E. Kasten et al., Restoration of vision II: Residual functions and training-induced visual field enlargement in brain-damaged patients, REST NEUROL, 15(2-3), 1999, pp. 273-287
Purpose: Brain damage is often accompanied by visual field defects which ha
ve been considered to be non-treatable. In recent years, however, new diagn
ostic methods have revealed hitherto unknown residual vision, which was fou
nd, for instance, in transition zones near the blind visual field sectors a
nd in spared islands of vision within the blind regions ("blindsight"). Fur
thermore, animal studies revealed a high degree of plasticity in the visual
system suggesting the possibility that recovery of vision may be induced b
y systematic visual training.
Methods: Here we summarize a series of studies with patients suffering from
visual field defects after brain lesion using some most recently developed
computer-based programs for the diagnosis and treatment of visual field de
fects. Specifically, high-resolution perimetry (HRP) was applied to first d
iagnose residual function in or near the "blind" sector of the visual field
. Thereafter, visual restitution training (VRT, see Kasten et al., Nature m
ed. 4, 1998, p. 1083) was used daily for 6 months to provide systematic sti
mulation of these areas of residual vision.
Results: In a number of studies, we have observed not only residual visual
functions within or near the field defect, but we were also able to follow
the course of spontaneous recovery of visual functions within weeks or mont
hs after visual system damage. Furthermore, even long after spontaneous rec
overy is complete, computer-based visual restitution training (VRT) in or n
ear the areas of residual vision results in a significant enlargement of in
tact areas, both after optic nerve damage and postchiasmatic lesions. Using
VRT, we found a border shift of about 5 degrees of visual angle which cann
ot be explained by eye movements or eccentric fixation. We observed a trans
fer of this training effects to other tasks such as form and color detectio
n, as well as to tests of visual exploration which were not specifically tr
ained. Moreover, 72 % of the patients reported subjective improvements of v
ision. Training-induced visual field enlargement persisted for at least one
year, even in the absence of training beyond 6 months of treatment.
Conclusions: The visual system possesses a remarkable plasticity which beco
mes apparent in visual field enlargement during spontaneous recovery and sp
ecific visual training. Animal studies indicate that a minimum number of re
sidual neurons surviving the lesion, in the order of 10 %, provides a suffi
cient substrate for recovery of vision. Though the precise mechanisms of tr
aining-induced visual field enlargement need to be further explored, VRT ca
n be introduced for routine clinical treatment of patients with visual fiel
d defects.