Search PubMed⌕ Search

PubMed · 10987578

Cortical function in epilepsy.

Abstract

Recent work with functional neuroimaging that relies on blood flow techniques, (15)O water positron emission tomography and functional magnetic resonance imaging has identified the lateralization and location of language functions. These technologies are increasingly being explored as alternatives to the more invasive intracarotid amytal procedure. Paradigms and sequences have been designed to identify the capacity of the hippocampus and mesial structures to support memory. Magnetoelectroencephalography offers the prospect of mapping language function in real time. Event-related data acquisition has also been employed to localize blood flow changes that are associated with interictal activity.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

W D Gaillard. 2000. Cortical function in epilepsy.. https://doi.org/10.1097/00019052-200004000-00013

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Histone H3K9 methyltransferases regulate cortical growth by coordinating heterochromatin formation and neural progenitor dynamics.

DNA packaging into heterochromatin is a fundamental mechanism of transcriptional silencing, yet its role in regulating neural progenitor behavior during brain development remains poorly understood. Trimethylation of histone H3 lysine 9 (H3K9me3), catalyzed by the methyltransferases SETDB1, SUV39H1, and SUV39H2, is a defining feature of heterochromatin, but functional redundancy among these enzymes has obscured their developmental roles. Here, we generated a cortex-specific triple knockout mouse model lacking Setdb1, Suv39h1, and Suv39h2 to directly interrogate H3K9me3 function during corticogenesis. Combined loss of H3K9 methyltransferases caused genome-wide depletion of H3K9me3, disruption of neural progenitor cell-cycle progression, and impaired cortical neurogenesis, resulting in microcephaly. H3K9 methyltransferases preserve neural progenitor identity and function by silencing clustered protocadherins, meiosis-associated genes, and a cell-cycle restraint program through H3K9me3 deposition. Loss of H3K9me3 promoted local chromatin opening and increased transcription factor occupancy, enabling transposable elements to acquire cryptic enhancer activity and modulate proximal gene expression. Together, these findings establish H3K9me3 heterochromatin as an active regulator of neural progenitor dynamics and lineage fidelity, revealing a central epigenetic mechanism that restricts aberrant transcriptional programs to ensure cortical growth.

Cerebral Cortex↗

Losing the error related negativity in the EEG of human subjects: an indicator for willed action.

When people make errors in a discrimination task, a negative-going waveform can be observed in scalp-recorded EEG that has been coined the error-related negativity (ERN). We hypothesized that the ERN only occurs with slips, that is unwilled action errors, but not if an error is committed willingly and intentionally. We investigated the occurrence of the ERN in a choice reaction time task that has been shown to produce an ERN and in an error simulation task where subjects had to fake errors while the EEG was recorded. We observed a loss of the ERN when errors were committed in willed actions but not in unwilled actions thus supporting the idea that the production of the ERN is tied to slips in unwilled actions but not mistakes in willed actions.

Cerebral Cortex↗

Event-related brain potentials in normal children during detection of inverse serial digits.

Three inverse serial digit detection tasks were evaluated with event-related brain potentials (ERPs) in 15 11-year-old children to determine how the increase of perceptual or memory demands could modify detection processing. Reaction times were significantly longer for the task that used visual blurring, compared to that with a greater memory demand. Difference-ERPs (target minus non-target conditions) showed three significant parietal components; one earlier positive peak at 162 ms interpreted as an index of working memory load; a same polarity 295 ms peak which probably represents a P3 analogous and a subsequent negative polarity component (520 ms) possibly involved with motor preparation. A fourth difference-component was a frontal positive peak at 680 ms, interpreted as related to task difficulty.

Cerebral Cortex↗