Abstract. This article presents operational diagnostic criteria for benign paroxysmal positional vertigo (BPPV), formulated by the Committee for Classification of Vestibular Disorders of the Bárány Society. The classification reflects current knowledge of clinical aspects and pathomechanisms of BPPV and includes both established and emerging syndromes of BPPV. It is anticipated that growing understanding of the disease will lead to further development of this classification.

Certain patients with balance disorders report a 'visual vertigo' in which their symptoms are provoked or aggravated by specific visual contexts (e.g. supermarkets, driving or movement of objects). In order to determine the causes of visual vertigo (VV), we assessed symptoms, anxiety and the influence of disorienting visual stimuli in 21 such patients. In 17 out of 21 patients, a peripheral vestibular disorder was diagnosed. Sixteen bilateral labyrinthine-defective subjects (LDS) and 25 normal subjects served as controls. Questionnaire assessment showed that the levels of trait anxiety and childhood motion sickness in the three subject groups were not significantly different. Reporting of autonomic symptoms and somatic anxiety was higher than normal in both patient groups but not significantly different between LDS and VV patients. Handicap levels were not different in the two patient groups, but the reporting of vestibular symptoms was higher in the VV than in the LDS group. The experimental stimuli required subjects to set the subjective visual vertical in three visual conditions: total darkness, in front of a tilted luminous frame (rod and frame test) and in front of a large disc rotating in the frontal plane (rod and disc test). Body sway was also measured in four visual conditions: eyes closed, eyes open, facing the tilted frame and during disc rotation. In psychophysical and postural tests, both LDS and VV patients showed: (i) a significant increase in the tilt of the visual vertical both with the static tilted frame and with the rotating disc; and (ii) an increased postural deviation whilst facing the tilted frame and the rotating disc. The ratio between sway path with eyes closed and eyes open (i.e. the stabilizing effect of vision) was increased in the LDS, but not in VV patients, compared with normal subjects. In contrast, the ratio between sway path during disc rotation and sway path during eyes open (i.e. the destabilizing effect of a moving visual stimulus) was increased in the VV patients but not in LDS. Taken together, these data show that VV patients have abnormally large perceptual and postural responses to disorienting visual environments. VV is not related to trait anxiety or a past history of motion sickness. The results indicate that VV emerges in vestibular patients if they have increased visual dependence and difficulty in resolving conflict between visual and vestibulo-proprioceptive inputs. It is argued that treating these patients with visual motion desensitization, e.g. repeated optokinetic stimulation, should be beneficial.

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Objective: The pathogenesis of idiopathic sudden sensorineural hearing loss (ISSHL) remains unknown, but vascular involvement is one of the main hypotheses. The main objective of this study was to investigate the association between ISSHL and cardiovascular and thromboembolic risk factors. Study Design: Multicentric case-control study. Methods: Ninety-six Caucasian patients with ISSHL and 179 sex- and age-matched controls were included. Patients were evaluated on the day of the inclusion and 1 week, 3 weeks and 3 months later. Clinical information concerning personal and familial cardiovascular and thromboembolic risk factors and concerning the ISSHL was collected. Blood samples were collected for genetic analysis of factor V Leiden and G20210A polymorphism in the factor II gene. The severity of the hearing loss was classified as mild (21–40 dB), moderate (41–70 dB), severe (71–90 dB) and profound or total (>90 dB). Hearing improvement was calculated as a relative improvement of hearing thresholds using the contralateral ear as baseline. Results: Systolic blood pressure was higher in patients (130 ± 1.7 mm Hg) than in controls (124 ± 1.1 mm Hg, p = 0.003). The personal/familial history of cardiovascular events was also more prevalent in patients (p = 0.023 and p = 0.014, respectively), whereas no difference was found in the prevalence of personal cardiovascular risk factors (hypertension, diabetes mellitus, hyperlipidemia, smoking habits). There was no correlation between the audiogram type, the hearing outcome and the presence of cardiovascular risk factors. No significant difference was observed in the personal/familial history or in the presence of thromboembolic risk factors. The prothrombin and factor V mutations were uncommon in both patients and controls. The final hearing threshold was only correlated with the severity of the initial hearing loss (p < 0.001), but not influenced by the presence of vertigo, audiogram type, time elapsed from onset of ISSHL to hospitalization or failure of a previous oral therapy. Hearing stabilization was obtained at 21 days in 92% of patients. Conclusion: These results support the theory of vascular involvement as the etiology of some cases of ISSHL. The sole predictive factor of poor final hearing is the severity of the initial hearing loss.

A rotatory-upbeat nystagmus in the context of PC BPPV, a horizontal nystagmus, whether geotropic or ageotropic, due to HC BPPV, and a positional downbeat nystagmus related to various central disorders are the 3 most common types of positional nystagmus. Geotropic horizontal positional nystagmus and, most certainly, horizontal positional nystagmus changing from geotropic to ageotropic or the reverse point to HC BPPV. In contrast, an ageotropic horizontal positional nystagmus that is not changing (from ageotropic to geotropic) may indicate a central lesion.

We report 3 patients who complained of positional vertigo shortly after head trauma. Positional maneuvers performed in the plane of the posterior canal (PC; Dix-Hallpike maneuver) and the horizontal canal (HC; patients were rolled to either side in a supine position with the head raised 30 degrees) revealed a complex positional nystagmus that could only be interpreted as the result of combined PC and HC benign paroxysmal positional vertigo (BPPV). Two patients had a right PC BPPV and an ageotropic HC BPPV, and 1 patient had a bilateral PC BPPV and a left geotropic HC BPPV. All 3 patients were rapidly free of vertigo after the PC BPPV was cured by the Epley maneuver and the geotropic HC BPPV was cured by the Vannucchi method. The ageotropic HC BPPV resolved spontaneously. Neuroimaging (brain computed tomography and/or magnetic resonance imaging scans) findings were normal in all 3 patients. From a physiopathological viewpoint, it is easy to conceive that head trauma could throw otoconial debris into different canals of each labyrinth and be responsible for these combined forms of BPPV. Consequently, in trauma patients with vertigo, it is mandatory to perform the Dix-Hallpike maneuver, as well as supine lateral head turns, in order to diagnose PC BPPV, HC BPPV, or the association of both. Early diagnosis and treatment of BPPV may help to reduce the postconcussion syndrome.

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