Post-Rotary Nystagmus and Concussion

You may be familiar with the concept of post-rotary nystagmus, in which spinning around in circles makes you dizzy from sloshing up your semicircular canals, and sets off a characteristic oscillating motion of your eyes when you stop spinning.  Here is a real-time recording of what the eyes of a normal child are doing during rotation and then immediately post-rotation, as projected onto a video monitor.

We know that visual fixation under normal viewing conditions serves to dampen post-rotary nystagmus and stabilize balance through visual-vestibular interaction.  Frenzel goggles are high power convex lenses that serve to magnify the subjects’ eyes making the post rotary nystagmus more visible to the examiner, and also to blur the visual field significantly to impair the dampening of post-rotary nystagmus.  Here is a video of a young adult’s eyes during post-rotary nystagmus, wearing Frenzel goggles.

In a search of the literature I was unable to find any publications on the effect of concussion on post-rotary nystagmus.  By way of this post I am theorizing that concussion impairs post-rotary nystagmus in a way similar to Frenzel goggles, rendering the individual as “being in a fog”, as occurs with the high plus lenses.  Specifically, impaired visual-vestibular interaction should inhibit the ability of the visual system to dampen post-rotary nystagmus.  This would increase the decay time of pos-rotary nystagmus, and would be measurable objectively.

One of the holy grails of concussion testing is an objective measure that does not require responses on the part of the individual suspected of being concussed, or interpretation of the individual’s responses.  I am proposing that post-rotary nystagmus can be measured objectively through a sensor, either in glasses or though a fixation target, and that a baseline measure can be established of the duration of post-rotary nystagmus (PRN).

When testing an athlete, I am proposing that concussion prolongs PRN time, and impedes stabilization of gaze than dampens PRN.  This has great potential to complement other tests used for both remove from play as well as return to play, or return to learn.  It is entirely independent of intellect, and requires limited if any instructional set, or interpretation of verbal responses.  Baseline data can be established for post-rotary nystagmus done in the standing or vertical position, as opposed to sitting in a chair, which would be more pertinent for athletes.  For return to learn or driving, being seated in a chair may be more pertinent.

12 thoughts on “Post-Rotary Nystagmus and Concussion

  1. Don’t OT’s consider prolonged post rotary nystagmus to indicate impaired vestibular function in non-concussed, but delayed kids? I wonder if they have some insight into this, at least the ones who work with TBI pts.

  2. Changes in duration of rotary nystagmus without a restricted or blurred field would certainly help document the visual involvement, the ability of visual fixation to damper nystagmus. I’m not sure what a blurred or restricted field measurement would tell us? Couldn’t damage to a specific area of the brain linking the canals to eye-movement system, damper the nystagmus in the first place?

  3. Len,
    Jean Ayers did some work with PRN back in the day which is where our norms come from. Our office has conducted thousands of PRN tests over the years and here is what we have found. “normal” (meaning non-neurologic insult diagnosis) patients should have a PRN of 7-10 seconds in all isolated canal positions. What we find clinically is that some patients (especially with a history of multiple tympanoplasty/ies) have wildly different results. Concussed patients can rarely finish the test if they have any motion sensitivity. My thought is that in the concussed patient (known or not known) the neural integrator has a hard time with controlling the signal from the vestibular system and therefore prolongs the signal (that is not allowing vision to integrate/refixate). I would love to see some formal studies on this.

    Also, after VT (cringe) we may still have some “non normal” numbers, but they are much more consistent (ie- 16 seconds in all positions rather than 15, 8, 22, 14, 10, 26 responses). Next student I have will be pulling some charts and doing research. Thanks

    • Thanks, Jason. I noted in my comments below to Michael that Ayres introduced this as part of her Southern California test battery. There is some controversy about norms for the SCPNT, as she called it, but I like the concept as a diffuse CNS indicator of vestibular function, as noted here:

      I did a literature review for use of the SCPNT in mTBI and came up empty. I agree with your thoughts on the significant impact that concussion should have on PRN, and it blows me away that there don’t seem to be any published studies on PRN and concussion.I am very interested in what you come up with as you do your chart review, and will look forward to what you come up with. Thanks again!

      • I’ve seen that article. Our office has done thousands of PRN tests and there are many, many factors that need to be considered. I would never do PRN testing on a patient with ABI. Too much. On the “normo-typic” population, whatever that may be, we find that we get 2 results: Hypo PRN responders (visual dominance) which we consider less than 7 seconds of PRN or hyper PRN responders >12 seconds (vestibular dominance). There are many sub-categories. We treat them very differently in therapy and have some really interesting results. Next OD student I get, I think, we will do a retrospective analysis of the data. I’ll likely need help. 😉

  4. I’ve been thinking about it for awhile. Consider that we’re talking about an athlete who is borderline for return to play. I doubt having him turn around a few times would be any worse than sending him back into play when he (or she) is not ready yet. This happens all to often. And PRN is a very direct physiologic measure requiring no cognitive response whatsoever. If consensus in the field is that even three revolution has the potential to do harm, another possibility is to use an OKN drum, which has a normal post OKN stabilization time to normal fixation which, I would also theorize, is delayed when an athlete is concussed. While OKN testing may make an mTBI patient transiently dizzy, there is nothing physical going on regarding spinning and brain edema or related issues.

  5. Your patent is on the right track,Jason, but if I understand it correctly you’re looking at quantifying the difference in angle between the two eyes objectively in real time as they’re de-coupled. I’m looking for something that requires the sensitivity to measure small high speed oscillatory movmement OU, and when it is nulled by stable fixation.

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