Department of Psychiatry, Center for Studies of Addiction, University of Pennsylvania School of Medicine, 3900 Chestnut Street, Philadelphia, PA 19104, USA.
Brain Struct Funct. 2013 Jan;218(1):97-104. doi: 10.1007/s00429-012-0385-6.
Voxel-based morphometry (VBM) studies have interpreted longitudinal medication- or behaviorally induced changes observed on T1-weighted magnetic resonance images (MRIs) as changes in neuronal structure. Although neurogenesis or atrophy certainly occurs, the use of T1-weighted scans to identify change in brain structure in vivo in humans has vulnerability: the T1 relaxation time for arterial blood and gray matter are not clearly distinguishable and therefore, apparent reported structural findings might be at least partially related to changes in blood flow or other physiological signals. To examine the hypothesis that apparent structural modifications may reflect changes introduced by additional mechanisms irrespective of potential neuronal growth/atrophy, we acquired a high-resolution T1-weighted structural scan and a 5-min perfusion fMRI scan (a measurement of blood flow), before and after administration of an acute pharmacological manipulation. In a within-subject design, 15 subjects were either un-medicated or were administered a 20 mg dose of baclofen (an FDA-approved anti-spastic) approximately 110 min before acquiring a T1-weighted scan and a pseudo continuous arterial spin labeled perfusion fMRI scan. Using diffeomorphic anatomical registration through exponentiated lie algebra within SPM7, we observed macroscopic, and therefore implausible, baclofen-induced decreases in VBM 'gray matter' signal in the dorsal rostral anterior cingulate (family wise error corrected at p<0.04, T = 6.54, extent: 1,460 voxels) that overlapped with changes in blood flow. Given that gray matter reductions are unlikely following a single dose of medication these findings suggest that changes in blood flow are masquerading as reductions in gray matter on the T1-weighted scan irrespective of the temporal interval between baseline measures and longitudinal manipulations. These results underscore the crucial and immediate need to develop in vivo neuroimaging biomarkers for humans that can uniquely capture changes in neuronal structure dissociable from those related to blood flow or other physiological signals.
基于体素的形态测量学（VBM）研究将 T1 加权磁共振成像（MRI）上观察到的药物或行为诱导的纵向变化解释为神经元结构的变化。尽管神经发生或萎缩肯定会发生，但使用 T1 加权扫描来识别人类体内大脑结构的变化存在弱点：动脉血和灰质的 T1 弛豫时间不能明确区分，因此，明显报道的结构发现可能至少部分与血流或其他生理信号的变化有关。为了检验以下假设，即明显的结构改变可能反映了除潜在神经元生长/萎缩之外的其他机制引入的变化，我们在给药前后获得了高分辨率 T1 加权结构扫描和 5 分钟灌注 fMRI 扫描（血流测量）。在一项基于个体的设计中，15 名受试者或未接受药物治疗，或在获得 T1 加权扫描和假性连续动脉自旋标记灌注 fMRI 扫描前约 110 分钟接受了 20 毫克剂量的巴氯芬（一种 FDA 批准的抗痉挛药物）。使用 SPM7 中的指数 Lie 代数的可变形解剖配准，我们观察到宏观的、因此不太可能的巴氯芬诱导的 VBM“灰质”信号在背侧额前扣带（经家族 wise 错误校正，p<0.04，T=6.54，范围：1460 个体素）中的减少，与血流变化重叠。鉴于单次给药后灰质减少不太可能，这些发现表明，无论基线测量和纵向操作之间的时间间隔如何，血流变化都会伪装成 T1 加权扫描中的灰质减少。这些结果强调了迫切需要为人类开发独特的体内神经影像学生物标志物，这些生物标志物可以分离与血流或其他生理信号相关的神经元结构变化。
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