Understanding the effects of anesthetic agents on the EEG through neural field theory

Anesthetic and analgesic agents act through a diverse range of pharmacological mechanisms. Existing empirical data clearly shows that such “microscopic” pharmacological diversity is reflected in their “macroscopic” effects on the human electroencephalogram (EEG). Based on a detailed mesoscopic neural field model we theoretically posit that anesthetic induced EEG activity is due to selective parametric changes in synaptic efficacy and dynamics. Specifically, on the basis of physiologically constrained modeling, it is speculated that the selective modification of inhibitory or excitatory synaptic activity may differentially effect the EEG spectrum. Such results emphasize the importance of neural field theories of brain electrical activity for elucidating the principles whereby pharmacological agents effect the EEG. Such insights will contribute to improved methods for monitoring depth of anesthesia using the EEG.

[1]  D. Liley,et al.  Drug-induced modification of the system properties associated with spontaneous human electroencephalographic activity. , 2003, Physical review. E, Statistical, nonlinear, and soft matter physics.

[2]  D. Liley,et al.  Modeling the effects of anesthesia on the electroencephalogram. , 2005, Physical review. E, Statistical, nonlinear, and soft matter physics.

[3]  Mathew P. Dafilis,et al.  A spatially continuous mean field theory of electrocortical activity , 2002, Network.

[4]  J. Fermaglich Electric Fields of the Brain: The Neurophysics of EEG , 1982 .

[5]  David T. J. Liley,et al.  A continuum theory of electro-cortical activity , 1999, Neurocomputing.

[6]  Donald O. Walter,et al.  Mass action in the nervous system , 1975 .

[7]  B. Antkowiak,et al.  Molecular and neuronal substrates for general anaesthetics , 2004, Nature Reviews Neuroscience.

[8]  E. Brown,et al.  Thalamocortical model for a propofol-induced α-rhythm associated with loss of consciousness , 2010, Proceedings of the National Academy of Sciences.

[9]  J. Cowan,et al.  Excitatory and inhibitory interactions in localized populations of model neurons. , 1972, Biophysical journal.

[10]  N. Franks General anaesthesia: from molecular targets to neuronal pathways of sleep and arousal , 2008, Nature Reviews Neuroscience.

[11]  Nicholas V Swindale Neural Synchrony, Axonal Path Lengths, and General Anesthesia: A Hypothesis , 2003, The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry.

[12]  K. Kuizenga,et al.  Quantitative electroencephalographic analysis of the biphasic concentration-effect relationship of propofol in surgical patients during extradural analgesia. , 1998, British journal of anaesthesia.

[13]  A. Mikulec,et al.  Riluzole Anesthesia: Use-Dependent Block of Presynaptic Glutamate Fibers , 1996, Anesthesiology.

[14]  R. Pearce,et al.  Dual actions of volatile anesthetics on GABA(A) IPSCs: dissociation of blocking and prolonging effects. , 1998, Anesthesiology.

[15]  R. Kötter,et al.  Connecting Mean Field Models of Neural Activity to EEG and fMRI Data , 2010, Brain Topography.

[16]  Ingo Bojak,et al.  Population based models of cortical drug response: insights from anaesthesia , 2008, Cognitive Neurodynamics.