Precision and binding as two dimensions of medial temporal lobe amnesia

项目摘要 人类内侧颞叶的病变会导致显著的且往往是长期的缺陷， 语言记忆延迟，称为内侧颞叶健忘症。虽然媒体模型 颞叶功能，如陈述性记忆理论，假设一个有限的作用， 对于内侧颞叶在记忆功能中的作用，认知科学中越来越多的共识 神经科学表明，这种缺陷还包括表征的损伤， 重要的认知领域，如感知，注意力，工作记忆， 语言和空间导航。在这里，我们提出了一个新的模型，以更好地说明 内侧颞叶病变所伴随的认知缺陷的范围。我们的模型 假设人类内侧颞叶功能最好描述为 包括代表性的精确性和约束力，预测赤字增加， 任务需求沿着这两个关键维度增加。Aim 1测试中的实验 我们的模型，特别侧重于测试的代表性精度的背景下， 记忆和导航使我们能够比较这些实验的结果 与陈述性记忆理论预测的结果相反。实验将包括测试 双侧内侧颞叶患者，包括那些病变主要 仅限于海马体，健康参与者的高分辨率功能磁共振成像研究， 更好地确定海马对精度贡献的机制基础， 约束力目标2将决定我们模型的预测能力， 基于fMRI的网络建模，以解释伴随单侧内侧 颞叶病变是在治疗过程中手术切除的结果， 难治性癫痫。该提案的预期成果是： 1)对内侧颞叶损伤后果的更完整描述， 特别是海马体，对认知的影响， 2）一个更完整的预测模型的影响 单侧颞叶切除术对切除术后认知结果的影响， 允许更大的灵活性来决定哪些患者应该接受反应性的 神经刺激（RNS）与切除术3）建模是否以及如何在内侧外 颞叶皮层网络可以补偿切除后失去的功能4） 潜在地，涉及认知干预的新疗法的灵感， 神经刺激靶向具有遗忘样症状的患者的完整皮质组织。

Project Abstract Lesions to the human medial temporal result in striking and often long-lasting deficits in delayed verbal memory, termed medial temporal lobe amnesia. While models of medial temporal lobe function, such as declarative memory theory, hypothesize a restricted role for the medial temporal lobe in memory function, a growing consensus in cognitive neuroscience suggests that such deficits also include impairments in representations important to other areas of cognition, such as perception, attention, working memory, language, and spatial navigation. Here, we propose a novel model to better account for the range of cognitive deficits that accompany medial temporal lobe lesions. Our model hypothesizes that human medial temporal lobe function can best be described as involving both representational precision and binding, predicting increasing deficits as task-demands increase along these two critical dimensions. Experiments in Aim 1 test our model with a particular focus on testing representational precision in the context of memory and navigation to allow us to compare the outcomes from these experiments against those predicted by declarative memory theory. Experiments will include testing with bilateral medial temporal lobe patients, including those with lesions primarily restricted to the hippocampus, and high-resolution fMRI studies in healthy participants to better determine the mechanistic basis of hippocampal contributions to precision and binding. Aim 2 will determine the predictive capacity of our model, in conjunction with fMRI-based network modeling, to explain deficits accompanying unilateral medial temporal lesions that occur as a result of surgical resections during treatment of pharmacologically intractable epilepsy. The anticipated outcomes from the proposal are: 1) a more complete account of the consequences of medial temporal lobe lesions, particularly to the hippocampus, on cognition than can be provided by neuropsychological measures alone 2) a more complete predictive model of the effects of unilateral temporal lobe resection on cognitive outcomes post-resection, possibly allowing greater flexibility in determining which patients should undergo responsive neurostimulation (RNS) vs. resection 3) modeling whether and how extra-medial temporal lobe cortical networks can compensate for lost function following resection 4) potentially, inspiration for novel therapies involving cognitive interventions or neurostimulation targeting intact cortical tissue in patients with amnestic-like symptoms.