MRI线性测量局部脑萎缩对早期阿尔兹海默病的诊断意义

目的评价ＭＲＩ线性测量脑萎缩程度对阿尔兹海默病（Ａｌｚｈｅｉｍｅｒｄｉｓｅａｓｅ，ＡＤ）患者的早期诊断价值。方法应用ＭＲＩ线性定量测量对３０例轻度痴呆的ＡＤ患者、２０例多发脑梗塞性痴呆（ＭＩＤ）和２０名正常老年人进行局部额叶（双额指数、额叶半球间宽度）、中颞叶（海马钩回间距、中颞叶最小厚度）及海马结构（海马高度、脉络膜裂宽度、海马脑干间距及颞角宽度）等指标测量。结果颞角宽度指标是区别ＡＤ患者与ＭＩＤ患者及正常老年人的最敏感的指标；其敏感性达９０％，特异性达８５％。如结合脉络膜裂宽度、海马高度、海马与脑干间距及海马钩回间距，其敏感性达９３％，特异性达９５％。结论ＭＲＩ线性定量测量局部海马萎缩能够作为早期诊断ＡＤ的准确可靠性指标之一。     

Frontal hypometabolism does not explain inhibitory dysfunction in Alzheimer disease

A series of tasks assessing inhibitory processes was administered to patients with Alzheimer disease and control subjects. Two groups of patients with Alzheimer disease were examined: patients with hypometabolism restricted to the posterior (temporal and parietal) cerebral areas and patients with hypometabolism in both posterior and anterior (frontal) cerebral areas. The performances of the patients with Alzheimer disease were inferior to those of control subjects on all inhibitory tasks, but the two groups of patients obtained similar scores. These data indicate that frontal lobe hypometabolism is not necessary to produce inhibitory impairment in Alzheimer disease. Consequently, inhibitory dysfunction could be the consequence of a (partial) disconnection process between posterior and anterior cerebral areas.     

Frontal lobe hypometabolism and impaired insight in Alzheimer disease.

OBJECTIVE: The authors examined the relationship between impaired insight regarding cognitive and functional deficits and frontal cortex hypometabolism in 41 patients with Alzheimer disease (AD). METHODS: Regional cerebral glucose metabolism was determined with (18F)fluorodeoxyglucose and positron emission tomography. Level of insight was measured with the clinician-rated Neurobehavioral Rating Scale, and severity of global cognitive impairment was determined with the Mini-Mental State Exam. RESULTS: Inaccurate insight was correlated with glucose metabolic rate in the right lateral frontal cortex (Brodmann areas 6 and 45, and the lateral aspect of Brodmann areas 8 and 9) after controlling for global cognitive dysfunction. CONCLUSIONS: The findings from this study help to further elucidate the neurobiological mechanisms underlying impaired insight in AD, indicating a link between this important clinical phenomenon and dysmetabolism in a focal region of the right prefrontal cortex.     

脑皮质下小血管病变与脑萎缩的相关性分析

目的探讨脑皮质下小血管病变与脑萎缩的相关性。方法通过10例临床确诊为脑萎缩的病人的调查,收集其临床基本资料及头颅磁共振成像(magnetic resonance imaging,MRI)的结果及图像,评判其脑皮质下小血管的病变情况。结果所有病例颅脑MRI均发现显著的弥漫性脑白质病变(white matter lesions,WML)和多发的脑腔隙性梗死灶(lacunarinfarcts,LI)。结论颅脑MRI提示,脑皮质下小血管病变与脑萎缩共存,提供了其与脑萎缩可能有关的临床依据。     

阿尔茨海默病的脑血流灌注研究

目的探讨AD患者脑血流灌注的特征性变化。方法选择20例确诊AD患者和10例认知正常者,对所有入组对象行SPECT脑血流灌注显像检查,对所得图像进行视觉分析和半定量分析,比较两组对象各脑区血流灌注情况的差异,并比较AD患者左、右脑叶脑血流灌注的差异。结果 (1)视觉分析结果显示,AD组以颞叶或顶叶脑血流灌注减低为主,各占55%,其中双侧颞顶叶血流灌注减低者占15%,单侧颞顶叶血流灌注减低占20%。正常认知组SPECT影像学表现各异,额叶、颞叶、顶叶、枕叶、丘脑、基底节血流灌注减少情况均存在,各占10%。但无双侧颞顶叶血流灌注减少者,40%表现完全正常。(2)半定量分析结果显示,AD组在右额叶、双侧颞顶叶、右枕叶血流灌注显著低于正常认知组(P<0.05),以右侧颞叶血流灌注降低最明显,左右颞顶叶血流低灌注程度对比无显著性差异。结论 AD患者的SPECT特征性表现为双侧对称性颞顶叶血流低灌注,其中右侧颞叶血流灌注下降最严重。     

Progression of corpus callosum atrophy in Alzheimer disease

BACKGROUND: Atrophy of the corpus callosum in the absence of primary white matter degeneration reflects loss of intracortical projecting neocortical pyramidal neurons in Alzheimer disease (AD). OBJECTIVES: To determine individual rates of atrophy progression of the corpus callosum in patients with AD and to correlate rates of atrophy progression with clinical disease severity and subcortical disease. METHODS: Magnetic resonance imaging-derived measurements of corpus callosum size were studied longitudinally in 21 patients clinically diagnosed as having AD (mean observation time, 17.0 +/- 8.5 months) and 10 age- and sex-matched healthy controls (mean observation time, 24.1 +/- 6.8 months). RESULTS: Corpus callosum size was significantly reduced in AD patients at baseline. Annual rates of atrophy of total corpus callosum, splenium, and rostrum were significantly larger in AD patients (-7.7%, -12.1%, and -7.3%, respectively) than in controls (-0.9%, -1.5%, and 0.6%, respectively). Rates of atrophy of the corpus callosum splenium were correlated with progression of dementia severity in AD patients (rho = 0.52, P<.02). The load of subcortical lesions at baseline (P<.05) predicted rate of anterior corpus callosum atrophy in healthy controls. Rates of atrophy of corpus callosum areas were independent of white matter hyperintensity load in patients with AD. CONCLUSIONS: Measurement of corpus callosum size allows in vivo mapping of neocortical neurodegeneration in AD over a wide range of clinical dementia severities and may be used as a surrogate marker for evaluation of drug efficacy.     

The topography of metabolic deficits in posterior cortical atrophy (the visual variant of Alzheimer's disease) with FDG-PET

BACKGROUND: The term "posterior cortical atrophy" (PCA) refers to a clinical syndrome in which higher order visual processing is disrupted owing to a neurodegenerative disorder, the most commonly associated pathology being Alzheimer's disease. OBJECTIVE: To map the topography of hypometabolic brain regions in a group of subjects with PCA who had undergone detailed neuropsychological characterisation. METHODS: Resting cerebral metabolism was measured with ((18)F)fluorodeoxyglucose-positron emission tomography (FDG-PET) in patients with PCA (n = 6), typical Alzheimer's disease (n = 10), and healthy controls (n = 10). The data were analysed using statistical parametric mapping (SPM99) and region of interest techniques. RESULTS: Clinically, the PCA subjects showed predominant visuospatial deficits (including features of Balint's syndrome) consistent with damage to the dorsal stream of visual processing. Compared with the controls, the PCA group showed marked glucose hypometabolism primarily affecting the posterior cerebral hemispheres (right worse than left). In addition, the PCA group showed two symmetrical areas of hypometabolism in the region of the frontal eye fields. Compared with typical Alzheimer's disease, the PCA group had selective hypometabolism in the occipito-parietal region (right much worse than left). CONCLUSIONS: The neuropsychological and PET findings are consistent with damage predominantly to the dorsal stream of visual processing. Frontal eye field hypometabolism secondary to loss of input from the occipito-parietal region may be the mechanism for the ocular apraxia seen in Balint's syndrome.     

Spatial patterns of atrophy,hypometabolism, and amyloid deposition in Alzheimer's disease correspond to dissociable functional brain networks

Recent neuroimaging studies of Alzheimer's disease (AD) have emphasized topographical similarities between AD‐related brain changes and a prominent cortical association network called the default‐mode network (DMN). However, the specificity of distinct imaging abnormalities for the DMN compared to other intrinsic connectivity networks (ICNs) of the limbic and heteromodal association cortex has not yet been examined systematically. We assessed regional amyloid load using AV45‐PET, neuronal metabolism using FDG‐PET, and gray matter volume using structural MRI in 473 participants from the Alzheimer's Disease Neuroimaging Initiative, including preclinical, predementia, and clinically manifest AD stages. Complementary region‐of‐interest and voxel‐based analyses were used to assess disease stage‐ and modality‐specific changes within seven principle ICNs of the human brain as defined by a standardized functional connectivity atlas. Amyloid deposition in AD dementia showed a preference for the DMN, but high effect sizes were also observed for other neocortical ICNs, most notably the frontoparietal‐control network. Atrophic changes were most specific for an anterior limbic network, followed by the DMN, whereas other neocortical networks were relatively spared. Hypometabolism appeared to be a mixture of both amyloid‐ and atrophy‐related profiles. Similar patterns of modality‐dependent network specificity were also observed in the predementia and, for amyloid deposition, in the preclinical stage. These quantitative data confirm a high vulnerability of the DMN for multimodal imaging abnormalities in AD. However, rather than being selective for the DMN, imaging abnormalities more generally affect higher order cognitive networks and, importantly, the vulnerability profiles of these networks markedly differ for distinct aspects of AD pathology. Hum Brain Mapp 37:35–53, 2016. © 2015 Wiley Periodicals, Inc.     

Hippocampal atrophy in Alzheimer disease: age matters

Hippocampal atrophy is a marker of Alzheimer disease (AD). It remains unclear whether this holds true for younger patients as well. Hippocampal volume was measured on MRI scans of 103 clinically diagnosed AD patients and 73 controls (aged 51 to 85 years). Aging and AD were independently associated with smaller hippocampal volume. Both young and old AD patients have hippocampal atrophy abnormal for age. Age-dependent criteria for hippocampal atrophy, suggestive of AD, are needed.     

The course of brain atrophy in Parkinson's disease

Summary In 110 parkinsonian patients (53 men, 57 women) aged 38–81 years, computer-tomographic follow-up investigations were done to assess the development of brain atrophy. The control examinations were done after an average of 28 months. At that time an increase in brain atrophic changes of different localization could be observed in 23% of the patients. In addition, it could be demonstrated that the increase in pathologic CT findings is to be observed especially in patients with higher age, a more marked impairment in psycho-organic capacity, more pronounced handicaps in the fine-motorial performances at the beginning of the study. From the neuroradiological point of view, patients with more marked pathologic CT findings upon the first examination, be these ventricular enlargement and/or cortical atrophy, more often showed a progression of brain atrophy.     

Distribution of brain atrophy in behavioral variant frontotemporal dementia

Marked brain atrophy occurs in frontotemporal dementia (FTD) yet substantial variation between cases is seen. Recently, a four-level staging scheme which reflects increasing disease duration, severity of dementia and degree of neurodegeneration was described. In the present study, the extent and magnitude of atrophy in behavioral variant FTD and its relationship to disease duration and pathological subtype was further evaluated by quantifying the volume of 30 anatomically-defined regions. A validated point count technique was applied to 17 patients with FTD (9 Pick's disease, 6 dementia lacking distinctive histology, 2 FTD with motor neuron disease) and 21 controls. Atrophy was seen in all brain regions except the inferior frontal cortex and area 37. As might be expected, increasing severity of atrophy occurred with increasing disease duration and stage however measurable atrophy was more widespread than indicated by the staging scheme. Furthermore, severity of atrophy was not related to pathological subtype. Frontal, limbic and temporal regions appeared to be severely affected early in the disease process with temporal lobe atrophy the best predictor of disease duration. White matter, more posterior regions and the subcortex were affected later in the disease. These findings demonstrate a pattern of selective vulnerability which progresses over time. Furthermore, they demonstrate that although patients with a similar clinical subtype may have differing underlying histopathology, the pattern, severity and progression of brain atrophy is the same. This suggests that the regional pattern of neurodegeneration, rather than the type of histopathology influences the clinical syndrome in FTD.