Developing a rational strategy for visual rehabilitation after cortical lesions

制定皮质损伤后视力康复的合理策略

基本信息

项目摘要

Visual field loss is a common corollary of stroke (Pollock et al,The Cochrane Library:John Wiley & Sons; 2011,p p. 1-83) that is prevalent in the VA population. Posterior and middle cerebral artery infarcts often injure visual cortical networks resulting in partial or complete homonymous hemianopia or quadrantanopia. The most common clinically significant visual cortical injury involves the primary visual cortex and adjacent regions (area V1+). Area V1 is the chief relay of visual input to higher (extrastriate) cortical areas, and V1 lesions result in a dense contralateral scotoma within which visual perception is severely impaired. The resulting visual deficit is long thought to be resistant to rehabilitation, i.e. to be essentially irreversible, and impairs quality of life significantly. Visual field loss impairs many activities of daily living, including the ability to ambulate safely, drive, read, cook, supervise minors, and others, markedly reducing the independence of the patient (Veterans Health Initiative 2002: Visual Impairment and Blindness). Loss of visual motion perception is particularly problematic for navigating the environment and for avoiding collision with moving objects. Here we focus on studying rehabilitation of visual motion perception. Several studies demonstrated that visual cortex can be driven from the interior of the scotoma, i.e. from areas of the visual field where there is no visual perception. One such area that can be visually modulated in the absence of V1 input is hV5/MT+, an area important for visual motion perception. Although this modulation is weak and does not generally confer useful vision (“blindsight”), it raises the hope that appropriately designed new rehabilitative strategies may be able to strengthen these partially functioning pathways promoting recovery. Recent work (Huxlin et al. J Neuroscience 29(13):3981-91, 2009) has shown that intensive training in a visual motion discrimination task can improve visual motion perception in some subjects with cortical V1 lesions (see fig 5-6). However, this work is still at the preliminary stage. Specifically, not all subjects appear to benefit (section C2), it is not clear which parts of the visual field are amenable to visual rehabilitation, and the mechanism of recovery remains unclear. Our goal here is twofold: 1) To pilot functional magnetic resonance imaging (fMRI) population receptive field mapping methods for identifying regions of the visual field that are more amenable to visual rehabilitation after lesions of the primary visual cortex (area V1+). 2) To probe the mechanisms underlying the recently reported rehabilitation-induced improvement in visual performance that occurs in some subjects (preliminary data fig. 5-7). We will address the following specific aims: Aim 1: We will show that functional magnetic resonance imaging (fMRI) population receptive field mapping methods can identify regions of the visual field that are more amenable to visual motion perception rehabilitation after lesions of the primary visual cortex (area V1+). Hypothesis 1: Regions of the scotoma that elicit visually driven fMRI activity in both spared area V1 and hV5/MT+ (see fig.1) will be easier to rehabilitate, and will reach higher behavioral thresholds, compared to regions that activate only area hV5/MT+. Aim 2: Study how the strength of visual modulation changes in early visual areas, in hV5/MT+, and in fronto- parietal networks subserving attention & higher-order visual processing, following rehabilitative training. Determine whether observed changes are correlated with recovery. Hypothesis 2: Training will increase the signal to noise ratio of the response to visual motion stimuli in area hV5/MT+, while responses in spared V1+ and early extrastriate areas will remain relatively unchanged. Increase in hV5/MT+ response strength will correlate best with recovery. The change in hV5/MT+ response strength will likely be mediated via top down pathways, potentially associated with attentional networks (see [43] [44] and preliminary data fig. 5-7). Our long-term goal is to use information obtained from fMRI methods to implement a principled strategy for developing rehabilitative treatments following visual cortex injury.
视野丧失是中风的常见推论(Pollock等人,Cochrane图书馆:John Wiley&Sons;2011,p 第1-83页),在退伍军人中普遍存在。大脑后动脉和大脑中动脉梗塞常损害视力 皮质网络导致部分或完全同名偏盲或象限视。最多的 常见的临床显著视觉皮质损伤累及初级视觉皮质和邻近区域(区域 V1+)。V1区是视觉输入到较高(纹状体外)皮质区域的主要中继站,V1区病变导致 致密的对侧暗点,其中视觉感觉严重受损。由此产生的视觉缺陷是 长期以来被认为是抗拒康复的,即基本上不可逆转的,并损害生活质量 意义重大。视野丧失损害了日常生活中的许多活动,包括安全行走、驾驶、 阅读、烹饪、监督未成年人和其他,明显降低病人的独立性(退伍军人健康 2002年倡议:视力障碍和失明)。视觉运动知觉的丧失对于 导航环境并避免与移动对象发生碰撞。在这里,我们专注于研究 视觉运动知觉康复。 几项研究表明,视觉皮质可以从暗点的内部驱动,即从 没有视觉知觉的视野。一个这样的区域可以在视觉上调制在 缺少V1输入是hV5/MT+,这是视觉运动知觉的一个重要区域。尽管这种调制是 虚弱,通常不提供有用的视力(“盲视”),它提出了希望,适当地设计 新的康复战略可能能够加强这些部分起作用的促进恢复的途径。 最近的工作(Huxlin等人神经科学杂志29(13):3981-91,2009)已经表明,在视觉上的强化训练 运动辨别任务可以改善部分大脑皮质V1病变受试者的视觉运动知觉(见 图5-6)。然而,这项工作仍处于初步阶段。具体地说,并不是所有的受试者都从中受益 (C2节),尚不清楚视野的哪些部分适合视力康复,以及 恢复的机制仍不清楚。我们的目标有两个:1)试验功能性磁共振 用于识别符合以下条件的视野区域的成像(FMRI)群体感受野映射方法 初级视皮层(V1+区)损伤后更容易接受视力康复。2)探查 最近报道的康复诱导的视觉表现改善的机制 在某些受试者中发生(初步数据图。5-7)。我们将解决以下具体目标: 目的1:我们将展示功能磁共振成像(FMRI)群体感受野标测 方法可以识别更适合视觉运动感觉康复的视野区域 在初级视皮层(V1+区)损伤后。假设1:视觉性暗点的区域 在备用区V1和hV5/MT+的驱动功能磁共振活动(见图1)将更容易恢复,并将达到 与仅激活区域hV5/MT+的区域相比,行为阈值更高。 目的2:研究视觉调制强度在早期视觉区域、hV5/MT+和额叶中的变化。 在康复训练后,顶叶网络服务于注意力和高级视觉处理。 确定观察到的变化是否与恢复相关。假设2:训练会增加 HV5/MT+区对视觉运动刺激的反应的信噪比,而备用V1+区的反应 而早期纹外区将保持相对不变。增加hV5/MT+反应强度将 与复苏的关联度最高。HV5/MT+反应强度的变化可能会通过自上而下的方式进行调节 可能与注意网络相关的通路(见[43][44]和初步数据图。5-7)。 我们的长期目标是利用从功能磁共振成像方法获得的信息来实施一项原则性的战略 发展视皮层损伤后的康复治疗。

项目成果

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Stelios Manolis Smirnakis其他文献

Stelios Manolis Smirnakis的其他文献

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{{ truncateString('Stelios Manolis Smirnakis', 18)}}的其他基金

Cell-specific Functional and Transcriptomic Analysis of Plasticity Pathways in MECP2-Duplication Syndrome
MECP2 重复综合征可塑性途径的细胞特异性功能和转录组分析
  • 批准号:
    10593623
  • 财政年份:
    2022
  • 资助金额:
    --
  • 项目类别:
CMA: Network plasticity in acquired epileptogenesis
CMA:获得性癫痫发生中的网络可塑性
  • 批准号:
    10343662
  • 财政年份:
    2021
  • 资助金额:
    --
  • 项目类别:
CMA: Network plasticity in acquired epileptogenesis
CMA:获得性癫痫发生中的网络可塑性
  • 批准号:
    10011986
  • 财政年份:
    2021
  • 资助金额:
    --
  • 项目类别:
Dense Analysis of Cortical Circuit Dysfunction in the MECP2-duplication Syndrome of Autism
自闭症 MECP2 重复综合征皮质回路功能障碍的密集分析
  • 批准号:
    10545061
  • 财政年份:
    2021
  • 资助金额:
    --
  • 项目类别:
Dense Analysis of Cortical Circuit Dysfunction in the MECP2-duplication Syndrome of Autism
自闭症 MECP2 重复综合征皮质回路功能障碍的密集分析
  • 批准号:
    10322152
  • 财政年份:
    2021
  • 资助金额:
    --
  • 项目类别:
CMA: Network plasticity in acquired epileptogenesis
CMA:获得性癫痫发生中的网络可塑性
  • 批准号:
    10553141
  • 财政年份:
    2021
  • 资助金额:
    --
  • 项目类别:
PROBING THE CELL-SPECIFIC CONTROL OF FOCAL CORTICAL SEIZURE EVENTS IN VIVO
探究体内局灶性皮质癫痫事件的细胞特异性控制
  • 批准号:
    10553167
  • 财政年份:
    2020
  • 资助金额:
    --
  • 项目类别:
PROBING THE CELL-SPECIFIC CONTROL OF FOCAL CORTICAL SEIZURE EVENTS IN VIVO
探究体内局灶性皮质癫痫事件的细胞特异性控制
  • 批准号:
    10438529
  • 财政年份:
    2020
  • 资助金额:
    --
  • 项目类别:
Developing a rational strategy for visual rehabilitation after cortical lesions
制定皮质损伤后视力康复的合理策略
  • 批准号:
    10454752
  • 财政年份:
    2020
  • 资助金额:
    --
  • 项目类别:
PROBING THE CELL-SPECIFIC CONTROL OF FOCAL CORTICAL SEIZURE EVENTS IN VIVO
探究体内局灶性皮质癫痫事件的细胞特异性控制
  • 批准号:
    9889763
  • 财政年份:
    2020
  • 资助金额:
    --
  • 项目类别:

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