Vision recovery in cortical blindness
皮质失明的视力恢复
基本信息
- 批准号:10634933
- 负责人:
- 金额:$ 2.31万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2022
- 资助国家:美国
- 起止时间:2022-09-01 至 2026-01-31
- 项目状态:未结题
- 来源:
- 关键词:AdultAffectAnimal ModelAttentionBlindnessCell DeathChronicComplexConsciousContralateralCortical BlindnessCuesDataDiscriminationDorsalGoalsGrantHemianopsiaHumanImageImpairmentInterventionKnowledgeLateral Geniculate BodyLeadershipLinkLocationMagnetic Resonance ImagingMeasurableMeasuresMethodsMotionMotor CortexNeuronsNoiseOptic tract structureOptical Coherence TomographyOutcomeParticipantPatientsPerceptionPerceptual learningPersonsPhysical therapyPropertyPsychological TransferPsychophysicsQuality of lifeRandomizedRecoveryResearchResidual stateRetinaRetinal Ganglion CellsRetrograde DegenerationStimulusStrokeTestingTimeTrainingVisionVisualVisual PathwaysVisual system structureWorkarea striatablindbrain magnetic resonance imagingclinical practicecostearly onseteffective therapyexpectationgazehuman modelimprovedinsightluminancenovelpatient populationpost strokepreservationrestorationsight restorationstroke rehabilitationvisual performance
项目摘要
In adulthood, stroke damage to the primary visual cortex (V1) causes a large, contralateral loss of conscious
vision referred to as hemianopia or cortical blindness (CB). Although this condition affects up to ½ million new
cases each year in the US alone, there is a total lack of accepted vision restoration therapies – in marked
contrast with early-onset physical therapies prescribed to those with motor cortex damage. Two decades of
work in chronic CB patients, whose deficits are deemed stable, permanent and thus amenable to scientific
study, have generated one method consistently able to recover vision after long-standing V1 damage: gaze-
contingent visual training to detect or discriminate stimuli in the blind field. Over the last 2 grant periods, we
have taken clear leadership in the field, providing hope that an effective therapy for CB may finally be on the
horizon. However, while characterizing training-induced recovery and its underlying mechanisms, we also
found that recovery in chronic CB requires months of daily training and the vision restored is low-contrast,
coarse, impaired by excessive internal processing noise and restricted to the blind field perimeter.
Accumulating evidence suggests that these limitations may occur because chronic patients have lost a
substantial portion of neurons that contribute to vision fundamentals not only in V1, but through retrograde
degeneration, in the dorsal lateral geniculate nucleus (dLGN) and retina. Our new pilot data show subacute CB
patients <6 months post-stroke to lack significant signs of degeneration, and more than half of subacutes
tested retained visual discrimination abilities in their blind field, which disappeared by the start of the chronic
period (6 months post-stroke). Moreover, when training was administered to subacutes, they recovered the
same discrimination abilities as chronics, but much faster, and with recovery extending deeper into their blind
field. These data form a strong premise for testing the hypothesis that substantial differences in plastic
potential between subacute and chronic V1-stroke visual systems can be exploited to maximize visual
restoration in CB, and that the extent of recovery attainable is limited by the amount of retrograde
degeneration sustained. We now propose to: (Aim 1) assess how visual performance relates to structural
evidence of retrograde degeneration in the subacute period post-V1-stroke. We will then (Aim 2) assess the
impact of subacute training on blind-field functions, the progression of retrograde degeneration and the
continued potential for training-induced recovery in the chronic period. Finally, we will (Aim 3) contrast
mechanistic substrates of perceptual learning in subacute & chronic CB. All in all, the work proposed is unique
in the field, which it stands to advance significantly by generating entirely new knowledge and understanding of
the change in visual plastic potential with time in the early period after permanent V1 damage in humans. This
knowledge is important both neuro-scientifically, and for devising more effective treatment and realistic
outcome expectations for this growing patient population.
在成年期,对主要视觉皮层(V1)的中风损害造成大量的,对方的损失
视力称为半岛或皮质失明(CB)。
仅在美国,每年的情况就会出现到总数缺乏加入视觉恢复疗法 -
与早期的物理疗法相比,与有运动皮层损害的人开处方
在慢性CB患者中的工作,其缺陷是稳定的,永久的,因此适合科学
研究,已经产生了一种能够在长期存在V1损害后能够恢复视力的方法:凝视 -
在过去的两个赠款期间,偶然的视觉训练在盲区中检测或区分刺激。
已经在该领域取得了明确的领导,为CB提供有效的疗法最终可能会出现
但是,在表征训练引起的恢复和潜在机制的同时,我们也是
发现慢性CB的恢复需要每天几个月的训练,并且需要进行调用,这是低对比度的,
粗糙,受到过度内部处理噪声的损害,并且仅限于盲场周长。
积累的证据表明,可能会发生这种限制,因为长期帕特斯人失去了
不仅在V1中,而且通过反编程中有助于视觉基础的大量神经元的大部分神经元
退化,在背侧基因核(DLGN)和视网膜中。
中风后<6个月的患者缺乏重大变性迹象,超过一半的亚纯净迹象
经过测试的盲区中保留的视觉耻辱能力,该领域在慢性开始时消失了
(击球后6个月)。
相同的歧视能力与年龄相同,但更快,并且恢复更深入地扩展到他们的盲人
字段。
可以利用亚急性和慢性V1-STROKE视觉系统之间的钾盐,以最大化视觉
CB中的恢复,并且可以实现的恢复程度受到逆转录的量的限制
退化稳定。我们现在建议:(目标1)
v1杆后,我们将(AIM 2)评估您的逆行变性证据。
亚急性训练对盲场功能的影响,后置变性的进展和您
持续的训练引起的恢复的潜力。
亚急性和慢性CB中知觉学习的机械基板。
在该领域,它可以通过产生全新的知识和对
在人类中永久性V1损害后的早期,视觉塑料潜力的变化。
知识在神经方面都很重要,并且要设计更有效的治疗和现实
对这个不断增长的患者人群的结果期望。
项目成果
期刊论文数量(0)
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Krystel R Huxlin其他文献
Krystel R Huxlin的其他文献
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{{ truncateString('Krystel R Huxlin', 18)}}的其他基金
Mechanisms of visual learning in cortical blindness
皮质失明的视觉学习机制
- 批准号:
8515422 - 财政年份:2011
- 资助金额:
$ 2.31万 - 项目类别:
Mechanisms of visual learning in cortical blindness
皮质失明的视觉学习机制
- 批准号:
8698756 - 财政年份:2011
- 资助金额:
$ 2.31万 - 项目类别:
Mechanisms of visual learning in cortical blindness
皮质失明的视觉学习机制
- 批准号:
8319327 - 财政年份:2011
- 资助金额:
$ 2.31万 - 项目类别:
Mechanisms of visual learning in cortical blindness
皮质失明的视觉学习机制
- 批准号:
8186221 - 财政年份:2011
- 资助金额:
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8500289 - 财政年份:2004
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