Timothy C. Hain, MD Page last modified: December 28, 2014
Impaired Fixation Suppression
The diagnosis of impaired fixation suppression is made by observing the effect of asking the subject to fix his eyes upon a clearly visible target, upon any ongoing nystagmus.The most commonly used test procedure is one described by Albert (1974). For at least one left and right-beating response (generally a caloric response), the patients nystagmus is recorded until shortly after the peak. At that time the examiner tells the patient ot open the eyes and fixat a small target for about 10 seconds. The fixation index is the ratio of nystagmus peak slow-phase velocity with fixation to nystagmus intensity with fixation removed (e.g. complete darkness or eyes closed). This number is often computed into a percentage by multiplying it by 100.
VENG -- FI = (eye-velocity while fixating)/(eye velocity at same point in dark)
Fixation suppression can also be calculated from rotatory chair tests by having the subject track a chair fixed laser projected on a wall.
R-chair FI = (peak eye-velocity while fixating)/(chair velocity)
However, this is a "different beast" than the fixation index from caloric testing, because the denomenator is different. Consider for example -- someone with bilateral vestibular loss.
The VENG-FI would be
0/0 -- indeterminent.
The R-chair FI would be
0/60, or 0.
Not the same thing at all.
The zero-divide problem is a gigantic one with the fixation index, and it is likely the reason why papers on the fixation index say that it is extremely variable (Schuchman and Uri, 1986).
There is evidence that there are multiple systems that participate in fixation suppression. Smooth pursuit can be used to suppress nystagmus, and some investigators have suggested that fixation suppression is redundant with the pursuit test. However, others have found that a different system, the "vestibular cancellation system", can also contribute to suppression (e.g. Tomlinson and Robinson, 1981)
For nystagmus induced by caloric input, Takemori and Cohen (1974) found the normal mean fixation index to be 48 + 10 percent. Similarly, Alpert reported the normal humans had a fixation index between 60 and 70 (Alpert, 1974). However, it is questionable whether these values are appropriate normal values for several reasons. It seems likely that fixation index should increase with age, as the pursuit declines with age, but fixation data according to age are not available. Similarly, fixation suppression is probably affected by the many other variables which affect pursuit. It also seems extremely likely that the efficiency of fixation is related to the intensity of nystagmus that one is attempting to suppress.
Peripheral vestibular nystagmus is usually well suppressed by fixation. Congenital nystagmus and many varieties of central nystagmus are unaffected by or even increased by fixation. Nystagmus which is increased by fixation is called "fixation nystagmus".
Here a strong congenital jerk-type nystagmus is seen during fixation (4 megabytes) . In this movie of jerk type Congenital nystagmus in dark (3 megabytes), the same patient as above is being recorded with a video system in complete darkness. Note that the nystagmus has nearly abated.
Maire and Duvoisin (1999) reported that visual suppression of static positional nystagmus is poor in central vestibular lesions and good in peripheral lesions. This seems reasonable, although it would seem unrealistic to rely on fixation suppression alone to differentiate between these two entities.
Bottom line: Based on many years of ENG lab experience, the author feels that fixation suppression of caloric responses adds very little to the diagnostic value of the test. Fixation suppression of rotatory chair responses, which is actually a different quantity -- eye velocity/chair velocity, is often valuable.