Journal article
Clinical and intracranial electrophysiological signatures of post-operative and post-ictal delirium
Clinical neurophysiology, Vol.171, pp.38-50
03/2025
DOI: 10.1016/j.clinph.2024.12.023
PMCID: PMC11893240
PMID: 39862841
Abstract
Objectives: (1) Gain insight into the mechanisms of postoperative delirium (POD). (2) Determine mechanistic overlap with post-ictal delirium (PID). Epilepsy patients undergoing intracranial electrophysiological monitoring can experience both POD and PID, and thus are suitable subjects for these investigations.
Methods: POD was assessed daily after surgery. PID was assessed following seizures. Resting state data were collected following delirium assessments, during a control period, and during sleep. Slow-wave activity (SWA: 1-4 Hz) and resting state functional connectivity were compared between different time points and according to delirium status.
Results: POD was present in 6 of 20 participants. Post-operatively, SWA was globally elevated in all participants but highest in POD+ participants. POD+ participants exhibited altered functional connectivity compared to POD-. These differences persisted even after resolution of delirium. PID was present in 7 of 15 participants and was predicted by seizures involving prefrontal cortex. PID+ participants exhibited higher post-ictal SWA versus PID-; no differences in functional connectivity were observed. Post-operative and post-ictal SWA was comparable to sleep in some participants.
Conclusions: Elevated SWA may predispose patients to both post-operative and post-ictal delirium and may indicate overlapping mechanisms.
Significance: Delirium treatments focused on SWA may be most effective for ameliorating cognitive symptoms.
Details
- Title: Subtitle
- Clinical and intracranial electrophysiological signatures of post-operative and post-ictal delirium
- Creators
- Matthew I. Banks - University of Wisconsin–MadisonEmily R. Dappen - University of IowaElie Matar - The University of SydneyBenjamin D. Hayum - University of Wisconsin–MadisonMichael H. Sutherland - University of Wisconsin–MadisonBryan M. Krause - University of Wisconsin–MadisonHiroto Kawasaki - University of IowaRobert D. Sanders - The University of SydneyKirill V. Nourski - University of Iowa
- Resource Type
- Journal article
- Publication Details
- Clinical neurophysiology, Vol.171, pp.38-50
- DOI
- 10.1016/j.clinph.2024.12.023
- PMID
- 39862841
- PMCID
- PMC11893240
- NLM abbreviation
- Clin Neurophysiol
- ISSN
- 1388-2457
- eISSN
- 1872-8952
- Publisher
- ELSEVIER IRELAND LTD
- Grant note
- National Institutes of Health: R01 GM109086, R01 AG063849, R01 DC004290
We are grateful to Joel Berger, Haiming Chen, Christopher Garcia, Matthew Howard, Heidi Lindroth, Junjie Liu, and Ariane Rhone for help with data collection, analysis, interpretation, and helpful comments on the manuscript. This work was supported by the National Institutes of Health (grant numbers R01 GM109086, R01 AG063849, R01 DC004290) . The study sponsors had no role in the collection, analysis and interpretation of data and in the writing of the manuscript.
- Language
- English
- Electronic publication date
- 01/20/2025
- Date published
- 03/2025
- Academic Unit
- Iowa Neuroscience Institute; Neurosurgery
- Record Identifier
- 9984775017402771
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