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Department of Anesthesiology

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Low-dose propofol-induced amnesia is not due to a failure of encoding: left inferior prefrontal cortex is still active.

TitleLow-dose propofol-induced amnesia is not due to a failure of encoding: left inferior prefrontal cortex is still active.
Publication TypeJournal Article
Year of Publication2008
AuthorsVeselis RA, Pryor KO, Reinsel RA, Mehta M, Pan H, Johnson R
Date Published2008 Aug
KeywordsAdult, Amnesia, Cerebrum, Dose-Response Relationship, Drug, Electroencephalography, Female, Humans, Hypnotics and Sedatives, Male, Positron-Emission Tomography, Prefrontal Cortex, Propofol, Psychomotor Performance, Thiopental

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: Seventeen volunteer participants (12 men; aged 30.4 +/- 6.5 yr) had regional cerebral blood flow measured using H2O 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 microg/ml target concentration), placebo with a divided attention task (n = 5), or thiopental at sedative doses (n = 6, 3 microg/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 h later (median recognition of 35% [interquartile range, 17-54%] of words presented during propofol vs. 65% [38-91%] before drug; P < 0.05). Statistical parametric mapping analysis identified a region of interest of 6.6 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, activation in the LIPFC should be minimal. Because 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.

Alternate JournalAnesthesiology
PubMed ID18648230
PubMed Central IDPMC2599915
Grant ListR01 GM058782-01A2 / GM / NIGMS NIH HHS / United States
R01 GM58782 / GM / NIGMS NIH HHS / United States