Monitoring Anesthetic Brain States - Effects of Different Anesthetics on the Brain

Monitoring Anesthetic Brain States - Effects of Different Anesthetics on the Brain is a topic covered in the Clinical Anesthesia Procedures.

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Propofol

Propofol

  1. Neurophysiology: Agonist at the gamma-aminobutyricacid (GABAA) receptors which function to enhance inhibition
    1. There is usually a balance between excitatory and inhibitory control of pyramidal neurons. Propofol enhances the inhibitory effects.
    2. Affects the thalamus by increasing inhibition which decreases excitatory inputs to the cortex.
  2. EEG signatures
    1. The EEG signatures are markers of altered arousal states induced by each anesthetic.
    2. Propofol displays a characteristic alpha oscillation (8 to 12 Hz) and a slow oscillation (0.5 to 1 Hz).
  3. Putative mechanism EEG effect
    1. During the normal awake state there is a constant exchange of information between the thalamus and cortex. Modeling studies have shown that the EEG alpha oscillations (8 to 12 Hz) observed with propofol likely represent an alpha oscillation between the thalamus and the frontal cortex.
    2. The slow oscillation seen with propofol is associated with neurons across the cortex being activated and inactivated at different times (up-down states). This fragments brain activity into asynchronous windows and impairs communication, which is also referred to as “cortical fragmentation” (Fig. 11.5).

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Propofol

Propofol

  1. Neurophysiology: Agonist at the gamma-aminobutyricacid (GABAA) receptors which function to enhance inhibition
    1. There is usually a balance between excitatory and inhibitory control of pyramidal neurons. Propofol enhances the inhibitory effects.
    2. Affects the thalamus by increasing inhibition which decreases excitatory inputs to the cortex.
  2. EEG signatures
    1. The EEG signatures are markers of altered arousal states induced by each anesthetic.
    2. Propofol displays a characteristic alpha oscillation (8 to 12 Hz) and a slow oscillation (0.5 to 1 Hz).
  3. Putative mechanism EEG effect
    1. During the normal awake state there is a constant exchange of information between the thalamus and cortex. Modeling studies have shown that the EEG alpha oscillations (8 to 12 Hz) observed with propofol likely represent an alpha oscillation between the thalamus and the frontal cortex.
    2. The slow oscillation seen with propofol is associated with neurons across the cortex being activated and inactivated at different times (up-down states). This fragments brain activity into asynchronous windows and impairs communication, which is also referred to as “cortical fragmentation” (Fig. 11.5).

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