Cerebral Temperature Dysregulation: MR Thermographic Monitoring in a Nonhuman Primate Study of Acute Ischemic Stroke.
Cerebral Temperature Dysregulation: MR Thermographic Monitoring in a Nonhuman Primate Study of Acute Ischemic Stroke.
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DOI：
10.3174/ajnr.a5059
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发表时间：
2017-04
期刊：
影响因子：
--
通讯作者：
Tong F
中科院分区：
文献类型：
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作者：
Dehkharghani S;Fleischer CC;Qiu D;Yepes M;Tong F
大脑的体温调节仍然知之甚少。体温失调与脑血管缺血的增强密切相关。我们在非人类灵长类动物（NHP）的MCA梗死模型中提出了一项多相磁共振热成像研究，假设可检测的脑温度干扰和脑系统温度解耦。3只恒河猴NHP用于三相MRI: 1)基线MRI (t-7)；2)微创血管内MCA脑卒中诱导后连续7小时MRI检查（10）；3)脑卒中后当天MRI （t1）随访。利用质子共振频率的化学位移，利用多体素光谱（半激光MRSI）实现了磁共振测温。使用混合效应模型表征脑和全身温度与时间和梗死体积的关系。在MCA梗死后，在所有三个受试者中观察到进行性脑热，明显超过全身温度波动。在脑卒中诱导后的时间内，观察到系统、半球和整体脑温度（所有回归的F-stat p.0005）与时间高度显著相关。将全身温度与同侧（p=.007）、对侧（p=.004）和梗死核心（p=.003）进行多次比较校正后，发现卒中发生后温度和时间之间的关系存在显著差异。梗死体积与全身（p≤0.01）和同侧（p= 0.04）脑温度有显著相关性，但与对侧脑温度无显著相关性（p= 0.08）。成功地进行了生理和连续的缺血后脑MR热成像，并在NHP梗死模型中进行了规定，以方便可翻译。结果证实了假设的温度干扰和脑-系统温度梯度的解耦。这些发现揭示了脑温度调节的发展模式，以及脑温度作为中枢神经系统损伤的神经成像生物标志物的适用性。
Cerebral thermoregulation remains poorly understood. Temperature dysregulation is deeply implicated in potentiation of cerebrovascular ischemia. We present a multi-phasic, MR thermographic study in a non-human primate (NHP) model of MCA infarction, hypothesizing detectable brain temperature disturbances and brain-systemic temperature decoupling. Three rhesus macaque NHP were sourced for three-phase MRI: 1) baseline MRI (t-7); 2) seven-hour continuous MRI following minimally-invasive, endovascular MCA stroke induction (t0); 3) post-stroke day MRI (t1) follow-up. MR thermometry was achieved by multi-voxel spectroscopy (semi-LASER MRSI) using the proton resonance frequency chemical shift. Relationship of brain and systemic temperatures with time and infarction volumes was characterized using a mixed-effects model. Following MCA infarction progressive cerebral hyperthermia was observed in all three subjects, significantly outpacing systemic temperature fluctuations. Highly significant associations were observed for systemic, hemispheric, and global brain temperatures (F-stat p.0005 for all regressions) relative to time from stroke induction. Significant differences in the relationship between temperature and time following stroke onset were detected when comparing systemic temperatures with ipsilateral (p=.007), contralateral (p=.004), and infarction core (p=.003) temperatures following multiple comparisons correction. Significant associations were observed between infarction volumes and both systemic (p≤.01) and ipsilateral (p=.04) brain temperatures, but not contralateral brain temperature (p=.08). Successful physiologic and continuous post-ischemic cerebral MR thermography was conducted, and prescribed in an NHP infarction model to facilitate translatability. The results confirm hypothesized temperature disturbance and decoupling of physiologic brain-systemic temperature gradients. These findings inform a developing paradigm of brain thermoregulation, and the applicability of brain temperature as a neuroimaging biomarker in CNS injury.