptogenesis. The purpose of our study is to clarify the relationship between slow shift, HFO and conventional electrocorticographic (ECoG) change. METHODS: A patient with right temporal lobe epilepsy who underwent presurgical evaluation with subdural electrodes was studied. Slow shift and HFO were evaluated in 16 habitual seizures with wideband EEG technique (bandpass filter of 0.016-600 Hz). RESULTS: Upon seizure occurrence in wideband ECoG, negative slow shifts coexisted with HFO (100-300 Hz) in the ictal onset zone in all investigated seizures. The former always preceded HFO and conventional initial EEG changes by mean value of 1.6 and 20.4s, respectively. The slow shifts and HFOs were observed only in the restricted ictal onset zone. CONCLUSIONS: In this particular patient, wideband EEG could delineate both ictal slow shift and HFO to define ictal onset zone, and the earliest occurrence of slow shifts may suggest an early role of glia in slow EEG shift generation than neurons. SIGNIFICANCE: The time difference of the onset between ictal HFO and slow shift may help to understand epileptogenesis.