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Because of its low cost and ease of use at the bedside, continuous electroencephalography (EEG) has become widely performed to measure electrical brain activity and to monitor neurological status of patients with severe brain injury.1 Nonetheless, the exact relationship tying spontaneous electroencephalographic activity recorded acutely after traumatic brain injury (TBI), the unfolding of secondary brain damage processes in the subacute and chronic settings,2 3 and functional outcome remains poorly understood. The present study begins bridging this gap, adopting a multimodal approach combining EEG spectral analysis,1 magnetic resonance (MR)-based measures of brain pathology2 3 and clinical outcome at 6 months. Specifically, we perform three analyses: (1) we assess the relationship between acute EEG spectral features and 6-month outcome; (2) we assess the relationship between acute EEG spectral features and subcortical atrophy over the first 6 months postinjury; and (3) we bring together EEG, MRI and other covariate variables in a multimodal analysis predicting 6-month outcome. Our results suggest that alpha and delta frequencies recorded acutely at the bedside predict left dorsal and ventral thalamic atrophy and functional recovery at 6 months postinjury.
In an observational, non-interventional, longitudinal study, we retrospectively analysed a convenience sample of 13 adult patients with severe TBI (21–77 years old; see online supplementary etable 1 and online supplementary information) admitted at the University of California Los Angeles (UCLA) Neurointensive Care Unit with an initial Glasgow Coma Scale (GCS) score of ≤8 or 9–14 with evidence of intracranial bleeding, and who did not show, within 8 hours of admission, GCS score >14 or brain death. Patients with epileptic seizures, pre-existing neurological disorder, overwhelming concurrent hepatic, metabolic encephalopathy, or burst-suppressing sedation were …
CS and ESL contributed equally.
Contributors MMM, CS, ESL and PMV conceived the study. CS, ESL and BJB analysed the data. All authors discussed and interpreted the results. CS, ESL and MMM drafted the manuscript. All authors provided critical feedback and input to the manuscript.
Competing interests None declared.
Funding This work received support from the James S McDonnell Foundation, Tiny Blue Dot Foundation and the Brain Injury Research Center (BIRC) at UCLA.
Patient consent Not required.
Ethics approval The protocol was approved by the University of California at Los Angeles Institutional Review Board.
Provenance and peer review Not commissioned; externally peer reviewed.
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