Timothy C. Hain, MD •Page last modified: August 1, 2022 Also see: gen

Rebound nystagmus is a primary position nystagmus which is provoked by prolonged eccentric gaze holding. It appears after the eyes are returned to primary position.

There are two methods of eliciting rebound. The traditional method, which we will call "finger rebound", is to have the patient follow ones finger to one side, hold gaze there for 10 seconds (with constant encouragement by the examiner to keep looking), and then rapid return to central gaze. At that point, the examiner looks for a nystagmus that beats away from the previous direction of gaze holding, lasting for at least 5 beats. This should occur on BOTH sides -- i.e. it should reverse. A key point to this procedure is that it is done in the light.


A much more sensitive method than using one's finger of eliciting rebound is to use video-frenzel goggles. (as shown above). We will call this "Video-Frenzel Rebound". This is done in the dark. Otherwise the technique is similar. The video-frenzels make it much easier to see small amounts of nystagmus, and the lack of light also makes it much easier to see nystagmus when the eyes return to the center. We think that this is much more sensitive than bedside (but we are unaware of a paper proving this to be the case). We don't think optical Frenzels are a good way of testing for Rebound. In essence, this is because there is the "worst of both worlds" -- there is light, and there is also a magnified periphery.

Normal subject -- no significant nystagmus appears after 10 seconds of eccentric gaze holding.

Normal subjects only rarely have rebound -- mainly after very prolonged gaze-holding which is a different paradigm than discussed above (Gordon et al, 1986; Shallo-Hoffmann, Schwarze et al. 1990; Suzuki 1991)


Abnormal subject -- on the top panel (position), there is gaze evoked nystagmus beating to the right. When the eye returns to center, there is a left-beating nystagmus. Eye velocity gradually declines during gaze holding to the right, and also decays after return to center. Image courtesy of Dr. Dario Yacovino. CT scan of subject to left showing damage to the right cerebellar hemisphere. Image courtesy of Dr. Dario Yacovino.


An abnormal amount of rebound in the light, as shown above and below, consists of at least 3 beats of clear nystagmus, with the slow-phases directed towards the previous position of gaze. It must reverse direction according to the direction of previous gaze. When using the video-frenzel goggles, at least 5 beats should be observed. These are rather arbitrary limits of course, that might benefit from a new study.

Rebound Nystagmus -- a right-beating nystagmus occurs after 10 seconds of gaze holding to the left. This patient had a cerebellar disturbance.
A left-beating nystagmus appears after 10 seconds of gaze holding to the right.

Supplemental material : Video of rebound nystagmus.

sca6 ReboundSupplemental material : Video of rebound nystagmus in patient with SCA-6, courtesy of Dr. Dario Yacovino.

Rebound after gaze holding for periods more prolonged than 30 sec, or for eccentricities larger than about 45 deg is of uncertain significance as normal subjects may exhibit rebound under such circumstances (Gordon et al, 1986). Vertical rebound is rare but it can also occur.

Asymmetrical rebound is not rebound nystagmus.

Asymetrical Rebound -- is not rebound

If the eyes do not reverse direction from both left and right, it isn't rebound nystagmus. Similarly, if the eyes don't reverse after both up and down, it isn't rebound either.

While one could certainly claim that it is just "asymmetrical rebound", implying that it shares the same mechanism as "rebound rebound", avoiding using this term is an executive decision aimed at reducing contamination of the rebound nomenclature by other phenomena. The main one to worry about is "latent" spontaneous nystagmus -- the concept here being that eccentric gaze hold disrupts fixation, and after returning to center, there might be a transient unidirectional nystagmus. We are not so sure about this theory, but we think it is prudent to stay narrow -- no asymmetrical rebound.

Causes of Rebound nystagmus

Rebound is nearly always pathological, and is mainly related to brainstem or cerebellar disease (Lin et al, 1999). Accordingly, if an unusually large gaze-evoked nystagmus is observed, one should automatically look for rebound nystagmus. On the other hand, gaze-evoked nystagmus without rebound is usually of little significance. Rebound is always associated with poor smooth pursuit, but the poor pursuit does not inevitably mean that the person will have rebound.

Rebound nystagmus in patient with myotonic dystrophy -- type II.

Rarely rebound rarely occurs in situations where there is no obvious cerebellar disease. We have found patients with myotonic dystrophy who have rebound, possibly due to ocular myotonia. An example of this is shown above. (Ajroud-Driss et al, 2008). Persons with myotonia are slow to relax previously contracted muscles. If this occurred in the eye muscles, as others have suggested (Versino et al, 2002) it might cause rebound nystagmus.

Rebound using the video goggles is usually a sensitive and specific sign of cerebellar disturbance. Clinical situations in which rebound is commonly encountered include MS involving the pons, typically a lesion of the middle cerebellar peduncle, and ischemic pontine hypertensive lesions. Rebound nystagmus is also a feature of EA2 (Episodic ataxia, type 2). Rebound also can occur in congenital nystagmus, but it is not at all a universal feature of CN.

Topics for research.

Rebound nystagmus is one of those supposedly specific signs that hasn't gotten a lot of attention. Some low hanging fruit for research projects:

  1. How common is Rebound noted when using the "finger" technique vs. the video Frenzel technique. We would guess the video-Frenzel is a whole lot more sensitive but less specific.
  2. How sensitive is Rebound to neurological disease (in a prospective fashion). We have these papers that say that Rebound is always pathological (Lin and Young, 1999). This seems unlikely for the more sensitive version of the rebound test. .
  3. One could improve the Rebound test by having a flashing light (e.g. see the Gordon et al abstract from 1986). How much better is this than conventional methodology ?
  4. How often is Rebound found in congenital nystagmus (we would guess, a lot in the people with unstable tracking).
  5. Is it true that optical Frenzel testing of Rebounds is even less sensitive than finger Rebound ?