Noninvasive Measurement of Brain Temperatureafter Stroke
Ronald J.T. Corbett
,a,
Phillip D. Purdya,
Abbot R. Laptooka,
Curtis Chaneya and
Damian Garciaa
a From the Departments of Radiology (R.J.T.C., P.D.P., C.C.), Neurosurgery (P.D.P.), and Pediatrics (A.R.L., D.G.), University of Texas Southwestern Medical Center at Dallas, Dallas, TX.

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FIG 1. 1H MR image of canine brain. A T2-weighted coronal image, obtained 24 hours after MCA embolization, shows hyperintense signal from the basal ganglia. The box shows the location of the voxel used for 1H MR spectroscopy data collection from the infarct; the same-sized voxel was collected from the analogous anatomic region contralateral to the infarct.
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FIG 2. Representative 1H MR spectra from infarcted and contralateral non-infarcted brain tissue using TEs of 136 ms and 272 ms (data from the same animal as that depicted in fig 1). The MR signals corresponding to H2O, TMA, creatine plus phosphocreatine, NAA, and related compounds, and lactate are identified. A five-times larger vertical scaling factor was used for the data collected using a TE of 272 ms, compared with the data collected using a TE of 136 ms.
A, 1H MR spectra of infarcted brain tissue (TE, 136).
B, 1H MR spectra of non-infarcted brain tissue (TE, 136).
C, 1H MR spectra of infarcted brain tissue (TE, 272).
D, 1H MR spectra of non-infarcted brain tissue (TE, 272).
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FIG 3. Comparison of the relationship between brain temperature measured from sensors implanted into the infarcted and contralateral non-infarcted tissue versus the chemical-shift differences between H2O and NAA (left) and between H2O and TMA (right). Only data collected using a TE of 136 ms are depicted. The lines show the best fit by linear regression analysis. There was no significant difference in the slope or elevation of the data collected from the infarct compared with the non-infarcted tissue.
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