10 research outputs found
A neuroanatomical construct for the amnesic effects of propofol,”
Background: This study was designed to identify neuroanatomical locations of propofol's effects on episodic memory by producing minimal and maximal memory impairment during conscious sedation. Drug-related changes in regional cerebral blood flow (rCBF) were located in comparison with rCBF increases during a simple word memory task. Methods: Regional cerebral blood flow changes were assessed in 11 healthy volunteers using H 2 15 O positron emission tomography (PET) and statistical parametric mapping (SPM99) at 600 and 1,000 ng/ml propofol target concentrations. Study groups were based on final recognition scores of auditory words memorized during PET scanning. rCBF changes during propofol administration were compared with those during the word memory task at baseline. Results: Nonoverlapping memory effects were evident: low (n ‫؍‬ 4; propofol concentration 523 ؎ 138 ng/ml; 44 ؎ 13% decrement from baseline memory) and high (n ‫؍‬ 7; 829 ؎ 246 ng/ml; 87 ؎ 6% decrement from baseline) groups differed in rCBF reductions primarily in right-sided prefrontal and parietal regions, close to areas activated in the baseline memory task, particularly R dorsolateral prefrontal cortex (Brodmann area 46; x, y, z ‫؍‬ 51, 38, 22). The medial temporal lobe region exhibited relative rCBF increases. Conclusions: As amnesia becomes maximal, rCBF reductions induced by propofol occur in brain regions identified with working memory processes. In contrast, medial temporal lobe structures were resistant to the global CBF decrease associated with propofol sedation. The authors postulate that the episodic memory effect of propofol is produced by interference wit
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Low-dose Propofol–induced Amnesia Is Not due to a Failure of Encoding
Background—Propofol may produce amnesia by affecting encoding. The hypothesis that propofol
weakens encoding was tested by measuring regional cerebral blood flow during verbal encoding.
Methods—17 volunteer participants (12 M, 30.4±6.5 years old) had regional cerebral blood flow
measured using H2O15 positron emission tomography during complex and simple encoding tasks
(deep vs. shallow level of processing), to identify a region of interest in the left inferior prefrontal
cortex (LIPFC). The effect of either propofol (n=6, 0.9 mcg/ml target concentration), placebo with
a divided attention task (n=5), or thiopental at sedative doses (n=6, 3 mcg/ml) on regional cerebral
blood flow activation in the LIPFC was tested. The divided attention task was expected to decrease
activation in the LIPFC.
Results—Propofol did not impair encoding performance or reaction times, but impaired recognition
memory of deeply encoded words 4 hours later (median recognition of 35% (17–54 interquartile) of
words presented during propofol versus 65% (38–91) before drug, p<0.05). Statistical parametric
mapping analysis identified a region of interest of 6.6 cu.cm. in the LIPFC (T=7.44, p=0.014).
Regional cerebral blood flow response to deep encoding was present in this region of interest in each
group before drug (T>4.41, p<0.04). During drug infusion only the propofol group continued to have
borderline significant activation in this region (T=4.00, p=0.063).
Conclusions—If the amnesic effect of propofol were solely due to effects on encoding, then
activation in LIPFC should be minimal. As LIPFC activation was not totally eliminated by propofol,
the amnesic action of propofol must be present in other brain regions and/or affect other memory
processes