Radiothermomapping of human brain: equipment and results
ABSTRACT The problems of investigation of temperature responses of a human head brain by the noninvasive method of dynamic multiprobe radiothermoimaging are considered. The equipment is described, the dynamic maps registered during a functional hyperventilation test are presented for patients with epileptogenic zones. Statistical data on thermoreactions of sick and healthy humans are presented. Comparison with the noninvasive measurements of human brain temperature using magnetic resonance spectroscopy is conducted.
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ABSTRACT: Elucidation of the role of cerebral hyperthermia as a secondary factor that worsens outcome after brain injury, and the therapeutic application of modest brain hypothermia would benefit from noninvasive measurements of absolute brain temperature. The present study was performed to evaluate the feasibility of using 1H magnetic resonance (MR) spectroscopy to measure absolute brain temperature in human subjects on a clinical imaging spectroscopy system operating at a field strength of 1.5 T. In vivo calibration results were obtained from swine brain during whole-body heating and cooling, with concurrent measurements of brain temperature via implanted probes. Plots of the frequency differences between the in vivo MR peaks of water and N-acetyl-aspartate and related compounds (NAX), or water and choline and other trimethylamines versus brain temperature were linear over the temperature range studied (28-40 degrees C). These relationships were used to estimate brain temperature from 1H MR spectra obtained from 10 adult human volunteers from 4 cm3-volumes selected from the frontal lobe and thalamus. Oral and forehead temperatures were monitored concurrently with MR data collection to verify normothermia in all the subjects studied. Temperatures determined using N-acetyl-aspartate or choline as the chemical shift reference did not differ significantly, and therefore results from these estimates were averaged. The brain temperature (mean +/- SD) measured from the frontal lobe (37.2 +/- 0.6 degrees C) and thalamus (37.7 +/- 0.6 degrees C) were significantly different from each other (paired t-test, p = 0.035). We conclude that 1H MR spectroscopy provides a viable noninvasive means of measuring regional brain temperatures in normal subjects and is a promising approach for measuring temperatures in brain-injured subjects.Journal of Cerebral Blood Flow & Metabolism 05/1997; 17(4):363-9. DOI:10.1097/00004647-199704000-00001 · 5.34 Impact Factor
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ABSTRACT: Brain temperature has been measured only occasionally in humans. After head trauma, a temperature gradient in brain temperature compared with body temperature of up to 3 degrees C degrees higher in the brain has been reported. Elevated temperature facilitates neuronal injury after ischemia. At present, no information concerning changes in brain temperature after acute stroke is available. In 15 patients who had suffered severe ischemic stroke in the MCA territory, intracerebral temperature was recorded with use of two different thermocouples, with intraventricular, epidural, and parenchymatous measurements. Body-core temperature (Foley catheter temperature) and jugular bulb temperature (n = 5) were recorded simultaneously. Measures for reducing brain temperature were compared. In all patients, brain temperature exceeded body-core temperature by at least up to 1 degrees C (range, 1.0 to 2.1 degrees C). Temperature in the ventricles exceeded epidural temperature by up to 2.0 degrees C. Brain temperature modulation was independent of single pharmacologic (paracetamol, metamizol) treatments. Only systemic cooling was effective and sustained hypothermic (33 to 34 degrees C) brain temperatures. After MCA stroke, human intracerebral temperature is higher than central body-core temperature. There is also a temperature gradient within the brain, with the ventricles warmer than the surface. Mild hypothermia in the treatment of severe cerebral ischemia with use of cooling blankets is both easy to perform and effective in the therapy of severe hemispheric infarction.Neurology 04/1997; 48(3):762-7. DOI:10.1186/cc9 · 8.30 Impact Factor