Response to galvanic vestibular stimulation in patients with unilateral vestibular loss

OBJECTIVES: This study sought to characterize various responses to galvanic vestibular stimulation (GVS) by comparing GVS-induced eye movements in healthy subjects and patients with vestibular function loss. The study also aimed to estimate the clinical significance of GVS tests. Finally, an effort was made to localize the primary excitation site of stimulation in the vestibular system. MATERIALS AND METHODS: Three parameters of response to GVS, spontaneous nystagmus, galvanic stimulating nystagmus (GSN), and postgalvanic stimulating nystagmus (PGSN), were evaluated in 20 normal subjects and 14 patients with complete unilateral vestibular function loss resulting from labyrinthectomy or vestibular neurectomy using a three-dimensional video-electronystagmography technique. RESULTS: In normal subjects, GSN was detected in all subjects and was directed toward the negative electrode. PGSN was also detected but was directed toward the opposite electrode. When the negative electrode was attached to the intact side in unilateral vestibular loss subjects, GSN was always directed toward the negative electrode and PGSN was never observed. When the negative electrode was attached to the lesion side, however, GSN was detected in only one case, and PGSN was observed and directed to the intact side in 13 patients. CONCLUSIONS: The response to GVS in vestibular loss patients differed from that in normal subjects, which suggests that GVS could be useful for estimating the extent of vestibular function loss. The fact that the patterns of GVS response differed so significantly suggests that the primary site of excitation is not central but is instead the peripheral vestibular organ.     

The influence of dorsal neck proprioceptive inputs on vestibular compensation--by three-dimensional analysis of neck-induced nystagmus

The influence of dorsal neck proprioceptive inputs on vestibular compensation was investigated in 21 patients with unilateral vestibular dysfunction. Subjects neither had history of spontaneous nystagmus nor of disequilibrium, indicating that they were in a good compensated stage. However, marked nystagmus was induced by applying vibratory stimulation to the dorsal neck of the patients, using a vibrator with a frequency of 110 Hz. The nystagmus was three-dimensional as analyzed by applying computerized eye movement analysis system. Twelve of 21 patients (57%) demonstrated three components of eye movement. All subjects showed a horizontal component directed towards the contralateral side of the vestibular lesion. Vertical and torsional components of the nystagmus were exhibited by 18 and 14 subjects, respectively. The average percentages of slow phase velocity of the horizontal, vertical and torsional components were 57%, 23% and 20%, respectively. No tendency towards any of the three components was observed. Furthermore, in order to investigate the relation between dorsal neck proprioceptive inputs and vestibular outputs, especially semicircular canal outputs, the author compared the direction of the nystagmus with the orientation of the semicircular canals. Normalized average velocity vectors of the nystagmus were calculated. In most subjects, the velocity vectors of the nystagmus were related to the horizontal semicircular canal. These results suggest that by controlling the neck proprioceptive inputs, neck vibration can cause discompensation in vestibularly well-compensated subjects with unilateral dysfunction secondary to vestibular lesion, and that neck proprioceptive inputs have a great influence on the horizontal vestibulo-ocular reflex pathways. However, in a few subjects the average vectors of the nystagmus were related to the vertical semicircular canals. This suggests that the proprioceptive inputs may also be related to the vertical vestibulo-ocular reflex pathways.     

Vestibular function after vestibular neuritis

Abstract

Objective: To measure horizontal semicircular canal function over days, weeks, and months after an acute attack of vestibular neuritis. Design: The video head impulse test (vHIT) was used to measure the eye movement response to small unpredictable passive head turns at intervals after the attack. Study sample: Two patients diagnosed with acute right unilateral vestibular neuritis. Results: There was full restoration of horizontal canal function in one patient (A) as shown by the return of the slow phase eye velocity response to unpredictable head turns, while in the other patient (B) there was little or no recovery of horizontal canal function. Instead this second patient generated covert saccades during head turns. Conclusion: Despite the objective evidence of their very different recovery patterns, both patients reported, at the final test, being happy and feeling well recovered, even though in one of the patients there was clear absence of horizontal canal function. The results indicate covert saccades seem a successful way of compensating for loss of horizontal canal function after unilateral vestibular neuritis. Factors other than recovery of the slow phase eye velocity are significant for patient recovery.     

Caloric and Search-Coil Head-Impulse Testing in Patients after Vestibular Neuritis

The objective of this study was to compare results of quantitative head-impulse testing using search coils with eye-movement responses to caloric irrigation in patients with unilateral vestibular hypofunction after vestibular neuritis. The study population consisted of an acute group (<3 days; N = 10; 5 male, 5 female; 26-89 years old) and a chronic group (>2 months; N = 14; 8 male, 6 female; 26-78 years old) of patients with unilateral vestibular hypofunction after vestibular neuritis. The testing battery included: (1) simultaneous measurement of eye and head rotations with search coils in a magnetic coil frame during passive Halmagyi-Curthoys head-impulse testing and (2) electronystagmography during bilateral monaural 44 degrees C-warm and 30 degrees C-cold caloric irrigation. The main outcome measures were (1) the gain of the horizontal vestibulo-ocular reflex during search-coil head-impulse testing and (2) the amount of canal paresis during caloric irrigation. All acute and chronic patients had a unilateral gain reduction during search-coil head-impulse testing. A pathological canal paresis factor was present in 100% of the acute patients but in only 64% of the chronic patients. The clinically suspected unilateral vestibular hypofunction resulting from vestibular neuritis was validated in all acute patients by both search-coil head-impulse and caloric testing. Hence, either of these tests is sufficient for diagnosis in the acute phase of vestibular neuritis. Chronic patients, however, were reliably identified only by search-coil head-impulse testing, which suggests that the low-frequency function of the labyrinths often becomes symmetrical, leading to a normal canal paresis factor.     

Three-Dimensional Vibration-Induced Vestibulo-ocular Reflex Identifies Vertical Semicircular Canal Dehiscence

Vertical semicircular canal dehiscence (VSCD) due to superior canal dehiscence (SCD) or posterior canal dehiscence (PCD) of the temporal bone causes vestibular and cochlear hypersensitivity to sound. This study aimed to characterize the vibration-induced vestibulo-ocular reflex (ViVOR) in VSCD. ViVORs in one PCD and 17 SCD patients, confirmed by CT imaging reformatted in semicircular canal planes, were measured with dual-search coils as binocular three-dimensional eye rotations induced by skull vibrations from a bone oscillator (B71—10 ohms) at 7 ms, 500 Hz, 135-dB peak-force level (re: 1 μN). The ViVOR eye rotation axes were computed by vector analysis and referenced to known semicircular canal planes. Onset latency of the ViVOR was 11 ms. ViVOR from VSCD was up to nine times greater than normal. The ViVOR’s torsional rotation was always contraversive-torsional (the eye’s upper pole rotated away from the stimulated ear), i.e. its direction was clockwise from a left and counterclockwise from a right VSCD, thereby lateralizing the side of the VSCD. The ViVORs vertical component distinguishes PCD from SCD, being downwards in PCD and upwards in SCD. In unilateral VSCD, the ViVOR eye rotation axis aligned closest to the dehiscent vertical semicircular canal axis from either ipsilateral or contralateral mastoid vibrations. However, in bilateral VSCDs, the ViVOR eye rotation axis lateralized to the ipsilateral dehiscent vertical semicircular canal axis. ViVOR was evoked in ossicular chain dysfunction, even when air-conducted click vestibulo-ocular reflex (VOR) was absent or markedly reduced. Hence, ViVOR could be a useful measurement to identify unilateral or bilateral VSCD even in the presence of ossicular chain dysfunction.     

Horizontal vestibulo-ocular reflex dynamics in acute vestibular neuritis and viral labyrinthitis: evidence of otolith-canal interaction

OBJECTIVE: To evaluate the dynamic properties of the horizontal vestibulo-ocular reflex (h-VOR) in the acute stage of two common labyrinthine diseases that provoke severe attacks of vertigo with spontaneous nystagmus: vestibular neuritis (vestibular loss alone) and viral labyrinthitis (cochleovestibular loss). MATERIAL AND METHODS: Sixty-three patients were investigated: 42 were diagnosed with vestibular neuritis and 21 with viral labyrinthitis. The h-VOR function was evaluated by conventional caloric and impulsive testing. A simplified model of vestibular function was used to analyze the vestibulo-ocular response to rotational stimulation. RESULTS: The results showed a significant difference in h-VOR characteristics between the two pathologies. Patients with vestibular neuritis exhibited a strong horizontal semicircular canal deficit, but no h-VOR asymmetry between the two rotational directions. In contrast, patients with viral labyrinthitis demonstrated moderate canal paresis and a marked h-VOR deficit in rotation toward the affected ear. CONCLUSION: These findings support the hypothesis that the h-VOR dynamic asymmetry that occurs after an acute unilateral inner ear lesion is not due to canal dysfunction alone, but involves complex adaptive changes in the central VOR that may implicate the otolith system. Based on histopathologic and clinical differences in the two pathologies reported in the literature, we postulate that this otolith-canal interaction is mainly linked to the loss of saccular function.     

The lesion site of vestibular dysfunction in Ramsay Hunt syndrome: a study by click and galvanic VEMP

Ramsay Hunt syndrome (RHS) is characterized by vestibulocochlear dysfunction in addition to facial paralysis and auricular vesicles. The present study investigated the lesion site of vestibular dysfunction in a group of 10 RHS patients. Caloric testing, vestibular evoked myogenic potentials by click sound (cVEMP) and by galvanic stimulation (gVEMP) were used to assess the function of the lateral semicircular canal, saccule, and their afferents. The results of caloric testing (all 10 cases showed canal paresis) mean the existence of lesion sites in lateral semicircular canal and/or superior vestibular nerve (SVN). Abnormal cVEMPs in 7 patients mean the existence of lesions in saccule and/or inferior vestibular nerve (IVN). Four of the 6 patients with absent cVEMP also underwent gVEMP. The results of gVEMP (2 absent and 2 normal) mean that the former 2 have lesions of the vestibular nerve, and the latter 2 have only saccular lesions concerning the pathway of VEMPs. Thus, our study suggested that lesion sites of vestibular symptoms in RHS could be in the vestibular nerve and/or labyrinth, and in SVN and/or IVN. In other words, in the light of vestibular symptoms, there is the diversity of lesion sites.     

Acoustic responses of vestibular afferents in a model of superior canal dehiscence.

HYPOTHESIS: Afferents innervating the superior semicircular canal are rendered especially sensitive to acoustic stimulation when there is a dehiscence of the superior canal. Other vestibular end organs are also more sensitive to acoustic stimulation. BACKGROUND: Dehiscence of the superior semicircular canal is associated with vertigo and nystagmus caused by loud sounds (Tullio phenomenon) or changes in middle ear or intracranial pressures. The mechanisms by which acoustic stimuli act on the vestibular end organs are unclear. The nystagmus caused by acoustic stimuli generally aligns with the affected superior canal. METHODS: Responses to acoustic stimuli in the superior vestibular nerves of anesthetized chinchillas were recorded before and after fenestration of the superior canal. RESULTS: Two acoustic response patterns were seen: rapid phase locking and slow tonic changes in firing rate. Phasic responses principally occurred in irregular afferents and tonic responses in regular afferents. Afferents from all of the vestibular end organs encountered could respond to acoustic stimuli, even before fenestration. However, fenestration lowered the thresholds for acoustic stimulation in superior canal afferents with phasic responses and increased the magnitude of tonic responses. CONCLUSIONS: Superior canal dehiscence may render the irregular afferents innervating the superior canal particularly sensitive to loud sounds. Rapid phase-locking responses may explain the short latency of nystagmus seen in patients with superior canal dehiscence syndrome. The mechanisms by which acoustic stimuli activate the vestibular end organs may differ from the damped endolymph motion associated with head acceleration.     

Vestibular Neuritis: Three-dimensional Videonystagmography and Vestibular Evoked Myogenic Potential Results

Eight patients diagnosed with vestibular neuritis received the newly developed three-dimensional videonystagmography (3D VNG) and vestibular evoked myogenic potential (VEMP) examination in order to localize the lesion site. Two (25%) of the 8 patients exhibited spontaneous nystagmus with 3 components, indicating that both the horizontal semicircular canal (HSCC) and anterior semicircular canal (ASCC) were affected. The remaining 6 patients (75%) displayed only horizontal nystagmus, meaning that only the HSCC was involved. Seven (88%) of the 8 patients had bilateral normal VEMPs, revealing sparing of the posterior semicircular canal (PSCC). In a comparative study, another seven patients with vestibular neuritis 1 year post-treatment also received the caloric test, 3D VNG and VEMP examination. Only one patient exhibited spontaneous nystagmus. An absent caloric response of the lesioned side persisted in 5 (71%) of the 7 patients. However, all patients showed normal VEMPs bilaterally. 3D VNG and VEMP examination indicates that vestibular neuritis mainly affects the superior division of the vestibular nerve, which innervates the HSCC and ASCC. Meanwhile, the function of the PSCC and saccule, innervated by the inferior vestibular nerve, is preserved.     

Horizontal vestibulo-ocular reflex dynamics in acute vestibular neuritis and viral labyrinthitis: evidence of otolith-canal interaction

Objective To evaluate the dynamic properties of the horizontal vestibulo-ocular reflex (h-VOR) in the acute stage of two common labyrinthine diseases that provoke severe attacks of vertigo with spontaneous nystagmus: vestibular neuritis (vestibular loss alone) and viral labyrinthitis (cochleovestibular loss).

Material and Methods Sixty-three patients were investigated: 42 were diagnosed with vestibular neuritis and 21 with viral labyrinthitis. The h-VOR function was evaluated by conventional caloric and impulsive testing. A simplified model of vestibular function was used to analyze the vestibulo-ocular response to rotational stimulation.

Results The results showed a significant difference in h-VOR characteristics between the two pathologies. Patients with vestibular neuritis exhibited a strong horizontal semicircular canal deficit, but no h-VOR asymmetry between the two rotational directions. In contrast, patients with viral labyrinthitis demonstrated moderate canal paresis and a marked h-VOR deficit in rotation toward the affected ear.

Conclusions These findings support the hypothesis that the h-VOR dynamic asymmetry that occurs after an acute unilateral inner ear lesion is not due to canal dysfunction alone, but involves complex adaptive changes in the central VOR that may implicate the otolith system. Based on histopathologic and clinical differences in the two pathologies reported in the literature, we postulate that this otolith-canal interaction is mainly linked to the loss of saccular function.     

Vestibular neuritis: three-dimensional videonystagmography and vestibular evoked myogenic potential results

Eight patients diagnosed with vestibular neuritis received the newly developed three-dimensional videonystagmography (3D VNG) and vestibular evoked myogenic potential (VEMP) examination in order to localize the lesion site. Two (25%) of the 8 patients exhibited spontaneous nystagmus with 3 components, indicating that both the horizontal semicircular canal (HSCC) and anterior semicircular canal (ASCC) were affected. The remaining 6 patients (75%) displayed only horizontal nystagmus, meaning that only the HSCC was involved. Seven (88%) of the 8 patients had bilateral normal VEMPs, revealing sparing of the posterior semicircular canal (PSCC). In a comparative study, another seven patients with vestibular neuritis 1 year post-treatment also received the caloric test, 3D VNG and VEMP examination. Only one patient exhibited spontaneous nystagmus. An absent caloric response of the lesioned side persisted in 5 (71%) of the 7 patients. However, all patients showed normal VEMPs bilaterally. 3D VNG and VEMP examination indicates that vestibular neuritis mainly affects the superior division of the vestibular nerve, which innervates the HSCC and ASCC. Meanwhile, the function of the PSCC and saccule, innervated by the inferior vestibular nerve, is preserved.     

Superior canal dehiscence reveals concomitant unilateral utricular loss (UUL)

Conclusion: We report enhanced symmetrical cervical vestibular evoked myogenic potential (cVEMP) but asymmetrical ocular VEMP (oVEMP) responses in a patient with CT-verified bilateral superior semicircular canal dehiscence (SCD) but with acute vestibular syndrome. This implies that absence of unilateral utricular macula function alone is sufficient to cause symptoms of acute vertigo. Acute vertigo should not automatically be presumed to originate from semicircular canal dysfunction. Objectives: To identify the cause of an acute vertigo attack in a patient with bilateral SCD. Methods: The functional state of all peripheral vestibular sense organs was tested using the video head impulse test (vHIT) for all semicircular canals and VEMPs to air-conducted sound (ACS) or bone-conducted vibration (BCV) to test all otolith organs. The cVEMP tested mainly saccular function and the oVEMP mainly utricular function. Results: All semicircular canals showed normal function. The cVEMPs showed enhanced, but symmetrical saccular function. In contrast, oVEMPs showed an enhanced but asymmetric n10 component – it was greatly reduced beneath the left eye, implying decreased function in the right utricular macula. That result was confirmed using very high frequency stimuli which are effective in SCD: 4000 Hz BCV stimuli showed that oVEMP n10 was present beneath the right eye but absent beneath the left eye.     

Symptoms,Findings and Treatment in Patients with Dehiscence of the Superior Semicircular Canal

Recently Minor and co-workers described patients with sound- and pressure-induced vertigo due to dehiscence of the superior semicircular canal. Identifying patients with this 'new' vestibular entity is important, not only because the symptoms are sometimes very incapacitating, but also because they can be treated. We present symptoms and findings in eight such patients, all of whom reported pressure-induced vertigo that increased during periods of upper respiratory infections. Pulse-synchronous tinnitus and gaze instability during head movements were also common complaints. All patients lateralized Weber's test to the symptomatic ear. In some of the patients the audiogram also revealed a small conductive hearing loss. However, the stapedius reflexes were always normal. A vertical/torsional eye movement related to the superior semicircular canal was seen in most of the patients in response to pressure changes and/or sound stimulation. One patient also had superior canal-related positioning nystagmus. Testing vestibular evoked myogenic potentials revealed in all patients a vestibular hypersensitivity to sounds. In the coronal high-resolution 1-mm section CT scans the dehiscence was visible on 1 to 4 sections. Moreover, the skull base was rather thin in this area and cortical bone separating the middle ear and the antrum from the middle cranial fossa was absent in many of the patients. Two of the patients have undergone plugging of the superior semicircular canal using a transmastoid approach and both patients were relieved of the pressure-induced symptoms.     

Electronystagmographic analysis of optokinetic and smooth pursuit eye movement disorders in vestibular lesions

The electronystagmographical analysis of the eye movements is an important method in the evaluation and topical diagnostic procedure of several vestibular lesions. The aim of the study was to compare the electronystagmographical results of the optokinetic and the smooth pursuit eye-movement, and their sensitivity in several vestibular disorders. The patients were divided into five groups: right and left unilateral and bilateral peripheral lesions, central vestibular dysfunction, and normal vestibular function. In patients with normal vestibular system the optokinetic eye movement was pathological in 9.53% of patients, while the smooth pursuit eye movements were pathological in 8.3% of patients with normal vestibular function. In unilateral lesions, 17.42% of the OKNs were pathological, compared with the smooth pursuit test's 20.3% pathological ratio. In the bilateral peripheral vestibular dysfunction the ratio of the pathological eye-movements was 28% equally with to two methods. In central vestibular lesions 22.72% of the patients had abnormal optokinetic eye movements, and the smooth pursuit eye movement was abnormal in 41.6%. Our results show that in the unilateral peripheral vestibular lesions the smooth pursuit eye movement examination seems to be more sensitive than the OKN test, while in central dysfunctions the smooth pursuit eye movement examination is more sensitive than OKN examination.     

Symptoms, findings and treatment in patients with dehiscence of the superior semicircular canal

Recently Minor and co-workers described patients with sound- and pressure-induced vertigo due to dehiscence of the superior semicircular canal. Identifying patients with this 'new' vestibular entity is important, not only because the symptoms are sometimes very incapacitating, but also because they can be treated. We present symptoms and findings in eight such patients, all of whom reported pressure-induced vertigo that increased during periods of upper respiratory infections. Pulse-synchronous tinnitus and gaze instability during head movements were also common complaints. All patients lateralized Weber's test to the symptomatic ear. In some of the patients the audiogram also revealed a small conductive hearing loss. However, the stapedius reflexes were always normal. A vertical/torsional eye movement related to the superior semicircular canal was seen in most of the patients in response to pressure changes and/or sound stimulation. One patient also had superior canal-related positioning nystagmus. Testing vestibular evoked myogenic potentials revealed in all patients a vestibular hypersensitivity to sounds. In the coronal high-resolution 1-mm section CT scans the dehiscence was visible on 1 to 4 sections. Moreover, the skull base was rather thin in this area and cortical bone separating the middle ear and the antrum from the middle cranial fossa was absent in many of the patients. Two of the patients have undergone plugging of the superior semicircular canal using a transmastoid approach and both patients were relieved of the pressure-induced symptoms.     

The influence of middle ear pressure on the vestibular nerve activity in cats

The influence of middle ear pressure on the vestibular nerve activities was investigated in anesthetized cats. The vestibular nerve activities were recorded intraaxonally and positive or negative pressure was applied to the middle ear cavity through a tympanic membrane perforation. The firing of vestibular nerve fibers, especially the regular type nerve that responded to horizontal semicircular canal stimulation, increased with positive pressure and decreased with negative pressure. Most vestibular nerves that responded to anterior or posterior semicircular canal stimulation were not influenced by changes in the middle ear pressure. These results indicate that middle ear pressure load is transmitted to the vestibular end organs and then to vestibular nerve.     

Torsional vestibulo-ocular reflex during whole-body oscillation in the upright and the supine position: II. Responses in patients after vestibular neuritis

In a recent study we demonstrated that otolith input modifies the torsional angular vestibulo-ocular reflex (torVOR) of healthy human subjects: Compared to turntable oscillations in supine position, oscillations in upright position increased the gain of torVOR by 0.1 and cancelled the phase lead originating from low-frequency semicircular canal signals. We asked whether these otolith-related changes of torVOR are still present in patients after vestibular neuritis (VN). Eight patients were sinusoidally oscillated about their naso-occipital axis in supine (canal-only stimulation) and upright (canal-and-otolith stimulation) position. Three-dimensional eye movements were recorded with dual search coils. The patients showed similar otolith-related gain and phase changes of the torVOR as healthy subjects: the gain increased by about 0.1 (p < 0.05) and the low-frequency phase lead from semicircular canal signals was abolished. These results indicate that otolith function after VN is still sufficient to interact with semicircular canal signals to optimize torsional gaze stabilization when the head is upright.     

Head-Shaking Nystagmus Depends on Gravity

In acute unilateral peripheral vestibular deficit, horizontal spontaneous nystagmus (SN) increases when patients lie on their affected ear. This phenomenon indicates an ipsilesional reduction of otolith function that normally suppresses asymmetric semicircular canal signals. We asked whether head-shaking nystagmus (HSN) in patients with chronic unilateral vestibular deficit following vestibular neuritis is influenced by gravity in the same way as SN in acute patients. Using a three-dimensional (3-D) turntable, patients (N = 7) were placed in different whole-body positions along the roll plane and oscillated (1 Hz, ±10°) about their head-fixed vertical axis. Eye movements were recorded with 3-D magnetic search coils. HSN was modulated by gravity: When patients lay on their affected ear, slow-phase eye velocity significantly increased upon head shaking and consisted of a horizontal drift toward the affected ear (average: 1.2°/s ±0.5 SD), which was added to the gravity-independent and directionally nonspecific SN. In conclusion, HSN in patients with chronic unilateral peripheral vestibular deficit is best elicited when they are lying on their affected ear. This suggests a gravity-dependent mechanism similar to the one observed for SN in acute patients, i.e., an asymmetric suppression of vestibular nystagmus by the unilaterally impaired otolith organs.     

Vestibular-evoked myogenic potentials in patients with dehiscence of the superior semicircular canal

Recently Minor and co-workers described patients with sound- and pressure-induced vertigo due to dehiscence of bone overlying the superior semicircular canal. Identifying patients with this "new" vestibular entity is important, not only because the symptoms can be very incapacitating, but also because they are surgically treatable. We present symptoms and findings for three such patients. On exposure to sounds, especially in the frequency range 0.5-1 kHz, they showed vertical/torsional eye movements analogous to a stimulation of the superior semicircular canal. They also showed abnormally large sound-induced vestibular-evoked myogenic potentials (VEMP), i.e. the short latency sternomastoid muscle response considered to be of saccular origin. The VEMP also had a low threshold, especially in the frequency range 0.5-1 kHz. However, in response to saccular stimulation by skull taps, i.e. when the middle ear route was bypassed, the VEMP were not enlarged. This suggests that the relation between the sound-induced and the skull tap-induced responses can differentiate a large but normal VEMP from an abnormally large response due to dehiscence of bone overlying the labyrinth, because only the latter would produce large sound-induced VEMP compared to those induced by skull taps.     

Caloric vertical nystagmus: the vertical semicircular canal in caloric testing

Vertical nystagmus elicited by caloric testing does not necessarily mean there is central pathology. In a patient with confirmed peripheral vestibular disease, caloric stimulation produced an intense vertical nystagmus, which showed all the features of a caloric nystagmus. The patient had bilateral mastoid cavities, allowing easy stimulation of the posterior semicircular canal, using air. At the same time, a unilateral horizontal semicircular canal functional loss was observed, raising the possibility of dissociated canal dysfunction.