老年人主观认知下降与慢性病共病的相关性分析

背景 主观认知下降（SCD）是阿尔茨海默病（AD）早期预防的目标阶段,AD与慢性病共病关系密切,但二者间相关性尚不十分明确。目的 探究老年人SCD与慢性病共病的相关性,为AD早期预防和干预提供理论依据。方法 于2021年1月至2022年6月,在广州市城市生活小区和养老机构以便利抽样法抽取≥60岁的老年人612例。采用基础版蒙特利尔认知评估量表（MoCA-B）、临床痴呆量表（CDR）、Hachinski缺血指数量表（HIS）评定客观认知功能水平,通过SCD标准诊断框架和SCD问卷（SCD-Q9）进行分组,将整体客观认知水平无异常、符合SCD标准诊断框架和SCD-Q9≥5分的老年人分入SCD组,将整体客观认知功能无异常和SCD-Q9<5分的老年人为认知无异常（CN）组。采用一般资料问卷收集老年人的社会人口学（性别、年龄、居住地、受教育年限、婚姻状况、退休前职业类型、月收入）和健康相关资料[体质指数、腰围、吸烟习惯、饮酒习惯、饮茶习惯、锻炼频率、午觉习惯及平均时长、睡眠质量、抑郁及焦虑症状、日常生活活动能力（ADL）],其中睡眠质量、抑郁症状、焦虑症状及ADL分别采用匹兹堡睡眠指数量表...     

Quantification of motor deficit in Parkinson's disease with a motor performance test series

Summary It was the purpose of the present study to quantify the expected motor deficit in parkinsonian patients with the computer assisted Motor Performance Test Series (MPS), version 05.87 by Schuhfried (1987) and to examine which of the motor test variables found correlate at a significance level of p<0.01 with items of motor examination recorded at neurological examination and activities of daily living of the Unified Parkinson's Disease Rating Scale (UPDRS), version 3.0.38 patients with idiopathic Parkinson's disease (PD) stages I–IV according to Hoehn and Yahr, aged 41 to 73 years were studied. The study design, i.e. initial rating by the physician followed immediately by testing of motor function with MPS was strictly adhered to in each patient.Physician's rating of rigor and the scores of the semiquantitative tests (finger taps, hand movements and alternating movements) as expression of hypokinesia and the activities of daily living correlated with the 3 factors of the Motor Performance Test Series at a highly significant level independent of disease stage. Tremor is only partly and never significantly reflected in the motor data measured. Stages I–II and II–IV (Hoehn and Yahr) differ significantly in the representative data of the Motor Performance Test Series.The results of the study support the assumption that MPS is a valid instrument for quantitative measurement of the motor deficit in parkinsonian patients, but that only some subtests are pathognomonic.     

The role of imperatives in psychopathology: A reply to Ellis

In his recent formulations of rational emotive therapy (RET), Ellis (1985) has increasingly emphasized what he believes to be the central role of necessitous thinking or musturbation in the development of depression. In his most recent article (Ellis, 1987), he suggests that necessitous thinking is the primary cognitive component of depression and that RET stands alone in its recognition of the role of this cognitive element. The present study addressed three issues raised by Ellis's paper: (1) Clarify whether necessitous thinking has been neglected by other cognitive theorists, (2) test empirically the role of necessitou thinking in depression relative to other established cognitive constructs, e.g., the cognitive triad (Beck, 1967), and (3) determine whether necessitous thinking is particularly salient in depression as compared with other forms of psychopathology. It was predicted that necessitous thinking would be found in other forms of psychology in addition to depression, and this was confirmed. The results are discussed as highlighting the importance of empirically testing theoretical predictions.From the Foundation for Cognitive Therapy.     

Brief report: cognitive functioning in children with Tourette's syndrome with and without comorbid ADHD

OBJECTIVE: To examine whether patients with Tourette's syndrome (TS) with and without comorbid attention deficit and hyperactivity disorder (ADHD) differ in cognitive functioning and whether a higher level of cognitive functioning is associated with severity of TS symptoms and psychosocial functioning. METHODS: Cognitive functioning, symptom severity, and psychosocial functioning were examined in 40 patients (33 boys, 7 girls; age range 6-18 years) with TS, of whom 17 had the comorbid diagnosis of ADHD. RESULTS: Patients with a comorbid ADHD diagnosis evidenced poorer performance than those with TS alone with respect to severity of TS symptoms, psychosocial functioning, verbal and performance intelligence, and word fluency, but not on tests of cognitive flexibility. Psychosocial functioning was predicted by symptom severity, but not by intelligence or fluency. CONCLUSIONS: Results confirm prior findings that comorbid ADHD is associated with more TS symptoms and worse psychosocial and cognitive functioning, and motivate whether cognitive flexibility plays a role in moderating the deleterious psychosocial effects of Tourette's syndrome and ADHD.     

DFNA54, a third locus for low-frequency hearing loss

Nonsyndromic hereditary hearing impairment (NSHHI) is a highly heterogeneous disorder with more than 90 loci mapped, of which nearly one-half of the responsible genes are identified. In dominant NSSHI hearing loss is typically biased towards the high frequencies while low-frequency hearing loss is unusual. Only two NSHHI loci, DFNA1 and DFNA6/14/38, are associated with predominantly low- frequency loss. We mapped the loci harboring the gene responsible for autosomal dominant low-frequency hearing loss in a multigenerational family. The pedigree of a Swiss family with low-frequency hearing loss was established. Using genomic DNA, DFNA1 and DFNA6/14/38 were excluded by linkage analysis or by direct sequencing of the responsible gene. Genome-wide linkage analysis was performed using commercially available microsatellite markers. Two-point linkage analysis demonstrated linkage to chromosome 5q31, the locus for DFNA15, with a lod score of 6.32 at recombination fraction =0 for marker D5S436. Critical recombinations were seen at markers D5S1972 and D5S410. Sequencing of the corresponding gene POU4F3 yielded no pathogenic mutation segregating with the affected members. In addition to Wolfram syndrome gene 1 (DFNA6/14/38) and diaphanous (DFNA1) there is evidence for a third gene involved in low-frequency hearing loss located at DFNA15. Because of the differences in auditory phenotype and the absence of pathogenic mutation in the coding region of POU4F3 it is likely that there is a second gene in 5q31, designated DFNA54, associated with NSHHI.     

Problem‐maintaining circles: Case illustrations of formulations that truly guide therapy

The cognitive behaviour therapy (CBT) emphasis on treatment relevance in assessment, and on evidence‐based intervention, has led to an increasing focus on problem maintenance factors (vs. precipitants) in both its models of psychopathology and in its individual case formulations. This article describes the reasons for this growing focus, and presents a generic CBT model based on the functional analysis of “problem‐maintaining circles” (PMCs) of causes. Some samples of the profuse literature implicating PMCs in many psychological disorders are presented, and the utility of PMC‐based functional analysis, case formulation, or modelling of psychopathology is advanced, not only as a guide to selection of therapeutic interventions, but as an alternative to standard psychiatric diagnosis. A sampling of a taxonomy of such PMCs is presented. And finally, the clinical application of PMC‐based functional analysis, case formulation, and treatment selection is illustrated in five case illustrations drawn from a recent clinical caseload.     

Children''s perceptions of chronic illness: the roles of disease symptoms, cognitive development, and information

This experiment considered the acceptance of chronically illchildren by their peers as a result of the peer's level of cognitivedevelopment, the type of disease, and the amount of informationprovided. The results of multivariate and univariate analysesof variance indicate that (a) children's comprehension of illnessescan be improved significantly with the provision of explanatoryinformation, although preoperational children are less ableto retain specifics, (b) preoperational children as well asuninformed children perceived themselves as significantly morevulnerable to contagion, (c) the more observable illness wasseen as significantly less attractive, and (d) provision ofinformation about the nature of a highly observable illnesstended to decrease rather than increase attraction.     

缺铁性贫血对学龄儿童某些认知能力影响的研究

本文采用双盲法对 IDA 和 NIDA学龄儿童各61名进行了认知能力测验及铁治疗前后的动态比较。结果表明:IDA 儿童识记再认、字母匹配反应时、数字扫描记忆和一般推理能力测验成绩较 NIDA 儿童差。经铁治疗的IDA 儿童,注意、短时记忆和心理动作反应速度均有明显提高。但对较高级认知能力的改善不明显。     

Hearing impairment as an early sign of alpha‐mannosidosis in children with a mild phenotype: Report of seven new cases

Alpha‐mannosidosis (AM) is a very rare (prevalence: 1/500000 births) autosomal recessive lysosomal storage disorder. It is characterized by multi‐systemic involvement associated with progressive intellectual disability, hearing loss, skeletal anomalies, and coarse facial features. The spectrum is wide, from very severe and lethal to a milder phenotype that usually progresses slowly. AM is caused by a deficiency of lysosomal alpha‐mannosidase. A diagnosis can be established by measuring the activity of lysosomal alpha‐mannosidase in leucocytes and screening for abnormal urinary excretion of mannose‐rich oligosaccharides. Genetic confirmation is obtained with the identification of MAN2B1 mutations. Enzyme replacement therapy (LAMZEDE^R) was approved for use in Europe in August 2018. Here, we describe seven individuals from four families, diagnosed at 3–23 years of age, and who were referred to a clinical geneticist for etiologic exploration of syndromic hearing loss, associated with moderate learning disabilities. Exome sequencing had been used to establish the molecular diagnosis in five cases, including a two‐sibling pair. In the remaining two patients, the diagnosis was obtained with screening of urinary oligosaccharides excretion and the association of deafness and hypotonia. These observations emphasize that the clinical diagnosis of AM can be challenging, and that it is likely an underdiagnosed rare cause of syndromic hearing loss. Exome sequencing can contribute significantly to the early diagnosis of these nonspecific mild phenotypes, with advantages for treatment and management.     

Concerted type I interferon signaling in microglia and neural cells promotes memory impairment associated with amyloid β plaques

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