Neural correlates of cognitive control deficits in pediatric mild traumatic brain injury.
Neural correlates of cognitive control deficits in pediatric mild traumatic brain injury.
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DOI：
10.1002/hbm.26504
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发表时间：
2023-12-01
影响因子：
4.8
通讯作者：
Mayer, Andrew R.
中科院分区：
文献类型：
--
作者：
van Der Horn, Harm J.;Dodd, Andrew B.;Wick, Tracey V.;Robertson-Benta, Cidney R.;Mcquaid, Jessica R.;Hittson, Anne K.;Ling, Josef M.;Zotev, Vadim;Ryman, Sephira G.;Erhardt, Erik B.;Phillips, John P.;Campbell, Richard A.;Sapien, Robert E.;Mayer, Andrew R.
越来越多的研究表明，小儿轻度创伤性脑损伤（pmTBI）引发的脑病理生理过程可能会超出通常的临床恢复时间轴。进一步阐明这些过程至关重要，因为发育中的大脑中持续继发性损伤可能导致的长期认知影响尚不清楚。在当前的fMRI研究中，对181例pmTBI患者在损伤后亚急性（SA; ~1周）和早期慢性（EC; ~4个月）阶段与认知控制相关的神经过程进行了研究。此外，在相同的时间点招募了一组162名年龄和性别匹配的健康对照（HC）。主动（后线索）和反应（后探测）的认知控制进行了检查，无论是一致或不一致的刺激使用多模态注意功能磁共振成像范例。为了研究大脑网络功能，使用了三重网络模型，包括执行和显着性网络（统称为认知控制网络）以及默认模式网络。此外，还进行了全脑体素分析。在主动和被动控制期间，在pmTBI之后的EC阶段，在默认模式网络内发现失活减少。体素分析显示，在主动控制期间，认知控制网络的额叶区域（左侧前补充运动区）亚急性低激活，在pmTBI后的EC阶段具有相反的效果。在反应性控制期间，在三重网络之外的区域中观察到类似的效果。在积极主动的控制激活组的差异仅限于视觉领域，而反应性控制的结果更明显的出席听觉刺激。任务相关激活与（持续性）脑震荡后症状之间不存在显著相关性。总体而言，目前的结果显示，无论临床恢复如何，pmTBI损伤后4个月内认知控制期间神经功能发生变化。我们认为，亚急性活动减少反映了由于损伤导致的低兴奋性的一般状态，而早期慢性过度激活代表了一种代偿机制，以防止默认模式干扰并保持认知控制。在这项纵向研究中，我们使用任务功能磁共振成像（task-fMRI）研究了小儿轻度创伤性脑损伤（pmTBI）后的认知控制。在损伤后4个月内，相对于健康对照，在pmTBI中发现了三重网络模型内的变化。这些变化与损伤严重程度有关，但与持续的脑震荡后症状无关。
There is a growing body of research showing that cerebral pathophysiological processes triggered by pediatric mild traumatic brain injury (pmTBI) may extend beyond the usual clinical recovery timeline. It is paramount to further unravel these processes, because the possible long‐term cognitive effects resulting from ongoing secondary injury in the developing brain are not known. In the current fMRI study, neural processes related to cognitive control were studied in 181 patients with pmTBI at sub‐acute (SA; ~1 week) and early chronic (EC; ~4 months) stages post‐injury. Additionally, a group of 162 age‐ and sex‐matched healthy controls (HC) were recruited at equivalent time points. Proactive (post‐cue) and reactive (post‐probe) cognitive control were examined using a multimodal attention fMRI paradigm for either congruent or incongruent stimuli. To study brain network function, the triple‐network model was used, consisting of the executive and salience networks (collectively known as the cognitive control network), and the default mode network. Additionally, whole‐brain voxel‐wise analyses were performed. Decreased deactivation was found within the default mode network at the EC stage following pmTBI during both proactive and reactive control. Voxel‐wise analyses revealed sub‐acute hypoactivation of a frontal area of the cognitive control network (left pre‐supplementary motor area) during proactive control, with a reversed effect at the EC stage after pmTBI. Similar effects were observed in areas outside of the triple‐network during reactive control. Group differences in activation during proactive control were limited to the visual domain, whereas for reactive control findings were more pronounced during the attendance of auditory stimuli. No significant correlations were present between task‐related activations and (persistent) post‐concussive symptoms. In aggregate, current results show alterations in neural functioning during cognitive control in pmTBI up to 4 months post‐injury, regardless of clinical recovery. We propose that subacute decreases in activity reflect a general state of hypo‐excitability due to the injury, while early chronic hyperactivation represents a compensatory mechanism to prevent default mode interference and to retain cognitive control. In this longitudinal study we investigated cognitive control after pediatric mild traumatic brain injury (pmTBI) using task‐fMRI. Changes within the triple‐network model were found in pmTBI relative to healthy controls, up to 4 months post‐injury. These changes were related to injury severity, but not to persistent post‐concussive symptoms.
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DOI：
10.1017/s1355617711001226
发表时间：
2011-11-01
影响因子：
2.6
作者：
Krivitzky, Lauren S.;Roebuck-Spencer, Tresa M.;Gioia, Gerard
通讯作者：
Gioia, Gerard
影响因子：
2.4
作者：
Babikian, Talin;Asarnow, Robert
通讯作者：
Asarnow, Robert
影响因子：
10.6
作者：
Mayer AR;Quinn DK
通讯作者：
Quinn DK
影响因子：
5.7
作者：
Cole, Michael W.;Schneider, Walter
通讯作者：
Schneider, Walter
影响因子：
1.2
作者：
Hoover, Eric C.;Souza, Pamela E.;Gallun, Frederick J.
通讯作者：
Gallun, Frederick J.