Visual vertigo: Symptom assessment, spatial orientation and postural control
Guerraz M., Yardley L., Bertholon P., Pollak L., Rudge P., Gresty MA., Bronsteinn AM.
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. Q uestionnaire 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.