Optimization of Inversion Time for Postmortem Fluid-attenuated Inversion Recovery (FLAIR) MR Imaging at 1.5T: Temperature-based Suppression of Cerebrospinal Fluid.

PURPOSE: Signal intensity (SI) and image contrast on postmortem magnetic resonance (MR) imaging are different from those of imaging of living bodies. We sought to suppress the SI of cerebrospinal fluid (CSF) sufficiently for fluid-attenuated inversion recovery (FLAIR) sequence in postmortem MR (PMMR) imaging by optimizing inversion time (TI). MATERIALS AND METHODS: We subject 28 deceased patients to PMMR imaging 3 to 113 hours after confirmation of death (mean, 27.4 hrs.). PMMR imaging was performed at 1.5 tesla, and T1 values of CSF were measured with maps of relaxation time. Rectal temperatures (RT) measured immediately after PMMR imaging ranged from 6 to 32°C (mean, 15.4°C). We analyzed the relationship between T1 and RT statistically using Pearson's correlation coefficient. We obtained FLAIR images from one cadaver using both a TI routinely used for living bodies and an optimized TI calculated from the RT. RESULTS: T1 values of CSF ranged from 2159 to 4063 ms (mean 2962.4), and there was a significantly positive correlation between T1 and RT (r = 0.96, P < 0.0001). The regression expression for the relationship was T1 = 74.4 * RT + 1813 for a magnetic field strength of 1.5T. The SI of CSF was effectively suppressed with the optimized TI (0.693 * T1), namely, TI = 0.693 * (77.4 * RT + 1813). CONCLUSION: Use of the TI calculated from the linear regression of the T1 and RT optimizes the FLAIR sequence of PMMR imaging.

Cerebral relaxation times from postmortem MR imaging of adults.

PURPOSE: We measured T1 and T2 values of cerebral postmortem magnetic resonance (PMMR) imaging and compared the data of cadavers with that of living human subjects. MATERIALS AND METHODS: We performed PMMR imaging of the brains of 30 adults (22 men, 8 women; mean age, 58.2 years) whose deaths were for reasons other than brain injury or disease at a mean of 29.4 hours after death. Before imaging, the bodies were kept in cold storage at 4°C (mean rectal temperature, 15.6°C). We measured T1 and T2 values in the brain bilaterally at 5 sites (bilateral caudate nucleus, putamen, thalamus and gray matter and white matter of the frontal lobe) and compared the data of PMMR imaging with that from MR imaging of the corresponding sites in 24 healthy volunteers (9 men, 15 women; mean age, 51.8 years). We also investigated the influence of body temperature on T1 and T2 values. RESULTS: Compared with MR imaging findings in the living subjects, PMMR imaging showed significantly shorter T1 values in the caudate nucleus, putamen, thalamus and gray matter and white matter of the frontal lobe and significantly longer T2 values in the gray matter and white matter of the frontal lobe; T2 values in the caudate nucleus, putamen, and thalamus showed no such differences. T1 values correlated significantly with body temperature in all 5 brain sites measured, but T2 values did not. CONCLUSION: Compared with findings of cerebral MR imaging in living adult subjects, those of PMMR imaging tended to demonstrate shorter T1 values and longer T2 values. We attribute this to increased water content of tissue, reduced pH, and reduced body temperature after death.

Optimization of inversion time for postmortem short-tau inversion recovery (STIR) MR imaging.

PURPOSE: Signal intensity and image contrast differ between postmortem magnetic resonance (PMMR) images and images acquired from the living body. We sought to achieve sufficient fat suppression with short-tau inversion recovery (STIR) PMMR imaging by optimizing inversion time (TI). MATERIAL AND METHODS: We subjected 37 deceased adult patients to PMMR imaging at 1.5 tesla 8 to 60 hours after confirmation of death and measured T1 values of areas of subcutaneous fat with relaxation time maps. Rectal temperature (RT) measured immediately after PMMR ranged from 6 to 31°C. We used Pearson's correlation coefficient to analyze the relationship between T1 and relaxation time (RT). We compared STIR images from 4 cadavers acquired with a TI commonly used in the living body and another TI calculated from the linear regression of T1 and RT. RESULTS: T1 values of subcutaneous fat ranged from 89.4 to 182.2 ms. There was a strong, positive, and significant correlation between T1 and RT (r = 0.91, P < 0.0001). The regression expression for the relationship was T1 = 2.6*RT + 90 at a field strength of 1.5T. The subcutaneous fat signal was suppressed more effectively with the optimized TI. CONCLUSION: The T1 value of subcutaneous fat in PMMR correlates linearly with body temperature. Using this correlation to determine TI, fat suppression with PMMR STIR imaging can be easily improved.

Postmortem magnetic resonance imaging dealing with low temperature objects.

In Japan, the medical examiner system is not widespread, the rate of autopsy is low, and many medical institutions therefore perform postmortem imaging using clinical equipment. Postmortem imaging is performed to clarify cause of death, select candidates for autopsy, make a guide map for autopsy, or provide additional information for autopsy. Findings are classified into 3 categories: cause of death and associated changes, changes induced by cardiopulmonary resuscitation, and postmortem changes. Postmortem magnetic resonance imaging shows characteristic changes in signal intensity related to low body temperature after death; they are low temperature images.

Characteristic signal intensity changes on postmortem magnetic resonance imaging of the brain.

PURPOSE: We investigated and identified postmortem changes on magnetic resonance imaging (MRI) of the brain to provide accurate diagnostic guidelines. MATERIALS AND METHODS: Our subjects were 16 deceased patients (mean age 57 years) who underwent postmortem computed tomography (CT), MRI, and autopsy, the latter of which showed no abnormalities in the brain. The subjects underwent CT and MRI 6-73 h after confirmation of death (mean 26 h), after being kept in cold storage at 4 degrees C. Postmortem MRI of the brain was performed using T1-weighted imaging (T1WI), T2WI, fluid attenuated inversion recovery (FLAIR) imaging, and diffusion weighted imaging (DWI) with parameters identical to those used for living persons. RESULTS: In all cases, postmortem CT showed brain edema and swelling. Postmortem MRI showed characteristic common signal intensity (SI) changes, including (1) high SI of the basal ganglia and thalamus on T1WI; (2) suppression of fat SI on T2WI; (3) insufficient SI suppression of cerebrospinal fluid on FLAIR imaging; (4) high SI rims along the cerebral cortices and the ventricular wall on DWI; and (5) an apparent diffusion coefficient decrease to less than half the normal value. CONCLUSION: Postmortem MRI of the brain in all cases showed characteristic common SI changes. Global cerebral ischemia without following reperfusion and low body temperature explain these changes.

Hyperattenuating aortic wall on postmortem computed tomography (PMCT).

PURPOSE: To quantitatively evaluate the finding of hyperattenuating aortic wall on postmortem computed tomography (PMCT) and investigate its causes. MATERIALS AND METHODS: Our subjects were 50 PMCT of non-traumatic deaths and 50 CT of living persons (live CT). The ascending aorta at the level of the carina was visually assessed regarding the presence or absence of hyperattanuating aortic wall and hematocrit effect on PMCT and live CT. The diameter, thickness of the aortic wall, and CT number (HU) of the aortic wall and the lumen were also measured. RESULTS: Hyperattenuating aortic wall was detected in 100% of PMCT and 2% of live CT. The diameter of the aortic wall was 2.9 +/- 0.5 cm on PMCT and 3.5 +/- 0.5 cm on live CT, showing a significant difference. The thickness of the aortic wall was 2 mm on PMCT. Hematocrit effect was observed in 46% of PMCT and in none of live CT. With PMCT, there was a significant difference between the CT numbers of the upper and lower half portions of the lumen (19.6 +/- 11.7/30.9 +/- 12.9), whereas, with live CT, there was no such significant difference (37.4 +/- 7.6/38.9 +/- 6.7), with the overall value of 38.2 +/- 6.7. The CT number of the aortic wall was 49.9 +/- 10.9 on PMCT. CONCLUSION: The causes of hyperattenuating aortic wall on PMCT are considered to be increased attenuation due to contraction of the aortic wall, a lack of motion artifact, and decreased attenuation of the lumen due to dilution of blood after massive infusion at the time of cardiopulmonary resuscitation.