The sensory thalamus and cerebral motor cortex are affected concurrently during induction of anesthesia with propofol: a case series with intracranial electroencephalogram recordings

  • Olivier Verdonck
  • Sean J. Reed
  • Jeffery Hall
  • Jean Gotman
  • Gilles PlourdeEmail author
Case Reports / Case Series



Brain imaging studies suggest that loss of consciousness induced by general anesthetics is associated with impairment of thalamic function. There is, however, limited information on the time course of these changes. We recently obtained intracranial electroencephalogram (EEG) recordings from the ventroposterolateral (VPL) nucleus of the thalamus and from the motor cortex during induction of anesthesia in three patients to study the time course of the alterations of cortical and thalamic function.

Clinical features

The patients were American Society of Anesthesiologists physical status I-II males aged 33-57 yr with intractable central pain caused by brachial plexus injury (patient 1 and 2) or insular infarct (patient 3). Anesthesia was induced with propofol (2.5-3.1 mg·kg−1 over 30-45 sec) followed, after loss of consciousness, by rocuronium for tracheal intubation. The data retained for analysis are from one minute before the start of propofol to 110 sec later during ventilation of the patients’ lungs before tracheal intubation. Spectral analysis was used to measure absolute EEG power. Propofol caused significant increases of cortical and thalamic power in the delta to beta frequency bands (1-30 Hz). These increases of cortical and thalamic power occurred either concomitantly or within seconds of each other. Propofol also caused a decrease in cortical and thalamic high-gamma (62-200 Hz) power that also followed a similar time course.


We conclude that induction of anesthesia with propofol in these patients was associated with concurrent alterations of cortical and sensory thalamic activity.


Rocuronium General Anesthetic Brachial Plexus Injury Gamma Power Bipolar Montage 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Le thalamus sensoriel et le cortex moteur cérébral sont simultanément affectés pendant l’induction de l’anesthésie au propofol: une série de cas fondée sur des enregistrements d’électroencéphalogrammes intracrâniens



Selon les études d’imagerie cérébrale, la perte de conscience induite par les anesthésiques généraux serait associée à une détérioration de la fonction du thalamus. Toutefois, nous ne disposons que d’informations limitées quant au profil temporel de ces modifications. Nous avons récemment obtenu les enregistrements d’électroencéphalogrammes (EEG) intracrâniens du noyau ventro-postéro-latéral (VPL) du thalamus et du cortex moteur pendant l’induction de l’anesthésie chez trois patients afin d’étudier le profil temporel des modifications des fonctions corticale et thalamique.

Éléments cliniques

Les patients étaient des hommes de statut physique I-II selon l’American Society of Anesthesiologists âgés de 33 à 57 ans et souffrant de douleur centrale réfractaire causée par une lésion du plexus brachial (patients 1 et 2) ou d’un infarctus insulaire (patient 3). L’anesthésie a été induite avec du propofol (2,5-3,1 mg·kg−1 sur 30-45 sec), lequel fut suivi, après la perte de conscience, par du rocuronium pour l’intubation trachéale. Les données retenues pour analyse couvrent la période allant d’une minute avant l’administration du propofol à 110 sec plus tard, pendant la ventilation des poumons des patients avant l’intubation trachéale. Nous avons utilisé une analyse spectrale pour mesurer la puissance absolue de l’EEG. Le propofol a provoqué des augmentations considérables de la puissance corticale et thalamique dans les bandes de fréquence delta à bêta (1-30 Hz). Ces augmentations de puissance corticale et thalamique sont survenues soit simultanément, soit à quelques secondes d’intervalle. Le propofol a également provoqué une réduction de la puissance corticale et thalamique gamma élevée (62-200 Hz), laquelle a également suivi un profil temporel semblable.


Nous concluons que l’induction de l’anesthésie au propofol chez ces patients a été associée à des modifications simultanées de l’activité corticale et thalamique sensorielle.



We thank José A. Correa, Director, McGill Statistical Consulting Service, for designing and conducting the statistical analysis. We thank the EEG technologists, Lorraine Allard and Nicole Drouin, for their expert help. We also thank the OR staff and our anesthesiologist colleagues involved with these patients for their cooperation. Finally, our warmest thanks go to the patients and their families for making this report possible. Olivier Verdonck was supported by a Preston Robb Fellowship from the Montreal Neurological Institute.

Conflicts of interest

None declared.


  1. 1.
    Angel A. Central neuronal pathways and the process of anaesthesia. Br J Anaesth 1993; 71: 148-63.PubMedCrossRefGoogle Scholar
  2. 2.
    Vahle-Hinz C, Detsch O, Siemers M, Kochs E. Contributions of GABAergic and glutamatergic mechanisms to isoflurane-induced suppression of thalamic somatosensory information transfer. Exp Brain Res 2007; 176: 159-72.PubMedCrossRefGoogle Scholar
  3. 3.
    Veselis RA, Reinsel RA, Beattie BJ, et al. Midazolam changes cerebral blood flow in discrete brain regions: an H2-15O positron emission tomography study. Anesthesiology 1997; 87: 1106-17.PubMedCrossRefGoogle Scholar
  4. 4.
    Fiset P, Paus T, Daloze T, et al. Brain mechanisms of propofol-induced loss of consciousness in humans: a positron emission tomographic study. J Neurosci 1999; 19: 5506-13.PubMedGoogle Scholar
  5. 5.
    Alkire MT, Hudetz AG, Tononi G. Consciousness and anesthesia. Science 2008; 322: 876-80.PubMedCentralPubMedCrossRefGoogle Scholar
  6. 6.
    Franks NP. General anaesthesia: from molecular targets to neuronal pathways of sleep and arousal. Nat Rev Neurosci 2008; 9: 370-86.PubMedCrossRefGoogle Scholar
  7. 7.
    Clark DL, Rosner BS. Neurophysiologic effects of general anesthetics: 1. The electroencephalogram and sensory evoked responses in man. Anesthesiology 1973; 38: 564-82.PubMedCrossRefGoogle Scholar
  8. 8.
    Nuwer MR. Evoked Potential Monitoring in the Operating Room. Raven Press; 1986.Google Scholar
  9. 9.
    Owen SL, Green AL, Nandi D, Bittar RG, Wang S, Aziz TZ. Deep brain stimulation for neuropathic pain. Neuromodulation 2006; 9: 100-6.PubMedCrossRefGoogle Scholar
  10. 10.
    Crone NE, Korzeniewska A, Franaszczuk PJ. Cortical gamma responses: searching high and low. Int J Psychophysiol 2011; 79: 9-15.PubMedCrossRefGoogle Scholar
  11. 11.
    Hudetz AG, Vizuete JA, Pillay S. Differential effects of isoflurane on high-frequency and low-frequency gamma oscillations in the cerebral cortex and hippocampus in freely moving rats. Anesthesiology 2011; 114: 588-95.PubMedCentralPubMedCrossRefGoogle Scholar
  12. 12.
    San-juan D, Chiappa KH, Cole AJ. Propofol and the electroencephalogram. Clin Neurophysiol 2010; 121: 998-1006.PubMedCrossRefGoogle Scholar
  13. 13.
    Bland JM, Altman DG. The use of transformation when comparing two means. BMJ 1996; 312: 1153.PubMedCrossRefGoogle Scholar
  14. 14.
    Hommel G. A stagewise rejective multiple test procedure based on a modified Bonferroni test. Biometrika 1988; 75: 383-6.CrossRefGoogle Scholar
  15. 15.
    Velly LJ, Rey MF, Bruder NJ, et al. Differential dynamic of action on cortical and subcortical structures of anesthetic agents during induction of anesthesia. Anesthesiology 2007; 107: 202-12.PubMedCrossRefGoogle Scholar
  16. 16.
    Hirano S, Shinotoh H, Eidelberg D. Functional brain imaging of cognitive dysfunction in Parkinson’s disease. J Neurol Neurosurg Psychiatry 2012; 83: 963-9.PubMedCrossRefGoogle Scholar
  17. 17.
    Nienborg H, Cumming BG. Psychophysically measured task strategy for disparity discrimination is reflected in V2 neurons. Nat Neurosci 2007; 10: 1608-14.PubMedCentralPubMedCrossRefGoogle Scholar
  18. 18.
    Rudolph U, Antkowiak B. Molecular and neuronal substrates for general anaesthetics. Nat Rev Neurosci 2004; 5: 709-20.PubMedCrossRefGoogle Scholar
  19. 19.
    Plourde G, Garcia-Asensi A, Backman S, et al. Attenuation of the 40-hertz auditory steady state response by propofol involves the cortical and subcortical generators. Anesthesiology 2008; 108: 233-42.PubMedCrossRefGoogle Scholar
  20. 20.
    Fell J, Widman G, Rehberg B, Elger CE, Fernandez G. Human mediotemporal EEG characteristics during propofol anesthesia. Biol Cybern 2005; 92: 92-100.PubMedCrossRefGoogle Scholar
  21. 21.
    Murphy M, Bruno MA, Riedner BA, et al. Propofol anesthesia and sleep: a high-density EEG study. Sleep 2011; 34: 283-291.PubMedGoogle Scholar
  22. 22.
    Breshears JD, Roland JL, Sharma M, et al. Stable and dynamic cortical electrophysiology of induction and emergence with propofol anesthesia. Proc Natl Acad Sci USA 2010; 107: 21170-5.PubMedCrossRefGoogle Scholar
  23. 23.
    Plourde G. Auditory evoked potentials. Best Pract Res Clin Anaesthesiol 2006; 20: 129-39.PubMedCrossRefGoogle Scholar
  24. 24.
    Reed SJ, Plourde G, Tobin S, Chapman CA. Partial antagonism of propofol anaesthesia by physostigmine in rats is associated with potentiation of fast (80-200 Hz) oscillations in the thalamus. Br J Anaesth 2013; 110: 646-53.PubMedCrossRefGoogle Scholar
  25. 25.
    Plourde G, Belin P, Chartrand D, et al. Cortical processing of complex auditory stimuli during alterations of consciousness with the general anesthetic propofol. Anesthesiology 2006; 104: 448-57.PubMedCrossRefGoogle Scholar
  26. 26.
    Ojemann GA, Ojemann J, Ramsey NF. Relation between functional magnetic resonance imaging (fMRI) and single neuron, local field potential (LFP) and electrocorticography (ECoG) activity in human cortex. Front Hum Neurosci 2013; 7: 34.PubMedCentralPubMedCrossRefGoogle Scholar

Copyright information

© Canadian Anesthesiologists' Society 2014

Authors and Affiliations

  • Olivier Verdonck
    • 1
    • 3
  • Sean J. Reed
    • 1
    • 4
  • Jeffery Hall
    • 2
  • Jean Gotman
    • 2
  • Gilles Plourde
    • 1
    Email author
  1. 1.Department of Anesthesia, Montreal Neurological Institute and HospitalMcGill UniversityMontrealCanada
  2. 2.Department of Neurology and Neurosurgery, Montreal Neurological Institute and HospitalMcGill UniversityMontrealCanada
  3. 3.Département d’anesthésiologieHôpital MaisonneuveMontrealCanada
  4. 4.Department of Neurology and Neurosurgery, Douglas Mental Health InstituteMcGill UniversityMontrealCanada

Personalised recommendations