Key result
Pharmacological targeting of GABA and adrenergic pathways may stabilize anesthesia levels and prevent awareness.
Discusses the theoretical models of memory formation and implicit memory during anesthesia.
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Should not alter anesthesia protocols yet; leaves open efficacy of targeted agents pending prospective trials.
This process, however, is completely outside of conscious control and therefore does not necessarily imply that our patient opens his eyes oris capable of interacting with the operator to show us the performance of the first phase of the program.According to the classic explanation of the AA genesis, the information is transferred from the sensory memory to the short-term memory through the process of attention, a cognitive process that consists in concentrating selectively on one aspect of a context, ignoring the other surrounding elements.The information in short-term memory is available for a short period of time (usually from 10 to 15 seconds, or sometimes up to a minute) and is destined to disappear forever, unless the engrams are transferred to the next phase of maintenance, the long-term memory.This step poses a big obstacle to Atkinson's model.While this system provides that consolidation-necessary for establishing long term memory-requires motivation, personal reference, interest and attention, it is well known that transferring of information to long term memory doesn't necessary require the presence of consciousness.Implicit memory (and the phenomenon of the awareness without recall) is an example of unconscious memory formation during anesthesia.
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A 2015 study conducted a review in Anesthesia awareness. Pharmacological interventions was evaluated. Pharmacological interventions targeting various neurotransmitter pathways, including GABA and adrenergic receptors, offer potential strategies to stabilize anesthesia levels and prevent anesthesia awareness.
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