TY - JOUR
T1 - Propofol-induced Changes in α-β Sensorimotor Cortical Connectivity
AU - Malekmohammadi, Mahsa
AU - AuYong, Nicholas
AU - Price, Collin M.
AU - Tsolaki, Evangelia
AU - Hudson, Andrew E.
AU - Pouratian, Nader
N1 - Funding Information:
This work was supported by the National Institute of Biomedical Imaging and Bioengineering (Bethesda, Maryland; grant No. K23 EB014326), National Institute of Neurological Disorders and Stroke (Bethesda, Maryland; grant No. R01NS097782)
Funding Information:
This work was supported by the National Institute of Biomedical Imaging and Bioengineering (Bethesda, Maryland; grant No. K23 EB014326), National Institute of Neurological Disorders and Stroke (Bethesda, Maryland; grant No. R01NS097782), and philanthropic support from Casa Colina Centers for Rehabilitation (Pomona, California). Dr. Malekmohammadi also was supported by a postdoctoral fellowship from American Parkinson Disease Association (New York, New York).
Publisher Copyright:
© 2018 Lippincott Williams and Wilkins. All rights reserved.
PY - 2018/2/1
Y1 - 2018/2/1
N2 - Background: Anesthetics are believed to alter functional connectivity across brain regions. However, network-level analyses of anesthesia, particularly in humans, are sparse. The authors hypothesized that propofol-induced loss of consciousness results in functional disconnection of human sensorimotor cortices underlying the loss of volitional motor responses. Methods: The authors recorded local field potentials from sensorimotor cortices in patients with Parkinson disease (N = 12) and essential tremor (N = 7) undergoing deep brain stimulation surgery, before and after propofol-induced loss of consciousness. Local spectral power and interregional connectivity (coherence and imaginary coherence) were evaluated separately across conditions for the two populations. Results: Propofol anesthesia caused power increases for frequencies between 2 and 100 Hz across the sensorimotor cortices and a shift of the dominant spectral peak in α and β frequencies toward lower frequencies (median ± SD peak frequency: 24.5 ± 2.6 Hz to 12.8 ± 2.3 Hz in Parkinson disease; 13.8 ± 2.1 Hz to 12.1 ± 1.0 Hz in essential tremor). Despite local increases in power, sensorimotor cortical coherence was suppressed with propofol in both cohorts, specifically in β frequencies (18 to 29 Hz) for Parkinson disease and α and β (10 to 48 Hz) in essential tremor. Conclusions: The decrease in functional connectivity between sensory and motor cortices, despite an increase in local spectral power, suggests that propofol causes a functional disconnection of cortices with increases in autonomous activity within cortical regions. This pattern occurs across diseases evaluated, suggesting that these may be generalizable effects of propofol in patients with movement disorders and beyond. Sensorimotor network disruption may underlie anesthetic-induced loss of volitional control.
AB - Background: Anesthetics are believed to alter functional connectivity across brain regions. However, network-level analyses of anesthesia, particularly in humans, are sparse. The authors hypothesized that propofol-induced loss of consciousness results in functional disconnection of human sensorimotor cortices underlying the loss of volitional motor responses. Methods: The authors recorded local field potentials from sensorimotor cortices in patients with Parkinson disease (N = 12) and essential tremor (N = 7) undergoing deep brain stimulation surgery, before and after propofol-induced loss of consciousness. Local spectral power and interregional connectivity (coherence and imaginary coherence) were evaluated separately across conditions for the two populations. Results: Propofol anesthesia caused power increases for frequencies between 2 and 100 Hz across the sensorimotor cortices and a shift of the dominant spectral peak in α and β frequencies toward lower frequencies (median ± SD peak frequency: 24.5 ± 2.6 Hz to 12.8 ± 2.3 Hz in Parkinson disease; 13.8 ± 2.1 Hz to 12.1 ± 1.0 Hz in essential tremor). Despite local increases in power, sensorimotor cortical coherence was suppressed with propofol in both cohorts, specifically in β frequencies (18 to 29 Hz) for Parkinson disease and α and β (10 to 48 Hz) in essential tremor. Conclusions: The decrease in functional connectivity between sensory and motor cortices, despite an increase in local spectral power, suggests that propofol causes a functional disconnection of cortices with increases in autonomous activity within cortical regions. This pattern occurs across diseases evaluated, suggesting that these may be generalizable effects of propofol in patients with movement disorders and beyond. Sensorimotor network disruption may underlie anesthetic-induced loss of volitional control.
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U2 - 10.1097/ALN.0000000000001940
DO - 10.1097/ALN.0000000000001940
M3 - Article
C2 - 29068830
AN - SCOPUS:85046132478
SN - 0003-3022
VL - 128
SP - 305
EP - 316
JO - Anesthesiology
JF - Anesthesiology
IS - 2
ER -