Network Effects of Brain Lesions Causing Central Poststroke Pain.
Network Effects of Brain Lesions Causing Central Poststroke Pain.
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DOI：
10.1002/ana.26468
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发表时间：
2022-11
影响因子：
11.2
通讯作者：
Fox, Michael D.
中科院分区：
文献类型：
--
作者：
Kim, Na Young;Taylor, Joseph J.;Kim, Yong Wook;Borsook, David;Joutsa, Juho;Li, Jing;Quesada, Charles;Peyron, Roland;Fox, Michael D.
测试引起中枢性卒中后疼痛（CPSP）的病变是否与特定的连接谱有关，这些连接是否与代谢变化有关，以及该网络是否与疼痛的神经调节靶点一致。使用了两个独立的病变数据集：1)来自已发表病例报告的皮质下病变，2)使用18F-氟脱氧葡萄糖PET-CT进行代谢成像的丘脑病变。使用标准连接组（n = 1000）评估每个病变部位与大脑其他部位之间的功能连接，并确定CPSP特有的连接。CPSP特有的代谢变化也被确定，并与病变连通性的差异有关。通过测试与现有脑刺激数据的一致性，并在7例CPSP患者中前瞻性地使用重复经颅磁刺激（rTMS）靶向该网络，探讨了该网络的治疗相关性。引起CPSP的病变位置显示出一种特定的大脑连接模式，这种模式在两个独立的病变数据集中是一致的（空间r = 0.82, p < 0.0001）。连通性差异与病变后代谢相关（r = - 0.48, p < 0.001）。这种基于病变的疼痛网络的地形与12个先前神经调节靶点和32名接受rTMS至初级运动皮质的患者的疼痛改善变异性一致（p < 0.05）。针对该网络的rTMS可改善6/7患者的CPSP。引起疼痛的病变与一个特定的大脑网络相连，该网络显示出代谢异常，并有望成为神经调节的目标。
To test whether lesions causing central post-stroke pain (CPSP) are associated with a specific connectivity profile, whether these connections are associated with metabolic changes, and whether this network aligns with neuromodulation targets for pain. Two independent lesion datasets were utilized: 1) subcortical lesions from published case reports and, 2) thalamic lesions with metabolic imaging using 18F- fluorodeoxyglucose PET-CT. Functional connectivity between each lesion location and the rest of the brain was assessed using a normative connectome (n = 1000) and connections specific to CPSP were identified. Metabolic changes specific to CPSP were also identified and related to differences in lesion connectivity. Therapeutic relevance of the network was explored by testing for alignment with existing brain stimulation data and by prospectively targeting the network with repetitive transcranial magnetic stimulation (rTMS) in 7 patients with CPSP. Lesion locations causing CPSP showed a specific pattern of brain connectivity that was consistent across two independent lesion datasets (spatial r = 0.82, p < 0.0001). Connectivity differences were correlated with post-lesion metabolism (r = −0.48, p < 0.001). The topography of this lesion-based pain network aligned with variability in pain improvement across 12 prior neuromodulation targets and across 32 patients who received rTMS to primary motor cortex (p < 0.05). Prospectively targeting this network with rTMS improved CPSP in 6/7 patients. Lesions causing pain are connected to a specific brain network that shows metabolic abnormalities and promise as a neuromodulation target.
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影响因子：
7.7
作者：
Johnson, Kevin A.;Baig, Mirza;Ramsey, Dave;Lisanby, Sarah H.;Avery, David;McDonald, William M.;Li, Xingbao;Bernhardt, Elisabeth R.;Haynor, David R.;Holtzheimer, Paul E., III;Sackeim, Harold A.;George, Mark S.;Nahas, Ziad
通讯作者：
Nahas, Ziad
影响因子：
5.7
作者：
Linnman, Clas;Moulton, Eric A.;Barmettler, Gabi;Becerra, Lino;Borsook, David
通讯作者：
Borsook, David
影响因子：
2.8
作者：
Kobayashi, Masahito;Fujimaki, Takamitsu;Ohira, Takayuki
通讯作者：
Ohira, Takayuki
DOI：
10.1073/pnas.1405003111
发表时间：
2014-10-14
影响因子：
11.1
作者：
Fox, Michael D.;Buckner, Randy L.;Pascual-Leone, Alvaro
通讯作者：
Pascual-Leone, Alvaro
影响因子：
8.3
作者：
Kuceyeski A;Kamel H;Navi BB;Raj A;Iadecola C
通讯作者：
Iadecola C