Propofol-induced Changes in α-β Sensorimotor Cortical Connectivity

Abstract

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.

Leveraging Nonhuman Primate Multisensory Neurons and Circuits in Assessing Consciousness Theory

“…These findings are concordant with a recent primate neuroimaging study demonstrating the breakdown of functional nodes (at the benefit of anatomically defined connections) during propofol, sevoflurane, and ketamine anesthesia (Uhrig et al, 2018), and a reduction in EEG directed functional connectivity across frontal and parietal areas during exposure to the same three drugs (Lee et al, 2013). Similarly, the seeming breakdown of frontoparietal/sensorimotor networks has been previously identified during propofol exposure in humans using electrocorticography (Malekmohammadi et al, 2018) and during ketamine exposure in nonhuman primates using multielectrode arrays (Schroeder et al, 2016), as in the current study (for further discussion of the effect of anesthetics on ignition in the context of GNW, particularly regarding interesting putative dose-dependent effects, see Mashour, 2018).…”

Altered Pallidocortical Low-Beta Oscillations During Self-Initiated Movements in Parkinson Disease

“…The bipolar signal pair were used for the analysis of PM/M1 (premotor/motor) activities (contact pair: immediately anterior to the central sulcus, spanning precentral gyrus). The details of imaging, DBS lead targeting, and anatomical localization of ECoG strip are provided in our prior publications ( Tsiokos et al, 2017 ; Malekmohammadi et al, 2018b , a ).…”

Pallidal stimulation in Parkinson disease differentially modulates local and network β activity

“…Following the procedure, a post-operative CT scan was obtained for additional confirmation of DBS electrode position. Anatomical localization of ECoG strip was done using a technique previously described [33, 34] (Figure 1 A). The central sulcus was identified and marked on the reconstructed cortical surface.…”