Hyperventilation Induced Nystagmus

Timothy C. Hain, MD Page last modified: January 5, 2008

This page is written for clinicians.

The way that I test for hyperventilation induced nystagmus in my dizzy clinic. There is also a MOVIE: hvt small.avi (15 meg) Hyperventilation induced nystagmus in person with left sided acoustic neuroma. This is a rather long (1.5 minute) clip. Many other movies can be found on the site DVD:

Hyperventilation (HVT) is thought to induce symptoms in certain populations of people through it's effect on lowering the concentration of carbon dioxide in the blood. Most authors report nystagmus, but there are also reports that it increases postural sway in both normal subjects and persons with bilateral vestibular loss. (Sakellari, V. and A. M. Bronstein, 1997)

The early literature suggested that this was a sign of psychogenic (psychiatric) disturbance (Drachman and Hart, 1972), but later workers using better technology to monitor eye movements suggest that nystagmus induced by hyperventilation is a good sign of vestibular disease (see review that follows). Some workers have suggested that hyperventilation increases the gain of vestibular responses, unmasking asymmetries ( Lempert and Brevern, 1996; Theunissen et al, 1986). This conclusion, if indeed the case, may be relevant to findings in persons with unilateral vestibular loss.

The main problem with this test is false positives. If a test can be common in normal persons as well as patients with disease, because there are generally more normal persons presenting for testing than patients with disease, the number of false positives can greatly exceed the true positives.

The conclusion of this review is that hyperventilation is an excellent test for vestibular disorders, when combined with other evidence to increase the specificity of the test.

What hyperventilation induced nystagmus (HVIN) looks like.

HVIN usually beats toward the side of lesion (Minor et al., 1999), as opposed to head-shaking nystagmus or vibration induced nystagmus, which initially beats away from the lesion. This has been suggested in the past as evidence that the mechanism for HVT nystagmus is to improve conduction in apartially demyelinated vestibular nerve.

This mechanism would predict the opposite direction for patients who have nystagmus after a complete vestibular lesion, as there is no longer a mechanism for improving vestibular function.

Hyperventilation induced nystagmus (slow phase velocity)

Methodology of the hyperventilation test

Most investigators simply ask patients to breath deeply and rapidly for 30 breaths, or for a given duration (i.e. 30 seconds to 3 minutes). This method clearly is somewhat difficult to quantify as some patients will avoid deeply breathing (perhaps out of anxiety), while others are "good" hyperventilators, and one may have to remind them to stop.

The way I do it in the clinic is to use a video-ENG device (as shown at the top of this page), which allows me to see the eye without allowing vision of the person who is being tested. After watching for spontaneous nystagmus in darkness for about 10 seconds, I hyperventilate the individual for 30 deep breaths, in complete darkness. I steady the patient by holding on to one of their shoulders while doing this as HVT often induces some ataxia. I observe (and record to DVD) the nystagmus during the whole procedure. Generally this test is combined with the vibration test. A "significant" change in nystagmus -- generally a reversal in direction, is counted as a positive HVIN. No change, minor downbeating nystagmus, or accentuation of already present nystagmus, is counted as a negative HVIN.

There have been few attempts to do this in a more rigorous way. Wilson and Kim (1981) studied ventilation testing with electronystagmography, and compared hyperventilation (which lowers PCO2), as well as oxygen (which increases PCO2). In a study of two groups totaling over 700 patients, they found that oxygen testing is only occasionally positive (2.5%) and is of little practical value. Hyperventilation testing was positive 8% of the time but rarely alone, and had no localizing value. When hyperventilation and oxygen tests are both positive, the nystagmus may be in opposite directions. In 6 of 18 patients with acoustic neurinomas, hyperventilation produced transitory direction-changing nystagmus.

Eye movements (nystagmus) may be recorded with many devices ranging from direct observation, Frenzel goggles, video systems, EOG, and scleral eye coil. As might be expected, the most sensitive method is recording in darkness using a low-noise method such as video or scleral eye coil. The least sensitive method is use of unaided observation or optical Frenzels, or EOG. Little has been published concerning use of video-eye movement recordings. This methodology would be expected to be useful.

Evidence for the utility of hyperventilation in vestibular disorders.

Many studies have documented the utility of hyperventilation in vestibular disorders as well as a relative paucity of nystagmus in persons who are otherwise normal.

Normal persons.

Bance et al. (1998). found HVT nystagmus in 3.5% of normal persons. Monday and Tetreault (1980) found no effect on caloric nystagmus after 90 seconds of hyperventilation. These studies suggest that the rate of false-positives is low. Of course, the frequency of false positives will depend greatly on the method of recording (see above).

Persons with acoustic neuromas. There have been many papers on this subject. These observations generally confirm our own clinical impression. Acoustic neuroma is simply an example of a vestibular problem that involves the 8th nerve. Other conditions -- meningioma's, any problem that affects the nerve, would be expected to have similar findings.

• Bance, M. L., M. O'Driscoll, et al., 1998 reported that 82% of patients prior to acoustic surgery had HVIN and that all patients post surgery had HVIN. This would suggest that HVIN does not require a demyelinated vestibular nerve. We suspect that in these latter patients, the nystagmus did not reverse direction with hyperventilation.
• Chee, N. W. and H. M. Tong (2002). Reported 2 patients with ipsilateral beating nystagmus after hyperventilation.
• Minor, L. B., T. Haslwanter, et al. (1999). Reported 6 patients with ipsilateral beating nystagmus after hyperventilation.
• Robichaud, J., H. DesRoches, et al. (2002). Found HVT nystagmus in both persons with acoustics and persons with vestibular lesions in the inner ear rather than nerve (defined by the rather weak sign of a 25% caloric weakness). They found 58% of persons with acoustic neuroma to be positive, as opposted to 18% of the caloric weakness group.
• Wilson, W. R. and J. W. Kim (1981). Found 6/18 patients with acoustics had a transient nystagmus. This study is suspect as EOG was used rather than newer video methodology.

Persons with other disorders.

• Skliut, I. A., V. B. Shalkevich, et al. (1987). Reported nystagmus and symptoms 36 patients with brain stem injuries of various origins. This is reasonable, but as brainstem disorders are rare causes of dizziness, and HVIN occurs in normal persons, other findings would have to be used to increase specificity.
• Walker, M. F. and D. S. Zee (1999). Reported the effect of hyperventilation on downbeat nystagmus in cerebellar disorders. In four of eight patients, hyperventilation produced an increase in the slow-phase velocity of downbeat nystagmus. They speculated that this effect may be mediated through metabolic effects on cerebellar calcium channels. In our clinical practice, we often have seen downbeating nystagmus in otherwise normal persons, induced by HVT.
• Hain - -unpublished observations. In my practice, I have often noted patients who have symptoms most easily explained by irritibility of the vestibular nerve, have HVIN which is oppositely directed to their spontaneous nystagmus (if present) or vibration induced nystagmus.

Bottom line for hyperventilation induced nystagmus:

Hyperventilation is a useful test in diagnosing disorders of the vestibular nerve. In our opinion, HVIN is mainly useful when it is found in persons with no other signs of vestibular disorder, and also a known acoustic neuroma or the "quick spin" symptom (which is suggestive of vestibular paroxysmia). In this context, it induceds a nystagmus that beats away from the side of lesion. The main problem with the test is it's positivity in otherwise normal persons. Because of this, it should be combined with other tests, such as vibration testing that induces a nystagmus in the opposited direction, to improve the specificity.

Research project opportunities

As noted above, HVT is a good dizziness test which has not been studied to a great extent, perhaps because it has been incorrectly assigned as a test for anxiety, by past studies using less sensitive methodology than we now have available. There are only about 20 very relevant papers in the literature accessed by Pubmed (as of 3-2006).

It would be interesting to know many things -- how sensitive is the response to the number of breaths ? How specific is the combination of HVT with another test (such as spontaneous nystagmus, head-shaking or vibration ?) -- especially the direction changing nystagmus. Does the test work for vestibular neuritis ? Can the unsteadiness induced by hyperventilation in various clinical contexts be quantified ? Is it meaningful ?

References:

• Bance, M. L., M. O'Driscoll, N. Patel, et al. (1998). "Vestibular disease unmasked by hyperventilation." Laryngoscope108(4 Pt 1): 610-4.
• Baranov, V. M., M. A. Tikhonov, E. I. Matsnev, et al. (1991). "[Role of external respiration in the formation of the autonomic component in motion sickness]." Kosm Biol Aviakosm Med25(5): 20-4.
• Chee, N. W. and H. M. Tong (2002). "Acoustic neuroma presenting as exercise-induced vertigo." J Laryngol Otol 116(8): 630-2.
• Drachman, D. A. and C. W. Hart (1972). "An approach to the dizzy patient." Neurology22(4): 323-34.
• Minor, L. B., T. Haslwanter, D. Straumann, et al. (1999). "Hyperventilation-induced nystagmus in patients with vestibular schwannoma." Neurology 53(9): 2158-68.
• Modugno, G. C., S. Marcellini, A. Pirodda, et al. (1988). "The influence of hyperventilation on caloric and optokinetic responses in normal and pathological subjects." Adv Otorhinolaryngol42: 108-15.
• Monday, L. A. (1979). "[Effect of hyperventilation on the vestibular system]." J Otolaryngol8(1): 71-6.
• Monday, L. A. and L. Tetreault (1980). "Hyperventilation and vertigo." Laryngoscope90(6 Pt 1): 1003-10.
• Robichaud, J., H. DesRoches and M. Bance (2002). "Is hyperventilation-induced nystagmus more common in retrocochlear vestibular disease than in end-organ vestibular disease?" J Otolaryngol31(3): 140-3.
• Sakellari, V. and A. M. Bronstein (1997). "Hyperventilation effect on postural sway." Arch Phys Med Rehabil78(7): 730-6.
• Sakellari, V., A. M. Bronstein, S. Corna, et al. (1997). "The effects of hyperventilation on postural control mechanisms." Brain120 ( Pt 9): 1659-73.
• Skliut, I. A., V. B. Shalkevich, S. A. Likhachev, et al. (1987). "[A subclinical sign of vestibular pathology of the brain stem]." Zh Nevropatol Psikhiatr Im S S Korsakova87(4): 542-4.
• Theunissen, E. J., P. L. Huygen and H. T. Folgering (1986). "Vestibular hyperreactivity and hyperventilation." Clin Otolaryngol Allied Sci11(3): 161-9.
• Walker, M. F. and D. S. Zee (1999). "The effect of hyperventilation on downbeat nystagmus in cerebellar disorders." Neurology53(7): 1576-9.
• Wilson, W. R. and J. W. Kim (1981). "Study of ventilation testing with electronystagmography." Ann Otol Rhinol Laryngol90(1 Pt 1): 56-9.

© 1996-2007, Timothy C. Hain