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 c
auses of visual vertigo (VV), we assessed symptoms, anxiety and the influen
ce of disorienting visual stimuli in 21 such patients. In 17 out of 21 pati
ents, a peripheral vestibular disorder was diagnosed. Sixteen bilateral lab
yrinthine-defective subjects (LDS) and 25 normal subjects served as control
s. Questionnaire assessment showed that the levels of trait anxiety and chi
ldhood motion sickness in the three subject groups were not significantly d
ifferent. Reporting of autonomic symptoms and somatic anxiety was higher th
an normal in both patient groups but not significantly different between LD
S and VV patients. Handicap levels were not different in the two patient gr
oups, but the reporting of vestibular symptoms was higher in the VV than in
the LDS group. The experimental stimuli required subjects to set the subje
ctive 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 dis
c rotating in the frontal plane (rod and disc test). Body sway was also mea
sured 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 v
isual vertical both with the static tilted frame and with the rotating disc
; and (ii) an increased postural deviation whilst facing the tilted frame a
nd 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 patien
ts have abnormally large perceptual and postural responses to disorienting
visual environments. VV is not related to trait anxiety or a past history o
f motion sickness. The results indicate that VV emerges in vestibular patie
nts if they have increased visual dependence and difficulty in resolving co
nflict between visual and vestibulo-proprioceptive inputs. It is argued tha
t treating these patients with visual motion desensitization, e.g. repeated
optokinetic stimulation, should be beneficial.