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Stroke damage to the primary visual cortex (V1) causes a loss of vision known as hemianopia or cortically-induced blindness. While perimetric visual field improvements can occur spontaneously in the first few months post-stroke, by 6 months post-stroke, the deficit is considered chronic and permanent. Despite evidence from sensorimotor stroke showing that early injury responses heighten neuroplastic potential, to date, visual rehabilitation research has focused on patients with chronic cortically-induced blindness. Consequently, little is known about the functional properties of the post-stroke visual system in the subacute period, nor do we know if these properties can be harnessed to enhance visual recovery. Here, for the first time, we show that ‘conscious’ visual discrimination abilities are often preserved inside subacute, perimetrically-defined blind fields, but they disappear by ∼6 months post-stroke. Complementing this discovery, we now show that training initiated subacutely can recover global motion discrimination and integration, as well as luminance detection perimetry, just as it does in chronic cortically-induced blindness. However, subacute recovery was attained six times faster; it also generalized to deeper, untrained regions of the blind field, and to other (untrained) aspects of motion perception, preventing their degradation upon reaching the chronic period. In contrast, untrained subacutes exhibited spontaneous improvements in luminance detection perimetry, but spontaneous recovery of motion discriminations was never observed. Thus, in cortically-induced blindness, the early post-stroke period appears characterized by gradual—rather than sudden—loss of visual processing. Subacute training stops this degradation, and is far more efficient at eliciting recovery than identical training in the chronic period. Finally, spontaneous visual improvements in subacutes were restricted to luminance detection; discrimination abilities only recovered following deliberate training. Our findings suggest that after V1 damage, rather than waiting for vision to stabilize, early training interventions may be key to maximize the system’s potential for recovery.

Damage to the primary visual cortex (V1) causes homonymous visual-field loss long considered intractable. Multiple studies now show that perceptual training can restore visual functions in chronic cortically-induced blindness (CB). A popular hypothesis is that training can harness residual visual functions by recruiting intact extrageniculostriate pathways. Training may also induce plastic changes within spared regions of the damaged V1. Here, we link changes in luminance detection sensitivity with retinotopic fMRI activity before and after visual discrimination training in eleven patients with chronic, stroke-induced CB. We show that spared V1 activity representing perimetrically-blind locations prior to training predicts the amount of training-induced recovery of luminance detection sensitivity. Additionally, training results in an enlargement of population receptive fields in perilesional V1, which increases blind-field coverage and may support further recovery with subsequent training. These findings uncover fundamental changes in perilesional V1 cortex underlying training-induced restoration of conscious luminance detection sensitivity in CB., In humans, stroke damage to V1 causes large visual field defects. Spared V1 activity prior to training predicts the amount of training-induced recovery in luminance detection sensitivity. Moreover, visual training changes population receptive field properties within residual V1 circuits.

Numerous behavioral studies have shown that visual function can improve with training, although perceptual refinements generally require weeks to months of training to attain. This, along with questions about long-term retention of learning, limits practical and clinical applications of many such paradigms. Here, we show for the first time in female and male human participants that just 10 d of visual training coupled with transcranial random noise stimulation (tRNS) over visual areas causes dramatic improvements in visual motion perception. Relative to control conditions and anodal stimulation, tRNS-enhanced learning was at least twice as fast, and, crucially, it persisted for 6 months after the end of training and stimulation. Notably, tRNS also boosted learning in patients with chronic cortical blindness, leading to recovery of motion processing in the blind field after just 10 d of training, a period too short to elicit enhancements with training alone. In sum, our results reveal a remarkable enhancement of the capacity for long-lasting plastic and restorative changes when a neuromodulatory intervention is coupled with visual training. SIGNIFICANCE STATEMENT Our work demonstrates that visual training coupled with brain stimulation can dramatically reduce the training period from months to weeks, and lead to fast improvement in neurotypical subjects and chronic cortically blind patients, indicating the potential of our procedure to help restore damaged visual abilities for currently untreatable visual dysfunctions. Together, these results indicate the critical role of early visual areas in perceptual learning and reveal its capacity for long-lasting plastic changes promoted by neuromodulatory intervention.

Transcranial random noise stimulation (tRNS), a relatively recent addition to the field of non-invasive, electrical brain stimulation, has been shown to improve perceptual and cognitive functions across a wide variety of tasks. However, the underlying mechanisms of visual improvements caused by tRNS remain unclear. To study this question, we employed a well-established, equivalent-noise approach, which measures perceptual performance at various levels of external noise and is formalized by the Perceptual Template Model (PTM). This approach has been used extensively to infer the underlying mechanisms behind changes in visual processing, including those from perceptual training, adaptation and attention. Here, we used tRNS during an orientation discrimination task in the presence of increasing quantities of external visual white noise and fit the PTM to gain insights into the effects of tRNS on visual processing. Our results show that tRNS improves visual processing when stimulation is applied during task performance, but only at high levels of external visual white noise—a signature of improved external noise filtering. There were no significant effects of tRNS on task performance after the stimulation period. Of interest, the reported effects of tRNS on visual processing mimic those previously reported for endogenous spatial attention, offering a potential area of investigation for future work.

Damage to the primary visual cortex (V1) causes profound, homonymous visual-field loss termed cortical blindness (CB). Though long considered intractable, multiple studies now show that perceptual training can recover visual functions in chronic CB. A popular hypothesis is that training recruits intact extrageniculostriate pathways. Alternatively, training may induce plastic changes within spared regions of the damaged V1. Here, we linked changes in luminance detection sensitivity with retinotopic fMRI activity in eleven chronic CB patients, before and after extensive visual discrimination training. Our results show that the strength of spared V1 activity representing perimetrically blind-field locations before training predicts the amount of training-induced recovery of luminance detection sensitivity. Additionally, training caused an enlargement of population receptive fields in perilesional V1 cortex, which increased blind-field coverage. These findings uncover fundamental changes in perilesional V1 cortex underlying training-induced restoration of conscious luminance detection sensitivity in cortically-blind patients.

Stroke damage to the primary visual cortex (V1) causes a loss of vision known as hemianopia or cortically-induced blindness (CB). While early, spontaneous, perimetric improvements can occur, by 6 months post-stroke, the deficit is considered chronic and permanent. Despite evidence from sensorimotor stroke showing that early injury responses heighten neuroplastic potential, to date, rehabilitation research has focused only on chronic CB patients. Consequently, little is known about the functional properties of subacute, post-stroke visual systems, and whether they can be harnessed to enhance visual recovery. Here, for the first time, we show that conscious visual discrimination abilities are partially preserved inside subacute, perimetrically-defined blind fields, disappearing by 6 months post-stroke. Complementing this discovery, we show that global motion discrimination training initiated subacutely leads to comparable magnitude of recovery as that initiated in chronic CB. However, it does so 6 times faster, generalizes to deeper, untrained regions of the blind field, and to other [untrained] aspects of motion perception, preventing their degradation upon reaching the chronic period. Untrained subacutes exhibited only spontaneous improvements in perimetry - spontaneous recovery of motion discriminations was never observed. Thus, in CB, the early post-stroke period appears characterized by gradual - rather than sudden - loss of visual processing. Subacute training stops this degradation, and is dramatically more efficient at eliciting recovery than identical training in the chronic period. Finally, spontaneous improvements in subacutes appear restricted to luminance detection, whereas recovering discrimination abilities requires deliberate training. Simply stated, after an occipital stroke, “time is VISION”.One Sentence SummaryThe first 3 months after an occipital stroke are characterized by a gradual - not sudden - loss of visual perceptual abilities and increased rehabilitative potential if visual discrimination training is administered in the blind field.

Numerous behavioral studies have shown that visual function can improve with training, although perceptual refinements generally require weeks to months of training to attain. This, along with questions about long-term retention of learning, limits practical and clinical applications of many such paradigms. Here, we show for the first time that just 10 days of visual training coupled with transcranial random noise stimulation (tRNS) over visual areas causes dramatic improvements in visual motion perception. Relative to control conditions and anodal stimulation, tRNS-enhanced learning was at least twice as fast, and, crucially, it persisted for 6 months after the end of training and stimulation. Notably, tRNS also boosted learning in patients with chronic cortical blindness, leading to recovery of motion processing in the blind field after just 10 days of training, a period too short to elicit enhancements with training alone. In sum, our results reveal a remarkable enhancement of the capacity for long-lasting plastic and restorative changes when a neuromodulatory intervention is coupled with visual training.

The incidence of cortically induced blindness is increasing as our population ages. The major cause of cortically induced blindness is stroke affecting the primary visual cortex. While the impact of this form of vision loss is devastating to quality of life, the development of principled, effective rehabilitation strategies for this condition lags far behind those used to treat motor stroke victims. Here we summarize recent developments in the still emerging field of visual restitution therapy, and compare the relative effectiveness of different approaches. We also draw insights into the properties of recovered vision, its limitations and likely neural substrates. We hope that these insights will guide future research and bring us closer to the goal of providing much-needed rehabilitation solutions for this patient population.

SummaryEarly psychologists, including Galton, Cattell, and Spearman, proposed that intelligence and simple sensory discriminations are constrained by common neural processes, predicting a close link between them [1, 2]. However, strong supporting evidence for this hypothesis remains elusive. Although people with higher intelligence quotients (IQs) are quicker at processing sensory stimuli [1–5], these broadly replicated findings explain a relatively modest proportion of variance in IQ. Processing speed alone is, arguably, a poor match for the information processing demands on the neural system. Our brains operate on overwhelming amounts of information [6, 7], and thus their efficiency is fundamentally constrained by an ability to suppress irrelevant information [8–21]. Here, we show that individual variability in a simple visual discrimination task that reflects both processing speed and perceptual suppression [22] strongly correlates with IQ. High-IQ individuals, although quick at perceiving small moving objects, exhibit disproportionately large impairments in perceiving motion as stimulus size increases. These findings link intelligence with low-level sensory suppression of large moving patterns—background-like stimuli that are ecologically less relevant [22–25]. We conjecture that the ability to suppress irrelevant and rapidly process relevant information fundamentally constrains both sensory discriminations and intelligence, providing an information-processing basis for the observed link.

The effects of attention, as well as its functional utility, are particularly prominent when selecting among multiple stimuli that compete for processing resources. However, existing studies have found that binocular rivalry—a phenomenon characterized by perceptual competition between incompatible stimuli presented to the two eyes—is only modestly influenced by selective attention. Here, we demonstrate that the relative resistance of binocular rivalry to selective modulations gradually erodes over the course of extended perceptual training that uses a demanding, feature-based attentional task. The final result was a dramatic alteration in binocular rivalry dynamics, leading to profound predominance of the trained stimulus. In some cases, trained observers saw the trained rival image nearly exclusively throughout 4-min viewing periods. This large change in binocular rivalry predominance was driven by two factors: task-independent, eye-specific changes in visual processing, as well as an enhanced ability of attention to promote predominance of the task-relevant stimulus. Notably, this strengthening of task-driven attention also exhibited eye specificity above and beyond that from observed sensory processing changes. These empirical results, along with simulations from a recently developed model of interocular suppression, reveal that stimulus predominance during binocular rivalry can be realized both through an eye-specific boost in processing of sensory information and through facilitated deployment of attention to task-relevant features in the trained eye. Our findings highlight the interplay of attention and binocular rivalry at multiple visual processing stages and reveal that sustained training can substantially alter early visual mechanisms.

Attentional influence over perception is particularly pronounced when sensory stimulation is ambiguous, where attention can reduce stimulus uncertainty and promote a stable interpretation of the world. However, binocular rivalry, an extensively studied visual ambiguity, has proved to be comparatively resistant to attentional modulation. We hypothesize that this apparent inconsistency reflects fluctuations in the degree of unresolved competition during binocular rivalry. Namely, attentional influence over rivalry dynamics should be limited to phases of relatively unresolved stimulus competition, such as ends of individual dominance periods. We found that transient, feature-based cues congruent with the dominant stimulus prolonged dominance durations, while cues matching the suppressed stimulus hastened its return to dominance. Notably, the effect of cues depended on when the cues are presented. Cues presented late, but not early, during a given episode of perceptual dominance influenced rivalry dynamics. This temporal pattern mirrors known changes in the relative competitive dynamics of rival stimuli, revealing that selective effects occur only during temporal windows containing weak resolution of visual competition. In conclusion, these findings reveal that unresolved competition, which gates attention across a variety of domains, is also crucial in determining the susceptibility of binocular rivalry to selective influences.

Damage to the primary visual cortex typically causes cortical blindness (CB) in the hemifield contralateral to the damaged hemisphere. Recent evidence indicates that visual training can partially reverse CB at trained locations. Whereas training induces near-complete recovery of coarse direction and orientation discriminations, deficits in fine motion processing remain. Here, we systematically disentangle components of the perceptual inefficiencies present in CB fields before and after coarse direction discrimination training. In seven human CB subjects, we measured threshold versus noise functions before and after coarse direction discrimination training in the blind field and at corresponding intact field locations. Threshold versus noise functions were analyzed within the framework of the linear amplifier model and the perceptual template model. Linear amplifier model analysis identified internal noise as a key factor differentiating motion processing across the tested areas, with visual training reducing internal noise in the blind field. Differences in internal noise also explained residual perceptual deficits at retrained locations. These findings were confirmed with perceptual template model analysis, which further revealed that the major residual deficits between retrained and intact field locations could be explained by differences in internal additive noise. There were no significant differences in multiplicative noise or the ability to process external noise. Together, these results highlight the critical role of altered internal noise processing in mediating training-induced visual recovery in CB fields, and may explain residual perceptual deficits relative to intact regions of the visual field.