Primary Image

Head Impulse Test / Head Thrust Test

Head Impulse Test / Head Thrust Test

Last Updated


The Head Impulse Test (HIT) is a widely used clinical assessment technique used to assess the angular vestibulo-ocular reflex (aVOR). Specifically, the HIT assesses horizontal semicircular canal (HSCC) and superior vestibular nerve function in response to discrete, small amplitude (~10◦), high acceleration (~3000-4000 ◦s2) rotational head impulses. During the HIT, the patient is asked to fix his or her eyes on a target (e.g. the examiner’s nose). The examiner will then generate a rapid head impulse while monitoring the patient’s eyes for a corrective or compensatory saccade (CS) response.A CS or “overt saccade” is a rapid eye movement generated by the brain to re-fixate the patient’s eyes on the intended target if the aVOR is unable to generate an adequate slow phase eye movement due to peripheral weakness or loss on ipsi-rotational side. Individuals with normal vestibular function should not generate a CS after a head impulse (the eyes should stay fixed on the target). People with vestibular hypofunction may generate a corrective saccade after the head is quickly rotated toward the affected (pathological) side and this is considered a (+) HIT.

This clinical test takes advantage of Ewald’s Second Law which states that for a given impulse in the plane of the HSCCs, a head movement generates a larger magnitude vestibular stimulus on the side to which the impulse was directed (i.e, ipsi-rotational)than it does on the contra-rotational side (opposite the direction of the head impulse). Stated another way, excitation is a stronger 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 (Goldberg and Fernandez, 1971). In persons with intact vestibular function, vestibular nerve firing frequencies are able to increase in accordance with increasing ipsi-rotational velocities or accelerations without saturating or requiring a compensatory saccade to stabilize gaze.

The clinical HIT is not scored. aVOR function is evaluated as normal or abnormal (i.e., hypofunctional) by noting the presence (+ finding) or absence (-finding) of a compensatory saccade. Use of more sophisticated technologies such as the sclearal search coil (SSC) or high speed video in a laboratory setting has provided measurement of aVOR gain and eye movement latencies to validate the HIT. Video is emerging as a more feasible clinical alternative to SSC use.

Link to Instrument

Instrument Details

Acronym HIT / HTT

Assessment Type

Performance Measure

Administration Mode

Paper & Pencil




  • Brain Injury Recovery
  • Pediatric + Adolescent Rehabilitation
  • Vestibular Disorders

Key Descriptions

  • The examiner must first explain to the patient that he or she will perform a series of small, but rapid rotational head movements. The patient should try to relax his or her neck muscles and try not to blink.
  • The examiner should clear the C-spine to ensure adequate pain free range of motion to perform the test. Additionally, the examiner is encouraged to perform a vertebral artery test to rule out vertebral artery insufficiency.
  • The clinician should position him/herself in front of the patient and instruct the patient to look at his/her nose. The examiner will grasp the patient’s head above the ears and position him into 30 degrees of cervical flexion bringing the horizontal canals into the horizontal (testing) plane (Schubert et al., 2004).
  • The clinician should position him/herself in front of the patient and instruct the patient to look at his/her nose. The examiner will grasp the patient’s head above the ears and position him into 30 degrees of cervical flexion bringing the horizontal canals into the horizontal (testing) plane (Schubert et al., 2004).
  • Rotate the patient’s head slowly left and right around a vertical axis ensuring cervical muscles are relaxed and gaze remains fixed on the tester’s nose during slow rotations.
  • Suddenly rotate the patient’s head ~10 degrees from mid-line while maintaining good visibility on the patient’s eyes. Rotation to the right tests the patient’s right vestibular end organ. Leftward rotation tests the left peripheral vestibular response.
  • The presence of a compensatory, re-fixating saccade back to the examiner’s nose when the head stops moving is a positive clinical sign indicative of peripheral vestibular weakness (vestibular hypofunction) on side to which the head was rotated. If a unilateral weakness is suspected based on possible compensatory saccade response, repeat the impulse to the side in question in an unpredictable manner (after a one or two impulses in the opposite direction) to confirm the presence of the compensatory saccade response. Note that this saccadic response may fatigue after 2-3 ipsi-lesional impulses. Emerging instrumentation (i.e., video HIT) is expected to improve the sensitivity of the HIT to micro saccades beyond what is observable by the un-aided eye of the examiner (MacDugall and Curthoys, 2012).

Equipment Required

  • None (non-instrumented) or video goggles (vHIT)

Time to Administer

1 minutes

Required Training

Reading an Article/Manual

Age Ranges


6 - 12



13 - 17



18 - 64


Elderly Adult

65 +


Instrument Reviewers

Initially reviewed by Matthew R Scherer PT, PhD, NCS and Jennifer L. Stoskus, PT, MSPT, DPT.

Body Part


ICF Domain

Body Structure
Body Function

Measurement Domain


Professional Association Recommendation

Recommendations for use of the instrument from the Neurology Section of the American Physical Therapy Association’s Multiple Sclerosis Taskforce (MSEDGE), Parkinson’s Taskforce (PD EDGE), Spinal Cord Injury Taskforce (PD EDGE), Stroke Taskforce (StrokEDGE), Traumatic Brain Injury Taskforce (TBI EDGE), and Vestibular Taskforce (Vestibular EDGE) are listed below. These recommendations were developed by a panel of research and clinical experts using a modified Delphi process.

For detailed information about how recommendations were made, please visit:




Highly Recommend




Reasonable to use, but limited study in target group  / Unable to Recommend


Not Recommended

Recommendations for use based on acuity level of the patient:



(CVA < 2 months post)

(SCI < 1 month post) 

(Vestibular < 6 weeks post)


(CVA 2 to 6 months)

(SCI 3 to 6 months)


(> 6 months)

(Vestibular > 6 weeks post)

Vestibular EDGE




Recommendations based on vestibular diagnosis




Benign Paroxysmal Positional Vertigo (BPPV)


Vestibular EDGE





Recommendations for entry-level physical therapy education and use in research:


Students should learn to administer this tool? (Y/N)

Students should be exposed to tool? (Y/N)

Appropriate for use in intervention research studies? (Y/N)

Is additional research warranted for this tool (Y/N)

Vestibular EDGE






  • Clear the cervical spine prior to administering the HIT.

  • Consider performing Vertebral Artery Test prior to administering the HIT.

  • Cervical Flexion to 30 degrees to bring the HSCC into the horizontal plane has been shown to improve the sensitivity of the HIT by optimizing inhibitory cutoff in the contralesional peripheral vestibular end organ (Schubert et al., 2004).

  • Ensure that the head impulse is un-predictable to reduce the likelihood of a compensatory saccade because this could reduce the sensitivity of the test (Schubert et al., 2004).

  • Emerging vHIT technology is being developed to improve diagnostic accuracy of the HIT by providing resolution of “covert” catch-up saccades which begin while the head is still moving. Covert saccades are not detectable by the naked eye even of a trained clinician; and may result in false negative HIT findings by degrading the magnitude of overt CS. vHIT may be a clinically effective and non-invasive means of objectively measuring the presence and vestibular dysfunction in a clinical setting (Weber et al., 2009).

  • HIT may also result in false positives with (+) findings reported in patients with acute cerebellar (9%) and brainstem strokes (39%) unrelated to peripheral vestibular dysfunction (Cnyrim, 2008; Newman-Toker, 2008).

  • vHIT may have the added benefit over non-instrumented HIT with elevated sensitivity to peripheral vestibular deficits during the acute phase of the lesion in the presence of spontaneous nystagmus (MacDougall, 2009).

Do you see an error or have a suggestion for this instrument summary? Please e-mail us!

Vestibular Disorders

back to Populations

Criterion Validity (Predictive/Concurrent)

Predictive Validity (Non-Instrumented)

Unilateral and Bilateral Vestibular Hypofunction (Schubert et al., 2004); = 79 with UVH, mean age = 65.3 years (16.2), = 32 with BVH, mean age = 66.7 years (13.3); and n = 65 with non-vestibular dizziness, mean age = 64.4 years (16.8).  

  • Good Sensitivity UVH: 71% (88% for complete loss)
  • Good Sensitivity BVH: 84% (100% for complete loss
  • Good Specificity, UVH and BVH: 82%  
  • Positive Predictive Value (All subjects): 87%
  • Negative Predictive Value (All subjects): 65%
  • Positive Liklihood Ratio: 4.16
  • Negative Liklihood Ratio: 0.30


Unilateral and Bilateral Vestibular Hypofunction (Jorns-Haderli et al., 2006; = 15 persons with UVH (= 5) or BVH (n = 10) mean age of 54 years, n = 9 healthy control subjects, mean age 33 years).

Bedside HIT (bHIT) Sensitivity in experts vs. non-experts. Quantified HIT (qHIT) with scleral search coils was used as the gold standard in this study.

  • Adequate Sn 63% (experts: > 6 mos training)
  • Adequate Sn 72%(non-experts)
  • Good Specificity 78% (experts)
  • Adequate Specificity 64% (non-experts)


Patients presenting with dizziness (Harvey et al., 1997; n = 105 patients; 35 male / 70 female, mean age 52.1 years). Air calorics were:

  • Poor Sensitivity 35%
  • Good Specificity 95%
    • Positive Predictive Value 64% (When HIT was positive there was a 64% chance of caloric weakness in that ear). 
    • Negative Predictive Value 86% (When HIT was negative there was an 86% chance of a normal caloric result).
    • When HIT and Head Shake Nystagmus (HSN) findings are in agreement the Specificity was 88%. When both HIT and HSN were abnormal, positive predictive value was 80%. Negative predictive value when both were normal was 88%.


Vestibular Schwannoma, Vestibular Neuritis and Meniere’s Disease (Benyon et al., 1998, n = 42 schwannoma, n = 8 VN, n = 18 Meniere’s Disease, n = 84 unclear dx, mean age 50.9 (13.7) years). 

Clinical Head Impulse validated by bithermal calorics.

  • Poor Sensitivity 34%
  • Excellent Specificity 100%


Vestibular Pseudoneuritis (VPN) (Cnyrim et al., 2008, n = 40 with vestibular neuritis mean age 54 (14) years, n= 43 with vestibular pseudoneuritis, mean age 53 (17) years).

  • Good Sensitivity: 61% (improves to 92% with battery of clinical tests including gaze (VOG), saccadic pursuit (VOG), skew deviation and SVV.
  • Excellent Specificity 92%


Predictive Validity (Instrumented - Scleral Search Coil and video HIT)

Vestibular neuritis, s/p unilateral intratympanic, gentamicin, and s/p bilateral gentamicin vestibulotoxicity (MacDougall et al., 2009, n = 8 healthy control participants, mean age not reported; n = 6 patients with vestibular neuritis mean age 52 years, n = 1 patient with Meniere’s Disease s/p unilateral intratympanic gentamicin aged 53 years; and n = 1 patient with bilateral vestibular loss due gentamicin vestibulotoxicity aged 72 years).

  • Excellent Sensitivity (HIT with Scleral Search Coil): 100%
  • Excellent Specificity (HIT with Scleral Search Coil): 100%
  • Excellent Sensitivity (HIT with video): 100% 
  • Excellent Specificity  (HIT with video): 100%  (95% confidence interval 0.69–1.0)

Construct Validity

Convergent Validity (Bithermal calorics, scleral search coil, clinical HIT)

Unilateral Vestibular Loss s/p vestibular neurectomy (Halmagyi & Curthoys, 1988; n = 24 participants (ages not reported); = 12 patients with UVL; n = 12 healthy control participants).

  • 100% (n = 12) of patients with UVL generated compensatory saccades opposite in direction to ipsi-lesional rotational head impulses (peak head velocity and acceleration of 300 / s and 3000 / s2).  UVL was confirmed by scleral search coil in addition to presence of the refixation saccade. Patient subjects generated appropriate compensatory slow phase eye movement responses to contralesional impulses. N = 12 healthy control participants generated appropriate equal and opposite slow phase eye movement responses to bilateral head impulses.  


Patients with Cerebellar Ataxia (CA) and co-morbid vestibulopathy (Kremmyda et al., 2012); n = 16 patients with CA with and without normal vestibular dysfunction established by air caloric responses. Mean age for patients with normal peripheral vestibular function (the Cerebellar Ataxia Caloric Response present or CACR+ group) was 69.8 +[JS1]  5.7 years; those with abnormal or absent caloric responses (CACR-) averaged 73.1 + 9.3 years of age. aVOR gain and compensatory saccade (CS) latency measured using scleral search coil. 

  • = 8 participants with absent or pathological caloric responses (CACR-) demonstrated significantly degraded aVOR gain and generated a CS significantly earlier after head impulse (mean latency of ~100 ms) vs. participants in CACR+ group (mean latency of ~200 ms)  (p < 0.05)
  • CS were observed in CA patients without caloric deficits suggesting that the HIT may be sensitive to dysfunction in the cerebellar flocculus in addition to sensitivity to peripheral vestibular weakness.
  • Examiner should administer HIT as a component of a comprehensive diagnostic assessment to decrease the likelihood of a false positive sign for peripheral vestibular dysfunction, clinicians are urged to confirm HIT findings with additional vestibular testing.


Convergent Validity: Video Head Impulse Testing (HIT with video and SSC recording)

Vestibular neuritis, s/p unilateral intratympanic, gentamicin, and s/p bilateral gentamicin vestibulotoxicity (MacDougall et al., 2009), n = 8 healthy control participants, mean age not reported; n = 6 patients with vestibular neuritis mean age 52 years, = 1 patient with Meniere’s Disease s/p unilateral intratympanic gentamicin aged 53 years; and n = 1 patient with bilateral vestibular loss due gentamicin vestibulotoxicity aged 72 years.

  • Simultaneous video and search coil recordings of eye movements were closely comparable (average concordance correlation coefficient r = 0.930). 
  • Mean VOR gains measured with search coils and video were not significantly different in normal (p =0.107) and patients (p = 0.073). With these groups.
  • Sensitivity and specificity of both the reference and index test were 1.0 (95% confidence interval 0.69–1.0). 

Video HIT (vHIT) measures detected both overt and covert saccades as accurately as coils.


Aw, S. T., Halmagyi, G. M., et al. (1996). "Three-dimensional vector analysis of the human vestibuloocular reflex in response to high-acceleration head rotations. II. responses in subjects with unilateral vestibular loss and selective semicircular canal occlusion." J Neurophysiol 76(6): 4021-4030. Find it on PubMed

Aw, S. T., Haslwanter, T., et al. (1996). "Three-dimensional vector analysis of the human vestibuloocular reflex in response to high-acceleration head rotations. I. Responses in normal subjects." J Neurophysiol 76(6): 4009-4020. Find it on PubMed

Beynon, G. J., Jani, P., et al. (1998). "A clinical evaluation of head impulse testing." Clin Otolaryngol Allied Sci 23(2): 117-122. Find it on PubMed

Cnyrim, C. D., Newman-Toker, D., et al. (2008). "Bedside differentiation of vestibular neuritis from central "vestibular pseudoneuritis"." J Neurol Neurosurg Psychiatry 79(4): 458-460. Find it on PubMed

Goldberg, J. M. and Fernandez, C. (1971). "Physiology of peripheral neurons innervating semicircular canals of the squirrel monkey. I. Resting discharge and response to constant angular accelerations." J Neurophysiol 34(4): 635-660. Find it on PubMed

Halmagyi, G. M. and Curthoys, I. S. (1988). "A clinical sign of canal paresis." Arch Neurol 45(7): 737-739. Find it on PubMed

Hammond, S. and Harro, C. (2005). "Vestibular Evaluation in Individuals With Mild Brain Injury." Journal of Neurologic Physical Therapy 29(4): 209.

Harvey, S. A., Wood, D. J., et al. (1997). "Relationship of the head impulse test and head-shake nystagmus in reference to caloric testing." Am J Otol 18(2): 207-213. Find it on PubMed

Jorns-Haderli, M., Straumann, D., et al. (2007). "Accuracy of the bedside head impulse test in detecting vestibular hypofunction." J Neurol Neurosurg Psychiatry 78(10): 1113-1118. Find it on PubMed

Kremmyda, O., Kirchner, H., et al. (2012). "False-positive head-impulse test in cerebellar ataxia." Front Neurol 3: 162. Find it on PubMed

Leigh, J. R. and Zee, D. S. (1999). The Neurology of Eye Movements : Text and CD-ROM: Text and CD-ROM, Oxford University Press, USA. MacDougall, H. G., Weber, K. P., et al. (2009). "The video head impulse test: diagnostic accuracy in peripheral vestibulopathy." Neurology 73(14): 1134-1141. Find it on PubMed

Newman-Toker, D. E., Kattah, J. C., et al. (2008). "Normal head impulse test differentiates acute cerebellar strokes from vestibular neuritis." Neurology 70(24 Pt 2): 2378-2385. Find it on PubMed

Palla, A. and Straumann, D. (2004). "Recovery of the high-acceleration vestibulo-ocular reflex after vestibular neuritis." J Assoc Res Otolaryngol 5(4): 427-435. Find it on PubMed

Robinson, D. A. (1963). "A method of measuring eye movemnent using a scieral search coil in a magnetic field." Bio-medical Electronics, IEEE Transactions on 10(4): 137-145.

Weber, K. P., MacDougall, H. G., et al. (2009). "Impulsive Testing of Semicircular‐Canal Function Using Video‐oculography." Annals of the New York Academy of Sciences 1164(1): 486-491.