Research Applications for Striatech Products

Stroke

Ischemic and hemorrhagic cerebrovascular events producing a wide spectrum of visual deficits, from homonymous hemianopia to subtle perceptual loss. Detected in 73% of acute stroke survivors and a major contributor to acquired visual disability.
Introduction

What is Stroke?

Stroke, encompassing ischemic infarction and hemorrhagic cerebrovascular events, is among the leading causes of acquired visual disability in adults worldwide. Ischemic stroke accounts for approximately 87% of all cerebrovascular events and disrupts neural function by depriving tissue of oxygen and glucose, triggering excitotoxic cascades, blood-brain barrier breakdown, neuroinflammatory signaling, and ultimately irreversible neuronal death. When these insults involve the posterior cerebral circulation, the occipital lobe, or the retinal and ophthalmic vasculature, the result is a spectrum of visual impairments. Rowe et al (2019, PLoS ONE) found that 73% of acute stroke survivors had detectable visual problems at bedside assessment, including impaired central vision (56%), eye movement abnormalities (40%), visual field loss (28%), and visual perceptual disorders (27%). Homonymous hemianopia (loss of the same visual half-field in both eyes) is the most recognized form of post-stroke visual field defect and arises from retrochiasmal pathway damage, most commonly affecting the optic radiations or primary visual cortex (V1) supplied by the posterior cerebral artery. Retinal ischemia contributes to visual impairment in approximately 16% of stroke patients, reflecting the shared ophthalmic artery origin of both the middle cerebral artery territory and the inner retinal blood supply. MCAO therefore simultaneously threatens both cerebral and retinal perfusion. This page focuses specifically on the visual-system consequences of stroke and cerebrovascular ischemia as a mechanism studied within the broader context of Trauma and Acute Injury and Vascular and Metabolic Disease. Key mechanisms include neurovascular uncoupling, ischemic retinal ganglion cell (RGC) loss, and post-ischemic demyelination of the visual pathway, linking this topic to broader neurovascular and axonal injury processes: Neurovascular injury, Retinal Ischemia-Reperfusion Injury, Retinal Ganglion Cell Pathology, Optic Nerve Damage, and Axon Degeneration.
Vision: A Window into the brain 

Why Are Visual Endpoints Relevant in Stroke Research?

Stroke is primarily studied as a CNS event – and most preclinical stroke researchers are not vision scientists. Yet the visual system offers a uniquely accessible window into the consequences of cerebral ischemia, for three independent reasons. First, the retina is a true extension of the CNS, derived from the same neuroectodermal tissue as the brain. The ophthalmic artery, the first branch of the internal carotid, arises proximal to the MCA; MCAO in rodents therefore simultaneously ischemia the ipsilateral retina alongside the striatum and cortex. Retinal ganglion cells and the optic nerve thus sustain ischemic damage whose magnitude tracks directly with cerebral infarct severity, making retinal visual function an accessible, non-invasive proxy for CNS injury depth. Bhatt et al (2012, Front Neurol) reviewed this anatomy in detail and confirmed that MCAO-induced retinal ischemia produces both functional and structural retinal damage in rodents, with functional changes detectable by behavioral visual testing. Second, the visual cortex (V1, V2, and surrounding extrastriate areas) is among the most metabolically vulnerable regions of the posterior cerebral territory. Photothrombotic stroke models targeting the visual cortex produce well-defined infarcts with reproducible visual field deficits that can be tracked longitudinally in behaving animals. Dhanesha et al (2023, Front Neurol) reviewed MCAO techniques in rodents and emphasized that even standard proximal MCAO reliably produces cortical and subcortical damage spanning visual processing regions. Third, the optomotor reflex – the basis of the OptoDrum assay – is driven by the retino-pretectal pathway and does not require cortical processing, meaning it reports on the retinal and subcortical visual-pathway integrity that feeds into cortical circuits. This makes it sensitive to the retinal and retino-recipient damage caused by stroke, even when primary cortical lesions are the research focus. For researchers whose primary interest is cerebral infarct volume, motor deficit, or neuroprotective pharmacology, OptoDrum-measured visual acuity provides a longitudinal, non-invasive behavioral endpoint that complements standard stroke outcome batteries without additional surgical procedures.
Animal Models

What Are Common Animal Models For Stroke?

The following models have documented stroke-related visual pathway involvement and are represented in the Striatech publication corpus for this cluster or in the closely related retinal ischemia-reperfusion injury cluster. For the full landscape of acute CNS injury models, see Trauma and Acute Injury.
  • Intraluminal filament MCAO (transient or permanent). The most widely used rodent focal ischemia model: a monofilament introduced via the internal carotid occludes the MCA origin, producing combined striatal and cortical infarction. Because the ophthalmic artery originates proximal to the MCA, MCAO also compromises ipsilateral retinal perfusion. Bhatt et al (2012, Front Neurol) confirmed functional and structural retinal damage in MCAO rats. The Striatech publication by Colon Ortiz et al (2022) characterizing neurovascular injury used an ischemic stroke model in which OptoDrum detected visual acuity deficits downstream of the cerebrovascular insult (Colon Ortiz et al, 2022, Cell Death Dis).
  • Photothrombotic cortical stroke. Systemic administration of a photosensitizing dye (Rose Bengal) combined with focal transcranial laser illumination generates a platelet-rich thrombus in cortical microvasculature, producing a well-demarcated infarct at the target region. When directed at the visual cortex or posterior parietal area, it creates reproducible cortical visual field defects. Dhanesha et al (2023, Front Neurol) note that photothrombosis offers stereotactic precision with low mortality, making it well-suited for studying visual cortex plasticity.
  • Endothelin-1 (ET-1) intracerebral injection. Perivascular or intracortical microinjection of the potent vasoconstrictor endothelin-1 induces focal, concentration-dependent ischemia via arterial vasospasm. When targeted to the visual cortex or posterior cerebral territory, it can model cortical visual deficits with controlled infarct size and gradual reperfusion kinetics that more closely mimic clinical transient ischemic events than the abrupt filament-based occlusion. Cook et al (2017, Sci Rep) established the ET-1 model in non-human primates; the analogous rodent protocol has been validated for reproducible focal lesions in mice (Horie et al, 2008, J Neurosci Methods). Visual readouts have not yet been formally incorporated into most ET-1 rodent studies, representing an unmet experimental opportunity for optomotor-based longitudinal tracking.
  • Combined stroke and retinal ischemia-reperfusion injury model. Yu et al (2022) used a model that produced concurrent cerebral and retinal ischemia-reperfusion injury, exploiting the shared vascular anatomy of the two territories. OptoDrum detected functional visual deficits and their subsequent partial rescue by cell-based neuroprotective therapy (Yu et al, 2022, Biomaterials). This model is discussed further in the retinal ischemia-reperfusion injury cluster.
Global ischemia models (2-vessel occlusion/2VO and 4-vessel occlusion/4VO) mimic cardiac arrest physiology but primarily damage hippocampal and striatal circuits; Lima et al (2021, PubMed) reported that the modified 4VO model did not produce noticeable changes in visual perception and caused no significant retinal structural damage, suggesting these models are less appropriate for visual endpoint studies. For the comprehensive model landscape, see Trauma and Acute Injury.
Research Questions

How Can Striatech Tools support Your Study?

Select a question that matches your research objective to see which instruments are relevant, what challenge they address, and what the published evidence shows.
01
Can Optomotor-Based Visual Acuity Serve as a Non-Invasive Biomarker of Neurovascular Injury Severity After Stroke?
Audience A - Vision-focused
Audience B - CNS/Systemic

Quick Answer

Yes. OptoDrum measures spatial visual acuity via the subcortical optomotor reflex in awake, freely moving rodents without animal training or invasive procedures. In an ischemic stroke model, visual acuity deficits measured by OptoDrum correlated with the extent of neurovascular injury, making this endpoint a sensitive, longitudinal indicator of cerebrovascular injury severity even when the retina is not the primary organ of interest.

The challenge

Preclinical stroke researchers typically rely on infarct volume (MRI or TTC staining), motor deficit scoring (Bederson scale, rotarod, cylinder test), and histological measures of neuronal death as primary outcome measures. These readouts either require terminal procedures (TTC, histology) or capture only a subset of functional deficits. The retinal and visual consequences of cerebral ischemia – even when substantial and clinically meaningful – remain systematically unmeasured in most preclinical stroke studies, representing a gap between the animal model and the ~60-73% of human stroke survivors who experience significant visual impairment (Rowe et al, 2019, PLoS ONE; Li et al, 2022, Eye). Because the ophthalmic artery originates proximal to the MCA, intraluminal filament MCAO in rodents simultaneously interrupts retinal and cerebral perfusion. Retinal ganglion cells (RGCs) are exquisitely sensitive to ischemia and begin undergoing apoptosis within hours of vascular occlusion. RGC loss reduces the magnitude of the optomotor reflex before any gross retinal structural change is visible, meaning functional visual testing can detect injury earlier than most histological endpoints. Critically, this sensitivity comes without the need for anesthesia, surgical access, or contrast agents – making it repeatable at any time point throughout the study. For a focused discussion of the RGC and optic nerve dimension of this process, see Retinal Ganglion Cell Pathology and Neurovascular Injury.

How Striatech products help

OptoDrum
Measures spatial visual acuity (cycles per degree) via the subcortical optomotor reflex in awake, freely moving mice or rats. Non-invasive; can be repeated daily to track the time course of visual deficit onset and recovery after stroke. Both eyes can be assessed independently, allowing comparison of ipsilateral (ischemic) vs contralateral retinal function.
AcuiSee
Measures visual acuity via an operant forced-choice paradigm that requires cortical visual processing. Where cortical stroke is the primary lesion and the research question concerns visual cortex recovery specifically, AcuiSee provides a cortically dependent endpoint that complements the subcortical OptoDrum readout. (No publications in stroke context to date; included on capability grounds.)
Non-aversive Animal Platform
Reduces handling stress during OptoDrum testing, improving data reliability in post-stroke animals that may exhibit heightened stress responses or motor deficits that complicate standard platform placement.

Evidence from the Literature

  • Remlinger et al (2023) Neurol. Neuroimmunol. Neuroinflamm.
    Feature →
  • Colón Ortiz et al (2022) Cell. Death Dis.
    Journal Club →
    The OptoDrum was used to measure visual acuity as a non-invasive functional biomarker of neurovascular injury severity after experimental stroke. The study demonstrated that ischemic neurovascular damage produces quantifiable visual function deficits detectable via optomotor testing, even when retinal injury is not the primary research focus.
  • Minhas et al. (2012) Front Neurol.
    Review of the MCAO model as a tool for studying retinal ischemia and confirmed that functional and structural retinal damage parallels cerebral infarct in this preparation. Establishes the anatomical basis for treating retinal visual function as a downstream readout of MCA territory injury.
  • Rowe et al. (2019) PLoS One.
    Multi-centre prospective study of 1033 stroke survivors: 73% had visual problems at bedside assessment, with impaired central vision most common (56%), confirming the clinical relevance of visual outcomes in stroke research.
  • Li et al. (2022) Eye (Lond).
    Cross-sectional NHANES-based study (n = 4570) found that stroke was associated with a 10-fold adjusted odds ratio for mild visual impairment and ~8.6-fold for moderate-to-severe visual impairment. Reinforces the mechanistic link between stroke severity and downstream visual pathway damage.
02
How Does Vascular-Neural Coupling Determine Visual-Circuit Vulnerability in Focal Cerebral Ischemia?
Audience A - Vision-focused
Audience B - CNS/Systemic

Quick Answer

The retina and visual cortex are highly metabolically active structures with limited collateral circulation. Focal cerebral ischemia disrupts neurovascular coupling at multiple levels of the visual pathway simultaneously – retinal perfusion, optic nerve axon conduction, and cortical processing – and the relative contribution of each level depends on infarct territory. OptoDrum provides a subcortical (retino-pretectal) functional readout that reports on retinal and pre-cortical pathway integrity, while AcuiSee can complement this with a cortically dependent endpoint.

The challenge

The concept of neurovascular coupling – the tight coordination of local neural activity with microvessel blood flow – is central to understanding both normal visual function and its disruption by stroke. RGCs have high ATP demands and are among the first neurons to fail during ischemia; inner retinal layers begin showing electrophysiological dysfunction within 5-10 minutes of complete vascular occlusion. Downstream, the optic nerve axons – unmyelinated in the retinal portion but myelinated after the lamina cribrosa – are vulnerable to ischemic demyelination, a mechanism shared with multiple sclerosis and relevant to the post-ischemic axon degeneration discussed in the axon degeneration cluster. Post-stroke neuroinflammation further uncouples the neurovascular unit: activated microglia and recruited peripheral immune cells release TNF-α, IL-1β, and reactive oxygen species that amplify ischemic cell death in the peri-infarct zone. For a detailed treatment of the neuroinflammation dimension, see the neurovascular injury cluster and the Vascular and Metabolic Disease overview. Disentangling retinal from cortical contributions to the visual deficit requires assays that can be independently assigned to each circuit level.

How Striatech products help

OptoDrum
Measures the subcortical optomotor reflex, which is primarily driven by retinal input through the nucleus of the optic tract and accessory optic system. Because it does not require cortical processing, any deficit it detects is attributable to retinal or pre-cortical pathway dysfunction – useful for isolating the retinal component of a post-stroke visual deficit.
AcuiSee
An operant forced-choice paradigm requiring active cortical visual discrimination. When combined with OptoDrum, allows dissection of cortical vs subcortical contributions: deficits on both assays implicate the retina/optic nerve; deficits on AcuiSee alone, with intact OptoDrum performance, point to cortical visual pathway damage. (Capability-based inclusion; no publications in stroke context to date.)
ScotopicKit
Rod-mediated scotopic visual testing via the OptoDrum. Rod photoreceptors are especially vulnerable to ischemia due to their high oxygen consumption; scotopic acuity assessment can reveal early-phase ischemic damage to the outer retina before photopic (cone-mediated) deficits become evident.

Evidence from the Literature

  • Remlinger et al (2023) Neurol. Neuroimmunol. Neuroinflamm.
    Feature →
  • Colón Ortiz et al (2022) Cell. Death Dis.
    Journal Club →
    Neurovascular injury after stroke was characterized, using OptoDrum to show that ischemic disruption of the neurovascular unit produces functional visual deficits. The retinal component of the deficit was measurable without ophthalmic surgical access, consistent with the retino-pretectal circuit being the primary substrate for OptoDrum responses.
  • Wijesundera et al. (2022) Front Neurol.
    Sixty acute ischemic stroke patients tested within the first week post-stroke: visual field sensitivity and visual acuity with luminance noise were impaired relative to controls, with ROC analysis showing 93% sensitivity and 83% specificity for stroke detection from combined visual and visuomotor endpoints. Demonstrates that visual metrics can serve as independent diagnostic indicators of stroke – supporting their use as preclinical outcome measures.
  • Busza et al. (2019) Neurorehabil Neural Repair.
    Proposed the visual pathway as a model system for studying post-stroke neuroplasticity because of its well-defined anatomy and accessibility to functional and structural endpoints. Specifically highlighted that approximately one-third of stroke patients suffer visual field impairment, yet the visual pathway is underused as a readout in preclinical rehabilitation research.
  • Minhas et al. (2012) Front Neurol.
    Confirmed that 2VO (bilateral carotid occlusion) causes functional retinal damage detectable by ERG (b-wave reduction) and structural retinal thinning, while MCAO causes combined cerebral and retinal ischemia.
03
How Can Visual Function Testing Strengthen Neuroprotective Drug Screens in Preclinical Stroke Models?
Audience A - Vision-focused
Audience B - CNS/Systemic

Quick Answer

Adding optomotor-based visual acuity as an endpoint to a standard stroke drug-screen battery provides a non-invasive, quantitative functional readout that is sensitive to treatment effects on the retinal and pre-cortical visual pathway without requiring terminal tissue collection. The Yu et al (2022) study demonstrated that cell-based neuroprotective therapy significantly improved visual function recovery in a combined stroke/ischemia-reperfusion model, confirming that OptoDrum can detect biologically meaningful therapeutic signals in ischemic CNS injury.

The challenge

The translation failure rate for neuroprotective drugs in stroke is high: more than 1000 compounds have shown efficacy in rodent models but failed in human trials. A key contributor to this gap is the narrow range of functional endpoints used in preclinical screens. Standard stroke models assess infarct volume, motor scores, and often a single cognitive test; visual function is rarely included despite the high clinical burden of post-stroke visual impairment. Incorporating a functional visual endpoint offers several advantages for drug screens: it is quantitative and continuous (unlike categorical clinical scoring), it can be repeated longitudinally without additional animal groups, it is sensitive to treatment at both the retinal and subcortical visual-circuit levels, and it avoids the anesthesia confounds of electrophysiological endpoints. For cell-based and gene-therapy approaches in particular, the retinal visual system provides an accessible window: subretinal or intravitreal delivery can be validated by functional OptoDrum readout, while a concurrent systemic or CNS-directed treatment can be evaluated for its effect on the same retinal endpoint. This dual-window approach – cerebroprotective and retino-protective effects measured with a single behavioral assay – is uniquely enabled by the neurovascular anatomy of focal ischemia. See also the therapeutic recovery angle in the retinal ischemia-reperfusion injury cluster.

How Striatech products help

OptoDrum
Provides a longitudinal, non-invasive visual acuity endpoint for drug and cell-therapy efficacy screens in stroke models. Detects functional recovery at the retinal and pre-cortical circuit level without terminal tissue collection. Repeatable on any experimental day, allowing time-course analysis of therapeutic window and recovery trajectory.
ScotopicKit
Extends OptoDrum to scotopic (rod-mediated) vision testing; allows assessment of rod-pathway neuroprotection independently of cone-mediated acuity – relevant when the therapeutic target is the rod-rich peripheral retina.
AcuiSee
Provides a cortically dependent operant acuity endpoint, enabling evaluation of neuroprotective efficacy at the cortical visual processing level for treatments targeting V1 or peri-infarct cortex. (Capability-based inclusion; no stroke publications to date.)
Non-aversive Animal Platform
Ensures reliable optomotor data quality throughout the treatment time-course in post-stroke animals that may exhibit motor impairment, heightened anxiety, or altered handling tolerance.

Evidence from the Literature

  • Remlinger et al (2023) Neurol. Neuroimmunol. Neuroinflamm.
    Feature →
  • Yu et al (2022) Biomaterials
    Striatech OptoDrum was used as the primary behavioral endpoint for cell-therapy efficacy in a combined stroke and retinal ischemia-reperfusion model. TNF-α-preconditioned neural stem cells significantly improved visual function recovery compared with untreated controls.
  • Saionz et al. (2022) Handb Clin Neurol.
    Review of visual restitution training approaches after V1 stroke, noting that intensive visual training can recover measurable vision even in chronic cortical blindness.
  • Busza et al. (2019) Neural Repair.
    Visual pathway recovery metrics are underexploited in preclinical stroke studies despite providing unique sensitivity to circuit-level treatment effects.
04
How Do Optomotor Response, Electroretinography, VEP, and Behavioral Batteries Compare as Visual Endpoints in Stroke Models?
Audience A - Vision-focused
Audience B - CNS/Systemic

Quick Answer

OptoDrum provides a non-invasive, automated, awake-animal endpoint for retinal and pre-cortical visual function that is uniquely suited to longitudinal stroke studies. ERG and VEP are more mechanistically informative at specific retinal layers or cortical levels but require anesthesia and head restraint, limiting repeated-measures designs. AcuiSee adds a cortically dependent operant component. Each method interrogates a different segment of the visual pathway and can be used complementarily depending on the research question.

The challenge

Stroke researchers who wish to add a visual endpoint to their study face a choice between methods that differ substantially in invasiveness, throughput, anesthesia requirements, the circuit level they sample, and their suitability for repeated longitudinal measurements. A mismatch between method and question – for example, using a purely retinal assay to measure visual cortex recovery – produces uninterpretable data. Understanding which assay is appropriate for which question is therefore a prerequisite for experimental design. The detailed comparison is presented in the Modality Comparison Table in Section 6 below.

How Striatech products help

OptoDrum
Subcortical, reflex-based, fully automated visual acuity and contrast sensitivity. No anesthesia; repeatable daily; provides the retinal and pre-cortical circuit level. Directly comparable to the OMR literature across stroke models.
AcuiSee
Cortical operant forced-choice acuity. Complements OptoDrum for cortical stroke lesions where the retino-pretectal pathway may be intact but V1 processing is disrupted. (No published stroke-context data; included on capability grounds.)
ScotopicKit
Scotopic (rod-mediated) optomotor testing. Adds the rod-pathway dimension to the comparison; useful when distinguishing outer vs inner retinal contributions to the post-stroke visual deficit.
DarkAdapt
Light-tight housing for controlled dark adaptation prior to scotopic OptoDrum testing with the ScotopicKit. Ensures comparability across animals and time points.

Evidence from the Literature

  • Remlinger et al (2023) Neurol. Neuroimmunol. Neuroinflamm.
    Feature →
  • Busza et al. (2019) Neural Repair.
    Proposed the visual pathway as a model system for post-stroke recovery research and highlighted the complementarity of functional and structural visual endpoints. Argued that quantitative, repeatable visual function measurement is more sensitive to circuit recovery than global clinical scoring.
  • Wijesundera et al. (2022) Front Neurol.
    Demonstrated that combined visual field and visual acuity endpoints provided 93% sensitivity and 83% specificity for acute ischemic stroke detection in a bedside clinical study.
  • Saionz et al. (2022) Handb Clin Neurol.
    Review of visual perceptual rehabilitation in cortical blindness, cataloguing how different measurement modalities – visual field perimetry, visual acuity, contrast sensitivity, and VEP – each capture different aspects of cortical and subcortical recovery.
Product Fit

Summary: Striatech Products supporting your research questions

Research Question OptoDrum ScotopicKit AcuiSee Photorefractor Keratometer DarkAdapt Non-aversive platform
Visual acuity biomarker (neurovascular injury) Yes Yes Yes
Vascular-neural coupling / circuit vulnerability Yes Yes Yes Yes Yes
Neuroprotective drug / cell-therapy screen Yes Yes Yes Yes
Endpoint comparison (OMR vs ERG vs VEP) Yes Yes Yes Yes
Measurement Modalities

Measuring Functional Visual Outcomes in Stroke: How Do Available Methods Compare?

Method Circuit level assessed Anesthesia required Longitudinal repeats Automation Animal training 3Rs impact
OptoDrum (Striatech) Retina + retino-pretectal (subcortical) No Daily if needed Fully automated Not required Reduces terminal endpoints; refinement via non-invasive measurement
AcuiSee (Striatech) Cortical visual processing No Yes (session-based) Semi-automated Required (10-14 days) Reduction potential for terminal assays of cortical function
Electroretinogram (ERG) Outer retina to inner nuclear layer Yes (typically) Limited (stress, anesthesia load) Semi-automated Not required Anesthesia adds burden; cannot be repeated frequently
Visual evoked potential (VEP) V1 cortex; full visual pathway Yes (typically) Limited; requires chronic electrode implant for repeats Manual/semi Not required Surgical implant; moderate burden; informative on cortical recovery
Behavioral batteries (Morris water maze visual cue, novel object, etc.) Cortical (cognitive-visual integration) No Yes (with interval) Manual or video-based Partial Confounded by motor deficits common in stroke models; non-specific for visual circuit
Histology / OCT (structural) Retinal layers (structural); RGC layer thinning Yes (for OCT: light sedation); terminal for histology OCT: yes; histology: terminal Semi-automated (OCT) Not required OCT complements functional assays; histology terminal – reduces if replaced by in-vivo methods
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Publications on Stroke

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Journal Clubs related to Stroke

Featured image for “Journal Club: The role of Nogo-A in visual deficits induced by retinal injury.”
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Thursday, 28 Jan 2021

Journal Club: The role of Nogo-A in visual deficits induced by retinal injury.

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Julius Baya Mdzomba, PhD - Université Laval
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Nogo-A, an inhibitor of neural growth, prevents regeneration after injury. Blocking of Nogo-A aides recovery, also in the visual system after retinal damage. Baya Mdzomba show with our OptoDrum that visual behavior benefits from Nogo-A neutralization after retinal damage typically found in diabetic retinopathy or glaucoma.
Keep exploring

Related application areas, neighbouring research chapters, and the questions researchers ask most.

Application Area

Stroke

Ischemic and hemorrhagic cerebrovascular events producing a wide spectrum of visual deficits, from homonymous hemianopia to subtle perceptual loss. Detected in 73% of acute stroke survivors and a major contributor to acquired visual disability.

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Research Chapters
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FAQs answered
Main Field where Stroke is studied
Vascular and Metabolic Disease: Diabetic Retinopathy and Stroke
Other relevant fields
CNS Trauma and Acute Injury: TBI, Optic Nerve Injury, Stroke