Disconjugate gaze

[Hork Bajir]

I know from reading old threads that folks on this forum have strong ANECDOTAL beliefs regarding disconjugate gaze, and what it means in terms of anesthetic depth/risk of laryngospasm/excitatory state/etc. I share some of these beliefs based on my own anecdotal experience. But what I'm wondering is this:

1) What is the presumed mechanism behind disconjugate gaze under anesthesia, and what (if anything) does it actually tell us about the neurophysiologic state?
2) Is there any hard data that appearance or disappearance of disconjugate gaze can tell us anything meaningful regarding the likelihood that a patient will respond in a certain way to a certain type of stimulus?

My literature search turned up surprisingly little on this topic... Seems like Guedel described it, and then everyone said "yep seems about right" and stopped there.

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[pgg]

If you look at people that have "stage 2" signs as a part of their normal lives, because of other pathologic states -

Gaze palsies are brainstem problems. Spastic movement disorders and dystonias are a bit higher up but still well south of cortex. The other signs consistent with stage 2, notably irregular respiratory drive and elevated heart rate, are also medulla mediated functions. Nausea & vomiting is all medulla.

I'm not a neurologist obviously, but it's always sort of made sense to me that the different signs we associate with stage 2 all come from the same general region of the brain.

 

[DM27]

The way that I ultimately view anesthesia is that, mainly with volatiles, is that you first anesthetize the human brain/seat of consciousness, followed by the lizard brain. When you see someone with a disconjugate gaze from an anesthetic agent, you have a lizard brain that is mostly awake, but a human brain that's still a bit behind.

You can also view anesthesia induction and emergence as the progression of a traumatic head injury in both directions (glasglow coma reliably decreases with induction as you progress through the levels of sedation, and returns in a similar, but less well organized manner as you progress through emergence.

I would say there is no hard data for any of this as you cannot reliably predict the speed that individual portions of the brain will begin to function in a coherent manner again between individuals. The same way many people act differently from each other when drunk.

 

[deleted875186]

Agreed, there is

I know from reading old threads that folks on this forum have strong ANECDOTAL beliefs regarding disconjugate gaze, and what it means in terms of anesthetic depth/risk of laryngospasm/excitatory state/etc. I share some of these beliefs based on my own anecdotal experience. But what I'm wondering is this:

1) What is the presumed mechanism behind disconjugate gaze under anesthesia, and what (if anything) does it actually tell us about the neurophysiologic state?
2) Is there any hard data that appearance or disappearance of disconjugate gaze can tell us anything meaningful regarding the likelihood that a patient will respond in a certain way to a certain type of stimulus?

My literature search turned up surprisingly little on this topic... Seems like Guedel described it, and then everyone said "yep seems about right" and stopped there.

I also tried to look up data on stage 2 before and found very little. I always foundered if propofol and opioid anesthesia really had any appreciable stage 2.