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Postmortem imaging is increasingly used in forensic practice as good complementary tool to conventional autopsy investigations. Over the last decade, postmortem cardiac magnetic resonance (PMCMR) imaging was introduced in forensic investigations of natural deaths related to cardiovascular diseases, which represent the most common causes of death in developed countries. Postmortem CMR application has yielded interesting results in ischemic myocardium injury investigations and in visualizing other pathological findings in the heart. This review presents the actual state of postmortem imaging for cardiovascular pathologies in cases of sudden cardiac death (SCD), taking into consideration both the advantages and limitations of PMCMR application.

Human arousal is essential to survival and mediated by the ascending arousal network (AAN) and its connections. It spans from the brainstem to the diencephalon, basal forebrain, and cerebral cortex. Despite advances in mapping the AAN in adults, it is unexplored in fetal and early infant life, especially with high‐resolution magnetic resonance imaging techniques. In this study, we conducted—for the first time—high‐resolution ex vivo diffusion MRI‐based analysis of the AAN in seven fetal, infant, and adult brains, incorporating probabilistic tractography and quantifying connectivity using graph theory. We observed that AAN structural connectivity becomes increasingly integrated during development, progressively reaching rostrally during the first postconceptional year. We quantitatively identified the dorsal raphe (DR) nucleus and ventral tegmental area (VTA) as AAN connectivity hubs already in the fetus persisting into adulthood. The DR appears to form a local hub of short‐range connectivities, while the VTA evolves as a long‐range global hub. The identified connectivity maps advance our understanding of AAN architecture changes due to normative human brain development, as well as disorders of arousal, such as coma and sudden infant death syndrome. We used high‐resolution ex vivo diffusion MRI and graph theory to analyze ascending arousal network development in fetal to adult brains, revealing increasing rostral integration postnatally and identifying the dorsal raphe nucleus and ventral tegmental area as persistent connectivity hubs from fetal stages through adulthood.

Forensic pathology increasingly uses postmortem magnetic resonance imaging (PMMRI), particularly in pediatric cases. It should be noted that each (sudden and unexpected) death of an infant or child should have a forensic approach as well. Current postmortem imaging protocols do not focus adequately on forensic queries. First, it is important to demonstrate or rule out bleeding, especially in the brain. Thus, when incorporating PMMRI, a blood sensitive sequence (T2* and/or susceptibility weighted imaging (SWI)) should always be included. Secondly, as intracranial air might mimic small focal intracerebral hemorrhages, PMMRI should be preceded by postmortem CT (PMCT) since air is easily recognizable on CT. This will be illustrated by a case of a deceased 3-week-old baby. Finally, note that postmortem scans will often be interpreted by clinical radiologists, sometimes with no specific training, which makes this case report relevant for a broader audience.

Abstract Postmortem imaging (PMI) is increasingly used in postmortem practice and is considered a potential alternative to a conventional autopsy, particularly in case of sudden cardiac deaths (SCD). In 2017, the Association for European Cardiovascular Pathology (AECVP) published guidelines on how to perform an autopsy in such cases, which is still considered the gold standard, but the diagnostic value of PMI herein was not analyzed in detail. At present, significant progress has been made in the PMI diagnosis of acute ischemic heart disease, the most important cause of SCD, while the introduction of postmortem CT angiography (PMCTA) has improved the visualization of several parameters of coronary artery pathology that can support a diagnosis of SCD. Postmortem magnetic resonance (PMMR) allows the detection of acute myocardial injury-related edema. However, PMI has limitations when compared to clinical imaging, which severely impacts the postmortem diagnosis of myocardial injuries (ischemic versus non-ischemic), the age-dating of coronary occlusion (acute versus old), other potentially SCD-related cardiac lesions (e.g., the distinctive morphologies of cardiomyopathies), aortic diseases underlying dissection or rupture, or pulmonary embolism. In these instances, PMI cannot replace a histopathological examination for a final diagnosis. Emerging minimally invasive techniques at PMI such as image-guided biopsies of the myocardium or the aorta, provide promising results that warrant further investigations. The rapid developments in the field of postmortem imaging imply that the diagnosis of sudden death due to cardiovascular diseases will soon require detailed knowledge of both postmortem radiology and of pathology.

The image contrast of postmortem magnetic resonance imaging (MRI) may differ from that of antemortem MRI because of circulator arrest, changes in postmortem tissue, and low-body-temperature scanning conditions. In fact, we have found that the signal intensity of white matter (WM) on T1-weighted spin-echo (T1WSE) images of the postmortem brain was lower than that of gray matter (GM), which resulted in image contrast reversal between GM and WM relative to the living brain. However, the reason for this phenomenon is unclear. Therefore, the aim of this study is to clarify the reason why image contrast reversal occurs between GM and WM of the postmortem brain. Twenty-three corpses were included in the study (mean age, 60.6 years; range: 19–60 years; mean rectal temperature at scan, 6.9℃; range: 4–11℃). On a 1.5 T MRI system, postmortem T1W-SE MRI of the brain was conducted in the 23 corpses prior to medico-legal autopsy. Next, T1 and T2 of the GM and WM at the level of the basal ganglia were determined in the same participants using inversion recovery and multiple SE sequences, respectively. The proton density (PD) was also calculated from the T1 and T2 images (in the same slice). T1W-SE image contrast between the GM and WM of all postmortem brains was inverted relative to the living brain. T1 (579 ms in GM and 307 ms in WM) and PD (64 in GM and 44 in WM) of the postmortem brain decreased compared with the living brain. While T1 of WM/GM remained below 1 even postmortem, the PD of WM/GM decreased. T2 (110 ms in GM and 98 ms in WM) of the postmortem brain did not differ from the living brain. The decrease in PD of WM/GM in the postmortem brain may be the major driver of contrast reversal between the GM and WM relative to the living brain. •WM/GM is preserved in postmortem brain T1W-SE images.•Postmortem brain T1 and PD are decreased.•Rates of postmortem water reduction differ between WM and GM.•Lower PD of postmortem brain WM drives contrast inversion between the GM and WM.

BackgroundThe aim of this study was to evaluate the sensitivity of postmortem computed tomography (PMCT), postmortem magnetic resonance imaging (PMMR) and PMCT angiography (PMCTA) compared with autopsy in cases of adult death investigations.MethodsFor this systematic review and meta-analysis, Embase, PubMed, Scopus, Web of Science and Medline were searched for eligible studies in October 2016; a follow-up literature search was conducted in March 2018. Studies referring to PMCT, PMCTA and/or PMMR of more than 3 cases with subsequent autopsy were included. Data were extracted from published texts in duplicate. The extracted outcomes were categorized as follows: soft tissue and organ findings, skeletal injuries, haemorrhages, abnormal gas accumulations and causes of death. The summary measure was sensitivity, if 3 or more studies were available. To combine studies, a random effects model was used. Variability and heterogeneity within the meta-analysis was assessed.ResultsOf 1053 studies, 66 were eligible, encompassing a total of 4213 individuals. For soft tissue and organ findings, there was a high pooled sensitivity with PMCTA (0.91, 95% CI 0.81–0.96), without evidence for between-study variability (Cochrane’s Q test p = 0.331, I2 = 24.5%). The pooled sensitivity of PMCT+PMMR was very high in skeletal injuries (0.97, CI 0.87–0.99), without evidence for variability (p = 0.857, I2 = 0.0%). In detecting haemorrhages, the pooled sensitivity for PMCT+PMMR was the highest (0.88, 95% CI 0.35–0.99), with strong evidence of heterogeneity (p < 0.05, I2 > 50%). Pooled sensitivity for the correct cause of death was the highest for PMCTA with 0.79 (95% CI 0.52–0.93), again with evidence of heterogeneity (p = 0.062, I2 > 50%).ConclusionDistinct postmortem imaging modalities can achieve high sensitivities for detecting various findings and causes of death. This knowledge should lead to a reasoned use of each modality. Both forensic evidence and in-hospital medical quality would be enhanced.

Objectives To investigate unenhanced postmortem 3-T MR imaging (pmMRI) for the detection of pulmonary thrombembolism (PTE) as cause of death. Methods In eight forensic cases dying from a possible cardiac cause but with homogeneous myocardium at cardiac pmMRI, additional T2w imaging of the pulmonary artery was performed before forensic autopsy. Imaging was carried out on a 3-T MR system in the axial and main pulmonary artery adapted oblique orientation in situ. In three cases axial T2w pmMRI of the lower legs was added. Validation of imaging findings was performed during forensic autopsy. Results All eight cases showed homogeneous material of intermediate signal intensity within the main pulmonary artery and/or pulmonary artery branches. Autopsy confirmed the MR findings as pulmonary artery thrombembolism. At lower leg imaging unilateral dilated veins and subcutaneous oedema with or without homogeneous material of intermediate signal intensity within the popliteal vein were found. Conclusions Unenhanced pmMRI demonstrates pulmonary thrombembolism in situ. PmMR may serve as an alternative to clinical autopsy, especially when consent cannot be obtained. Key Points • Postmortem MRI (pmMRI) provides an alternative to clinical autopsy • Fatal pulmonary thrombembolism (PTE) can now be diagnosed using postmortem MRI (pmMRI). • Special attention has to be drawn to the differentiation of postmortem clots.

Our current understanding of the spread and neurodegenerative effects of tau neurofibrillary tangles (NFTs) within the medial temporal lobe (MTL) during the early stages of Alzheimer’s Disease (AD) is limited by the presence of confounding non-AD pathologies and the two-dimensional (2-D) nature of conventional histology studies. Here, we combine ex vivo MRI and serial histological imaging from 25 human MTL specimens to present a detailed, 3-D characterization of quantitative NFT burden measures in the space of a high-resolution, ex vivo atlas with cytoarchitecturally-defined subregion labels, that can be used to inform future in vivo neuroimaging studies. Average maps show a clear anterior to poster gradient in NFT distribution and a precise, spatial pattern with highest levels of NFTs found not just within the transentorhinal region but also the cornu ammonis (CA1) subfield. Additionally, we identify granular MTL regions where measures of neurodegeneration are likely to be linked to NFTs specifically, and thus potentially more sensitive as early AD biomarkers. Using high-resolution ex vivo MRI and serial histology, Ravikumar et al. characterise 3D tau spread across histologically defined medial temporal lobe subregions thus providing a postmortem reference for in vivo studies on early Alzheimer’s disease.

Quantitative susceptibility mapping (QSM) measures bulk susceptibilities in the brain, which can arise from many sources. In iron-rich subcortical gray matter (GM), non-heme iron is a dominant susceptibility source. We evaluated the use of QSM for iron mapping in subcortical GM by direct comparison to tissue iron staining. We performed in situ or in vivo QSM at 4.7T combined with Perls' ferric iron staining on the corresponding extracted subcortical GM regions. This histochemical process enabled examination of ferric iron in complete slices that could be related to susceptibility measurements. Correlation analyses were performed on an individual-by-individual basis and high linear correlations between susceptibility and Perls' iron stain were found for the three multiple sclerosis (MS) subjects studied (R2=0.75, 0.62, 0.86). In addition, high linear correlations between susceptibility and transverse relaxation rate (R2*) were found (R2=0.88, 0.88, 0.87) which matched in vivo healthy subjects (R2=0.87). This work validates the accuracy of QSM for brain iron mapping and also confirms ferric iron as the dominant susceptibility source in subcortical GM, by demonstrating high linear correlation of QSM to Perls' ferric iron staining. [Display omitted] •In situ or in vivo QSM is compared with Perls' iron stain in subcortical gray matter.•Full slice Perls' iron staining enabled spatial maps of ferric iron to relate directly to MRI.•High linear correlations are found between QSM and Perls' iron stain in postmortem subjects with multiple sclerosis.•High linear correlations are also found between QSM and R2* for both postmortem and in vivo subjects.

Remyelination of cortical lesions in people with multiple sclerosis (pwMS) has been shown to be extensive. In this work, we aimed to assess whether postmortem quantitative MRI (qMRI) can help detect those areas. We imaged six fixed whole brains of deceased pwMS by 3T‐MRI using magnetization transfer ratio (MTR, 570 μm isotropic), myelin water fraction (MWF, 1000 μm isotropic), quantitative T1 (qT1, 670 μm isotropic), quantitative susceptibility mapping (QSM, 330 μm isotropic) and radial diffusivity (RD, 1300 or 1400 μm isotropic) maps. Immunohistochemistry for myelin proteins was performed in 129 tissue blocks including the cortex and enabled the detection of cortical demyelination (DM), cortical remyelination (RM), and normal‐appearing cortex (NAC). We identified 25 DM, 25 RM, and for each of these areas, a corresponding NAC near the lesion. Wilcoxon paired tests showed that: (a) qT1 and RD were higher and QSM lower in DM versus NAC (all p < 0.001), whereas RD was higher and QSM lower in RM versus NAC (p = 0.048 and p < 0.01 respectively); (b) mean qT1 in RM did not differ from mean qT1 in NAC (p = 0.074); (c) MWF and MTR were not different between DM and RM. We compared the delta between DM versus NAC (∆DM) and the delta between RM versus NAC (∆RM) using a Mann–Whitney test, in which RM showed a partial recovery of qT1 only (∆qT1 DM > ∆qT1 RM, p = 0.045). Mixed‐effect models confirmed the findings obtained using univariate analyses. qT1 and QSM, but not RD, correlated with MBP intensity (r = −0.28, p < 0.01 and r = 0.29, p < 0.01 respectively). A Bonferroni correction was performed for multiple testing. Our data show that qT1 is altered in demyelinated but not in remyelinated cortical areas, while QSM and RD are affected by any cortical abnormalities. Accordingly, qT1 might be considered a potential imaging biomarker of cortical RM. In a post‐mortem study using multiparametric qMRI of whole fixed human brains from people with multiple sclerosis (pwMS), we found evidence that quantitative T1 (qT1) is sensitive to remyelination in the cortex. In contrast, QSM and radial diffusivity were affected by cortical pathology independently of remyelination. Our data suggest that qT1 could be used to study myelin changes over time in the cortex of pwMS.