In the present study, we used positron emission tomography to investigate changes in regional cerebral blood flow (rCBF) during a general anesthetic infusion set to produce a gradual transition from the awake state to unconsciousness. Five right-handed human volunteers participated in the study. They were given propofol with a computer-controlled infusion pump to achieve three stable levels of plasma concentrations corresponding to mild sedation, deep sedation, and unconsciousness, the latter defined as unresponsiveness to verbal commands. During awake baseline and each of the three levels of sedation, two scans were acquired after injection of an H215O bolus. Global as well as regional CBF were determined and correlated with propofol concentrations. In addition, blood flow changes in the thalamus were correlated with those of the entire scanned volume to determine areas of coordinated changes. In addition to a generalized decrease in global CBF, large regional decreases in CBF occurred bilaterally in the medial thalamus, the cuneus and precuneus, and the posterior cingulate, orbitofrontal, and right angular gyri. Furthermore, a significant covariation between the thalamic and midbrain blood flow changes was observed, suggesting a close functional relationship between the two structures. We suggest that, at the concentrations attained, propofol preferentially decreases rCBF in brain regions previously implicated in the regulation of arousal, performance of associative functions, and autonomic control. Our data support the hypothesis that anesthetics induce behavioral changes via a preferential, concentration-dependent effect on specific neuronal networks rather than through a nonspecific, generalized effect on the brain.
These findings suggest that the unconsciousness produced by propofol is mediated at least in part via interruption of central cholinergic muscarinic transmission.
Femoral nerve block (FNB) does not consistently produce anesthesia of the obturator nerve. In this single-blind, randomized, controlled study we added a selective obturator nerve block (ONB) to FNB to analyze its influence on postoperative analgesia after total knee replacement (TKR). Before general anesthesia, 90 patients undergoing TKR received FNB (Group 1), FNB and selective ONB (Group 2), or placebo FNB (Group 3). Postoperative analgesia was further provided by morphine IV via patient-controlled analgesia. Analgesic efficacy and side effects were recorded in the first 6 h after surgery. Adductor strength decreased by 18% +/- 9% in Group 1 and by 78% +/- 22% in Group 2 (P < 0.0001). Total morphine consumption was reduced in Group 2 compared with Groups 1 and 3 (P < or = 0.0001). Patients in Group 2 reported lower pain scores than those in Groups 1 and 3 (P = 0.0003). The incidence of nausea was more frequent in Groups 1 and 3 (P = 0.01). We conclude that FNB does not produce complete anesthesia of the obturator nerve. Single-shot FNB does not provide additional benefits on pain at rest over opioids alone in the early postoperative period. The addition of an ONB to FNB improves postoperative analgesia after TKR.
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.
Previous studies reporting an incidence of obturator nerve block after three-in-one block may have mistaken a femoral nerve block for an obturator nerve block in 100% of cases when the cutaneous distribution of the obturator nerve was assessed on the medial aspect of the thigh. The only way to effectively evaluate obturator nerve function is to assess adductor strength.
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