猪心肌梗死多普勒组织成像与组织化学变化

目的：运用多普勒组织成像（DTI）和组织化学染色对急性心肌梗死（AMI）动态变化进行检测。方法：10头开胸猪结扎左冠状动脉前降支（LAD）,复制急性心肌梗死模型。于结扎后2、20、90、180min,用DTI技术测定前间壁收缩期运动速度（Vs)、舒张早、晚期运动速度（VE、VA）;从前间壁取材5块,常规石蜡包埋、切片、HE及组织化学染色、对病变进行分析。结果：LAD结扎前,DTI－二维显示收缩期、舒张期室壁运动协调,彩色充盈。结扎后,前间壁室壁变薄,色彩暗淡,着色异常,甚或缺失。DTI－频谱检测结扎2、20min,Vs,VE明显降低（P＜0．05）,至90、180min时运动速度降低更加显著（P＜0．01）,而VA无显著差异（P＞0．05）。病理显示心肌细胞、血管内皮及平滑肌细胞有不同程度的坏死,并伴有血栓形成、心内膜及心外膜炎。结论：DTI与组织化学对照分析,能准确反映缺血、梗死区域心肌不同时间变化规律。精确测定心肌运动速度。     

A multivariate hypothesis testing framework for tissue clustering and classification of DTI data

The primary aim of this work is to propose and investigate the effectiveness of a novel unsupervised tissue clustering and classification algorithm for diffusion tensor MRI (DTI) data. The proposed algorithm utilizes information about the degree of homogeneity of the distribution of diffusion tensors within voxels. We adapt frameworks proposed by Hext and Snedecor, where the null hypothesis of diffusion tensors belonging to the same distribution is assessed by an F‐test. Tissue type is classified according to one of the four possible diffusion models, the assignment of which is determined by a parsimonious model selection framework based on Schwarz Criterion. Both numerical phantoms and diffusion‐weighted imaging (DWI) data obtained from excised rat and pig spinal cords are used to test and validate these tissue clustering and classification approaches. The unsupervised clustering method effectively identifies distinct regions of interest (ROIs) in phantoms and real experimental DTI data. Copyright © 2009 John Wiley & Sons, Ltd.     

Brain structure in asymptomatic FMR1 premutation carriers at risk for fragile X-associated tremor/ataxia syndrome

Fragile X-associated tremor/ataxia syndrome (FXTAS), a late-onset movement disorder affecting FMR1 premutation carriers, is associated with cerebral and cerebellar lesions. The aim of this study was to test whether computational anatomy can detect similar patterns in asymptomatic FMR1 premutation carriers (mean age 46.7 years) with qualitatively normal -appearing grey and white matter on brain MRI. We used a multimodal imaging protocol to characterize brain anatomy by automated assessment of gray matter volume and white matter properties. Structural changes in the hippocampus and in the cerebellar motor network with decreased gray matter volume in lobule VI and white matter alterations of the corresponding afferent projections through the middle cerebellar peduncles are demonstrated. Diffuse subcortical white matter changes in both hemispheres, without corresponding gray matter alterations, are only identified through age × group interactions. We interpret the hippocampal fimbria and cerebellar changes as early alterations with a possible neurodevelopmental origin. In contrast, progression of the diffuse cerebral hemispheric white matter changes suggests a neurodegenerative process, leading to late-onset lesions, which may mark the imminent onset of FXTAS.     

White matter tract signatures of the progressive aphasias

The primary progressive aphasias (PPA) are a heterogeneous group of language-led neurodegenerative diseases resulting from large-scale brain network degeneration. White matter (WM) pathways bind networks together, and might therefore hold information about PPA pathogenesis. Here we used diffusion tensor imaging and tract-based spatial statistics to compare WM tract changes between PPA syndromes and with respect to Alzheimer's disease and healthy controls in 33 patients with PPA (13 nonfluent/agrammatic PPA); 10 logopenic variant PPA; and 10 semantic variant PPA. Nonfluent/agrammatic PPA was associated with predominantly left-sided and anterior tract alterations including uncinate fasciculus (UF) and subcortical projections; semantic variant PPA with bilateral alterations in inferior longitudinal fasciculus and UF; and logopenic variant PPA with bilateral but predominantly left-sided alterations in inferior longitudinal fasciculus, UF, superior longitudinal fasciculus, and subcortical projections. Tract alterations were more extensive than gray matter alterations, and the extent of alteration across tracts and PPA syndromes varied between diffusivity metrics. These WM signatures of PPA syndromes illustrate the selective vulnerability of brain language networks in these diseases and might have some pathologic specificity.     

Multimodal MRI assessment for first episode psychosis: A major change in the thalamus and an efficient stratification of a subgroup

Multi‐institutional brain imaging studies have emerged to resolve conflicting results among individual studies. However, adjusting multiple variables at the technical and cohort levels is challenging. Therefore, it is important to explore approaches that provide meaningful results from relatively small samples at institutional levels. We studied 87 first episode psychosis (FEP) patients and 62 healthy subjects by combining supervised integrated factor analysis (SIFA) with a novel pipeline for automated structure‐based analysis, an efficient and comprehensive method for dimensional data reduction that our group recently established. We integrated multiple MRI features (volume, DTI indices, resting state fMRI—rsfMRI) in the whole brain of each participant in an unbiased manner. The automated structure‐based analysis showed widespread DTI abnormalities in FEP and rs‐fMRI differences between FEP and healthy subjects mostly centered in thalamus. The combination of multiple modalities with SIFA was more efficient than the use of single modalities to stratify a subgroup of FEP (individuals with schizophrenia or schizoaffective disorder) that had more robust deficits from the overall FEP group. The information from multiple MRI modalities and analytical methods highlighted the thalamus as significantly abnormal in FEP. This study serves as a proof‐of‐concept for the potential of this methodology to reveal disease underpins and to stratify populations into more homogeneous sub‐groups.     

Increased segregation of structural brain networks underpins enhanced broad cognitive abilities of cognitive training

A major challenge in the cognitive training field is inducing broad, far‐transfer training effects. Thus far, little is known about the neural mechanisms underlying broad training effects. Here, we tested a set of competitive hypotheses regarding the role of brain integration versus segregation underlying the broad training effect. We retrospectively analyzed data from a randomized controlled trial comparing neurocognitive effects of vision‐based speed of processing training (VSOP) and an active control consisting of mental leisure activities (MLA) in older adults with MCI. We classified a subset of participants in the VSOP as learners, who showed improvement in executive function and episodic memory. The other participants in the VSOP (i.e., VSOP non‐learners) and a subset of participants in the MLA (i.e., MLA non‐learners) served as controls. Structural brain networks were constructed from diffusion tensor imaging. Clustering coefficients (CCs) and characteristic path lengths were computed as measures of segregation and integration, respectively. Learners showed significantly greater global CCs after intervention than controls. Nodal CCs were selectively enhanced in cingulate cortex, parietal regions, striatum, and thalamus. Among VSOP learners, those with more severe baseline neurodegeneration had greater improvement in segregation after training. Our findings suggest broad training effects are related to enhanced segregation in selective brain networks, providing insight into cognitive training related neuroplasticity.     

Long-term coordinated microstructural disruptions of the developing neocortex and subcortical white matter after early postnatal systemic inflammation

Severe postnatal systemic infection is highly associated with persistent disturbances in brain development and neurobehavioral outcomes in survivors of preterm birth. However, the contribution of less severe but prolonged postnatal infection and inflammation to such disturbances is unclear. Further, the ability of modern imaging techniques to detect the underlying changes in cellular microstructure of the brain in these infants remains to be validated. We used high-field ex-vivo MRI, neurohistopathology, and behavioral tests in newborn rats to demonstrate that prolonged postnatal systemic inflammation causes subtle, persisting disturbances in brain development, with neurodevelopmental delays and mild motor impairments. Diffusion-tensor MRI and neurite orientation dispersion and density imaging (NODDI) revealed delayed maturation of neocortical and subcortical white matter microstructure. Analysis of pyramidal neurons showed that the cortical deficits involved impaired dendritic arborization and spine formation. Analysis of oligodendrocytes showed that the white matter deficits involved impaired oligodendrocyte maturation and axonal myelination. These findings indicate that prolonged postnatal inflammation, without severe infection, may critically contribute to the diffuse spectrum of brain pathology and subtle long-term disability in preterm infants, with a cellular mechanism involving oligodendrocyte and neuronal dysmaturation. NODDI may be useful for clinical detection of these microstructural deficits.