Head-Impulse Test (HIT)

This material is intended for clinicians and vestibular scientists.

Timothy C. Hain, MD

Page last modified: May 17, 2008

The HIT is a bedside technique used to diagnose reduction in vestibular function in one ear vs. the other. It is one of several bedside methods offering similar information. The table below provides our opinions regarding their general clinical characteristics.

Method:

The patient's head is rapidly rotated by the examiner (abruptly and with high acceleration) about 20 degrees to the right or left. The patient is told to fixate on the examiners nose. After the head stops, the examiner watches the patient's eye to see whether or not a refixation saccade is needed to get the patient's eye on the examiners nose. A reliable and significant refixation saccade is judged as positive.

This test is requires a subjective judgement on the part of the examiner, who also controls the stimulus.

The HIT test also is vulnerable to prediction as patients who know which way their head will be turned, can generate "covert" saccades. (Weber et al, 2008). Another name for these saccades are "vestibular catch-up saccades". (Tian and Crane, 2000)

The HIT test also requires rapid head movements, which may cause neck pain in persons with arthritis. So far, we are unaware of any reports of carotid or vertebral dissection due to the HIT, but we would expect that it would have a similar prevalence of vascular compromise as do similar chiropractic maneuvers.

Variants of the HIT:

Allowing the patient to rotate their own head (active head rotation) is not as sensitive as the passive HIT as patients can use prediction to normalize their performance (Black et al. 2005).

Instrumentation (scleral eye coil recording) can make this test capable of detecting disturbances of vertical canals (Cremer et al, 1998). Practically however, it is not possible to use scleral eye coils in routine clinical practice. Similarly, motorized devices can be used to automate the test (Aalto et al, 2002). Again, this is impractical for clinical use.

The "head-heave" test is a similar procedure, where the head is displaced sideways rather than rotated. The heave is about 5-6 cm in excursion. Like the HIT, the head-heave test depends on a subjective judgement of the examiner, and is likely affected by prediction (although the test is very little studied).

Mechanism

The HIT, like head-shaking nystagmus, is a method of measuring asymmetries in vestibular gain.  The asymmetry in vestibular gain was first observed by Ewald (Ewald 1892), and is referred to as Ewald’s second law. In its specific form it states that ampullopetal endolymph flow in the horizontal canal causes a greater response than ampullofugal endolymph flow (Ewald 1892; Baloh and Honrubia 2001). In its general form it states that excitation is a relatively better vestibular stimulus than is inhibition (Leigh and Zee 2006).  Ewald’s second law is thought to be due to the inability of inhibitory stimuli to decrease vestibular nerve firing rates to less than zero (Baloh, Honrubia et al. 1977; Hain and Spindler 1993).

Bilateral mathematical model of vestibular processing from Hain (Hain, Fetter et al. 1987). This early model does not include acceleration in the canal transfer function, but otherwise contains the general features described below.

We can take these ideas and convert them into a more quantitative form. We will not do this formally, but just try to get the general concepts converted into a mathematical form. First, firing rate in the vestibular nerve is mainly proportional to head velocity, but there is also a component due to head acceleration. So one can (approximately) say that:

Firing rate = K0+Kv*head-velocity + Ka * head-acceleration

(Vestibular physiologists would shudder at this oversimplification). In the figure above, the acceleration term has been left out -- so to model the HIT, one would need to add an extra term to the canal transfer function as well as to the central processing in order to take out the acceleration sensitivity (so that eye velocity doesn't become proportional to head acceleration).

Continuing, because firing rate has a lower limit of 0 spiks/second, there is a saturation of the overall response for the nerve. In the diagram above, this is the little box with the curved line (nonlinearity) inside of it.

Net firing rate = saturation*Firing rate

The vestibular system is hooked up in "push-pull" so that the firing rate for one side is subtracted from the other. In other words:

central firing rate = right-left.

This is the circle with the +- in the center. When both vestibular nerves are working, net firing rate (right-left) shows a saturation in both direction.

When just one vestibular nerve is working, there is a strong response for rotation in that excites the remaining nerve (i.e. contralateral to the lesion for the lateral canal), and a weaker response for rotation for rotation towards the lesion.

Other machinery in the model above that are not necessary to cover right now are the cross-connected boxes that implement velocity storage. This is needed to explain head-shaking nystagmus, but irrelevant to the HIT.

This (fairly) simple theory explains the HIT in quantitative terms.

Literature:

The HIT is reported to be very sensitive to complete vestibular loss but insensitive to mild or moderate vestibular loss (Beynon et al, 1998; Hamid 2005; Harvey et al, 1997).

As a general comment, because this test depends so heavily on either subjective judgements on the part of the examiner, or inaccessible technology (scleral eye coils), its utility is probably limited to use by "vestibular experts".

Conclusions:

The HIT appears to be most useful as part of a rapid battery of bedside tests (as described above). (Mandala et al. 2008). By combining several quick clinical tests, the "dizzy doctor" can quickly determine the status of the inner ear.

References

1. Aalto, H., T. Hirvonen, et al. (2002). "Motorized head impulse stimulator to determine angular horizontal vestibulo-ocular reflex." J Med Eng Technol 26(5): 217-22.
2. Aw, S. T., M. Fetter, et al. (2001). "Individual semicircular canal function in superior and inferior vestibular neuritis." Neurology 57(5): 768-74.
3. Baloh, R. W. and V. Honrubia (2001). Clinical Neurophysiology of the Vestibular System, Oxford University Press.
4. Baloh, R. W., V. Honrubia, et al. (1977). "Ewald's second law re-evaluated." Acta Otolaryngol 83(5-6): 475-479.
   
5. Beynon, G. J., P. Jani, et al. (1998). "A clinical evaluation of head impulse testing." Clin Otolaryngol Allied Sci 23(2): 117-22.
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7. Cremer, P. D., G. M. Halmagyi, et al. (1998). "Semicircular canal plane head impulses detect absent function of individual semicircular canals." Brain 121 ( Pt 4): 699-716.
8. Ewald, J. R. (1892). Physiologische Untersuchungen über das Endorgan des Nervus octavus. Wiesbaden, Germany, Bergmann.
9. Hain, T. C. and J. Spindler (1993). Head-shaking nystagmus. The Vestibulo-Ocular Reflex and Vertigo. J. A. Sharpe and H. O. Barber. New York, Raven Press: 217-228.
10. Hain, T. C., M. Fetter, et al. (1987). "Head-shaking nystagmus in patients with unilateral peripheral vestibular lesions." American Journal of Otolaryngology 8(1): 36-47.
11. Harvey, S. A., D. J. Wood, et al. (1997). "Relationship of the head impulse test and head-shake nystagmus in reference to caloric testing." Am J Otol 18(2): 207-13.
12. Jorns-Haderli, M., D. Straumann, et al. (2007). "Accuracy of the bedside head impulse test in detecting vestibular hypofunction." J Neurol Neurosurg Psychiatry 78(10): 1113-8.
13. Karlberg, M., S. T. Aw, et al. (2002). "Vibration-induced shift of the subjective visual horizontal: a sign of unilateral vestibular deficit." Arch Otolaryngol Head Neck Surg 128(1): 21-7.
14. Kingma, H., A. Meulenbroeks, et al. (2000). "Vestibular ocular reflexes in Meniere's disease patients evaluated by passive high frequency head rotation (yaw) and sidewards acceleration." Acta Otolaryngol Suppl 544: 19-26.
15. Lehnen, N., S. T. Aw, et al. (2004). "Head impulse test reveals residual semicircular canal function after vestibular neurectomy." Neurology 62(12): 2294-6.
16. Leigh, R. J. and D. S. Zee (2006). The Neurology of Eye Movements, Oxford University PresHamid, M. (2005). "More than a 50% canal paresis is needed for the head impulse test to be positive." Otol Neurotol 26(2): 318-9.
17. Mandala, M., D. Nuti, et al. (2008). "Effectiveness of careful bedside examination in assessment, diagnosis, and prognosis of vestibular neuritis." Arch Otolaryngol Head Neck Surg 134(2): 164-9.
18. Migliaccio, A. A., C. C. Della Santina, et al. (2005). "The vestibulo-ocular reflex response to head impulses rarely decreases after cochlear implantation." Otol Neurotol 26(4): 655-60.
19. Perez, N. and J. Rama-Lopez (2003). "Head-impulse and caloric tests in patients with dizziness." Otol Neurotol 24(6): 913-7.
20. Tian, J., B. T. Crane, et al. (2000). "Vestibular catch-up saccades in labyrinthine deficiency." Exp Brain Res 131(4): 448-57.
21. Weber, K. P., S. T. Aw, et al. (2008). "Head impulse test in unilateral vestibular loss: vestibulo-ocular reflex and catch-up saccades." Neurology 70(6): 454-63.