Human immunodeficiency virus-associated distal sensory polyneuropathy (HIV-DSP) affects up to 50% of people with HIV and is associated with depression, unemployment, and generally worsened quality of life. Previous work on the cortical mechanism of HIV neuropathy found decreased gray matter volume in the bilateral midbrain, thalamus, and posterior cingulate cortex, but structural connectivity in this context remains under-studied. Here we examine alterations in white matter microstructure using diffusion imaging, hypothesizing that cortical white matter degeneration would be observed in continuation of the peripheral white matter atrophy previously observed in HIV-DSP. Male HIV seropositive patients (n = 57) experiencing varying degrees of HIV neuropathy underwent single-shell diffusion tensor imaging with 51 sampling directions. The scans were pooled using tractography and connectometry to create a quantitative map of white matter tract integrity, measured in generalized fractional anisotropy (GFA). The relationship between GFA and neuropathy severity was evaluated with linear regression. Correction for multiple comparisons was done using false discovery rate (FDR), a statistical method commonly used in genomics and imaging to minimize false positives when thousands of individual comparisons are made. Neuropathy severity was associated with decreased GFA along thalamocortical radiations leading along the lateral thalamus to sensorimotor cortex, with r = -0.405 (p < 0.001; FDR), as well as with the superior bilateral cingulum (r = -0.346 (p < 0.05; FDR)). Among a population of HIV neuropathy patients, greater neuropathy severity was correlated with lower white matter integrity running from midbrain to somatosensory cortex. This suggests ascending deafferentation extending from damaged peripheral nerves further downstream than seen previously, into the axons of third-order neurons. There is also evidence of cingulum degeneration, implying some more complex mechanism beyond the ascending atrophy observed here.

人类免疫缺陷病毒相关的远端感觉多发性神经病 (HIV-DSP) 影响高达 50% 的 HIV 感染者，并与抑郁、失业和生活质量普遍恶化有关。先前关于艾滋病毒神经病变的皮质机制的研究发现，双侧中脑、丘脑和后扣带皮层的灰质体积减少，但这种情况下的结构连接性仍未得到充分研究。在这里，我们使用扩散成像检查白质微观结构的变化，假设在先前在 HIV-DSP 中观察到的外周白质萎缩的延续中将观察到皮质白质变性。患有不同程度 HIV 神经病变的男性 HIV 血清阳性患者 (n = 57) 接受了 51 个采样方向的单壳扩散张量成像。使用纤维束成像和连接测定法汇集扫描结果，以创建白质纤维束完整性的定量图，并以广义分数各向异性 (GFA) 进行测量。通过线性回归评估 GFA 和神经病变严重程度之间的关系。使用错误发现率（FDR）对多重比较进行校正，这是一种基因组学和成像中常用的统计方法，可在进行数千个单独比较时最大限度地减少误报。神经病变的严重程度与沿着丘脑外侧丘脑通向感觉运动皮层的丘脑皮质辐射的 GFA 减少有关，r = -0.405 (p < 0.001; FDR)，以及双侧上扣带回 (r = -0.346 (p < 0.05; FDR))。罗斯福））。在艾滋病毒神经病变患者群体中，神经病变严重程度越高，从中脑到体感皮层的白质完整性越低。这表明上行传入神经阻滞从受损的周围神经延伸到比之前看到的更下游，进入三级神经元的轴突。还有扣带回退化的证据，这意味着除了此处观察到的上行萎缩之外，还存在一些更复杂的机制。