AJNR. American journal of neuroradiology最新文献

Background and purpose: The underlying transcriptomic signatures driving brain functional alterations in MS and neuromyelitis optica spectrum disorder (NMOSD) are still unclear.

Materials and methods: Regional fractional amplitude of low-frequency fluctuation (fALFF) values were obtained and compared among 209 patients with MS, 90 patients with antiaquaporin-4 antibody (AQP4)+ NMOSD, 49 with AQP4- NMOSD, and 228 healthy controls from a discovery cohort. We used partial least squares (PLS) regression to identify the gene transcriptomic signatures associated with disease-related fALFF alterations. The biologic process and cell type-specific signature of the identified PLS genes were explored by enrichment analysis. The correlation between PLS genes and clinical variables was explored. A prospective independent cohort was used to validate the brain fALFF alterations and the repeatability of identified genes.

Results: MS, AQP4+ NMOSD, and AQP4- NMOSD showed decreased fALFF in cognition-related regions and deep gray matter, while NMOSD (both AQP4+ and AQP4-) additionally demonstrated lower fALFF in the visual region. The overlapping PLS1- genes (indicating that the genes were overexpressed as regional fALFF decreased) were enriched in response to regulation of the immune response in all diseases, and the PLS1- genes were specifically enriched in the epigenetics profile in MS, membrane disruption and cell adhesion in AQP4+ NMOSD, and leukocyte activation in AQP4- NMOSD. For the cell type transcriptional signature, microglia and astrocytes accounted for the decreased fALFF. The fALFF-associated PLS1- genes directly correlated with Expanded Disability Status Scale of MS and disease duration across disorders.

Conclusions: We revealed the functional activity alterations and their underlying shared and specific gene transcriptional signatures in MS, AQP4+ NMOSD, and AQP4- NMOSD.

Background and purpose: Neuropsychiatric complications of SARS-CoV-2 infection, also known as neurologic postacute sequelae of SARS-CoV-2 infection (NeuroPASC), affect 10%-60% of infected individuals. There is growing evidence that NeuroPASC is a multi system immune dysregulation disease affecting the brain. The behavioral manifestations of NeuroPASC, such as impaired processing speed, executive function, memory retrieval, and sustained attention, suggest widespread WM involvement. Although previous work has documented WM damage following acute SARS-CoV-2 infection, its involvement in NeuroPASC is less clear. We hypothesized that macrostructural and microstructural WM differences in NeuroPASC participants would accompany cognitive and immune system differences.

Materials and methods: In a cross-sectional study, we screened a total of 159 potential participants and enrolled 72 participants, with 41 asymptomatic controls (NoCOVID) and 31 NeuroPASC participants matched for age, sex, and education. Exclusion criteria included neurologic disorders unrelated to SARS-CoV-2 infection. Assessments included clinical symptom questionnaires, psychometric tests, brain MRI measures, and peripheral cytokine levels. Statistical modeling included separate multivariable regression analyses of GM/WM/CSF volume, WM microstructure, cognitive, and cytokine concentration between-group differences.

Results: NeuroPASC participants had larger cerebral WM volume than NoCOVID controls (β = 0.229; 95% CI: 0.017-0.441; t = 2.16; P = .035). The most pronounced effects were in the prefrontal and anterior temporal WM. NeuroPASC participants also exhibited higher WM mean kurtosis, consistent with ongoing neuroinflammation. NeuroPASC participants had more self-reported symptoms, including headache, and lower performance on measures of attention, concentration, verbal learning, and processing speed. A multivariate profile analysis of the cytokine panel showed different group cytokine profiles (Wald-type-statistic = 44.6, P = .046), with interferon (IFN)-λ1 and IFN-λ2/3 levels higher in the NeuroPASC group.

Conclusions: NeuroPASC participants reported symptoms of lower concentration, higher fatigue, and impaired cognition compatible with WM syndrome. Psychometric testing confirmed these findings. NeuroPASC participants exhibited larger cerebral WM volume and higher WM mean kurtosis than NoCOVID controls. These findings suggest that immune dysregulation could influence WM properties to produce WM volume increases and consequent cognitive effects and headaches. Further work will be needed to establish mechanistic links among these variables.

Background and purpose: To date, only a few small studies have attempted deep learning-based automatic segmentation of white matter hyperintensity (WMH) lesions in patients with cerebral infarction; this issue is complicated because stroke-related lesions can obscure WMH borders. We developed and validated deep learning algorithms to segment WMH lesions accurately in patients with cerebral infarction using multisite data sets involving 8421 patients with acute ischemic stroke.

Materials and methods: We included 8421 patients with stroke from 9 centers in Korea. 2D UNet and squeeze-and-excitation (SE)-UNet models were trained using 2408 FLAIR MRIs from 3 hospitals and validated using 6013 FLAIR MRIs from 6 hospitals. WMH segmentation performance was assessed by calculating the Dice similarity coefficient (DSC), the correlation coefficient, and the concordance correlation coefficient compared with a human-segmented criterion standard. In addition, we obtained an uncertainty index that represents overall ambiguity in the voxel classification for WMH segmentation in each patient based on the Kullback-Leibler divergence.

Results: In the training data set, the mean age was 67.4 (SD, 13.0) years, and 60.4% were men. The mean (95% CI) DSCs for UNet in internal testing and external validation were, respectively, 0.659 (0.649-0.669) and 0.710 (0.707-0.714), which were slightly lower than the reliability between humans (DSC = 0.744; 95% CI, 0.738-0.751; P = .031). Compared with the UNet, the SE-UNet demonstrated better performance, achieving a mean DSC of 0.675 (95% CI, 0.666-0.685; P < .001) in the internal testing and 0.722 (95% CI, 0.719-0.726; P < .001) in the external validation; moreover, it achieved high DSC values (ranging from 0.672 to 0.744) across multiple validation data sets. We observed a significant correlation between WMH volumes that were segmented automatically and manually for the UNet (r = 0.917, P < .001), and it was even stronger for the SE-UNet (r = 0.933, P < .001). The SE-UNet also attained a high concordance correlation coefficient (ranging from 0.841 to 0.956) in the external test data sets. In addition, the uncertainty indices in most patients (86%) in the external data sets were <0.35, with an average DSC of 0.744 in these patients.

Conclusions: We developed and validated deep learning algorithms to segment WMH in patients with acute cerebral infarction using the largest-ever MRI data sets. In addition, we showed that the uncertainty index can be used to identify cases in which automatic WMH segmentation is less accurate and requires human review.

Photon-counting CT (PCT) allows for improved spatial and contrast resolution compared with traditional energy-integrating detector CT. PCT offers markedly improved visualization of previously described structures, as well as those that were previously beyond the resolution of imaging. Although the anatomic details of the external ear and middle ear structures have been described previously, the rich detail of these structures has not been comprehensively reviewed in the radiology literature. The microarchitecture of the middle ear ossicles and bony protuberances are particularly well visualized on PCT. This review updates the existing literature with a detailed anatomic review of the external ear and the middle ear on temporal bone CT.