HINTS Examination in Acute Vestibular Neuritis: Do Not Look Too Hard for the Skew

An ocular tilt reaction (OTR) is a triad of a skew deviation, head tilt, and ocular counter-roll that can be partial or complete. An OTR can occur anywhere along the utriculo-ocular motor pathways from the labyrinth to the interstitial nucleus of Cajal but is almost always central in origin. In acute vestibular neuritis (AVN), case reports have described patients with an OTR due to AVN, although it is unclear whether this examination finding is common or rare.

Original Contribution Section Editors: Clare Fraser, MD Susan Mollan, MD HINTS Examination in Acute Vestibular Neuritis: Do Not Look Too Hard for the Skew Kemar E. Green, DO, Daniel R. Gold, DO Background: An ocular tilt reaction (OTR) is a triad of a skew deviation, head tilt, and ocular counter-roll that can be partial or complete. An OTR can occur anywhere along the utriculo-ocular motor pathways from the labyrinth to the interstitial nucleus of Cajal but is almost always central in origin. In acute vestibular neuritis (AVN), case reports have described patients with an OTR due to AVN, although it is unclear whether this examination finding is common or rare. Methods: The vestibular and ocular motor features of 7 patients presenting with AVN are described. Results: Each of the 7 patients presented with typical features of AVN, including contralesional unidirectional spontaneous nystagmus and an ipsilesional abnormal head impulse test, although each patient also had a complete OTR. None of the patients had vertical diplopia or a skew deviation that was measurable with alternate cover testing (i.e., abnormal “test of skew” according to the Head Impulse, Nystagmus, Test of Skew examination); however, all had a subtle 1 prism diopter hyperphoria that was only measurable with a Maddox rod test. Conclusion: Seven cases of typical AVN with an OTR are presented, and in the authors’ experience, the presence of a subtle OTR is a common feature of AVN in these patients. Journal of Neuro-Ophthalmology 2021;41:e672–e678 doi: 10.1097/WNO.0000000000001013 © 2020 by North American Neuro-Ophthalmology Society A complete ocular tilt reaction (OTR) consists of 1) a skew deviation, 2) head tilt, and 3) an ocular counter-roll. When present, the OTR is almost always due to a destructive lesion involving the utriculo-ocular motor pathways (1,2) as they course through the posterior fossa (more commonly due to brainstem than cerebellum Department of Neurology (KEG, DRG), The John Hopkins University School of Medicine, Baltimore, Maryland; and Departments of Neurosurgery, Ophthalmology, Otolaryngology—Head and Neck Surgery, Emergency Medicine, and Medicine (DRG), The John Hopkins University School of Medicine, Baltimore, Maryland. The authors report no conflicts of interest. Address correspondence to Kemar E. Green, DO, Department of Neurology, The John Hopkins University School of Medicine, Baltimore, MD 21287; E-mail: [e-mail] e672 lesions). Rarely, a paroxysmal ocular tilt reaction (pOTR) can be seen as the result of an irritative lesion along the same pathways, for instance due to a hemorrhage involving the interstitial nucleus of Cajal (INC, see video link— https://collections.lib.utah.edu/ark:/87278/s6gt9z78). A destructive lesion involving the graviceptive pathways (utricle ± vertical [anterior and posterior] semicircular canals [SCCs]) will result in a static imbalance, which commonly causes a nonparalytic vertical ocular misalignment—a skew deviation—and vertical diplopia. It is generally believed that a “peripheral” lesion (e.g., labyrinth or vestibular nerve) rarely causes a skew deviation (2–4), although it is well known that a vestibular nerve section can cause a transient skew deviation (5,6). The utriculo-ocular motor pathway begins in the labyrinth, and its afferents first travel with the superior division of the vestibular nerve and then with the eighth cranial nerve and synapse in the ipsilateral vestibular nucleus. Fibers leaving the vestibular nucleus decussate at the pontomedullary junction and ascend through the contralateral medial longitudinal fasciculus (MLF) to innervate the cyclotorsional ocular motor nuclei (nucleus of cranial nerve 4 and subnuclei of cranial nerve 3, including superior rectus, inferior rectus, and inferior oblique) and the INC that is responsible for vertical and torsional gaze holding (Fig. 1). Lesions caudal to the decussation (labyrinth, eighth cranial nerve [examples below], and medulla) will have an ipsiversive OTR (e.g., right lateral medullary stroke—right head tilt, top poles of both eyes rotate toward the right ear, and right hypotropia), whereas lesions rostral to the decussation (MLF and INC) will have a contraversive OTR (e.g., left INC stroke—right head tilt, top poles of both eyes rotate toward the right ear, and left hypertropia, see video example https://collections.lib.utah. edu/ark:/87278/s6mm0pz4). The hypotropic (lower) eye will be ipsilateral to a lesion that is caudal to (lower than) the decussation—that is, the low–low rule. The hypertropic (higher) eye will be ipsilateral to a lesion that is rostral to (higher than) the decussation—that is, the high–high rule. Green and Gold: J Neuro-Ophthalmol 2021; 41: e672-e678 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. Original Contribution FIG. 1. Anatomical structures relevant to the utriculo-ocular motor pathway—from peripheral utricle to ocular motor nuclei and INC. III, oculomotor nuclei; IV, trochlear nuclei; VI, abducens nuclei; INC, interstitial nucleus of Cajal; IO, inferior oblique; IR, inferior rectus; MLF, medial longitudinal fasciculus; SO, superior oblique; SR, superior rectus; VN, vestibular nuclei. From the Neuro-ophthalmology Virtual Education Library: NOVEL (online) Available at: https:// novel.utah.edu/Gold/. Adaptations are themselves works protected by copyright. So to publish this adaptation, authorization must be obtained both from the owner of the copyright in the original work and from the owner of copyright in the translation or adaptation. In the rare pOTR, the ocular tilt reaction (OTR) will occur in a direction opposite to what is expected based on the above rules (which apply to a destructive lesion)—for example, excitation/irritation of the left INC causes an ipsiversive OTR, although the lesion is rostral to the decussation (3,7,8). A patient can have a partial or complete OTR, both of which are often accompanied by a tilted subjective visual vertical (SVV), which can be thought of as a perceptual consequence of the OTR. The SVV can be measured using the bucket test (9) and evaluates the patient’s perception of verticality compared with earth vertical. The SVV is almost always tilted in the same direction as the ocular counter-roll and/or head tilt (8). In the setting of the acute vestibular syndrome (AVS: constant vertigo, unsteadiness, nausea/ vomiting, head motion intolerance, and spontaneous nystagmus), the 3-step ocular motor Head Impulse, Nystagmus, Test of Skew (HINTS) examination should be applied to differentiate peripheral (e.g.,) from central (e.g., acute vestibular neuritis [AVN] stroke) etiologies (10–12). This bedside assessment is more sensitive and specific than Green and Gold: J Neuro-Ophthalmol 2021; 41: e672-e678 diffusion-weighted MRI in detecting a central cause of vertigo within the first 72 hours (11,12). In the AVS, when otoscopy is normal—without suggestion of Ramsay Hunt syndrome or labyrinthitis—yet there is associated hearing loss, labyrinthine ischemia should be assumed until proven otherwise. Adding a bedside assessment of auditory function (using finger rub) to the HINTS examination (i.e., HINTS “Plus”), further increases the sensitivity to detect a central etiology from 96.5% using HINTS to 99.2% using HINTS Plus, whereas the specificity to detect a central etiology is 98.5% with HINTS and 97% with HINTS Plus (11). We examined 7 consecutive AVN patients for the presence of a "peripheral" OTR (Table 1), and here we describe three illustrative cases in which the skew deviation was too small to be detected by the bedside HINTS examination (test of skew) but was present with Maddox rod testing (for information on how to perform this test, go to https://collections.lib.utah.edu/ark:/87278/s6jm6h96). The ocular counter-roll was diagnosed based on fundus photography, whereas small head and SVV tilts verified the complete OTR. The intention of this article is not to highlight a new pitfall of the HINTS examination (pearls and pitfalls have previously been described in detail [1315]). Rather, we present these cases to highlight that 1) involvement of the utricle in typical cases of AVN commonly causes a subtle OTR and 2) although skew deviations seem to be common in AVN when measured with a Maddox rod, the previously described “test of skew” in the HINTS examination will not identify these (potentially misleading) “peripheral” skews. Therefore, this article describes a clinical pearl in acute vestibular neuritis rather than a failure (pitfall) of the HINTS examination to differentiate peripheral from central etiologies. CASE 1 A 48-year-old man with hypertension, dyslipidemia, and prediabetes developed continuous vertigo that gradually worsened over 60 minutes. He presented to the emergency department (ED) within hours of the onset. Associated symptoms included nausea and vomiting, head motion intolerance, and unsteadiness but no diplopia or other symptoms suggestive of brainstem or cerebellar ischemia. Urgent brain MRI and CT angiography of the head and neck indicated normal results, and oto-neurology consultation was requested. Video-oculography (VOG) and a video head impulse test (vHIT—for more information on this vestibular function test, go to https://collections.lib.utah. edu/ark:/87278/s62n91vq) were performed in the ED, demonstrating unidirectional mixed horizontal–torsional left-beating nystagmus (LBN, peak slow phase velocity [SPV] in primary gaze of 11°/s with fixation removed) that followed Alexander’s law (i.e., more LBN in left gaze), and there was no vertical ocular misalignment seen on the VOG recording with alternate cover testing. With vHIT, e673 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. Original Contribution TABLE 1. Showing the clinical profile of all 7 cases of a “peripheral” ocular tilt reaction in acute vestibular neuritis Case 1 2 3 4 5 6 7 Spontaneous Nystagmus vHIT Hypofunction Alternate Cover (Vertical) Maddox Rod (Vertical, PD) OCR (Fundus Photos) Head Tilt SVV (Bucket Test) OTR Diagnosis LBN RBN RBN LBN RBN LBN LBN Right HC Left HC & AC Left HC & AC Right HC & AC Left HC Right HC & AC Right HC Normal Normal Normal Normal Normal Normal Normal 1 LH 1 RH 1 RH 1 LH 0.5 RH 2 LH 1 LH Ipsiversive Ipsiversive Ipsiversive Ipsiversive Ipsiversive Ipsiversive Not done Right Left Left Right Left Right Right 5° rightward 10–15° leftward 10–15° leftward Not done 5° leftward 5–10° rightward 5–10° rightward Ipsiversive Ipsiversive Ipsiversive Ipsiversive Ipsiversive Ipsiversive Ipsiversive Right AVN Left AVN Left AVN Right AVN Left AVN Right AVN Right AVN AC, anterior canal; AVN, acute vestibular neuritis; HC, horizontal canal; LH, left hyperphoria; OCR, ocular counter roll; OTR, ocular tilt reaction, LBN, left-beating nystagmus; OTR, ocular tilt reaction; PD, prism diopters; RBN, right-beating nystagmus; RH, right hyperphoria; SVV, subjective visual vertical; vHIT, video head-impulse test. horizontal canal (HC) gains were 0.65 to the left and 0.24 to the right (with corrective saccades). There was no hearing loss or other aural symptoms, and an otoscopy finding was normal. Bedside assessment of auditory function was normal. He was diagnosed with right-sided AVN based on a peripheral pattern of the HINTS “Plus” (Head Impulse [abnormal], Nystagmus [unidirectional], Test of Skew [no vertical refixation movement during alternate cover test], and Plus [no hearing loss]) examination and was discharged from the ED with steroids. At an outpatient follow-up 2 days later, he reported improvement of symptoms. vHIT was performed in the planes of all six SCCs (Fig. 2) and showed gains of 0.89 to the left and 0.39 to the right (with corrective saccades), and FIG. 2. Six canal video head impulse testing for Case 1 showing low-gain (,0.7) and corrective saccades (covert—occurring during the head movement that is invisible with the bedside HIT, and overt—occurring after the head movement) in the plane of the right HC with sparing of the right AC and PC. AC, anterior canal; HC, horizontal canal; PC, posterior canal. e674 Green and Gold: J Neuro-Ophthalmol 2021; 41: e672-e678 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. Original Contribution FIG. 3. Fundus photographs for Case 1 who also had an abnormal head impulse test to the right, unidirectional left-beating nystagmus, mild right head tilt, rightward SVV tilt observed with the bucket test. Two days after vertigo onset there is conjugate ocular counter-roll with the top poles rotated toward the right ear (mild left incycloduction and slightly more right excycloduction as determined by the angle between optic nerve and fovea). Two weeks after the onset, the ocular counter-roll (and other features of the OTR) resolved. OTR, ocular tilt reaction; SVV, subjective visual vertical. normal gains in the planes of the right vertical canals and no corrective saccades. Although there was no clear vertical ocular misalignment with alternate cover testing (during VOG in the ED or at the bedside as an outpatient), with a Maddox rod at near, there was a concomitant 1 prism diopter (PD) left hyperphoria (also measured in right and left head tilt). This left hyperphoria was compatible with a peripheral skew deviation given the right-sided peripheral localization (i.e., low–low) in addition to the following findings that suggested an ipsiversive OTR: mild right head tilt in the ED (resolved by the outpatient visit); 5° rightward SVV tilt observed with the bucket test (both eyes open); and fundus photographs demonstrated ocular counter-roll with the top poles rotated toward the right ear (i.e., left incycloduction and right excycloduction, Fig. 3). The involvement of the HC and utricle suggested that the superior division of the vestibular nerve was mainly affected, despite sparing of the right anterior canal (AC). He was seen 2 weeks later, at that time there was significant symptomatic improvement. Repeat fundus photographs demonstrated resolution of the ocular counter-roll (Fig. 3), and Maddox rod testing vertically was orthophoric in all directions of gaze, with resolution of the 1 PD left hyperphoria. Vestibular evoked myogenic potentials (VEMPs) and calorics were not performed. Green and Gold: J Neuro-Ophthalmol 2021; 41: e672-e678 CASE 2 A 60-year-old man with hypothyroidism presented to the ED with a “sensation of mild motion sickness” that developed into a “violent clockwise spinning” over 30– 60 minutes. He presented to the ED within hours of the onset. One week before presentation, he experienced cold symptoms. Associated symptoms included nausea and vomiting, head motion intolerance, and unsteadiness but no diplopia or other symptoms suggestive of brainstem or cerebellar ischemia. Urgent brain MRI and CT angiography of the head and neck indicated normal results, and otoneurology consultation was requested. Bedside examination demonstrated an abnormal HIT to the left, unidirectional mixed horizontal–torsional right-beating nystagmus (RBN) (following Alexander’s law), and a negative test of skew with alternate cover testing. There was no hearing loss or other aural symptoms, and otoscopy was normal. Bedside assessment of auditory function was normal. He was diagnosed with left-sided AVN based on a peripheral pattern of the HINTS examination and was started on prednisone. At an outpatient follow-up (6 days from the symptom onset), vertigo and nystagmus were significantly improved. VOG showed unidirectional RBN with a peak SPV of 23°/s (fixation removed in the primary gaze), increasing to e675 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. Original Contribution 26°/s with horizontal head shaking. Six canal vHIT showed HC gains of 0.88 to the left (with corrective saccades) and 1.49 to the right; AC gains of 0.41 to the left (with corrective saccades) and 0.96 to the right; and posterior canal (PC) gains of 0.97 to the left and 0.81 to the right. Although there was no vertical ocular misalignment with alternate cover testing, with a Maddox rod at near, there was a concomitant 1 PD right hyperphoria (also measured in right and left head tilt). This right hyperphoria was compatible with a peripheral skew deviation given the leftsided vestibulopathy in addition to the following findings that suggested a complete ipsiversive OTR: mild left head tilt; bucket test showed a 12–13° leftward SVV tilt with both eyes open; and fundus photographs demonstrated ocular counter-roll with the top poles deviated toward the left ear (i.e., right incycloduction and left excycloduction). At a 1-month follow-up, symptoms had almost completely resolved, and there was no head tilt, ocular counterroll, or hyperphoria with a Maddox rod. The preferential involvement of HC, AC, and the utricle was suggestive of a superior division pattern of vestibular neuritis. VEMPs and calorics were not performed. CASE 3 A 72-year-old man with hypertension presented to the ED with continuous “spinning” for 6 days that was abrupt in the onset. Associated symptoms included nausea and vomiting, head motion intolerance, and unsteadiness but no diplopia or other symptoms suggestive of brainstem or cerebellar ischemia. Oto-neurology consultation was requested, and VOG performed in the ED demonstrated unidirectional mixed horizontal–torsional RBN (peak SPV in the primary gaze with fixation removed was 27°/s) that followed Alexander’s law, and there was no vertical ocular misalignment with alternate cover testing. vHIT performed in the planes of the HC showed gains of 0.38 to the left (with corrective saccades) and 0.84 to the right. There was no vertical ocular misalignment seen on the VOG recording with alternate cover testing. There was no hearing loss or other aural symptoms, and otoscopy was normal. Bedside assessment of auditory function was normal. He was diagnosed with left-sided AVN based on a peripheral pattern of the HINTS “Plus” examination and was discharged from the ED without steroids or the need for additional imaging. At an outpatient follow-up (8 days from the symptom onset), symptoms continue to improve. VOG showed unidirectional RBN that increased with horizontal head shaking. Six canal vHIT showed HC gains of 0.42 to the left (with corrective saccades) and 0.81 to the right; AC gains of 0.66 to the left (with corrective saccades) and 0.84 to the right; and PC gains of 0.73 to the left and 0.83 to the right. Although there was no vertical ocular misalignment with alternate cover testing (during VOG in the ED or at the bedside as an outpatient), with a Maddox rod at near, e676 there was a concomitant 1 PD right hyperphoria (also measured in a right and left head tilt). This right hyperphoria was compatible with a peripheral skew deviation given the left-sided vestibulopathy in addition to the following findings that suggested a complete ipsiversive OTR: mild left head tilt; bucket test showed a 12–13° leftward SVV tilt with both eyes open; and fundus photographs demonstrated ocular counter-roll with the top poles deviated toward the left ear. At a 6-week follow-up visit, symptoms were almost completely resolved, and there was no head tilt, ocular counter-roll, or hyperphoria with a Maddox rod. The preferential involvement of HC, AC, and the utricle was suggestive of a superior division pattern of vestibular neuritis. VEMPs and calorics were not performed. DISCUSSION The incidence of a “peripheral” OTR in the setting of AVN is unknown. It is true that vertical diplopia due to a skew deviation is rare in typical vestibular neuritis, yet in our experience, an asymptomatic 1–2 PD hyperphoria is quite common acutely. It is believed that a skew deviation almost always represents damage to the central utriculo-ocular motor pathways, perhaps in part because of the topography of these fibers, long course through the brainstem and cerebellum, and/or their relative vulnerability (2). Or, it may be that unless there is significant peripheral damage to utricle and/or vertical SCC pathways, an OTR will not manifest (4). Each of our patients had an ipsiversive OTR (i.e., the expected pattern as the utricle pathways were still uncrossed) that was related to an eighth cranial neuropathy from AVN, and in each case the pattern of dysfunction was mainly in the distribution of the superior vestibular nerve. The vestibular nerve is divided into superior and inferior divisions, with the former innervating AC, HC, utricle, and a small portion of the saccule, whereas the latter innervates the PC and most of the saccule. In many cases, AVN is believed to be due to a postinfectious inflammation of the eighth cranial nerve, with sparing of the auditory portion of the nerve. It has been shown that pure superior division vestibular neuritis is far more common than pure inferior division vestibular neuritis. One theory is that the relatively longer course of the superior division creates greater vulnerability; however, both divisions are commonly affected to some degree as demonstrated in a prospective cross-sectional study of patients with AVN (16). This study reported isolated superior vestibular neuritis in 41.9% of patients, isolated inferior vestibular neuritis in 2.3%, and involvement of both divisions in 55.8%. Therefore, the utricle fibers may be affected to some degree in most of these cases. In our cases, the combination of ipsiversive OTR and involvement of the HC ± AC suggested that the superior division was in fact involved. Green and Gold: J Neuro-Ophthalmol 2021; 41: e672-e678 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. Original Contribution Although a skew deviation suggests a central etiology (usually stroke) in the HINTS examination, in the authors’ experience, the occurrence of a partial or complete OTR is very common in typical cases of vestibular neuritis (i.e., contralesional unidirectional mixed horizontal– torsional nystagmus with an abnormal ipsilesional HIT). In fact, in the experience of one of the authors (D.G.), when the superior division is involved in typical vestibular neuritis (HC ± AC involvement), subtle features of a partial or complete OTR are almost always present acutely (,1–2 weeks). Most of the cases that we have seen have had a 1–2 PD hyperphoria appreciated only with the Maddox rod. In each case, the hypophoric eye is ipsilesional to the vestibulopathy (in accordance with the low–low rule), and there is resolution of vertical misalignment, ocular counter-roll, and head and SVV tilt over weeks. For these reasons, the vertical ocular misalignment, albeit subtle, is almost certainly due to a skew deviation rather than an unrelated small hyperphoria. It has been shown that diplopia is rare in patients with vertical ocular misalignments of this magnitude (3). Cervical and ocular VEMPs are used to evaluate the function of saccule and utricle pathways, respectively, and could help determine the extent of superior and/or inferior division involvement. In the AVS, VEMPs can be helpful when the etiology or localization are ambiguous, particularly to aid in the diagnosis of pure inferior division vestibular neuritis (e.g., abnormal ipsilesional cervical VEMP and hypofunction of the PC and normal ipsilesional ocular VEMP and sparing of the HC and AC). In our series, each patient followed a typical vestibular neuritis course with significant improvement over weeks, so VEMPs would not have altered their diagnosis or management. Furthermore, previous studies did not find a close correlation between ocular VEMPs and ocular counter-roll in vestibular neuritis (17,18). A skew deviation large enough to be detected in the HINTS examination would likely cause vertical diplopia, and this should be considered central until proven otherwise. However, rarely a patient with AVN may experience a measureable skew that causes diplopia (10,12) (see example: https://collections.lib.utah.edu/ark:/87278/s6ht70fx), but this symptomatic “peripheral” skew should be a diagnosis of exclusion and MRI is warranted in such patients. In our cases, there was an OTR without diplopia and alternate cover testing was normal even when performed with VOG. It has been shown that mean vertical deviations detected by a Maddox rod (1.2 ± 1.6 PD) were smaller than those detected by a search coil (2.0 ± 1.4 PD) (19); however, the sensitivity and specificity of VOG in detecting skew deviations remains unknown. CONCLUSION When the astute clinician looks closely for features of the OTR in AVN, aided by tools including the Maddox rod (skew deviation), indirect ophthalmoscopy or fundus Green and Gold: J Neuro-Ophthalmol 2021; 41: e672-e678 photography (ocular counter-roll), and the bucket test (SVV), it seems likely that a partial or complete OTR can be appreciated in most (if not all) patients with superior division involvement. However, most neurologists, ophthalmologists, otolaryngologists, or neuro-ophthalmologists do not see these patients in the first few days after the onset and features of the OTR resolve quickly. Or, if the patients are seen acutely in the ED by one of these specialists, these tools are commonly unavailable or unfamiliar to the examiner. Although we believe that the incidence of a subtle (Maddox rod) skew deviation is quite high in AVN, the HINTS examination should still be applied. Alternate cover testing will identify those skew deviations that cause vertical diplopia (.3–4 PD), whereas appearing normal in those patients with a small asymptomatic peripheral skew (,1–2 PD). Performing the HINTS examination as originally described (10–12) will ensure that patients with small asymptomatic (peripheral) skew deviations are not misclassified as “central.” These cases highlight a clinical pearl in AVN.not a pitfall of the HINTS examination. STATEMENT OF AUTHORSHIP Category 1: a. Conception and design: K. E. Green; b. Acquisition of data: K. E. Green; c. Analysis and interpretation of data: K. E. Green and D. R. Gold. Category 2: a. Drafting the manuscript: K. E. Green and D. R. Gold; b. Revising it for intellectual content: K. E. Green and D. R. Gold. Category 3: a. Final approval of the completed manuscript: D. R. Gold. REFERENCES 1. Brodsky MC, Donahue SP, Vaphiades M, Brandt T. Skew deviation revisited. Surv Ophthalmol. 2006;51:105–128. 2. 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