帕金森病患者轻度认知功能损害

目的 探讨帕金森病(PD)患者伴轻度认知功能损害(MCI)即PD-MCI的特征及其相关因素.方法 采用多种量表[MMSE、Hoehn-Yahr分期、Webster评分、PD统一评分量表-运动(UPDRS-motor)及剑桥老年认知检查量表中文版(CAMCOG-C)]评估PD患者的病情严重程度、运动和认知功能;应用Petersen改良标准诊断PD-MCI.结果 89例PD患者中,认知正常(PDCOGNL)56例(63%),PD-MCI 20例(22%),PD痴呆(PDD)13例(15%).PD-MCI组较PDCOGNL组在定向、语言、记忆、注意、执行、思维、知觉等方面均存在明显损害,两组年龄和起病年龄差异无统计学意义,受教育程度差异有统计学意义(PD-MCI:4.4±4.3,PDCOGNL:7.1±4.9;q=3.270,P<0.05);PD-MCI组的年龄、起病年龄及受教育程度较PDD组差异均无统计学意义;而PDD组较PDCOGNL组在年龄、起病年龄、受教育程度等方面差异均有统计学意义(q=-4.913、-4.997、4.740,均P<0.01);3组间病程差异无统计学意义.Hoehn-Yahr分期、Webster评分及UPDRS-motor评分与PD认知功能均存在负相关.结论 PD-MCI是PD认知正常与PDD之间的过渡状态,存在多个区域的认知损害;高龄、起病年龄迟、受教育程度低可能是PD认知损害的危险因素;疾病严重程度及运动功能与PD认知功能存在着负相关.     

Mild cognitive impairment and vascular cognitive impairment in stroke patients

In 150 older stroke patients (>75) without dementia, the proportion of people meeting different criteria for early cognitive impairment varied from 17% to 23% depending upon the individual criteria used. Given this large disparity, prospective studies to clarify the utility of different criteria as a predictor of subsequent dementia are a priority.     

Educational level and cognitive impairment in patients with Parkinson disease

Background and purposeParkinson disease (PD) is a risk factor for dementia. In addition, specific cognitive deficits can occur in PD patients without dementia. A patient's level of education could have an influence on the development of cognitive impairment in PD. The aim of this study was to examine the relationship between the level of education and cognitive performance in non-demented patients with PD.Material and methodsThirty-seven consecutive, nondemented PD patients and 40 healthy controls fulfilled the inclusion criteria and were enrolled in the case-control study. Each of the controls and PD patients were classified, for the purpose of this study, into one of three groups (low, intermediate, higher), categorized by the number of years of education. There were no differences in education and age between the controls and PD patients. All of the subjects were evaluated with a battery of neuropsychological tests: Mini-Mental State Examination, Trail Making Tests, Stroop Test, Mental Rotation Test, and Verbal Fluency Test.ResultsLess (low and intermediate) education was correlated with poor results from tests. The comparison of all groups of PD patients and controls demonstrated that PD subjects received lower test scores, especially for the low and intermediate groups. However, no statistically significant difference was reached between educationally advanced PD patients and the appropriate control subjects.ConclusionsAs compared to the controls, most non-demented PD patients presented executive-type cognitive dysfunction. The higher educational level, however, was associated with a lower risk of cognitive deterioration. We conclude that higher education might have protective effects in cognitive decline in PD.     

Measuring mild cognitive impairment in patients with Parkinson's disease

We examined the frequency of Parkinson disease with mild cognitive impairment (PD‐MCI) and its subtypes and the accuracy of 3 cognitive scales for detecting PD‐MCI using the new criteria for PD‐MCI proposed by the Movement Disorders Society. Nondemented patients with Parkinson's disease completed a clinical visit with the 3 screening tests followed 1 to 3 weeks later by neuropsychological testing. Of 139 patients, 46 met Level 2 Task Force criteria for PD‐MCI when impaired performance was based on comparisons with normative scores. Forty‐two patients (93%) had multi‐domain MCI. At the lowest cutoff levels that provided at least 80% sensitivity, specificity was 44% for the Montreal Cognitive Assessment and 33% for the Scales for Outcomes in Parkinson's Disease‐Cognition. The Mini‐Mental State Examination could not achieve 80% sensitivity at any cutoff score. At the highest cutoff levels that provided specificity of at least 80%, sensitivities were low (≤44%) for all tests. When decline from estimated premorbid levels was considered evidence of cognitive impairment, 110 of 139 patients were classified with PD‐MCI, and 103 (94%) had multi‐domain MCI. We observed dramatic differences in the proportion of patients who had PD‐MCI using the new Level 2 criteria, depending on whether or not decline from premorbid level of intellectual function was considered. Recommendations for methods of operationalizing decline from premorbid levels constitute an unmet need. Among the 3 screening tests examined, none of the instruments provided good combined sensitivity and specificity for PD‐MCI. Other tests recommended by the Task Force Level 1 criteria may represent better choices, and these should be the subject of future research. © 2013 Movement Disorder Society     

Mitochondrial impairment in patients and asymptomatic mutation carriers of Huntington's disease.

Huntington's disease (HD) is an autosomal dominantly inherited neurodegenerative disorder caused by a CAG repeat expansion in the IT-15 gene; however, it remains unknown how the mutation leads to selective neurodegeneration. Several lines of evidence suggest impaired mitochondrial function as a component of the neurodegenerative process in HD. We assessed energy metabolism in the skeletal muscle of 15 HD patients and 12 asymptomatic mutation carriers in vivo using 31P magnetic resonance spectroscopy. Phosphocreatine recovery after exercise is a direct measure of ATP synthesis and was slowed significantly in HD patients and mutation carriers in comparison to age- and gender-matched healthy controls. We found that oxidative function is impaired to a similar extent in manifest HD patients and asymptomatic mutation carriers. Our findings suggest that mitochondrial dysfunction is an early and persistent component of the pathophysiology of HD.     

Insight and cognitive impairment: effects on quality-of-life reports from mild cognitive impairment and Alzheimer's disease patients

This study follows previous work to determine the effect of patient insight and cognitive impairment on the reliability and validity of self-reported quality of life (QOL) from patients diagnosed with Alzheimer's disease (AD) and mild cognitive impairment (MCI). AD and MCI patients (N = 68) and their caregivers participated. Patients with impaired insight provided QOL ratings that were less reliable than those provided by patients with better insight. Patient-caregiver agreement for. QOL reports was used as an index of validity. Neither better insight nor lesser cognitive impairment suggested better agreement. Thus, even when patient insight is intact, patient reports are unlikely to agree with caregiver reports. Patient and caregiver reports about patient QOL may represent 2 unique, yet potentially valid, perspectives.     

Mild cognitive impairment and cognitive reserve in Parkinson's disease

Patients with Parkinson’s disease (PD) typically present with motor symptoms, but non-motor symptoms, including cognitive impairment, autonomic dysfunction and neuropsychiatric symptoms, are usually also present, when looked for carefully. The objective of this paper is to provide an up-to-date, comprehensive review of two undecided issues about cognitive impairment in PD patients without dementia: the concept of Mild Cognitive Impairment (MCI) and the concept of Cognitive Reserve (CR). Empirical findings support the value of the concept of MCI in this population, from the early untreated stages onwards. Further studies are needed to establish 1) the clinical-neuroimaging characteristics of MCI subtypes in PD, in comparison to those MCI subtypes in patients without PD; 2) whether different types of MCI in PD are associated with different rates of cognitive decline during the progression of the disease. Preliminary empirical evidence also shows that education might exert a protective effect on cognitive decline in PD and that less educated subjects are at increased risk for developing dementia, lending support to the CR hypothesis, in this population as well. Further studies are necessary to investigate how CR modulates cognitive decline in PD and other frontal-subcortical disorders, e.g. by identifying possible differential effects of CR on different cognitive domains.     

Retinal thickness in patients with mild cognitive impairment and Alzheimer's disease

Objectives

Mild cognitive impairment (MCI) may represent a transition to early Alzheimer's disease (AD). The retinal nerve fiber layer (RNFL) is composed of axons originating in retinal ganglion cells that eventually form the optic nerves. Previous studies have shown that degenerative changes occur in optic nerve fibers and manifested as thinning of RNFL in patients with AD. The objective of this study was to assess the relationship between MCI, AD and loss of RNFL.

Patients and methods

In this study, patients fulfilling diagnostic criteria for MCI (n = 24), AD (n = 30) and cognitively normal age-matched controls (n = 24) have undergone neuro-ophthalmologic and optical coherence tomography (OCT) examinations to measure RNFL thickness.

Results

There was a significant decrease in RNFL thickness in both study groups (AD and MCI) compared to the control group, particularly in the inferior quadrants of the optic nerve head, while the superior quadrants were significantly thinner only in AD. Although AD patients may have more severe changes than MCI cases, the differences were statistically nonsignificant. Furthermore among AD patients, there was no relation to the severity of the dementia.

Conclusions

Our data confirm the retinal involvement in AD, as reflected by loss of axons in the optic nerves.     

Cognitive impairment in carriers of glucocerebrosidase gene mutation in Parkinson disease patients

AimParkinson disease (PD) is the common neurodegenerative disease with motor and numerous non-motor symptoms, including cognitive impairment. Mutation of glucocerebrosidase (GBA) gene is the most common genetic risk factor of sporadic PD. The aim of this study was to assess clinical features of PD associated with GBA mutation.MethodsOne hundred and thirty-eight PD patients were involved and examined by the movement disorder specialist using several scales including Unified Parkinson Disease Rating Scale (UPDRS) part II and III, Hoehn and Yahr (H&Y) staging, Mini-Mental State Examination (MMSE) and Hamilton Depression Scale (HDS). The exons 8 and 9 of GBA was sequenced and screened for variants.ResultsThe GBA variants were found in 16 (11.6%) PD patients: N370S mutation in 5 (3.6%) and T369M variant in 11 (7.9%). No significant differences between the group of mutation carriers and non-carriers were found in relation to clinical features except for dementia (MMSE score < 26) occurring more often in N370S mutation carriers (60.0% vs 19.6%, p = 0.03).ConclusionThe N370S GBA mutation is the risk factor for cognitive impairment in PD patients.     

Dementia and cognitive impairment in Parkinson disease

Changes in cognitive function and disturbances in behavior are commonly seen in parkinsonian patients and they are inherent features of the disease. Estimates on the prevalence of dementia in this disorder are quite variable, ranging from 15 to 25%. Advanced age, depression, severity of akinesia, and the presence of dopaminomimetic psychosis, are considered as risk factors in the development of cognitive deterioration within this patient population. Cognitive dysfunction may manifest as relatively circumscribed deficits or overt dementia. The finding of mild cognitive deficits is common in Parkinson's disease, such as reduced flexibility, psychomotor slowing, reduction in learning capacity and information retrieval, and disturbances in visuospatial tasks. The most prevalent cognitive disturbance is an impairment in visuospatial tasks, not necessarily related to the degree of motor disability. Dementia, when present early on in the course of the disease may suggest alternative diagnoses (Diffuse Lewy body dementia, Alzheimer's disease with extrapyramidal features, Fronto-temporal dementia, etc.), while in those cases in whom the dementing disorder develops at a later stage, it is assumed to be an integral part of the disease, albeit corresponding to variable pathogenetic mechanisms.     

MRI and cognitive impairment in Parkinson's disease

Patients with Parkinson's disease (PD) may present impairment in cognitive functions even at early stages of the disease. When compared with the general population, their risk of dementia is five to six times higher. Recent investigations using structural MRI have shown that dementia in PD is related to cortical structural changes and that specific cognitive dysfunctions can be attributed to atrophy in specific structures. We review the structural MRI studies carried out in PD using either a manual region of interest (ROI) approach or voxel‐based morphometry (VBM). ROI studies have shown that hippocampal volume is decreased in patients with PD with and without dementia; in addition, hippocampal atrophy correlated with deficits in verbal memory. VBM studies have demonstrated that dementia in PD involves structural changes in limbic areas and widespread cortical atrophy. Findings in nondemented patients with PD are less conclusive, possibly because cognitively heterogeneous groups of patients have been studied. Patients with PD with cognitive impairment and/or visual hallucinations present greater brain atrophy than patients without these characteristics. These findings suggest that cortical atrophy is related to cognitive dysfunction in PD and precedes the development of dementia. Structural MRI might therefore provide an early marker for dementia in PD. © 2009 Movement Disorder Society     

帕金森病患者的抑郁与认知功能障碍

目的探讨帕金森病(PD)患者的抑郁与认知功能障碍之间的关系。方法对60名PD患者和38名对照组进行抑郁和认知功能评定。结果PD组HAMD均分(16.8±0.6),对照组(7.2±2.8);PD组的认知功能与对照组相比下降;PD并抑郁患者的认知功能与PD并非抑郁患者的认知功能相比有显著性差异(P<0.05)。结论PD患者存在抑郁与认知功能障碍,抑郁可能是导致认知功能下降的重要因素。     

Alzheimer's disease and mild cognitive impairment

As our society ages, age-related diseases assume increasing prominence as both personal and public health concerns. Disorders of cognition are particularly important in both regards, and Alzheimer's disease is by far the most common cause of dementia of aging. In 2000, the prevalence of Alzheimer's disease in the United States was estimated to be 4.5 million individuals, and this number has been projected to increase to 14 million by 2050. Although not an inevitable consequence of aging, these numbers speak to the dramatic scope of its impact. This article focuses on Alzheimer's disease and the milder degrees of cognitive impairment that may precede the clinical diagnosis of probable Alzheimer's disease, such as mild cognitive impairment.     

帕金森病伴轻度认知功能障碍的研究进展

帕金森病伴发的轻度认知功能障碍，对患者的基本生活功能影响较小，但往往会演变成 帕金森痴呆，从而显著影响患者的生存质量及预后。因此，了解这一疾病，并对其进行早期干预具有十 分重要的意义。现从帕金森病轻度认知功能障碍的定义、临床表型、诊断标准、鉴别诊断、发病机制、危 险因素及治疗等方面进行综述，为相关研究提供参考。     

帕金森病轻度认知损害

轻度认知损害是帕金森病最为常见的非运动症状之一,是影响帕金森病患者日常生活活动能力的主要因素.轻度认知损害是介于正常老龄化与痴呆之间的过渡阶段,一般生活能力保持良好、发生轻度认知损害的帕金森病患者被称为帕金森病轻度认知损害,其临床特征可表现为不同认知领域损害,如工作记忆和(或)注意力、执行能力、言语、记忆力及视空间能力障碍等.在本文中,我们通过文献复习从流行病学、病理学、临床表现特点,以及辅助检查及诊断标准等方面对帕金森病轻度认知损害进行概述.     

Differential cognitive impairment in Alzheimer's disease and Huntington's disease

The differentiation between cortical and subcortical dementias requires that the cognitive characteristics of dementias attributable to different causes be discriminable. For large samples of Alzheimer's disease and Huntington's disease patients, distinct cognitive profiles were obtained on the Mini-Mental State Exam. The profile differences were independent of severity of dementia and were sufficiently robust to classify patients as Alzheimer's disease or Huntington's disease with 84% accuracy. The qualitative differences in cognitive functioning may also be typical of other cortical and subcortical dementias.     

帕金森病轻度认知损害

认知功能障碍是帕金森病较为常见的非运动症状,影响帕金森病患者生活质量、增加照料者负担。帕金森病认知功能障碍可以表现为轻度认知损害,也可以表现为痴呆。帕金森病轻度认知损害见于疾病早期,随着病情进展发病率逐渐升高,可进展为帕金森病痴呆。帕金森病轻度认知损害的诊断标准包括纳入标准、排除标准和损害水平判断。非药物治疗如运动锻炼和认知行为疗法可以改善帕金森病轻度认知损害症状,其药物治疗尚待进一步研究。