Pain Clinical Trial
Official title:
Modulation of Long-term Memory by the Experience of Pain During Sedation With Anesthetics
The purpose of this study is to determine the effects of pain on facilitating long-term auditory memory in the presence and absence of distinct intravenous anesthetics. The ability to identify previously presented words from a list assessed the degree of memory formation. In a subset of subjects, functional magnetic resonance imaging was used to identify the neural correlates of memory inhibition or facilitation by the combination of pain and anesthetic used.
This study adds specific details to the current incomplete body of knowledge examining the
effect of pain on memory formation under the influence of anesthetic agents.
Pain and anesthetic agents were administered as experimental variables in this study. Healthy
adult subjects were played repeated lists of words and performed several decision-making
tasks that encourage memory encoding. Some words were consistently paired with painful
electric shock, and was anticipated to improve subsequent memory performance specifically for
those items. The same experiment was repeated in all subjects during the administration of
1-2 possible agents that reduce memory formation: dexmedetomidine, a predominantly sedative
agent, and midazolam, a well-known amnestic agent, and ketamine, a well-known dissociative
analgo-sedative. The extent to which pain modulates memory performance under the effects of
the anesthetic agents was the primary outcome of interest.
Further, a subset of the subjects performed the same experimental procedures while undergoing
functional magnetic resonance imaging, which continuously reflects neuronal activity
throughout the brain. Classic memory areas were predicted to be activated by the auditory
processing task, but how these neural circuits change under the two anesthetic agents with
the concomitant experience of pain were of interest. It was anticipated that pain recruits a
parallel memory pathway using limbic structures, known for their involvement in fear
conditioning. Additionally, stronger and more diffuse cortical processing likely occurs with
concomitant pain, as level of sedation was reduced by this strong stimulus. Discovering the
anatomic correlates specific to each experimental variable (pain and anesthetic), and their
interplay, may help refine our model of brain function during the dynamics of pain and
sedation.
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