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Evidence for a novel subcortical mechanism for posterior cingulate cortex atrophy in HIV peripheral neuropathy.
Journal of Neurovirology ( IF 3.2 ) Pub Date : 2020-06-10 , DOI: 10.1007/s13365-020-00850-3
John R Keltner 1, 2, 3 , Alan Tong 1 , Eelke Visser 4 , Mark Jenkinson 4 , Colm G Connolly 5 , Alyssa Dasca 1 , Aleks Sheringov 1 , Zachary Calvo 1 , Earl Umbao 1 , Rohit Mande 1 , Mary Beth Bilder 1 , Gagandeep Sahota 1 , Donald R Franklin 1 , Stephanie Corkran 1 , Igor Grant 1 , Sarah Archibald 1 , Florin Vaida 6 , Gregory G Brown 1 , J Hampton Atkinson 1, 2 , Alan N Simmons 1, 2 , Ronald J Ellis 7 ,
Affiliation  

We previously reported that neuropathic pain was associated with smaller posterior cingulate cortical (PCC) volumes, suggesting that a smaller/dysfunctional PCC may contribute to development of pain via impaired mind wandering. A gap in our previous report was lack of evidence for a mechanism for the genesis of PCC atrophy in HIV peripheral neuropathy. Here we investigate if volumetric differences in the subcortex for those with neuropathic paresthesia may contribute to smaller PCC volumes, potentially through deafferentation of ascending white matter tracts resulting from peripheral nerve damage in HIV neuropathy. Since neuropathic pain and paresthesia are highly correlated, statistical decomposition was used to separate pain and paresthesia symptoms to determine which regions of brain atrophy are associated with both pain and paresthesia and which are associated separately with pain or paresthesia. HIV+ individuals (N = 233) with and without paresthesia in a multisite study underwent structural brain magnetic resonance imaging. Voxel-based morphometry and a segmentation/registration tool were used to investigate regional brain volume changes associated with paresthesia. Analysis of decomposed variables found that smaller midbrain and thalamus volumes were associated with paresthesia rather than pain. However, atrophy in the PCC was related to both pain and paresthesia. Peak thalamic atrophy (p = 0.004; MNI x = − 14, y = − 24, z = − 2) for more severe paresthesia was in a region with reciprocal connections with the PCC. This provides initial evidence that smaller PCC volumes in HIV peripheral neuropathy are related to ascending white matter deafferentation caused by small fiber damage observed in HIV peripheral neuropathy.



中文翻译:

HIV 周围神经病变中后扣带回萎缩的新皮质下机制的证据。

我们之前曾报道神经性疼痛与较小的后扣带皮层 (PCC) 体积相关,这表明较小/功能失调的 PCC 可能通过受损的思维游走而导致疼痛的发展。我们之前的报告中的一个空白是缺乏证据证明 HIV 周围神经病变中 PCC 萎缩的发生机制。在这里,我们研究了神经性感觉异常患者皮层下的体积差异是否可能导致较小的 PCC 体积,这可能是通过 HIV 神经病变中周围神经损伤引起的上行白质束的去传入。由于神经性疼痛和感觉异常高度相关,统计分解用于区分疼痛和感觉异常症状,以确定哪些脑萎缩区域与疼痛和感觉异常相关,哪些区域与疼痛或感觉异常分别相关。HIV+个体(N  = 233)在一项多站点研究中有和没有感觉异常的情况下接受了结构性脑磁共振成像。基于体素的形态测量和分割/配准工具用于研究与感觉异常相关的区域脑容量变化。对分解变量的分析发现,较小的中脑和丘脑体积与感觉异常有关,而不是与疼痛有关。然而,PCC 的萎缩与疼痛和感觉异常有关。峰值丘脑萎缩 ( p  = 0.004; MNI x  = - 14, y  = - 24, z = - 2) 更严重的感觉异常发生在与 PCC 有相互联系的地区。这提供了初步证据,即 HIV 周围神经病变中较小的 PCC 体积与在 HIV 周围神经病变中观察到的小纤维损伤引起的上行白质去传入有关。

更新日期:2020-06-10
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