社区慢性精神分裂症患者的需求调查

目的：了解社区慢性精神分裂症患者的需求情况。方法：对１２０例符合ＣＣＭＤ－２－Ｒ精神分裂症诊断标准的患者完成调查。依据社会功能缺陷量表（ＳＤＳＳ）总分划分轻残组，中残组，重残组。以Ｃａｍｂｅｒｗｅｌｌ需求评定量表（ＣＡＮ），生活质量评定量表（ＱＯＬＳ），以及阳性阴性症状评定量表（ＰＡＮＳＳ）作为评定工具。结果：ＣＡＮ需求项目评定结果：３组间家庭照料，日常生活，解决精神症状，了解疾病和治疗信息，社会     

老年慢性精神分裂症的脑电地形图和多项诱发电位研究

为了解老年慢性精神分裂症患者与正常老人在脑电图（ＥＥＧ）、脑电地形图（ＢＥＡＭ）、视觉和听觉诱发电位（ＶＥＰ、ＡＥＰ）、脑干听觉反应（ＡＢＲ）和认知电位Ｐ３００（Ｐ３００）检测中的不同表现，对４０例正常老人及３４例老年慢性精神分裂症患者作６项电生理检测。结果发现，患者ＥＥＧ异常率达６６．７％，其ＢＥＡＭ趋向凹字形低密度带，ＶＥＰ（潜伏期Ｐ１、Ｐ２）、Ｐ３００（靶潜伏期Ｎ１—Ｐ２—Ｎ２—Ｐ３）均前移，ＡＥＰ（潜伏期Ｎ２、Ｐ３）延迟，ＡＥＰ、ＶＥＰ和Ｐ３００的Ｐ２、Ｐ３波幅均减低，均有显著性差异（Ｐ＜０．０５或Ｐ＜０．０１）。患者的ＡＢＲ于中央区左右侧不对称，绝对波幅波Ⅰ降低（Ｐ＜０．０１），这与本组对象ＣＴ结果吻合。采用多项诱发电位检测技术能较可靠反映精神分裂症患者脑的功能，可辅助患者的认知功能评定     

世界卫生组织老年认知功能评价成套神经心理测验的临床初步应用

目的 验证世界卫生组织老年认知功能评价成套神经心理测验（ＷＨＯ－ＢＣＡＩ）并探讨阿尔茨海默病（ＡＤ）早期认知功能改变的特点。方法 采用ＷＨＯ－ＢＣＡＩ对２６例轻中度,ＡＤ患者（ＡＤ组）２７例轻度认知功能损害的老年人（ＭＣＩ组）和８３名认知功能正常的老年人（ＮＣ组）进行测试,结果 在全部（２５项）测验中３例组间比较差异均有非常显著性（Ｐ〈０．０１）,两两比较,ＡＤ组与ＭＣＩ组（除１项（视觉再认）外和     

Alzheimer病的神经心理学和有关检查的相关性研究：（2）认知功能…

探讨Ａｌｚｈｅｉｍｅｒ病与正常人的认知功能与ＣＴ变化的相关性。方法共有４３例ＡＤ患者与４１例正常老人分别完成一组神经心理测验与头颅ＣＴ检测。结果ＮＣ组认知功能与个别ＣＴ测量值相关。ＡＤ组认知功能与大多数ＣＴ测量值具相关性，尤其是第Ⅲ脑室，脑沟，侧脑室，ＡＤ愈严重，脑萎缩愈明显。头颅ＣＴ检测对推断ＡＤ患者智能下降程度有帮助。     

精神分裂症免疫指标与精神症状的关系

为探讨精神分裂症精神病理与免疫指标的相关性、评估抗精神病药对免疫指标的影响及其与疗效的关系，用固定剂量氟哌啶醇治疗５０例慢性精神分裂症患者１２周，在治疗前后测查Ｔ细胞亚群和白细胞介素２（ＩＬ－２）分泌细胞，并采用简明精神病评定量表（ＢＰＲＳ）、阳性症状评定量表（ＳＡＰＳ）和阴性症状评定量表（ＳＡＮＳ）进行评定。结果显示，治疗前ＣＤ３阳性细胞（ＣＤ＋３）、ＣＤ４阳性细胞（ＣＤ＋４）、ＣＤ４／ＣＤ８阳性细胞比值（ＣＤ４／ＣＤ８）和ＩＬ－２分泌细胞均明显低于正常人，治疗后ＣＤ＋４呈显著性增高；治疗前ＣＤ４／ＣＤ８与ＳＡＰＳ总分呈显著负相关，ＢＰＲＳ、ＳＡＰＳ和ＳＡＮＳ减分率与治疗前ＣＤ＋３细胞数均呈显著正相关，ＳＡＮＳ减分率与治疗前ＣＤ＋４细胞数亦呈正相关。研究表明，抗精神病药在改善患者精神症状的同时，也使其免疫功能得到改善；临床症状改善程度与治疗前的免疫功能状态相关。     

脑干听觉诱发电位在阿尔茨海默病和老年精神分裂症患者中的应用

目的探讨阿尔茨海默病（ＡＤ）和老年精神分裂症（ＳＳ）脑干听觉诱发电位（ＢＡＥＰ）的特点。方法应用丹麦电生理仪及Ｃｌｉｃｋ短声刺激，测查３２例ＡＤ、３４例ＳＳ和４０名正常老年人（ＮＣ）的ＢＡＥＰ。结果ＡＤ组患者波形变异大，绝对潜伏期波Ⅲ、波Ⅳ和波Ⅵ明显延迟，主波绝对波幅波Ⅴ平均波幅分别低于ＳＳ组和ＮＣ组１８％和３４％，波Ⅱ、波Ⅳ、波Ⅴ、波Ⅵ和Ⅶ绝对波幅也显著低于ＳＳ组和ＮＣ组，与ＮＣ组间差异有显著性。ＳＳ组波Ⅲ、波Ⅵ绝对潜伏期较ＮＣ组延迟，绝对波幅波Ⅶ平均波幅低于ＮＣ组２０％。结论老年精神疾病ＢＡＥＰ异常表现在听神经至桥脑下段之间     

不同认知功能老年慢性精神分裂症的临床特征分析

目的分析不同认知功能的老年慢性精神分裂症的临床特征及脑ＣＴ表现。方法比较１５例认知功能缺损的精神分裂症患者与１９例认知功能相对保存的精神分裂症患者的一般情况、临床症状、日常活动能力及脑ＣＴ改变。结果与保存组相比，缺损组教育程度低，女性比例高，起病较慢，起病诱因多，非偏执型比例高，阴性症状较多，日常活动能力下降更显著，脑萎缩明显，统计检验有显著意义。结论认知功能缺损和相对保存的老年慢性精神分裂症很可能具有异源性病因。     

脑干听觉诱导电位在阿尔茨海默病和老年精神分裂症患者中的 …

目的 探讨阿尔茨海默病（ＡＤ）和老年精神分裂症（ＳＳ）脑干听觉诱导电位（ＢＡＥＰ）的特点。方法 应用丹麦电生理仪及Ｃｌｉｃｋ短声刺激，测查３２例ＡＤ、３４例ＳＳ和４０名正常老年人（ＮＣ）的ＡＢＥＰ。结果 ＡＤ组患者波形变异大，绝对潜伏期波Ⅲ、波Ⅳ和波Ⅵ明显延迟，主波绝对波幅波Ⅴ平均波幅分别低于ＳＳ组和ＮＣ组１８％和３４％，波Ⅱ、波Ⅱ、波Ⅳ、波Ⅴ、波Ⅵ和Ⅶ绝对波幅也显著低于ＳＳ组和ＮＣ组，与ＮＣ组间     

家庭干预对首发精神分裂症近期与远期疗效影响的对照研究

目的 探讨家庭干预对首发精神分裂症的近期与远期疗效的影响。方法 对符合ＣＣＭＤ－２的５０例首发精神分裂症住院病人（Ａ组）进行为期８周的积极家庭干预及出院后维持干预，与采取传统方式治疗的５０例首发精神分裂症病人对照（Ｂ组），用ＢＰＲＳ、ＳＡＮＳ、ＣＧＩ量表评定其临床疗效，并进行２年随访。结果 经８周住院治疗，Ａ、Ｂ两组ＢＰＲＳ总分、ＳＡＮＳ总分、ＣＧＩ－ＳＩ、ＣＢＧＩ－ＧＩ减分有显著差异，Ａ组疗效好     

老年急性脑血管病并多器官功能衰竭患者SIL-2R和T细胞亚群的测定

采用ＥＬＩＳＡ和ＡＰＡＡＰ法对３２例老年急性脑血管病（ＡＣＶＤ）并多器官功能衰竭（ＭＯＦ）患者及４０例老年和３５例非老年ＡＣＶＤ患者血清可溶性白细胞介素２受体（ＳＩＬ２Ｒ）及Ｔ细胞亚群水平进行了测定。并与３０例对照组比较。结果显示，疾病各组除ＣＤ３外ＳＩＬ２Ｒ和ＣＤ８均较对照组明显升高，ＣＤ４／ＣＤ８比值则明显下降，其中以老年ＡＣＶＤ并ＭＯＦ组变化最为显著，与老年和非老年ＡＣＶＤ组比较，亦有显著性差异；ＣＤ４水平老年ＡＣＶＤ并ＭＯＦ组较老年和非老年ＡＣＶＤ组及对照组明显降低，老年和非老年ＡＣＶＤ组与对照组比较无显著性差异；上述指标也与老年ＡＣＶＤ并ＭＯＦ患者的预后密切相关     

The cortical neuroanatomy of neuropsychological deficits in mild cognitive impairment and Alzheimer's disease: a surface-based morphometric analysis

Patients with probable Alzheimer's disease (AD) and the amnesic form of mild cognitive impairment (aMCI) often demonstrate several types of neuropsychological deficits. These deficits are often related to cortical atrophy, induced by neuronal degradation. The purpose of this study is to investigate whether different anatomic patterns of cortical atrophy are associated with specific neuropsychological deficits. The participants were 170 patients with AD and 99 patients with aMCI. All participants underwent the Seoul Neuropsychological Screening Battery (SNSB), which includes tests that assess attention, language, visuospatial functions, verbal and visual memory, and frontal/executive functions. Cortical atrophy (thinning) was quantified by measuring the thickness of the cortical mantle across the entire brain using automated, three-dimensional magnetic resonance imaging. The relationship between cortical thickness and neuropsychological performance was analysed using stepwise multiple linear regression analyses. These analyses (corrected P < .001) showed that several specific brain regions with cortical thinning were associated with cognitive dysfunction including: digit span backward, verbal and picture recall, naming and fluency, drawing–copying, response inhibition and selective attention. Some of the other functions, however, were not associated with specific foci of cortical atrophy (digit span forward, the word reading portion of the Stroop test, word and picture recognition). Our study, involving a large sample of participants with aMCI and AD, provides support for the postulate that cortical thinning-atrophy in specific anatomic loci are pathological markers for specific forms of cognitive dysfunction.     

Cortical thinning associated with mild cognitive impairment in Parkinson's disease

The aim of this study was to investigate patterns of cortical atrophy associated with mild cognitive impairment in a large sample of nondemented Parkinson's disease (PD) patients, and its relation with specific neuropsychological deficits. Magnetic resonance imaging (MRI) and neuropsychological assessment were performed in a sample of 90 nondemented PD patients and 32 healthy controls. All underwent a neuropsychological battery including tests that assess different cognitive domains: attention and working memory, executive functions, memory, language, and visuoperceptual‐visuospatial functions. Patients were classified according to their cognitive status as PD patients without mild cognitive impairment (MCI; n = 43) and PD patients with MCI (n = 47). Freesurfer software was used to obtain maps of cortical thickness for group comparisons and correlation with neuropsychological performance. Patients with MCI showed regional cortical thinning in parietotemporal regions, increased global atrophy (global cortical thinning, total gray matter volume reduction, and ventricular enlargement), as well as significant cognitive impairment in memory, executive, and visuospatial and visuoperceptual domains. Correlation analyses showed that all neuropsychological tests were associated with cortical thinning in parietotemporal regions and to a lesser extent in frontal regions. These results provide neuroanatomic support to the concept of MCI classified according to Movement Disorders Society criteria. The posterior pattern of atrophy in temporoparietal regions could be a structural neuroimaging marker of cognitive impairment in nondemented PD patients. All of the neuropsychological tests reflected regional brain atrophy, but no specific patterns were seen corresponding to impairment in distinct cognitive domains. © 2014 International Parkinson and Movement Disorder Society     

Cinguloparietal atrophy distinguishes Alzheimer disease from semantic dementia

BACKGROUND: Progressive brain atrophy is associated with Alzheimer disease (AD) and other dementias. Regional differences in brain atrophy may reflect clinical features of disease. OBJECTIVE: To identify regions of cerebral atrophy that are associated with AD vs other dementias. SETTING: University hospital dementia clinic. PARTICIPANTS: Eleven patients with AD and 11 with semantic dementia (SD), matched for age, sex, education, and degree of overall cognitive impairment and 15 normal controls. METHODS: Voxel-based morphometry was used to compare patterns of gray matter loss, measured on T1-weighted magnetic resonance images, between patients with AD or SD, a subtype of frontotemporal lobar degeneration, and controls. Statistically significant differences in regional gray matter concentration, after multiple-comparisons correction, between groups of subjects were identified. RESULTS: Patients with AD were more impaired than those with SD on tests of visuospatial function and on simple calculations. Consistent with these neuropsychological deficits, the most significant area of atrophy in the AD group was the left parietal cortex vs controls (z = 5.0; P =.04). Compared with SD, AD was associated with more atrophy in the left parietal lobe (z = 5.6; P =.04) and bilaterally in the posterior cingulate/precuneus (z = 5.1; P =.04). A discriminant function analysis demonstrated that the degree of atrophy of right posterior cingulate, left parietal lobe, right amygdala, and right anterior temporal lobe structures correctly classified 96% of the patients. CONCLUSION: Alzheimer disease is associated with a specific pattern of cortical atrophy compared with SD.     

Neuropsychological functions in variant Alzheimer's disease with spastic paraparesis

Few data exist on the effects of specific Alzheimer's disease (AD)-related mutations on cognitive function. We present neuropsychological test results in eight members of a large kindred with variant Alzheimer's disease (VarAD) due to a deletion of the presenilin 1 (PS-1) gene, encompassing exon 9. The disease was neuropathologically characterized by the presence of large, unusual, "cotton wool" plaques (CWP). Four surviving patients were prospectively tested, and retrospective neuropsychological data were collected from additional four deceased patients. The neuropsychological evaluation was based on tests of verbal and visual memory, abstract thinking, and visuoconstructive and spatial functions. In addition, psychiatric symptoms were evaluated. In four patients, brain glucose metabolism was examined by positron emission tomography (PET). PET showed temporoparietal hypometabolism typical of AD. In addition, variable patterns of hypometabolism (hemispherical asymmetry and occipital accentuation) were related to individual deficits of cognitive performance. However, all these early-onset patients (age range 43-63 years) with a deletion mutation of PS-1 gene showed prominent memory impairment and deficits in visuoconstructive and intellectual functions.     

Comparison of dementia with Lewy bodies to Alzheimer's disease and Parkinson's disease with dementia.

We compared the clinical and neuropsychological pattern of dementia with Lewy bodies (DLB) to Alzheimer's disease (AD) and Parkinson's disease with dementia (PD-d). Sixteen patients clinically diagnosed with DLB were compared with two groups of patients with PD-d (n = 15) and AD (n = 16) matched for level of dementia. Isolated cognitive impairment was the most common form of presentation in AD (93.8%) and DLB (31.3%) groups, while parkinsonism was in 100% of PD-d subjects. Psychoses associated with cognitive impairment at the beginning of the disease were more frequent in DLB patients (31.3%) than in AD (6.3%) and PD-d (0%) groups. There were no significant differences in Unified Parkinson Disease Rating Scale motor-subscale scores between DLB and PD-d patients. DLB and PD-d patients performed significantly worse on attentional functions and better on memory tests than AD. DLB patients also showed lower scores than AD subjects on visual memory, visuoperceptive, and visuoconstructive tests. No significant differences were found between PD-d group and DLB subjects on any neuropsychological test. We were unable to find any differences in cognitive tasks between PD-d and DLB subjects. Clinical features and neuropsychological deficiencies of DLB (attentional, visuoperceptive, and visuoconstructive deficits) and PD (attentional deficits) compared to AD (amnesic syndrome) can contribute to accurate identification of these entities and to the understanding of the neuropathological and neurochemical substrate underlying these diseases.     

Hippocampal and cortical atrophy predict dementia in subcortical ischemic vascular disease

BACKGROUND: The cause of dementia in subcortical ischemic vascular disease (SIVD) is controversial. OBJECTIVES: To determine whether cognitive impairment in SIVD 1) correlates with measures of ischemic brain injury or brain atrophy, and/or 2) is due to concomitant AD. METHODS: Volumetric MRI of the brain was performed in 1) elderly subjects with lacunes (L) and a spectrum of cognitive impairment-normal cognition (NC+L, n = 32), mild cognitive impairment (CI+L, n = 26), and dementia (D+L, n = 29); 2) a comparison group with probable AD (n = 28); and 3) a control group with normal cognition and no lacunes (NC). The authors examined the relationship between the severity of cognitive impairment and 1) volume, number, and location of lacunes; 2) volume of white matter signal hyperintensities (WMSH); and 3) measures of brain atrophy (i. e., hippocampal, cortical gray matter, and CSF volumes). RESULTS: Among the three lacune groups, severity of cognitive impairment correlated with atrophy of the hippocampus and cortical gray matter, but not with any lacune measure. Although hippocampal atrophy was the best predictor of severity of cognitive impairment, there was evidence for a second, partially independent, atrophic process associated with ventricular dilation, cortical gray matter atrophy, and increase in WMSH. Eight autopsied SIVD cases showed variable severity of ischemic and neurofibrillary degeneration in the hippocampus, but no significant AD pathology in neocortex. The probable AD group gave evidence of only one atrophic process, reflected in the severity of hippocampal atrophy. Comparison of regional neocortical gray matter volumes showed sparing of the primary motor and visual cortices in the probable AD group, but relatively uniform atrophy in the D+L group. CONCLUSIONS: Dementia in SIVD, as in AD, correlates best with hippocampal and cortical atrophy, rather than any measure of lacunes. In SIVD, unlike AD, there is evidence for partial independence between these two atrophic processes. Hippocampal atrophy may result from a mixture of ischemic and degenerative pathologies. The cause of diffuse cortical atrophy is not known, but may be partially indexed by the severity of WMSH.     

Executive dysfunction in early Alzheimer's disease.

Twenty five patients with probable mild Alzheimer''s disease were assessed for deficits in executive functioning and the impact of these deficits on performance in other neuropsychological domains. The Wisconsin card sorting test, the release from proactive interference paradigm, the verbal fluency test, and the Stroop test were adopted to classify patients with (AD+) and without (AD-) executive deficits. Seven of the patients showed an impairment in executive function (AD+), defined as a performance below the cut off score in at least two of these tests. There were no significant differences in clinical assessments, demographic features, or other cognitive functions between patients. Executive dysfunction may be an early additional feature in a subgroup of patients with mild Alzheimer''s disease. Impairment on frontal lobe tests does not seem to be related to the severity or duration of disease, or to a different pattern of impairment in other cognitive domains.     

Grey-matter atrophy in Alzheimer's disease is asymmetric but not lateralized

In Alzheimer's disease (AD), brain atrophy has been proposed to be left lateralized. Here, we reinvestigated the asymmetry and lateralization (i.e., asymmetry directed toward one hemisphere) of grey-matter (GM) distribution in 35 patients with AD, 24 patients with amnestic mild cognitive impairment (aMCI, a state of increased risk for AD), and 30 age-matched healthy controls (HC). We analyzed GM distribution by applying voxel-based morphometry (VBM) including analyses for asymmetry and lateralization. When comparing MCI with AD patients, VBM revealed GM loss in the entorhinal, temporoparietal, dorsofrontal, and occipital cortices as well as in the precuneus; when comparing HCs with MCI patients, we found similar differences, which were less pronounced especially within the temporoparietal cortex and precuneus. Analyses of regional asymmetry and regional lateralization as well as global lateralization did not yield significant results. However, lobar asymmetry of the temporal, parietal, and occipital lobes increased from HC to AD. Moreover, in aMCI and AD patients, performance of language-based neuropsychological tests correlated with lateralization of GM loss to the left hemisphere. We conclude that, in principle, brain atrophy in AD is asymmetric rather than lateralized. At the individual level however, asymmetry contributes to cognitive deficits.     

Hippocampal atrophy and ventricular enlargement in normal aging, mild cognitive impairment (MCI), and Alzheimer Disease

Alzheimer disease (AD) is the most common type of dementia worldwide. Hippocampal atrophy and ventricular enlargement have been associated with AD but also with normal aging. We analyzed 1.5-T brain magnetic resonance imaging data from 46 cognitively normal elderly individuals (NC), 33 mild cognitive impairment and 43 AD patients. Hippocampal and ventricular analyses were conducted with 2 novel semiautomated segmentation approaches followed by the radial distance mapping technique. Multiple linear regression was used to assess the effects of age and diagnosis on hippocampal and ventricular volumes and radial distance. In addition, 3-dimensional map correction for multiple comparisons was made with permutation testing. As expected, most significant hippocampal atrophy and ventricular enlargement were seen in the AD versus NC comparison. Mild cognitive impairment patients showed intermediate levels of hippocampal atrophy and ventricular enlargement. Significant effects of age on hippocampal volume and radial distance were seen in the pooled sample and in the NC and AD groups considered separately. Age-associated differences were detected in all hippocampal subfields and in the frontal and body/occipital horn portions of the lateral ventricles. Aging affects both the hippocampus and lateral ventricles independent of AD pathology, and should be included as covariate in all structural, hippocampal, and ventricular analyses when possible.     

Impaired cognitive performance in Parkinson's disease is related to caudate dopaminergic hypofunction and hippocampal atrophy

Frontal lobe dysfunction and other cognitive deficits have been described in Parkinson's disease (PD), which may lead to dementia. Both striatal dopaminergic deficiency and regional or global brain volume loss have been suggested to contribute to cognitive decline in PD. We therefore performed a neuropsychological evaluation, structural brain MRI and Fdopa PET in patients with PD and healthy elderly volunteers. PD patients had impaired cognitive performance in many neuropsychological tests compared to controls, not limited just to frontal lobe function tests. Caudate Fdopa correlated positively with performance in verbal (immediate and delayed) and visual memory. Patients with PD showed atrophy in the hippocampus and the prefrontal cortex and hippocampal atrophy was related to impaired memory. Our findings suggest that striatal dopaminergic depletion and global brain volume loss contribute to cognitive impairment in non-demented PD patients, but dysfunction of extra-striatal dopaminergic or non-dopaminergic systems probably plays a role especially in more generalized cognitive impairment.