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Timothy C. Hain, MD 
Page last modified:
November 21, 2009
This page is written for clinicians.
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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.
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.
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| 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. There is a tiny risk of triggering a seizure, as for example, in persons with "petit mal" epilepsy. For this reason, we suggest that the examiner stand close to the subject and be ready to assist.
I 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. They should be fast and deep. I steady the patient by holding on to one of their shoulders or the top of their head 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.
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.
In the author's clinical practice, HVT is done on nearly all new patients. Here are his observations:
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.
We have noticed (but not published) that patients with tumors of the 8th nerve who have been treated with Gamma Knife nearly always have HVT. An very strong example of HVT induced nystagmus is shown here in this movie. The nystagmus beats toward the side of radiation.
Persons with other disorders.
Nothing has been written concerning treatment of HVIN. If HVIN is due to nerve irritibility, nerve stabilization agents should work. As HVIN is triggered by hypocapnea and associated metabolic alkalosis, methods of avoiding this should work. As HVIN is a nystagmus, drugs that suppress nystagmus might work. As HVIN is probably associated with partially damaged nerves, vestibular nerve section (i.e. taking out an acoustic neuroma) should work too.
Methods of avoiding hypocapnea include "breathing into a paper bag", and drugs that induce acidosis such as acetazolamide.
None of these treatments has been assessed in a quantitative fashion, and their utility is therefore simply a matter of conjecture as well as anecdotal evidence.
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.
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 ?
How do drugs affect HVIN ?
How much unsteadiness is induced by HVT (perhaps use a posturography system), in normal subjects and in patients with acoustic neuroma ?
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