V. Bonhomme et al., Propofol anesthesia and cerebral blood flow changes elicited by vibrotactile stimulation: A positron emission tomography study, J NEUROPHYS, 85(3), 2001, pp. 1299-1308
We investigated the effects of the general anesthetic agent propofol on cer
ebral structures involved in the processing of vibrotactile information. Us
ing positron emission tomography (PET) and the H-2 O-15 bolus technique, we
measured regional distribution of cerebral blood flow (CBF) in eight healt
hy human volunteers. They were scanned under five different levels of propo
fol anesthesia. Using a computer-controlled infusion, the following plasma
levels of propofol were targeted: Level W (Waking, 0 mug/ml), Level 1 (0.5
mug/ml), Level 2 (1.5 mug/ml), Level 3 (3.5 mug/ml), and Level R (Recovery)
. At each level of anesthesia, two 3-min scans were acquired with vibrotact
ile stimulation of the right forearm either on or off. The level of conscio
usness was evaluated before each scan by the response of the subject to a v
erbal command. At Level W, all volunteers were fully awake. They reported b
eing slightly drowsy at Level 1, they had a slurred speech and slow respons
e 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 t
he left thalamus and in several cortical regions, including the left primar
y somatosensory cortex and the left and right secondary somatosensory corte
x. During anesthesia, propofol reduced in a dose-dependent manner rCBF in t
he thalamus as well as in a number of visual, parietal, and prefrontal cort
ical regions. At Level 1 through 3, propofol also suppressed vibration-indu
ced increases in rCBF in the primary and secondary somatosensory cortex, wh
ereas the thalamic rCBF response was abolished only at Level 3, when volunt
eers lost consciousness. We conclude that propofol interferes with the proc
essing of vibrotactile information first at the level of the cortex before
attenuating its transfer through the thalamus.