ArticleJournal of neurophysiology2015
Infraslow EEG activity modulates cortical excitability in postanoxic encephalopathy.
Article in Journal of neurophysiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 24 citations in OpenAlex.
- Infraslow Closed-Loop Brain Training for Anxiety and Depression (ISAD): A pilot randomised, sham-controlled trial in adult females with internalizing disorders.Cognitive, affective & behavioral neuroscience · 2025Trial
- Data driven multiscale modelling of paroxysmal brain transitions using DC-coupled electrophysiological data.PloS one · 2026Article
- Article
- Impact of DC-Coupled Electrophysiological Recordings for Translational Neuroscience: Case Study of Tracking Neural Dynamics in Rodent Models of Seizures.Frontiers in computational neuroscience · 2022Article
- Quantitative Electroencephalogram Trends Predict Recovery in Hypoxic-Ischemic Encephalopathy.Critical care medicine · 2019Article
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Infraslow activity represents an important component of physiological and pathological brain function. We study infraslow activity (<0.1 Hz) in 41 patients with postanoxic coma after cardiac arrest, including the relationship between infraslow activity and EEG power in the 3-30 Hz range, using continuous full-band scalp EEG. In all patients, infraslow activity (0.015-0.06 Hz) was present, irrespective of neurological outcome or EEG activity in the conventional frequency bands. In two patients, low-amplitude (10-30 μV) infraslow activity was present while the EEG showed no rhythmic activity above 0.5 Hz. In 13/15 patients with a good outcome and 20/26 patients with a poor one, EEG power in the 3-30 Hz frequency range was correlated with the phase of infraslow activity, quantified by the modulation index. In 9/14 patients with burst-suppression with identical bursts, bursts appeared in clusters, phase-locked to the infraslow oscillations. This is substantiated by a simulation of burst-suppression in a minimal computational model. Infraslow activity is preserved in postanoxic encephalopathy and modulates cortical excitability. The strongest modulation is observed in patients with severe postanoxic encephalopathy and burst-suppression with identical bursts.
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