Search

Objective: To report the outcome of posterior semicircular canal occlusion surgery for intractable benign positional vertigo, regarding vertigo cure rate and hearing and balance outcomes., Methods: Retrospective review of 53 patients presenting with benign positional vertigo, unresponsive to repositioning manoeuvres, who eventually underwent posterior canal occlusion, over a 20 year period., Results: From 1991 to 2011, 5364 benign positional vertigo patients were treated in our balance disorders clinic; 53 of those who failed to respond to repositioning underwent posterior canal occlusion. All 53 were cured of their benign positional vertigo. Nine suffered some symptomatic permanent hearing loss (>20 dB at low and >25 dB at high frequencies). Ten patients suffered caloric vestibular function deterioration, with mild but permanent subjective imbalance in five; a further 10 patients with no post-operative caloric test changes also had some permanent imbalance. Benign positional vertigo later developed in the operated ear lateral canal in two patients and in the opposite ear posterior canal in eight patients. Two patients needed bilateral sequential posterior canal occlusion., Conclusion: Posterior canal occlusion is a highly effective treatment for intractable benign positional vertigo, with what is probably an acceptable risk to hearing and balance: five of six patients will have no hearing problem and nine of 10 no balance problem after surgery.

Objective: To describe the spatial and temporal characteristics of benign positional nystagmus (BPN) subtypes in benign positional vertigo (BPV) due to vestibular lithiasis affecting one or more semicircular canals (SCCs)., Background: Activation of SCC receptors by sequestered otoconia, either freely moving (canalithiasis) or cupula-adherent (cupulolithiasis) during head position changes with respect to gravity, is the accepted cause of BPV. Although accurate identification and interpretation of BPN is critical to BPV therapy, no rigorous, kinematically correct three-dimensional spatio-temporal analysis of BPN in all its forms exists., Methods: Using dual-search scleral coils, the authors recorded BPN provoked by Dix-Hallpike or supine ear-down test in a two-axis whole-body rotator in 44 patients with refractory BPV. To localize the SCC affected, BPN rotation axes were compared to SCC axes, axes orthogonal to average SCC planes., Results: Sixteen patients had upbeat, geotropic-torsional BPN in the Dix-Hallpike test to one side and five to both sides, with BPN rotation axes clustered around the lowermost posterior SCC axis. Seven had direction-changing horizontal BPN, three geotropic (canalithiasis) and four apogeotropic (cupulolithiasis), with rotation axes around the lowermost and uppermost horizontal SCC axis. Seven had predominantly downbeating BPN with rotation axes clustered around one superior SCC axis. Nine had upbeat, horizontal-torsional BPN with rotation axes located between posterior and horizontal SCC axes of the lowermost ear suggesting simultaneous lithiasis in both SCCs. BPN vector-guided repositioning therapy was successful in 43 patients., Conclusion: Benign positional vertigo can affect one or more semicircular canals and three-dimensional recording with vector analysis of the benign positional nystagmus (BPN) can guide canalith repositioning therapy especially in refractory cases with atypical BPN.

Vertigo is an illusion of rotation due to a disorder of the vestibular system, almost always peripheral. In the history it must be distinguished from pre-syncope, seizures and panic attacks. A single attack of acute, isolated spontaneous vertigo lasting a day or more is due either to vestibular neuritis or cerebellar infarction; distinguishing between the two requires mastery of the head impulse test. Recurrent vertigo is mostly due to benign paroxysmal positioning vertigo (BPPV), Meniere's disease or migraine. With a good history, a positional test, an audiogram and a caloric test, it is usually possible to distinguish between these. BPPV is the single most common cause of recurrent vertigo and can usually be cured immediately with a particle repositioning manoeuvre. Posterior circulation ischaemia very rarely causes isolated vertigo attacks and when it does the attacks are brief and frequent and the history is short.

We describe 4 patients who all simultaneously developed a sudden total or partial unilateral sensorineural hearing loss and an unusual acute peripheral vestibulopathy in the same ear characterized by posterior semicircular canal benign paroxysmal positional vertigo with intact lateral semicircular canal function. Two patients also had ipsilateral loss of otolith function. The vertigo resolved in all 4 patients after particle-repositioning maneuvers. The findings of audiometry and vestibular tests indicated that the lesion responsible for this syndrome was probably located within the labyrinth itself rather than within the vestibulocochlear nerve and that it was more likely a viral vestibulocochlear neurolabyrinthitis than a labyrinthine infarction.

Objectives: To determine the clinical significance of an isolated directional preponderance (DP) on bithermal caloric testing. An isolated caloric DP was defined as a DP, calculated according to the standard Jongkees formula, of > or = 40%, with a spontaneous nystagmus (SN) in darkness of < or = 2 degrees/s and a canal paresis (unilateral weakness) of < or = 25%., Study Design: A retrospective analysis of all 15,542 bithermal caloric tests performed in the authors' department in the previous 10 years to identify all tests with an isolated DP of > or = 40%. This was followed by a review of the clinical data on the 144 patients identified with such a result and then by a telephone or postal follow-up study of these patients. The study group eventually comprised 114 patients; these were patients in whom a clinical diagnosis could be made at the time the caloric test was done, or who responded to requests for follow-up information. The 34 patients in whom a clinical diagnosis could not be made at the time of the caloric test, and who did not respond to requests for follow-up information, were excluded., Study Setting: A balance disorders clinic in a tertiary referral hospital., Intervention: All patients underwent standard bithermal caloric testing. Some of the patients also underwent rotational testing., Outcome Measures: A clinical diagnosis for the cause of the isolated DP, made either at the time of the caloric test or on the basis of information supplied at follow-up by the patient or by the referring physician., Results: Of 114 patients, 39 had benign paroxysmal positioning vertigo, 14 had Ménière's disease, and 5 had migrainous vertigo. Five patients had central nervous system (CNS) disorders, and this was clinically apparent at the time of the caloric test in 4, so that only 1 patient with an isolated DP developed evidence of a CNS disorder after the caloric test was done. In the other 54 patients, no definite diagnosis could be made, but 41 of these 54 were either completely well or much better at follow-up., Conclusions: An isolated DP on caloric testing is usually a transient, benign disorder. About half the patients with an isolated DP have either Ménière's disease or benign paroxysmal positioning vertigo; in most of the other half, no definite diagnosis is made but most of these patients will do well. Only approximately 5% have a CNS lesion and in almost all this is apparent at the time the caloric test is done. In a relapsing-remitting peripheral vestibular disorder such as benign paroxysmal positioning vertigo or Ménière's disease, the mechanism of an isolated DP could be enhanced dynamic gain of ipsilesional medial vestibular nucleus neurons, perhaps as a result of intermittent hyperfunction of primary semicircular canal vestibular afferents. The authors postulate that an isolated DP reflects a gain asymmetry between neurons in the medial vestibular nucleus on either side, caused either by increased sensitivity on one side or by reduced sensitivity on the other, perhaps as an adaptive change in response to abnormal input. In an accompanying article, the authors implement a realistic neural network model in which it is possible to simulate an isolated DP by adjusting the dynamic sensitivity of type 1 medial vestibular nucleus neurons on one side or of type 2 medial vestibular nucleus neurons on the other.

Benign paroxysmal positional vertigo (BPPV) originating from the posterior semicircular canal (pSCC) is a common vestibular disorder that is easy to diagnose and usually easy to treat. The majority of patients with BPPV have no known inner ear disease; they have "primary" or "idiopathic" BPPV. However, a minority does have objective evidence of an inner ear disease on the same side as the BPPV and this group has "secondary" or "symptomatic" BPPV. Previous publications differ on the prevalence of secondary BPPV and about the types of inner ear diseases capable of causing it. In order to determine what proportion of patients have secondary as opposed to primary BPPV and which inner ear diseases are capable of causing secondary BPPV, we searched our database for the 10-year period from 1988 to 1997 and found a total of 2847 patients with BPPV. Of these, 81 (3%) had definite pSCC-BPPV secondary to an ipsilateral inner ear disease. Sixteen had Menière's disease, 24 had an acute unilateral peripheral vestibulopathy, 12 had a chronic unilateral peripheral vestibulopathy, 21 had chronic bilateral peripheral vestibulopathy and 8 had unilateral sensorineural hearing loss. It seems that any inner ear disease that detaches otoconia and yet does not totally destroy pSCC function can cause BPPV and that a case can be made for audiometry and caloric testing in all patients with BPPV.

Objective: Complete unilateral loss of vestibular function results in a phase advance (reduced time constant) of the horizontal slow-phase nystagmus response to yaw-axis rotation. The objective of this study was to determine whether partial losses of lateral semicircular canal function would result in proportional reductions in the time constant. SETTING AND STUDY DESIGN: This was a retrospective study of consecutive patients' records at two tertiary referral centers for vestibular disorders., Patients: Four hundred fifty-four patients who presented for evaluation of vertigo or imbalance or both and who were found to have partial or complete unilateral canal paresis on caloric testing., Main Outcome Measures: In 372 patients, the gain and time constant of the horizontal nystagmus response was measured using a 5-second velocity ramp of constant yaw-axis acceleration. Caloric responses to standard bithermal irrigations at 30 degrees and 44 degrees were obtained using an open-loop irrigation system. In a second group of 82 patients, the gain and time constant of the horizontal vestibulo-ocular reflex were measured using a sum-of-sines (pseudorandom) yaw-axis acceleration. The caloric response was measured using a closed-loop system., Results: In both groups, the peak gain of the nystagmus response was independent of the level of the canal paresis. However, the time constant of the response both toward and away from the lesioned side decreased proportionally with increasing canal paresis., Conclusion: This result supports the hypothesis that bilateral symmetrical peripheral vestibular input is a necessary condition for the mechanisms or processes underlying normal horizontal slow-phase velocity storage.

To define better the benefits and risks of intratympanic gentamicin injection treatment of intractable vertigo or drop attacks due to Ménière's disease, we reviewed the charts of 18 patients whom we have now observed for > 1 year after having completed this mode of therapy. There were nine women and nine men aged 29-81 years; all had poor hearing in the affected ear. Of the 18 patients, 14 have had no further vertigo or drop attacks (11 patients after a single set of three to five injections, another three after a further set of one to five injections). The treatment could be effective even if it did not abolish caloric responses from the treated ear, even if it did not produce an acute vestibular deafferentation syndrome afterwards, and even after a failed vestibular nerve section. After treatment, five of the 18 patients developed oscillopsia and ataxia--symptoms and signs of (presumably permanent) chronic vestibular insufficiency; this proportion is not obviously lower than that after vestibular neurectomy or surgical labyrinthectomy. Of the 18 patients, 12 showed no change in the 1-kHz threshold and 13 showed no change in the 4-kHz threshold. When hearing did deteriorate, the threshold rose by more than 30 dB at 1 kHz in four patients and at 4 kHz in six patients. We conclude and confirm that intratympanic gentamicin injections are a convenient and, in most cases, effective and safe treatment for intractable vertigo or drop attacks due to Ménière's disease.

To document the outcome of vestibular nerve section from the patient's point of view we reviewed 102 patients who had undergone vestibular nerve section 1 to 10 years after operation. Only 3 patients had experienced further vertigo attacks: 2 of these were cured by a further, this time translabyrinthine vestibular nerve section; 1 patient developed multiple sclerosis. In contrast, about 50% of patients developed some subjective problem with balance while standing or walking; in 15% it was present all the time and of moderate severity. Despite this, over 85% of patients reported that they felt much better or back to normal after the operation and were satisfied with the outcome. The development and application of objective preoperative measures of vestibular and, in particular, vestibulospinal function might improve patient selection for vestibular nerve section and thus reduce the number of dissatisfied patients.

In recent years, owing to significant technological developments and an increased number of investigators entering the field, there have been spectacular advances in our understanding of the basic anatomy and physiology of the vestibular system. Unfortunately, these advances in basic science are slow to impact the clinical management of patients. We have selected a few important advances in clinical neurotology that have impacted the diagnosis and treatment of patients with vestibular disorders. This material was originally presented at the "Mechanisms of Vestibular Function and Dysfunction" symposium of the 1994 Neural Control of Movement meeting in Waikoloa, Hawaii.

The responses to rapid, passive, unpredictable, low amplitude (10-20 degrees), high acceleration (3,000-4,000 degrees/s2) head rotations were used to study the human vestibulo-ocular reflex (VOR) in pitch and yaw plane after unilateral posterior semicircular canal occlusion (uPCO) in 10 subjects. The results from these 10 uPCO subjects were compared with those from 18 normal subjects. The VOR gains at a head velocity of 200 degrees/s in the uPCO subjects were: pitch upward = 0.62 +/- 0.06, pitch downward = 0.87 +/- 0.11, yew ipsilesion = 0.78 +/- 0.06, yaw contralesion = 0.79 +/- 0.10 and in normal subjects were: pitch upward = 0.92 +/- 0.06, pitch downward = 0.96 +/- 0.04, yaw right = 0.88 +/- 0.05, yaw left = 0.91 +/- 0.12 (group means +/- twotailed 95% confidence intervals). The results showed that the pitch-vVOR gain was significantly (p < 0.05) decreased in response to upward head impulses whereas in response to downward, ipsilesion and contralesion head impulses were not significantly different (p > 0.05) from the normals. This study shows that there is 30% permanent residual deficit of the upward pitch-vVOR with an up-down asymmetry in pitch-vVOR gain following inactivation of a single posterior semicircular canal and that compensation of pitch-vVOR function is incomplete.

Purpose: To review the extent and mechanism of the recovery of vestibular function after sudden, isolated, spontaneous, unilateral loss of most or all peripheral vestibular function – usually called acute vestibular neuritis. Methods: Critical review of published literature and personal experience. Results: The symptoms and signs of acute vestibular neuritis are vertigo, vomiting, nystagmus with ipsiversive slow-phases, ipsiversive lateropulsion and ocular tilt reaction (the static symptoms) and impairment of vestibulo-ocular reflexes from the ipsilesional semicircular canals on impulsive testing (the dynamic symptoms). Peripheral vestibular function might not improve and while static symptoms invariably resolve, albeit often not totally, dynamic symptoms only improve slightly if at all. Conclusions: The persistent loss of balance that some patients experience after acute vestibular neuritis can be due to inadequate central compensation or to incomplete peripheral recovery and vestibular rehabilitation has a role in the treatment of both. [ABSTRACT FROM AUTHOR]