Corbett R J, Purdy P D, Laptook A R, Chaney C, Garcia D
Department of Radiology, University of Texas Southwestern Medical Center at Dallas, 75235-9085, USA.
AJNR Am J Neuroradiol. 1999 Nov-Dec;20(10):1851-7.
Brain temperature may be an important factor governing the extent of neuronal injury associated with stroke. The goal of this study was to develop a noninvasive method for measuring brain temperature, both to characterize the extent to which temperature changes after stroke and to test protocols designed to reduce brain temperature. We used an animal model to test the ability of 1H MR spectroscopy to measure temperature from infarcted brain tissue at 24 hours after insult.
Unilateral permanent focal ischemia in the middle cerebral artery territory was induced in adult dogs by intravascular delivery of microfibrillar collagen. MR imaging performed at 24 hours after insult was used to guide the implantation of temperature probes into the basal ganglia infarct and into the same anatomic location on the contralateral side. Serial non-water-suppressed 1H MR spectra were obtained from 1.3-cm3 voxels using an echo time of 136 and 272 ms, alternately, from the infarcted and contralateral non-infarcted tissue during a period when brain temperature was raised and lowered by whole-body heating and cooling.
The chemical shift difference between the 1H MR spectroscopy signal of water and N-acetylaspartate or water and trimethylamines was plotted against brain temperature for two voxel locations. The slope and intercept of the plots obtained for infarcted and non-infarcted brain were not significantly different (P < .05, t test), and there was no difference between the slope and intercept of plots made from data collected with an echo time of 136 or 272 ms.
The results of this study indicate that brain temperature can be measured from regions of brain containing infarcted tissue, at least up to 24 hours after ischemia. It should be possible to apply the 1H MR spectroscopy method used in the present study to measure brain temperature after stroke.
脑温可能是决定与中风相关的神经元损伤程度的一个重要因素。本研究的目的是开发一种测量脑温的非侵入性方法,以描述中风后温度变化的程度,并测试旨在降低脑温的方案。我们使用动物模型来测试氢质子磁共振波谱(1H MR spectroscopy)在损伤后24小时测量梗死脑组织温度的能力。
通过血管内注入微纤维胶原,在成年犬大脑中动脉区域诱导单侧永久性局灶性缺血。损伤后24小时进行的磁共振成像用于引导将温度探头植入基底节梗死灶以及对侧相同解剖位置。在通过全身加热和冷却使脑温升高和降低的期间,交替从梗死组织和对侧非梗死组织的1.3立方厘米体素中获取系列非水抑制氢质子磁共振波谱,回波时间分别为136和272毫秒。
针对两个体素位置,将水与N - 乙酰天门冬氨酸或水与三甲胺的氢质子磁共振波谱信号之间的化学位移差与脑温作图。梗死脑和非梗死脑所获得的图的斜率和截距无显著差异(P < .05,t检验),并且使用回波时间136或272毫秒收集的数据所制作的图的斜率和截距之间也无差异。
本研究结果表明,至少在缺血后24小时内,可以从含有梗死组织的脑区测量脑温。应用本研究中使用的氢质子磁共振波谱方法来测量中风后的脑温应该是可行的。