(i) neural mechanisms of filling-in at the blind spot are probably involved explaining this perceptual phenomenon; (ii) any neuronal changes occurring at the edge of the lesion only affected filling-in within the scotoma area.
BACKGROUND: Iridocorneal endothelial syndrome is characterized by the proliferation and spreading of an abnormal corneal endothelial membrane across the iridocorneal angle and iris surface, resulting in iridocorneal adhesions, glaucoma, pupillary distortion, varying degrees of iris atrophy, and occasionally corneal decomposition with edema. These changes may possibly affect the long-term prognosis of penetrating keratoplasty in an adverse fashion.
METHODS: We reviewed the clinical course of 12 consecutive eyes (12 patients) which underwent penetrating keratoplasty for corneal edema associated with the iridocorneal endothelial syndrome (mean postoperative follow up = 30 months).
RESULTS: The grafts remained clear in 10 patients (83%) and the visual acuity was 20/40 or better in nine patients (75%). The endothelial cell losses averaged 13% at 6 months and 17% at 1 year after surgery. Simultaneous extracapsular cataract extraction and posterior chamber lens implantation at the time of keratoplasty posed no measurable compromise to the overall postoperative prognosis. Causes of poor visual acuity after surgery included glaucoma and graft failure (immune and nonimmune).
CONCLUSIONS: The prognosis of penetrating keratoplasty in the iridocorneal endothelial syndrome appears to be very favorable in the majority of eyes. (Refract Corneal Surg. 1993;9:129-132.)
Perceptual filling in is facilitated at the corresponding area of retinal scotomas. The neural mechanisms of this visual facilitation might be similar to those found following somatosensory cortex partial deafferentation.
The results show that: (i) stereoscopic presentation does not influence the target filling-in latency; (ii) differences between dorsal and ventral visual stream might influence target filling-in latency.
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