Damage to the optic radiations or primary visual cortex leads to blindness in all or part of the contralesional visual field. Such damage disconnects the retina from its downstream targets and, over time, leads to trans-synaptic retrograde degeneration of retinal ganglion cells. To date, visual ability is the only predictor of retinal ganglion cell degeneration that has been investigated after geniculostriate damage. Given prior findings that some patients have preserved visual cortex activity for stimuli presented in their blind field, we tested whether that activity explains variability in retinal ganglion cell degeneration over and above visual ability. We prospectively studied 15 patients (four females, mean age = 63.7 years) with homonymous visual field defects secondary to stroke, 10 of whom were tested within the first two months after stroke. Each patient completed automated Humphrey visual field testing, retinotopic mapping with functional magnetic resonance imaging, and spectral-domain optical coherence tomography of the macula. There was a positive relation between ganglion cell complex (GCC) thickness in the blind field and early visual cortex activity for stimuli presented in the blind field. Furthermore, residual visual cortex activity for stimuli presented in the blind field soon after the stroke predicted the degree of retinal GCC thinning six months later. These findings indicate that retinal ganglion cell survival after ischaemic damage to the geniculostriate pathway is activity dependent.
The division of labour between the dorsal and ventral visual pathways is well established. The ventral stream supports object identification, while the dorsal stream supports online processing of visual information in the service of visually guided actions. Here, we report a case of an individual with a right inferior quadrantanopia who exhibited accurate spontaneous rotation of his wrist when grasping a target object in his blind visual field. His accurate wrist orientation was observed despite the fact that he exhibited no sensitivity to the orientation of the handle in a perceptual matching task. These findings indicate that non-geniculostriate visual pathways process basic volumetric information relevant to grasping, and reinforce the observation that phenomenal awareness is not necessary for an object's volumetric properties to influence visuomotor performance.
Post-stroke homonymous hemianopia is disabling and complete spontaneous recovery is rare (12.5%). Other than acute revascularization, no proven treatments are available to enhance recovery. Compensatory training may lead to modest functional improvements, but does not restore native function. As such, therapies effective beyond the acute stage are desperately needed. In this phase IIa single-center, double-blinded, randomized, placebo-controlled pilot clinical trial, we tested whether fluoxetine (FLX) enhances visual recovery after an ischemic stroke by facilitating cortical remapping as measured by fMRI. We randomized 10 consecutive adults in a 1:1 ratio to 90 days of FLX 20 mg daily
vs
placebo within 5 days of a stroke in the PCA (
n
= 9) or MCA (
n
= 1) territory causing an isolated homonymous field defect. Only one subject was treated with tPA. The primary outcome measure was percent improvement in perimetric mean deviation (PMD) as measured by automated Humphrey perimetry at 6 months. Eight subjects completed the study. Intention-to-treat analysis of the primary outcome measure showed a non-significant benefit of FLX (
n
= 4) over placebo (70.5 ± 21.1%
vs
30.1 ± 23.5%; one-tailed
t
-test,
p
= 0.12). Complete recovery occurred more frequently than expected in both groups (75%
vs
25%), but was significantly greater than 12.5% only in the FLX group (
p
= 0.007
vs p
= 0.41). Percent improvement in PMD significantly correlated with scores on the 25-item Visual Functioning Questionnaire, a vision-targeted measure of health-related quality of life (
r
2
= 0.74;
p
= 0.012). Subjects in both groups who fully recovered showed fMRI evidence of cortical remapping by expansion and shifting of the center of their ipsilesional V1 receptive fields. In those with partial recovery, fMRI showed no cortical remapping, but a return of function in normal retinotopic locations, possibly due to recovery of “stunned” tissue. In conclusion, these results illustrate the feasibility of our approach, suggest a trend in favor of FLX, and have the potential to inform the design of a multi-center trial. Our fMRI analysis raises testable hypotheses about post-stroke recovery and suggests that FLX may improve outcomes by enabling the same kind of plasticity that underlies spontaneous recovery.
Background: Poststroke homonymous hemianopia is disabling, and complete spontaneous recovery is rare. In this randomized, placebo-controlled, double-blind, pilot clinical trial, we tested whether fluoxetine enhances vision recovery after stroke. Methods: We randomized 17 consecutive adults 1:1 to 90 days of fluoxetine 20 mg daily vs placebo within 10 days of an ischemic stroke causing isolated homonymous hemianopia. The primary end point was percent improvement in 24-2 automated perimetry at 6 months. Twelve participants completed the study. Clinical trial registration NCT02737930.Results: Intention-to-treat analysis of the primary end point, percent improvement in perimetric mean deviation, showed a nonsignificant benefit of fluoxetine (64.4%, n = 5) com-pared with placebo (26.0%, n = 7, one-tailed 95% confidence interval (CI) = (22.13, N), P = 0.06). The original blind field completely recovered in 60% receiving fluoxetine and 14% receiving placebo (odds ratio = 7.22, one-tailed 95% CI = (0.50, N)). Conclusion: These results suggest a trend in favor of fluoxetine for vision recovery after stroke and have the potential to inform the design of a larger multicenter trial.
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