Computational support, not primacy, distinguishes compensatory memory reorganization in epilepsy.
Computational support, not primacy, distinguishes compensatory memory reorganization in epilepsy.
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DOI：
10.1093/braincomms/fcab025
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发表时间：
2021
影响因子：
4.8
通讯作者：
Sperling MR
中科院分区：
文献类型：
--
作者：
Tracy JI;Chaudhary K;Modi S;Crow A;Kumar A;Weinstein D;Sperling MR
颞叶癫痫与情景记忆受损有关。然而，尽管存在颞叶病变，仍有相当多的亚群能够保持足够的记忆。先前的认知重组工作中缺少的是对状态完好的颞叶癫痫患者与记忆受损患者的直接比较。人们对区域激活、功能连接和/或网络重新配置知之甚少，这些区域激活、功能连接和/或网络重新配置实现了主要计算的变化或驱动自适应可塑性和补偿记忆的支持功能。我们在执行配对关联记忆任务期间对 54 名单侧颞叶癫痫患者和 24 名匹配的健康对照者使用任务功能 MRI，以解决三个问题：（i）哪些区域在颞叶癫痫中实现配对关联记忆，它们是否会随着表现的好坏而变化，（ii）在记忆编码过程中是否存在独特的功能连接，通过保留主要记忆计算或允许完整记忆反应的支持计算来解释完整状态，以及（iii）记忆编码过程中哪些特征最独特：是区域激活的幅度和位置，还是与海马体等关键结构的增强功能连接的存在？研究显示，与受损状态相比，非优势半球区域（右后颞区）涉及区域活动的增加和与海马体的调节通讯的增加，这对于左颞叶癫痫患者的完整记忆最为重要。该剖面涉及的区域既不是左半球记忆区域的对侧同源区域，也不是传统上被认为是情景记忆计算主要区域。这些激活或功能连接增加的区域均与健康对照组的优势记忆无关。我们对不同表现水平的强调使我们深入了解了两种形式的认知重组：计算优先性，其中左颞叶癫痫相对于健康对照几乎没有变化，以及计算支持，其中完整的左颞叶癫痫患者表现出适应性异常。这些分析分离出独特的区域激活和介导功能连接，从而在左颞叶癫痫中实现真正的代偿性重组。研究结果为记忆缺陷提供了一个新的视角，明确表明记忆缺陷不仅是由于功能中枢的敲除而引起的，而且是由于未能实例化一组复杂的重组反应而引起的。这些反应提供了计算支持以确保成功的记忆。我们证明，通过跟踪表现水平，我们可以增进对癫痫的适应性大脑反应和神经可塑性的理解。通过区分不同级别的记忆性能，Tracy 等人。分离出与癫痫完整记忆独特相关的大脑网络特征。他们强调了认知重组的两种形式（计算首要性；计算支持），并表明完整的记忆需要适应性异常，而受损的记忆则涉及无法产生补偿性、支持性的大脑反应。
Temporal lobe epilepsy is associated with impairment in episodic memory. A substantial subgroup, however, is able to maintain adequate memory despite temporal lobe pathology. Missing from prior work in cognitive reorganization is a direct comparison of temporal lobe epilepsy patients with intact status with those who are memory impaired. Little is known about the regional activations, functional connectivities and/or network reconfigurations that implement changes in primary computations or support functions that drive adaptive plasticity and compensated memory. We utilized task functional MRI on 54 unilateral temporal lobe epilepsy patients and 24 matched healthy controls during the performance of a paired-associate memory task to address three questions: (i) which regions implement paired-associate memory in temporal lobe epilepsy, and do they vary as a function of good versus poor performance, (ii) is there unique functional connectivity present during memory encoding that accounts for intact status by preservation of primary memory computations or the supportive computations that allow for intact memory responses and (iii) what features during memory encoding are most distinctive: is it the magnitude and location of regional activations, or the presence of enhanced functional connections to key structures such as the hippocampus? The study revealed non-dominant hemisphere regions (right posterior temporal regions) involving both increased regional activity and increased modulatory communication with the hippocampi as most important to intact memory in left temporal lobe epilepsy compared to impaired status. The profile involved areas that are neither contralateral homologues to left hemisphere memory areas, nor regions traditionally considered computationally primary for episodic memory. None of these areas of increased activation or functional connectivity were associated with advantaged memory in healthy controls. Our emphasis on different performance levels yielded insight into two forms of cognitive reorganization: computational primacy, where left temporal lobe epilepsy showed little change relative to healthy controls, and computational support where intact left temporal lobe epilepsy patients showed adaptive abnormalities. The analyses isolated the unique regional activations and mediating functional connectivity that implements truly compensatory reorganization in left temporal lobe epilepsy. The results provided a new perspective on memory deficits by making clear that they arise not just from the knockout of a functional hub, but from the failure to instantiate a complex set of reorganization responses. Such responses provided the computational support to ensure successful memory. We demonstrated that by keeping track of performance levels, we can increase understanding of adaptive brain responses and neuroplasticity in epilepsy. By distinguishing different levels of memory performance, Tracy et al. isolate the brain network characteristics uniquely associated with intact memory in epilepsy. They highlight two forms of cognitive reorganization (computational primacy; computational support) and show that intact memory requires adaptive abnormalities, and impaired memory involves failure to generate compensatory, supportive brain responses.
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影响因子：
3.4
作者：
Doucet GE;Skidmore C;Evans J;Sharan A;Sperling MR;Pustina D;Tracy JI
通讯作者：
Tracy JI
影响因子：
3.5
作者：
Gorgolewski K;Burns CD;Madison C;Clark D;Halchenko YO;Waskom ML;Ghosh SS
通讯作者：
Ghosh SS
影响因子：
5.3
作者：
Law, JR;Flanery, MA;Stark, CEL
通讯作者：
Stark, CEL
影响因子：
5.3
作者：
Burke, John F.;Sharan, Ashwini D.;Kahana, Michael J.
通讯作者：
Kahana, Michael J.
影响因子：
48
作者：
Esteban, Oscar;Markiewicz, Christopher J.;Gorgolewski, Krzysztof J.
通讯作者：
Gorgolewski, Krzysztof J.