1

Introduction

The phenomenon of nystagmus after rapid head shaking in the horizontal plane was first observed by Barany in 1907 and standardized in the diagnosis of vestibulopathy by Kamei et al in 1964. To perform the examination, the head of the seated patient is tilted forward 30°, then actively or passively rotated 45° toward each side 20 to 30 times at a rate of 1 to 2 Hz . The bedside head-shaking nystagmus (HSN) test is usually performed by having the patient wear Frenzel’s lenses (very high-diopter magnifying glass) or by direct visualization, but observation of nystagmus may also be made with laboratory instruments such as electrooculography, scleral coils, or videonystagmography (VNG) . The presence of HSN has been shown to correspond to asymmetry in the vestibular-ocular reflex (VOR) . However, several studies have demonstrated varying sensitivity and specificity when using the HSN test in the diagnosis of peripheral vestibulopathy. Discrepancies among these studies may be explained by differences in population samples, methodology, and the reference criterion standard. The clinical relevance of the bedside HSN is that it is a simple test that does not require expensive instrumentation and can be performed by any clinician. Although HSN has been documented by electrooculography in healthy controls in one series , it is generally accepted that a positive bedside HSN correlates with peripheral vestibular hypofunction .

The etiology of HSN is thought to be related to both Ewald second law and an asymmetry in the central velocity storage mechanism . Ewald second law of labyrinth function states that ampulopetal deflection of the horizontal semicircular canal cupula (excitatory stimulus) is a greater stimulus than ampulofugal deflection (inhibitory stimulus). In patients with asymmetric peripheral vestibular function, head rotation toward the stronger ear results in excitatory activity that outweighs that elicited by head rotation toward the impaired ear. The resulting asymmetric neural inputs alter central velocity storage at the level of the second-order vestibular neurons in the brainstem. After head shaking ceases, this stored asymmetry is revealed by the VOR, causing nystagmus with a fast component in the direction of the stronger ear. The plane of the nystagmus is in the plane of the affected canal, in this case horizontal. Typically, the fast component of the nystagmus is toward the stronger side, although reversal of the direction, biphasic (direction-changing), or vertical nystagmus can be present. It is still debated whether some of these qualitative and quantitative features of the HSN have clinical correlates.

A positive HSN has been correlated with the degree of peripheral vestibular asymmetry , and in one series, it helped differentiate functional vs psychogenic dizziness . Furthermore, Kristinsdottir et al reported that older patients who sustained falls and hip fractures were more likely to have a positive HSN and increased sway (indicating a vestibular asymmetry) than age-matched controls. These observations suggest that the bedside HSN test may provide information regarding both the presence and severity of a vestibular disorder among subsets of patients with balance disorders.

In this study, we recorded HSN with Frenzel’s lenses to evaluate the usefulness of HSN as a simple bedside screening examination available to all clinicians. We aimed to determine if a positive bedside HSN correlated with the degree of self-perceived dizziness disability in this homogenous cohort of patients with unilateral peripheral vestibulopathy and chief complaint of dizziness. Our secondary objective was to study the sensitivity and specificity of the bedside HSN test when compared with “criterion standards” such as the caloric test of the VNG and the analysis of the VOR by rotary chair test. If it can be assumed that unilateral caloric weakness, diminished VOR gain, and/or VOR asymmetry are diagnostic of vestibular dysfunction, we wanted to determine if the bedside HSN test can effectively predict these VNG abnormalities.

2

Materials and methods

We reviewed medical records of adult patients who presented to the University of Miami Ear Institute with primary complaint of vertigo or disequilibrium and who had documented unilateral or asymmetric reduced caloric responses by VNG between January 2006 and December 2008. This study’s protocol was approved by the institutional review board. The study population composes of 53 patients who met the inclusion criteria: (1) 18 years or older, (2) symptoms of vertigo or disequilibrium for at least 2 months before presentation, (3) unilateral or asymmetric peripheral vestibular hypofunction defined by the caloric test of the VNG (see below), (4) complete HSN and VNG tests, and (5) complete questionnaires of self-perceived dizziness handicap and functional level. Subjects were excluded if they had conditions that may impair or contribute to their disability beyond unilateral peripheral vestibular hypofunction such as benign paroxysmal positional vertigo, bilateral peripheral hypofunction, central nervous system disease, and musculoskeletal or visual impairment. We also ascertained 10 healthy adults of both sexes without symptoms of dizziness or disequilibrium and without history of vestibular disease; the bedside HSN test was performed in controls, and the results were recorded just like it was done for patients.

Patients and controls underwent a complete history and neurotologic physical examination that included the bedside HSN test. Data collected included demographics, symptoms at presentation, clinical findings, bedside HSN results, and vestibular diagnosis (this latter for patients). A positive HSN test was defined as the presence of at least 3 beats of nystagmus after 30 cycles of passive head rotation at a rate of 1 to 2 Hz with head tilted 30° forward in the plane of the horizontal semicircular canal. All subjects were examined with Frenzel’s lenses in partial darkness.

Examiners blinded to the bedside HSN results performed and analyzed the VNG results. Eye movements were recorded binocularly. The VNG (iVNG; Balanceback, Boca Raton, FL) test battery included spontaneous nystagmus with and without visual fixation, gaze-evoked nystagmus, oculomotor testing (saccades, smooth pursuit, gaze, and optokinetics), positioning and positional testing, and bithermal open-water caloric tests at temperatures of 44°C and 30°C. Rotational chair testing (I-Portal NOTC; Neuro Kinetics Inc, Pittsburgh, PA) was also used to assess VOR. Sinusoidal harmonic acceleration testing was performed at 6 frequencies ranging from 0.01 to 0.32 Hz. The maximum slow phase velocity of nystagmus was calculated for each set of tests and then analyzed using the manufacturer’s normative data. Abnormal caloric testing was considered diagnostic of unilateral canal paresis when the interaural difference in nystagmus response (degrees per second of the slow phase velocity) for the 2 temperatures was 30% or greater using Jongkees’ formula . Abnormal responses in the rotary chair test were considered diagnostic of nonlocalizing peripheral vestibulopathy if the results for VOR phase, gain, and symmetry fell outside 2 SDs of mean for at least 2 adjacent frequencies of stimulation. Furthermore, we classified this cohort with unilateral caloric weakness into 2 functional groups: (1) uncompensated vestibular disease, if VOR asymmetry was identified in at least 2 adjacent frequencies, and (2) compensated vestibular disease, if no VOR asymmetry was found. All of the patients underwent the vestibular battery described above, and controls only underwent the caloric test.

2

Materials and methods

We reviewed medical records of adult patients who presented to the University of Miami Ear Institute with primary complaint of vertigo or disequilibrium and who had documented unilateral or asymmetric reduced caloric responses by VNG between January 2006 and December 2008. This study’s protocol was approved by the institutional review board. The study population composes of 53 patients who met the inclusion criteria: (1) 18 years or older, (2) symptoms of vertigo or disequilibrium for at least 2 months before presentation, (3) unilateral or asymmetric peripheral vestibular hypofunction defined by the caloric test of the VNG (see below), (4) complete HSN and VNG tests, and (5) complete questionnaires of self-perceived dizziness handicap and functional level. Subjects were excluded if they had conditions that may impair or contribute to their disability beyond unilateral peripheral vestibular hypofunction such as benign paroxysmal positional vertigo, bilateral peripheral hypofunction, central nervous system disease, and musculoskeletal or visual impairment. We also ascertained 10 healthy adults of both sexes without symptoms of dizziness or disequilibrium and without history of vestibular disease; the bedside HSN test was performed in controls, and the results were recorded just like it was done for patients.

Patients and controls underwent a complete history and neurotologic physical examination that included the bedside HSN test. Data collected included demographics, symptoms at presentation, clinical findings, bedside HSN results, and vestibular diagnosis (this latter for patients). A positive HSN test was defined as the presence of at least 3 beats of nystagmus after 30 cycles of passive head rotation at a rate of 1 to 2 Hz with head tilted 30° forward in the plane of the horizontal semicircular canal. All subjects were examined with Frenzel’s lenses in partial darkness.

Examiners blinded to the bedside HSN results performed and analyzed the VNG results. Eye movements were recorded binocularly. The VNG (iVNG; Balanceback, Boca Raton, FL) test battery included spontaneous nystagmus with and without visual fixation, gaze-evoked nystagmus, oculomotor testing (saccades, smooth pursuit, gaze, and optokinetics), positioning and positional testing, and bithermal open-water caloric tests at temperatures of 44°C and 30°C. Rotational chair testing (I-Portal NOTC; Neuro Kinetics Inc, Pittsburgh, PA) was also used to assess VOR. Sinusoidal harmonic acceleration testing was performed at 6 frequencies ranging from 0.01 to 0.32 Hz. The maximum slow phase velocity of nystagmus was calculated for each set of tests and then analyzed using the manufacturer’s normative data. Abnormal caloric testing was considered diagnostic of unilateral canal paresis when the interaural difference in nystagmus response (degrees per second of the slow phase velocity) for the 2 temperatures was 30% or greater using Jongkees’ formula . Abnormal responses in the rotary chair test were considered diagnostic of nonlocalizing peripheral vestibulopathy if the results for VOR phase, gain, and symmetry fell outside 2 SDs of mean for at least 2 adjacent frequencies of stimulation. Furthermore, we classified this cohort with unilateral caloric weakness into 2 functional groups: (1) uncompensated vestibular disease, if VOR asymmetry was identified in at least 2 adjacent frequencies, and (2) compensated vestibular disease, if no VOR asymmetry was found. All of the patients underwent the vestibular battery described above, and controls only underwent the caloric test.