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The Clinical Examination

HINTS in the Acute Vestibular Syndrome: Pearls and Pitfalls

Kung, Nathan H. MD; Van Stavern, Gregory P. MD; Gold, Daniel R. DO

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Journal of Neuro-Ophthalmology: June 2018 - Volume 38 - Issue 2 - p 244-250
doi: 10.1097/WNO.0000000000000608
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Editor's Note:

This is a good deal of overlap between the fields of neuro-ophthalmology and neuro-otology. I believe that the value of HINTS testing is underappreciated by our subspecialty. Therefore, I asked experts in the field to educate us on the practical aspects of this clinical test and review its neuroanatomy and neurophysiology. HINTS testing underscores the importance of conducting a careful physical examination in the clinic before ordering expensive and, at times, invasive studies.

The acute vestibular syndrome (AVS) is characterized by the rapid onset of vertigo, nausea/vomiting, nystagmus, unsteady gait, and head motion intolerance lasting more than 24 hours (1). The etiology is often vestibular neuritis, but posterior fossa stroke accounts for approximately 20% of cases (2).

The mnemonic HINTS stands for Head Impulse, Nystagmus, Test of Skew and is a 3-step bedside ocular motor examination technique. It is designed to distinguish between central and peripheral etiologies. If performed by subspecialists within the first 72 hours of onset of symptoms, it has a higher sensitivity and specificity of identifying central causes of the AVS compared to diffusion-weighted (DW)-MRI (1). In addition, worrisome central signs can be recalled by the mnemonic INFARCT (Impulse Negative, Fast-phase Alternating, Refixation on Cover Test). A recently described fourth component also assesses for the presence of acute sensorineural hearing loss, which is ipsilateral to unilateral vestibular loss, when present. The onset of new hearing loss in the setting of the acute vestibular syndrome has been found to indicate a high likelihood of labyrinthine ischemia, especially in patients with vascular risk factors. When assessed as 4 component maneuver, the HINTS test is then known as the HINTS-plus examination (3).

For the examiner to be confident of a peripheral localization, all 3 elements of the traditional HINTS examination must fit with a “peripheral” pattern (Table 1). If any element indicates a “central” etiology or is inconsistent with a peripheral pattern, then, the etiology is central until proven otherwise (1). Hearing loss, if present, also indicates a high likelihood of a dangerous (vascular) etiology (albeit peripheral, given the labyrinthine localization of infarction) (3).



Case 1

A 67-year-old man reported 3 days of dizziness and oscillopsia. He denied any associated diplopia, ptosis, weakness, imbalance, or hearing loss. He had no significant medical history and took no medications.

He had horizontal right-beating nystagmus (RBN) in primary gaze. His RBN increased in right gaze (in accordance with Alexander law) and decreased significantly (but remained RBN) in left gaze. The nystagmus was similar with (fixation-blocking) Frenzel goggles. Cross-cover testing demonstrated normal vertical alignment. Head-impulse testing (HIT) was normal. Hearing was intact bilaterally. The remainder of the neuro-ophthalmic and neurologic examinations was unremarkable without ptosis, anisocoria, or ataxia (see NOVEL video,

Given the normal HIT, a “negative” result that is highly suggestive of a central etiology in the AVS, urgent neuroimaging was obtained and showed an acute 1 × 0.6-cm right middle cerebellar peduncle (MCP) hemorrhage (Fig. 1). The fact that there was no clear increase in his nystagmus with fixation removed was another feature suggestive of a central etiology, although this distinction can be ambiguous in the acute setting.

FIG. 1.
FIG. 1.:
Axial brain CT without contrast shows a hemorrhage in the right middle cerebellar peduncle.

Case 1 Summary:

  1. Findings that suggest a benign etiology:
    • Unidirectional nystagmus in accordance with Alexander law
    • Negative test of skew
    • Absence of acute hearing loss (e.g., labyrinthine ischemia)
  2. Findings that suggest a dangerous etiology:
    • Normal (negative) HIT
  3. Final diagnosis
    • Brainstem hemorrhage.

Case 2

A 55-year-old woman was evaluated in the emergency department for severe vertigo and dizziness. She denied hearing loss but reported postural instability while walking. She had a history of hypertension but had no other significant medical history.

She had horizontal left-beating nystagmus (LBN) in primary gaze. Her LBN increased in left gaze and diminished but remained left beating in right gaze. The nystagmus was more evident with (fixation-blocking) Frenzel goggles. Cross-cover testing demonstrated normal vertical alignment. Her HIT showed a catch-up saccade with head impulses to the right, a positive or “abnormal” HIT result (see NOVEL video, Hearing was intact. The remainder of the neurologic examination was normal aside from gait imbalance, although she could walk independently. She was diagnosed with right-sided vestibular neuritis, and her vertigo, nystagmus, and gait imbalance improved significantly over the next few weeks.

Case 2 Summary

  1. Findings that suggest a benign etiology:
    • Unidirectional (contralesional) nystagmus in accordance with Alexander law
    • Negative test of skew
    • Abnormal (positive) ipsilesional HIT
    • Absence of acute hearing loss (e.g., labyrinthine ischemia)
  2. Findings that suggest a dangerous etiology:
    • None
  3. Final diagnosis:
    • Acute vestibular neuritis.


Case 3

A 67-year-old woman presented to the emergency department with 1 day of fever, right ear pain, and binocular diplopia. She was seen by an otolaryngologist and found to have painful otorrhea with malignant right otitis externa, otitis media, middle-ear effusion, mastoid effusion, and mixed conductive/sensorineural right-sided hearing loss. Surgical drainage and debridement was performed, which confirmed bacterial labyrinthitis due to Group A Streptococcus and Pseudomonas. The patient was referred to us 1 week after the onset of her symptoms, given persistent diplopia.

At the time of the neuro-ophthalmic consultation, she had subtle LBN that increased in left gaze (in accordance with Alexander law) and decreased but remained LBN in right gaze. There was no obvious increase in the LBN with (fixation-blocking) Frenzel goggles, although quantitative recordings were not performed and nystagmus was subtle. She also had a concordantly abnormal HIT to the right (see NOVEL video, However, cross-cover testing showed a 12-prism diopter left hypertropia that was in the pattern of a skew deviation. Double Maddox rod testing showed 10 degrees of left incyclodeviation with 10 degrees of right excyclodeviation, consistent with ocular counterroll. In combination with her right head tilt, the ocular counterroll and skew deviation represented a complete ocular tilt reaction. The remainder of the neuro-ophthalmic and neurologic examinations was unremarkable without ptosis or anisocoria.

The combination of unidirectional LBN with abnormal HIT to the right typically suggests a peripheral etiology. However, given the presence of skew deviation with a complete ocular tilt reaction, neuroimaging was performed to exclude ischemia or intracranial extension of her infection, which was negative. Although a false-negative DW-MRI was possible, this was believed to be highly unlikely since 1 week had passed since the onset of symptoms. Cerebral transverse and sigmoid venous sinus thrombosis as well as petrous apicitis (Gradenigo syndrome) were also important to consider, given the active infection and hearing loss, but there was no indication of these on MRI (4,5). Her hearing loss and vestibular deficits were believed to be labyrinthine in etiology, a conclusion supported by the severity of her bacterial labyrinthitis.

This patient had a “peripheral” skew deviation, a finding that has been reported in cases of severe peripheral utricle or utricle pathway injury such as with severe bacterial labyrinthitis, therapeutic surgical or chemical labyrinthectomy, vestibular neurectomy, selective canal plugging, or complications of stapedectomy (6–8). With typical vestibular neuritis due to a viral etiology, small and asymptomatic skews are possible because of milder injury to the utricular pathways but are typically transient and subtle (e.g., a self-resolving 1-2 prism diopter ipsilateral hypophoria with Maddox rod testing—personal experience from one of the authors [DG]). Large skew deviations usually result from involvement of the utricle-ocular motor pathways, especially those involving the vestibular nucleus or interstitial nucleus of Cajal. Therefore, when vertical diplopia is reported or when a vertical refixation saccade is seen with cross-cover testing, the etiology should be considered central until proven otherwise.

Another potential pitfall in this study was timing and context: HINTS was specifically evaluated in the context of AVS, and the sensitivity and specificity were based on examinations performed within 72 hours of symptom onset in patients with isolated dizziness and vertigo who were suspected primarily of having vestibular neuritis or a posterior fossa stroke syndrome. It has not been validated in a large series of patients presenting with less common etiologies, such as following bacterial labyrinthitis, otologic surgery, therapeutic labyrinthectomy, or varicella zoster infection (e.g., with Ramsay Hunt syndrome). It also has not been specifically validated in younger patients (<18 years). Therefore, HINTS should not be solely relied on outside the 72-hour time window or validated clinical context (including age). Even in these situations, however, the individual elements of HINTS (especially when positive or abnormal) still retain descriptive and diagnostic values. HINTS also cannot be relied on in patients with episodic vestibular syndromes which can last from seconds to hours and may be due to such etiologies as vestibular migraine, Meniere disease or transient ischemic attacks (spontaneous onset), or benign paroxysmal positional vertigo (triggered).

The patient's hearing loss in this case was believed to be due to bacterial infection of the labyrinth rather than brainstem or cochlear ischemia, so the assessment of auditory function must be interpreted in the patient's specific clinical context. Given her painful bacterial otorrhea, the most likely etiology of her overall symptoms was bacterial labyrinthitis.

Case 3 Summary

  1. Findings that suggest a benign etiology:
    • Unidirectional (contralesional) nystagmus in accordance with Alexander law
    • Abnormal ipsilesional HIT
  2. Findings that suggest a dangerous etiology:
    • Abnormal vertical ocular alignment consistent with skew deviation
    • Presence of acute hearing loss, although explained by labyrinthine infection (rather than labyrinthine ischemia) in this case
  3. Final diagnosis
    • Bacterial labyrinthitis.

Case 4

A 13-year-old girl, with a 1 day history of acute vertigo, nausea, and vomiting, had spontaneous RBN in primary gaze which increased in right gaze, although she had LBN in left gaze and upbeat nystagmus in up gaze. The nystagmus was unchanged with (fixation-blocking) Frenzel goggles. Skew deviation was absent with cross-cover testing, although there was a positive HIT to the left (see NOVEL video, There was no saccadic dysmetria, and pursuit was saccadic only in the direction of the fast phases, that is, to the right and up. There was no change in her spontaneous RBN with horizontal head shaking, and her neurologic examination showed decreased left facial sensation and gait ataxia. Brain MRI demonstrated high-signal foci in the periventricular and subcortical white matter and in the left MCP, where there was an area which demonstrated restricted diffusion and faint enhancement (Fig. 2). These findings were consistent with demyelination.

FIG. 2.
FIG. 2.:
A. Diffusion-weighted images reveal restricted diffusion in the caudal to mid-pons in the region of the eighth nerve fascicle. There is an area of increased signal (arrow) involving the left middle cerebellar peduncle on axial T2 MRI (B) and mild enhancement (arrowhead) on postcontrast axial T1 scan (C). D. Schematic drawing shows the location of the eighth nerve fascicle in the lateral, inferior pons. VIII, eighth nerve; VII, seventh nerve; VI, sixth nerve, CTT, central tegmental tract, MLF, medial longitudinal fasciculus.

Based on her clinical presentation and neuroimaging results, her vestibular symptoms were most likely due to involvement of the MCP and intraparenchymal (fascicular) course of the eighth cranial nerve. Lumbar puncture showed a mild pleocytosis and oligoclonal bands. She was treated with intravenous steroids for presumed demyelinating disease and experienced gradual improvement over time. She was subsequently diagnosed with multiple sclerosis.

Although there was a positive (or abnormal) HIT toward the left, there was also gaze-evoked nystagmus which suggests a central localization. An MCP lesion is a well-described etiology of the AVS in multiple sclerosis, and her abnormal HIT probably related to adjacent eighth fascicle involvement (9).

In patients presenting with AVS, a negative (normal) HIT is highly suggestive of a central etiology. However, a positive HIT can be seen with ischemic or hemorrhagic stroke, multiple sclerosis, and other central processes involving the vestibular nucleus, root entry zone, and with infarcts involving the anterior inferior cerebellar artery (AICA) territory causing labyrinthine ischemia (6).

Even when the HIT is abnormal in the AVS, a dangerous etiology is still suggested by acute sensorineural hearing loss, presence of a skew deviation, central patterns of nystagmus (e.g., gaze-evoked, gaze-evoked, torsional or vertical nystagmus), and/or central patterns of head-shaking nystagmus (HSN) (4). These central patterns of HSN include the following: 1) vertical nystagmus produced by horizontal head shaking (known as perverted HSN), 2) nystagmus that changes direction from baseline after head shaking (for example, spontaneous LBN transitions to RBN), and 3) vigorous HSN in the absence of unilateral vestibular loss (10,11).

Case 4 Summary

  1. Findings that suggest a benign etiology:
    • Abnormal HIT
    • Absence of acute hearing loss (e.g., labyrinthine ischemia)
    • Negative test of skew
  2. Findings that suggest a central etiology:
    • Gaze-evoked nystagmus
  3. Final diagnosis
    • Acute brainstem demyelination.


The HINTS examination is a 3-step ocular motor examination that can differentiate central (e.g., posterior fossa stroke and demyelinating lesion) from peripheral (e.g., vestibular neuritis) etiologies of the AVS, with a higher sensitivity and specificity than DW-MRI when performed within the first 72 hours (1). When combined with an assessment of unilateral hearing loss in HINTS-plus examination, the sensitivity of the examination further increases with minimal tradeoff in specificity (6).

In a large validation study performed by subspecialists, the 3-step HINTS examination had a 96.8% sensitivity and 98.5% specificity for detection of a central etiology for AVS, whereas HINTS-plus examination had a 99.2% sensitivity and 97.0% specificity for detection of a central etiology for AVS, most commonly due to stroke (3). By contrast, DW-MRI had only 85.7% sensitivity in the first 24–72 hours, and the ABCD2 (age, blood pressure, clinical features, duration of symptoms, and diabetes) score had only 61.1% sensitivity and 62.3% specificity (3).

The physiologic basis of the basic 3-step examination rests primarily on semicircular canal and utricular pathway imbalance. Acute horizontal canal (HC) hypofunction causes dynamic semicircular canal imbalance, demonstrated by a positive or abnormal ipsilateral HIT. Static HC imbalance causes a contralesional unidirectional horizontal–torsional nystagmus, which is contralateral to the positive HIT (4). Skew deviation is the result of utricle-ocular motor pathway imbalance and should be absent with an acute peripheral vestibulopathy with the following exceptions: cases of chemical or surgical labyrinthectomy or neurectomy, or a particularly destructive peripheral etiology such as bacterial labyrinthitis (6–8).

As demonstrated in the cases above, the first step is to access the nystagmus. Spontaneous nystagmus should be present for the 3-step HINTS test to be valid, and the nystagmus should be evaluated in primary and eccentric gaze. The nystagmus associated with vestibular neuritis is unidirectional, has mixed horizontal-torsional components, and should follow Alexander law in which the nystagmus increases in the direction of the fast phase and decreases without reversal in the direction of the slow phase (e.g., RBN is maximal in right gaze and less pronounced in left gaze), such as in Case 2. However, small unilateral posterior fossa lesions commonly produce unidirectional nystagmus as well (12). AICA infarctions usually produce contralesional nystagmus, which may be in accordance with Alexander law. However, in a large series of patients with AICA infarctions, 6 of 55 patients had ipsilesional nystagmus (13), which may have been due to selective lesions of the superior and medial vestibular nuclei (14), damage to inhibitory or balancing pathways between the vestibular nuclei and/or vestibulocerebellum (15), or potentially local irritation due to hemorrhage (Case 1).

In addition, when assessing nystagmus, if gaze-evoked nystagmus is present, or if spontaneous nystagmus is vertical, vertical-torsional, or pure torsional, then, this should be considered central. Although it has been traditionally taught that peripheral vestibular nystagmus is suppressed with fixation and accentuated with removal of fixation (e.g., with occlusive ophthalmoscopy, Frenzel, or infrared video-oculography goggles), central vestibular nystagmus due to a posterior fossa lesion can behave in the same way. Although an increase in peripheral vestibular nystagmus with removal of fixation is almost always evident weeks or months after the symptom onset, a significant difference between fixation and fixation removal may not be appreciated in the acute setting without eye movement recordings (16).

The second step is to assess for a skew deviation, which is a nonparalytic (usually) comitant vertical misalignment of the eyes due to interruption of the pathways between the utricle of the inner ear and the ocular motor nuclei. Vertical alignment is best assessed by cross-cover testing, whereby each eye is alternately covered while the patient fixates on a distant target (see NOVEL video, Although skew deviation can rarely be due to a peripheral etiology, as discussed in Case 3, demonstration of a vertical refixation saccade or new-onset vertical diplopia should be considered central until proven otherwise.

Cross-cover testing in the primary position is generally sufficient for the non–neuro-ophthalmologist, but because it is possible that a false-positive result could occur from longstanding vertical strabismus or an unrecognized congenital fourth nerve palsy, quantification of the hyperdeviation in all directions of gaze and with head tilt is preferred. Measuring cyclodeviation using double Maddox rod testing, monocular bucket testing (17), or assessing the angle between the optic nerve and fovea (by ophthalmoscopy or with fundus photography) can also have localizing value—the hypertropic eye is incyclodeviated with a skew deviation, whereas it is excyclodeviated with a fourth nerve palsy (18). Unilateral lesions affecting the peripheral vestibular system and medullary pathways may result in an ipsilateral hypodeviation (e.g., right lateral medullary syndrome with right hypotropia—caudal to the decussation of utricle-ocular motor pathways), whereas unilateral lesions affecting the midbrain and mesencephalic structures may result in ipsilateral hypertropia (e.g., right medial longitudinal fasciculus lesion with right hyperdeviation and right internuclear ophthalmoplegia—rostral to the decussation of utricle-ocular motor pathways). Lesions in the pons may result in either ipsilateral hypotropia or hypertropia depending on whether the otolith pathways are affected caudal or rostral to their decussation, respectively (19).

The last step is to perform the HIT. Although generally well tolerated, the HIT is usually the last of the 3 maneuvers to be assessed, given the fact that patients' symptoms are usually aggravated by head movements. The patient should be sitting upright and is (usually) asked to fixate on the examiner's nose. The examiner grasps the patient's head and quickly thrusts/rotates the head from the center to the left or right or starts 10–20° eccentric and thrusts back to the center (the preferred method in older patients with cervical spine disease or poor range of motion; when robust nystagmus is present in eccentric gaze; or in the novice examiner to minimize the risk of cervical discomfort or injury), each time observing the eyes to make sure that they stay on the examiner's nose (see NOVEL video, (20).

In addition, the rotational speed of the head impulse must be high (but with low amplitude), and the HIT should be unpredictable in timing and amplitude, thereby uncovering covert saccades when present. Covert saccades occur during head movements and commonly develop as a compensatory response after unilateral vestibular loss. Covert saccades can make the HIT appear normal (which would suggest a central etiology), although overt saccades can usually be uncovered by an experienced examiner (by varying the amplitude of the impulses) and covert and overt saccades are both apparent with video HIT. Blinking during the HIT may also make the test appear falsely normal (or central), as the patient's corrective saccade may occur during the patient or examiner's blink.

However, if a patient is inattentive and cannot maintain fixation on the examiner's nose, the test may appear falsely abnormal (or peripheral) because the patient will saccade away from the target during or before the head impulse and then return with a refixation saccade once the head rotation is complete.

In the AVS, a negative or normal HIT is highly suggestive of a central etiology, whereas a positive or abnormal result is usually reassuring for a benign peripheral etiology. However, as discussed in Case 4, a positive HIT can be seen with central or dangerous processes involving the vestibular nucleus, root entry zone (or other intraparenchymal) lesions of the eighth cranial nerve, and with AICA territory infarcts involving the labyrinth (6–8). In these cases, however, other clues to a central etiology are almost always found with a comprehensive ocular motor and vestibular examination including an assessment of auditory function. (6). A negative HIT can rarely be seen with a benign peripheral etiology, especially with an inferior division vestibular neuritis in which the HC function is spared. However, this is another case in which the etiology should be presumed to be central until proven otherwise.

Other potentially misleading HINTS results can be seen in the case of a skew deviation with severe peripheral injury (Case 3), with hearing loss due to bacterial infection of the labyrinth (Case 3), or with a positive HIT that is central in origin (Case 4). In addition, studies have shown that nearly half of patients with confirmed central vestibulopathy due to stroke may have unidirectional nystagmus (10). Therefore, observation of unidirectional nystagmus that follows Alexander law can be either peripheral or central in origin. Even so, the specificity of the HINTS examination in daily practice remains high, with very few false-positive or false-negative results (1–3,6,21,22). However, findings of gaze-evoked nystagmus, vertical, or pure torsional nystagmus are considered highly suggestive of a central etiology.

Head-shaking nystagmus, although not part of the HINTS examination, can also be useful for differentiating central and peripheral etiologies of AVS. The examiner passively shakes the patients' head at ∼2 Hz for 15–20 seconds and then looks for nystagmus (see NOVEL video, This transiently accentuates vestibular asymmetry and may reveal distinctive patterns of central and peripheral nystagmus. Ideally, this test is performed with fixation removed, which is easily accomplished with bedside techniques (following the head-shaking procedure) and include occlusive ophthalmoscopy (viewing one optic nerve while occluding the other eye), placing a 20-diopter ophthalmic lens over one eye while occluding the fellow eye, or with Frenzel goggles (23). These can help unmask peripheral nystagmus and magnify the movements under observation. Downbeat or upbeat HSN (also known as “perverted” nystagmus) implies a central etiology (11). Horizontal nystagmus in the opposite direction of the spontaneous baseline nystagmus and a vigorous HSN in the absence of unilateral vestibular loss are also patterns suggesting a central etiology following the headshake maneuver (10,11).

In conclusion, although HINTS testing demonstrates outstanding sensitivity and specificity in the evaluation of the AVS, the results of testing must still be considered in the setting of the overall clinical context and in the setting of a more detailed ocular motor, otologic, and neurologic examination, particularly if a false-positive or false-negative HINTS result is suspected. In an era of increasing costs from neuroimaging, however, this valuable tool should allow for more focused diagnostic testing and decision making, helping to avoid near-misses of MRI-negative strokes, while also helping to avoid unnecessary testing in patients with benign peripheral pathology.


Category 1: a. Conception and design: Nathan H. Kung, Gregory P. Van Stavern, and Daniel R. Gold; b. Acquisition of data: Nathan H. Kung, Gregory P. Van Stavern, and Daniel R. Gold; and c. Analysis and interpretation of data: Nathan H. Kung, Gregory P. Van Stavern, and Daniel R. Gold. Category 2: a. Drafting the manuscript: Nathan H. Kung, Gregory P. Van Stavern, and Daniel R. Gold and b. Revising the manuscript for intellectual content: Nathan H. Kung, Gregory P. Van Stavern, and Daniel R. Gold. Category 3: a. Final approval of the completed manuscript: Nathan H. Kung, Gregory P. Van Stavern, and Daniel R. Gold.


The authors thank Belinda C. Sinks, AuD, Audiologist in the Department of Otolaryngology—Head and Neck Surgery at Washington University in St. Louis, for helping to identify suitable teaching cases for this article.


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