Restoration of vision II: Residual functions and training-induced visual field enlargement in brain-damaged patients

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.