Electroencephalographic Signatures of Dexmedetomidine and Propofol Sedation: A Structured Narrative Review

Laveeza Fatima; Maria Abad; Syed Hassan Tanvir Ramzi; Ihtisham Ud Din; Abdul Wasay Toor; Nosheen Munir

doi:10.61919/fa0r1b65

Authors

Laveeza Fatima Doctor of Medicine (MD), I.K. Akhunbaev Kyrgyz State Medical Academy, Bishkek, Kyrgyzstan Author
Maria Abad MBBS, Nishtar Medical University, Multan, Pakistan Author
Syed Hassan Tanvir Ramzi Medical Officer, The Cancer Clinic, Multan, Pakistan Author
Ihtisham Ud Din Institute of Health Sciences, Swat Campus, Khyber Medical University, Swat, Pakistan Author
Abdul Wasay Toor Assistant Professor Anaesthesiology, CMH Lahore Medical College and Institute of Dentistry, Lahore, Pakistan Author
Nosheen Munir Senior Registrar Anesthesiology, CMH Lahore Medical College Institute of Dentistry, Lahore, Pakistan Author

DOI:

https://doi.org/10.61919/fa0r1b65

Keywords:

Dexmedetomidine; Propofol; Electroencephalography; Conscious Sedation; Bispectral Index; Spectral Analysis; Anesthesia Monitoring.

Abstract

Background: Carpenters perform repetitive and forceful upper-limb activities that may increase the risk of lateral Background: Dexmedetomidine and propofol are frequently used intravenous sedatives with distinct molecular targets and effects on arousal networks. Although both agents can achieve clinically comparable sedation, their electroencephalographic manifestations differ in spectral composition, spatial organization, processed index behavior, functional connectivity, and emergence dynamics. These differences are clinically important because simplified depth-of-sedation indices may not represent equivalent neurophysiological states across drug classes. Objective: This structured narrative review aimed to critically synthesize contemporary evidence regarding the raw and processed electroencephalographic signatures associated with dexmedetomidine and propofol sedation in adults. Methods: PubMed/MEDLINE, Scopus, Web of Science, and CENTRAL were searched for English-language human studies and relevant reviews published principally between January 2014 and May 2024. Foundational earlier studies were considered when necessary to explain established propofol EEG mechanisms. Literature selection prioritized direct comparative studies, controlled volunteer investigations, prospective clinical studies, secondary EEG analyses, and mechanistically informative reports addressing spectral power, spectral edge frequency, bispectral index, entropy, coherence, functional connectivity, and emergence trajectories. Findings were organized through a structured thematic synthesis rather than statistical pooling. Results: Dexmedetomidine was commonly associated with increased slow-delta activity accompanied by frontal spindle- or alpha-range oscillations and relative preservation of selected coherence measures. Propofol produced prominent slow-wave activity with concentration- and state-dependent frontal alpha oscillations, reduced faster-frequency activity, and greater disruption of selected long-range cortical interactions. At comparable clinical sedation levels, bispectral index and spectral edge frequency values frequently differed between agents. Evidence concerning entropy, connectivity, and emergence trajectories was informative but less extensively replicated. Conclusion: Dexmedetomidine and propofol produce distinct, context-dependent EEG profiles that should not be interpreted through interchangeable processed-index thresholds. Drug-specific EEG interpretation may improve sedation assessment, but standardized prospective studies linking electrophysiological patterns with patient-centered outcomes remain necessary

References

1. Purdon PL, Sampson A, Pavone KJ, Brown EN. Clinical electroencephalography for anesthesiologists: Part I: background and basic signatures. Anesthesiology. 2015;123(4):937-60. doi:10.1097/ALN.0000000000000841.

2. Maze M, Tranquilli W. Alpha-2 adrenoceptor agonists: defining the role in clinical anesthesia. Anesthesiology. 1991;74(3):581-605.

3. Akeju O, Pavone KJ, Westover MB, Vazquez R, Prerau MJ, Harrell PG, et al. A comparison of propofol- and dexmedetomidine-induced electroencephalogram dynamics using spectral and coherence analysis. Anesthesiology. 2014;121(5):978-89. doi:10.1097/ALN.0000000000000419.

4. Maksimow A, Snapir A, Särkelä M, Kentala E, Koskenvuo J, Posti J, et al. EEG spectral entropy and heart rate variability differentiate sedation levels during dexmedetomidine and propofol infusions. Acta Anaesthesiol Scand. 2019;63(4):478-88. doi:10.1111/aas.13288.

5. Lee JM, Ahn HJ, Yang M, Kim JA, Kim HJ, Lee J, et al. Intraoperative electroencephalographic patterns of dexmedetomidine in comparison with propofol in patients undergoing major spinal surgery. J Clin Med. 2021;10(21):4926. doi:10.3390/jcm10214926.

6. Kim HJ, Kim Y, Lee SH, Kim J, Lee JH, Kim JT, et al. Comparison of electroencephalographic changes and recovery profiles between dexmedetomidine and propofol sedation during spinal anesthesia. Medicine (Baltimore). 2021;100(40). doi:10.1097/MD.0000000000027476.

7. Ni K, Cooter M, Gupta DK, Thomas J, Hopkins TJ, Miller TE, et al. Electroencephalographic dynamics during propofol and dexmedetomidine sedation for intracranial aneurysm embolization. J Neurosurg Anesthesiol. 2022;34(1):46-52. doi:10.1097/ANA.0000000000000721.

8. Hesse S, Kreuzer M, Hight D, Gaskell A, Devari P, Singh D, et al. Association of electroencephalogram trajectories during emergence from dexmedetomidine or propofol sedation with postoperative delirium: a secondary analysis. Anesthesiology. 2022;136(2):272-82. doi:10.1097/ALN.0000000000004079.

9. Scheinin A, Kallionpää RE, Li D, Kallioinen M, Kaisti K, Långsjö J, et al. Differentiating drug-related and state-related effects of dexmedetomidine and propofol on the electroencephalogram. Anesthesiology. 2018;129(1):22-36.

10. Evered LA, Chan MTV, Han R, Chu MHM, Cheng BP, Scott DA, et al. Anaesthetic depth and delirium after major surgery: a randomised clinical trial. Br J Anaesth. 2021;127(5):704-12. doi:10.1016/j.bja.2021.07.021.

11. Page MJ, McKenzie JE, Bossuyt PM, Boutron I, Hoffmann TC, Mulrow CD, et al. The PRISMA 2020 statement: an updated guideline for reporting systematic reviews. BMJ. 2021;372. doi:10.1136/bmj.n71.

12. Campbell M, McKenzie JE, Sowden A, Katikireddi SV, Brennan SE, Ellis S, et al. Synthesis without meta-analysis in systematic reviews: reporting guideline. BMJ. 2020;368. doi:10.1136/bmj.l6890.

13. Sterne JAC, Savović J, Page MJ, Elbers RG, Blencowe NS, Boutron I, et al. RoB 2: a revised tool for assessing risk of bias in randomised trials. BMJ. 2019;366.

14. Sterne JAC, Hernán MA, Reeves BC, Savović J, Berkman ND, Viswanathan M, et al. ROBINS-I: a tool for assessing risk of bias in non-randomised studies of interventions. BMJ. 2016;355. doi:10.1136/bmj.i4919.

15. Tang C, Hu X, Zhang Y. Comparative effects of dexmedetomidine and propofol on hemodynamics and postoperative recovery in patients undergoing laparoscopic surgery: a systematic review and meta-analysis. J Clin Anesth. 2021;75:110487. doi:10.1016/j.jclinane.2021.110487.