Propofol Anesthesia and Cerebral Blood Flow Changes Elicited by Vibrotactile Stimulation: A Positron Emission Tomography Study

Abstract

We investigated the effects of the general anesthetic agent propofol on cerebral structures involved in the processing of vibrotactile information. Using positron emission tomography (PET) and the H(2)(15)O bolus technique, we measured regional distribution of cerebral blood flow (CBF) in eight healthy human volunteers. They were scanned under five different levels of propofol anesthesia. Using a computer-controlled infusion, the following plasma levels of propofol were targeted: Level W (Waking, 0 microg/ml), Level 1 (0.5 microg/ml), Level 2 (1.5 microg/ml), Level 3 (3.5 microg/ml), and Level R (Recovery). At each level of anesthesia, two 3-min scans were acquired with vibrotactile stimulation of the right forearm either on or off. The level of consciousness was evaluated before each scan by the response of the subject to a verbal command. At Level W, all volunteers were fully awake. They reported being slightly drowsy at Level 1, they had a slurred speech and slow response at Level 2, and they were not responding at all at Level 3. The following variations in regional CBF (rCBF) were observed. During the waking state (Level W), vibrotactile stimulation induced a significant rCBF increase in the left thalamus and in several cortical regions, including the left primary somatosensory cortex and the left and right secondary somatosensory cortex. During anesthesia, propofol reduced in a dose-dependent manner rCBF in the thalamus as well as in a number of visual, parietal, and prefrontal cortical regions. At Level 1 through 3, propofol also suppressed vibration-induced increases in rCBF in the primary and secondary somatosensory cortex, whereas the thalamic rCBF response was abolished only at Level 3, when volunteers lost consciousness. We conclude that propofol interferes with the processing of vibrotactile information first at the level of the cortex before attenuating its transfer through the thalamus.

Total neuroenergetics support localized brain activity: Implications for the interpretation of fMRI

“…Human positron emission tomography (PET) studies measuring changes in CBF at different levels of propofol anesthesia did not show increasing increments to sensory stimulation at deeper levels of anesthesia (35), as would be expected from our results. However, the authors acknowledged that localized changes in CBF were confounded by elevated blood pCO 2 (that increased with depth of anesthesia), which in turn raised CBF globally.…”

Cortical and Subcortical Connectivity Changes during Decreasing Levels of Consciousness in Humans: A Functional Magnetic Resonance Imaging Study using Propofol

“…Our experiment cannot distinguish between direct propofol modulation of the striatum itself and striatal deafferentation secondary to drug activity at another site such as the cortex, brainstem or indeed the thalamus (Abulafia et al, 2009). This is a parallel problem to that raised by Bonhomme and colleagues, who found cortical activation to be reduced at lower doses than those required to reduce activation within the thalamus (Bonhomme et al, 2001).…”

“…Fiset et al (1999) found that propofol preferentially decreased regional cerebral blood flow (rCBF) in the thalamus, midbrain, cuneus, precuneus, posterior cingulate, and orbitofrontal cortex. Bonhomme et al (2001) found that propofol reduced rCBF changes during vibrotactile stimulation at doses below those required to suppress the thalamic rCBF response. We aimed to extend these important findings, harnessing the superior temporal resolution of functional magnetic resonance imaging (fMRI) to test the hypothesis that decreases in functional connectivity occur with deepening sedation.…”

Propofol-Induced Frontal Cortex Disconnection: A Study of Resting-State Networks, Total Brain Connectivity, and Mean BOLD Signal Oscillation Frequencies

“…Regional cerebral blood flow (rCBF) PET studies have shown that propofol-induced unresponsiveness is associated most with decreased blood flow in the thalamus and PCC/precuneus (Bonhomme et al, 2001;Fiset et al, 1999;Kaisti et al, 2003;Schlunzen et al, 2012;Xie et al, 2011). Most severe reductions in glucose use were seen in the thalamus, parietal and frontal DMN regions, and occipital lobe (Schlunzen et al, 2012;Sun et al, 2008).…”