帕金森病患者认知功能障碍与失匹配负波相关性研究

目的:探讨失匹配负波(MMN)与额叶认知功能测试对在评价帕金森病患者(Parkinson's disease,PD)的认知功能中的作用及其临床价值。方法:设28例早期非痴呆非抑郁帕金森病患者和31例年龄、教育年限相匹配的正常对照组分别进行额叶认知功能测试和失匹配负波测定。结果:非痴呆非抑郁帕金森病患者与正常对照组比较:额叶认知测试评分较差,MMN的潜伏期延长,差异有显著性意义;波幅下降,但无统计学意义;MMN潜伏期延长与额叶认知功能障碍程度呈正相关。结论:失匹配负波(MMN)能够客观地反映非痴呆非抑郁帕金森病人早期额叶认知功能障碍。     

帕金森病和皮质下缺血性血管性痴呆患者的失匹配性负波的比较

目的研究比较皮质下缺血性血管性痴呆（SIVD）患者和帕金森病患者认知功能障碍时在失匹配负波（MMN）的特征。方法17例非痴呆非抑郁帕金病患者,26例SIVD患者和21例年龄、教育年限相匹配的正常对照组分别进行失匹配负波（MMN）成分的潜伏期、波幅检测。结果SIVD组与对照组相比,MMN潜伏期延长,波幅明显降低,差异均有统计学意义（P〈0．01）;帕金森病组与对照组相比,MMN潜伏期延长（P〈0．01）;波幅虽呈下降趋势,但无统计学意义。SIVD组与帕金森病组相比,潜伏期延长,波幅明显降低,有显著意义（P〈0．01）。结论失匹配负波（MMN）能够客观地反映非痴呆非抑郁帕金森病人早期额叶认知功能障碍,更能反映SIVD患者在大脑信息处理的早期阶段对所输入信息的感觉记忆及自动选择所存在的障碍,其电生理特征对认知障碍的鉴别有一定价值。     

帕金森病合并抑郁患者认知功能和P300的研究

目的 探讨帕金森病（PD）合并抑郁患者认知功能和P300的改变。方法 对67例PD患者依据Zung抑郁自评量表（SDS）和汉密顿抑郁量表（HAMD）评分分为PD抑郁组（22例）和PD非抑郁组（45例），分别对两组患者进行认知功能评定和P300检测，并对结果进行比较和相关性分析。结果 本组PD患者简明智力状态量表（MMSE）评分尚在正常范围，但明显低于正常对照组（P〈0．05），PD抑郁组MMSE评分更低（P〈0.01）；与正常对照组比较，PD组P300潜伏期延长、波幅降低（均P〈0．05），PD抑郁组改变更为明显（均P〈0．01）；PD组P300潜伏期与MMSE评分呈负相关（r=-0．413，P〈0．05），波幅与MMSE评分呈正相关（r=0．398，P〈0．05）。结论 PD患者存在认知功能障碍，以记忆损害最为明显；抑郁对认知功能有负性影响，P300检测可以早期发现PD患者的认知功能障碍。     

帕金森病患者额叶认知功能和事件相关电位相关性研究

目的:探讨事件相关电位(P300)和额叶认知测试对帕金森病患者认知障碍评价的意义。方法:对31例非痴呆非抑郁帕金森病患者和25例年龄、性别、受教育程度相匹配的正常对照进行P300检测,同时采用词语流畅性、连线测验、Stroop字色干扰测验对病例组和对照组分别进行测试。结果:病例组与对照组比较:额叶认知功能评分较差,P300潜伏期延长(P<0.05),波幅下降;P300潜伏期与额叶认知功能障碍程度呈正相关。结论:非痴呆非抑郁帕金森病患者存在认知功能障碍。这种障碍可能是额叶功能受损后的表现。     

非痴呆非抑郁帕金森病患者额叶认知功能变化的研究

目的　探讨帕金森病 (PD)患者认知功能变化的特点 ,以及额叶认知测试对PD患者认知障碍评价的意义。方法　采用对额叶认知障碍比较敏感的神经心理方法 :词语流畅性、连线测验、Stroop字色干扰测验对 3 1例非痴呆非抑郁PD患者和 2 5名年龄、性别、受教育程度相匹配的正常对照进行测试。结果　非痴呆非抑郁PD患者与对照组比较额叶认知功能评分较差 (词语流畅性P <0 0 5、连线试验P <0 0 1、Stroop字色干扰测试P <0 0 1)。结论　非痴呆非抑郁的PD患者额叶认知功能显著降低 ,其机制可能与额叶 纹状体多巴胺环路中递质紊乱有关。     

帕金森病患者的事件相关电位研究

为探讨帕金森病（PD）患者认识功能障碍的电生理改变，分别对32例PD非痴呆患者，30例PD痴呆患者及28例健康人的事件相关电位（ERP）进行了分析。结果显示PD痴呆患者N2，P3潜伏期明显延长（P＜0．05），P3。潜伏期与其简易精神状态量表评分存在显著位负相关（P＜0．05）．另外，0对PD痴呆患者ERP及CT的对比研究表明，PD痴呆患者ERP阳性检出率高于CT。认为ERP能客观地反映出PD痴呆患者认知功能的损害．     

非痴呆非抑郁帕金森病患者额叶认知功能变化的研究靠

目的探讨帕金森病(PD)患者认知功能变化的特点,以及额叶认知测试对PD患者认知障碍评价的意义.方法采用对额叶认知障碍比较敏感的神经心理方法词语流畅性、连线测验、Stroop字色干扰测验对31例非痴呆非抑郁PD患者和25名年龄、性别、受教育程度相匹配的正常对照进行测试.结果非痴呆非抑郁PD患者与对照组比较额叶认知功能评分较差(词语流畅性P＜0.05、连线试验P＜0.01、Stroop字色干扰测试P＜0.01).结论非痴呆非抑郁的PD患者额叶认知功能显著降低,其机制可能与额叶-纹状体多巴胺环路中递质紊乱有关.     

急性脑卒中后脑诱发电位失匹配负波的变化观察

目的观察急性脑卒中后患者脑诱发电位失匹配负波的变化特点。方法对70例脑卒中患者和40例正常人进行失匹配负波（MMN）检查。结果与正常对照组比较，脑卒中患者脑诱发电位的MMN潜伏期延长、波幅降低，2组比较差异有统计学意义（P〈0．05）。结论脑卒中患者存在认知功能损害，MMN是敏感的检测工具。     

抑郁障碍患者五种脑诱发电位指标的临床随访研究

目的探讨抑郁障碍患者5种脑诱发电位指标及其治疗前后的特点。方法应用美国脑诱发电位仪，记录38例抑郁障碍患者（患者组）和33名正常对照者（对照组）的听觉诱发电位（AEP）、视觉诱发电位（VEP）、事件相关电位P300（ERP-P300）、失匹性负波（MMN）和关联性负变（CNV）。对其中18例患者随访至缓解期（治疗第9周末）。结果（1）与对照组相比，患者组出现AEP-N1潜伏期长[对照组（88±18）ms，患者组（104±25）ms]，N1-P2波幅低[对照组（5．3±1．9）μV，患者组（3．7±1．6）μV]；VEP-N1潜伏期长[对照组（125±19）ms，患者组（141±21）ms]，N1-P2波幅低[对照组（8．4±2．9）μV，患者组（6．9±2．6）μV]；P300-P3b潜伏期长[对照组（316±26）ms，患者组（330±21）ms]，P3．和P弘的波幅均低；CNV中的M1和M2波幅低，反应时间（RT）长[对照组（213±81）ms，患者组（306±126）ms]，均P〈0．01和P〈0．05。（2）随访部分患者，AEP中的N1-P2波幅、VEP中的N1潜伏期、P300中的P3b潜伏期，MMN波幅及CNV的波幅和RT等，与治疗前比较，差异有统计学意义（P〈0．05和P〈0．01）。结论抑郁障碍患者的AEP、VEP、P300和CNV，较正常对照组有改变。治疗后随抑郁症状的改善，与认知功能有关的指标也有相应的改善。     

帕金森病患者认知功能与脑电活动及脑影像学改变的相关性研究

目的研究帕金森病（Parkinsondisease,PD）患者认知功能、脑电活动及脑影像学的相关性。方法对70例PD患者及40例正常人进行中文版简易智能状态检查（MMSE）量表、BEAM频谱分析及脑影像学检查,对经MMSE初步测查后可疑认知功能障碍者进一步行成套神经心理学评估（FOM、RVR、DST、BD、BNT、HAMD）。结果PD痴呆组的神经心理学评估分值明显降低,痴呆组慢波（δ、θ频段）相对功率谱较非痴呆组明显增高（P〈0.01）,而快波（β1、β2频段）的相对功率谱显著降低（P〈0.05）;痴呆组额叶、颞叶的皮质萎缩及皮质下萎缩程度明显增加,且合并脑白质疏松症（LA）者明显高于非痴呆组;PD认知功能损害与额叶脑沟宽度、外侧裂宽度、三脑室宽度、脑室指数、前角指数及δ波功率值相关。结论神经心理学测验有利于发现PD患者的认知功能障碍,PD认知功能障碍与额颞叶皮质萎缩、皮质下机构萎缩程度、δ波功率及抑郁障碍密切相关,合并LA者痴呆发生率高。     

Hippocampal and prefrontal atrophy in patients with early non-demented Parkinson's disease is related to cognitive impairment

BACKGROUND: Early stage patients with Parkinson's disease (PD) show cognitive impairment in frontal lobe functions and memory tests. Hippocampal atrophy is seen in medicated patients with advanced PD. OBJECTIVES: To examine whether prefrontal or hippocampal atrophy are already present in early stage PD, and whether such atrophy is associated with cognitive impairment. METHODS: Twenty non-medicated, non-demented patients with early stage PD and 22 neurologically healthy age matched controls were studied. All subjects underwent magnetic resonance imaging to study hippocampal and prefrontal atrophy. Atrophy was evaluated by a neuroradiologist using a five point scale. In addition, the patients underwent a neuropsychological test battery sensitive to frontal lobe functions and memory. RESULTS: Patients with PD had atrophy in the right and the left prefrontal cortex. In the right hippocampus, the mean atrophy score was 1.15 in PD and 0.45 in controls. Corresponding figures for the left hippocampus were 1.05 for PD and 0.64 for controls. In PD, the left hippocampus atrophy correlated with verbal memory and prefrontal atrophy correlated with impaired performance in a test measuring vigilance. CONCLUSIONS: Non-medicated, non-demented patients with early stage PD show hippocampal and prefrontal atrophy. Impaired memory is related to hippocampal atrophy, whereas sustained attention is related to prefrontal atrophy.     

Alterations of the sense of self and personality in Parkinson's disease

PURPOSE: We hypothesized that alterations of subcomponents ('harm-avoidance') of personality and the sense of Self in patients with PD would be associated with executive cognitive dysfunction. METHODS: Thirty-four patients with PD and 17 age-matched controls with chronic disease were assessed with a set of neuropsychologic, personality and mood tests as well as an experimental assessment of the sense of Self. RESULTS: On personality and self tests, PD patients evidenced higher harm avoidance, lower novelty seeking scores, and lower recall rates of personally experienced events from childhood than controls and this PD personality profile was associated with poor performance on neuropsychologic tests of executive prefrontal function. PD patients, however, did not differ significantly from controls in their subjectively felt congruence between their present Selves and their hoped-for Selves. CONCLUSIONS: We suggest that harm-avoidance personality and Self-related changes of PD are due, in part, to a memory disorder associated with frontal dysfunction.     

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.     

Striatal [123I]β-CIT SPECT and prefrontal cognitive functions in Parkinson's disease

Summary. Twenty non-demented patients with idiopathic Parkinson's disease (PD) underwent single photon emission computed tomography (SPECT) with [¹²³I]β-CIT to further investigate the contribution of nigrostriatal dysfunction to cognitive and motor deficits. Compared to matched controls PD patients showed normal verbal intelligence, short-term memory and phasic alertness. There were significant (p < 0.05) deficits in tests of verbal working memory (digit ordering, reading span), strategic memory (story recall) and executive functions (card sorting), indicating a "prefrontal" cognitive deficit. Significant (p < 0.05) correlations were observed between dopamine transporter (DAT) density in the putamen and motor deficits as well as between DAT density in both striatal compartments (head of the caudate nucleus and putamen) and prefrontal functioning. Age was a major contributing factor to both cognitive status and nigrostriatal integrity as measured by [¹²³I]β-CIT SPECT. These results support the view that the striatum is part of a neuronal network that is mediating prefrontal cognitive functions. Received February 26, 1999; accepted August 18, 1999     

Cognitive functions in Parkinson's disease: Relation to disease severity and hallucination

ObjectiveWe wished to relate severity of Parkinson's disease (PD) with cognitive function in relation to cerebral blood flow (CBF).MethodsEighty-one consecutive PD patients were enrolled in this study. We used Mini-Mental State Examination (MMSE) and Wechsler Adult Intelligence Scale-Third edition (WAIS-III) to evaluate cognitive functions, and three-dimensional stereotactic ROI template (3DSRT) and Statistical Parametric Mapping (SPM) 8 to evaluate single photon emission CT (SPECT) recordings of regional CBF.ResultsThe mean MMSE score of PD patients was 27.4 ± 2.4. The scores of most patients were higher than 23/30. On the other hand, the mean Full-scale IQ of PD patients was 88.4 ± 17.3 in WAIS-III, which was lower than that of normal controls. In particular, visuospatial function score of most patients was lower. There was significant correlation between cognitive scores and Hoehn & Yahr stage and hallucinatory episodes. PD Patients with stage III and IV showed significant deterioration in cognitive functions compared to stage II patients. Analysis of CBF revealed relative reductions in perfusion in the cerebral cortex relative to that in normal control. SPM 8 showed that cognitive functions in PD patients were positively correlated with rCBF in the thalamus and cingulate gyrus.ConclusionsThis is the study to demonstrate the cognitive impairments in PD patients using WAIS-III. Visuospatial dysfunction might be caused by decrease in rCBF in the parietal and occipital lobes and dorsolateral prefrontal cortex. The severity of cognitive impairments in PD patients was correlated with disease severity and hallucinatory episodes.     

Neuropsychological follow up in patients with Parkinson's disease, striatonigral degeneration-type multisystem atrophy, and progressive supranuclear palsy

OBJECTIVES: Impairment of executive function is frequent in Parkinson's disease (PD), striatonigral degeneration-type multisystem atrophy (SND), and progressive supranuclear palsy (PSP); sometimes frank dementia is also present. However, the progression of cognitive decline has not been adequately studied. The objectives were to delineate the progression of cognitive impairment in these parkinsonisms and to elucidate interdisease differences. METHODS: Twenty three patients with SND and 21 with PSP, referred consecutively, and 18 patients with PD matched for severity of parkinsonism were compared on a comprehensive battery of cognitive tests and motor invalidity scales. A mean of 21 months later (range 18-24 months) the patients were called for retesting. RESULTS: Only 12 patients with PD (66.6%), 14 with SND (60.8%), and 11 with PSP (52.4%) were retested; those who dropped out refused, had died, or were too disabled. The patients with PSP performed worse than patients with PD or SND in the short tale, verbal fluency, visual search, and Benton tests at first evaluation. Overall cognitive performance was similar in the PD and SND groups except that the SND group did significantly worse on the verbal fluency test. Between group comparison of changes in scores from first to second evaluation showed that patients with PSP deteriorated significantly in the Nelson test compared with patients with PD or SND, and that patients with PSP or SND declined significantly on the visual search test compared with patients with PD. There was no difference between the groups for motor decline. Two patients with PSP were demented (DSM IV criteria) at first evaluation and six at second evaluation; no patients with PD or SND were demented at either evaluation. CONCLUSIONS: The greater decline of patients with PSP in attention, set shifting, and categorisation abilities is probably related to the conspicuous frontal deafferentation associated with direct premotor and prefrontal involvement, and to dysfunction of the midbrain ascending activating system, known to occur in PSP.     

Cognitive deficits in patients with essential tremor

OBJECTIVE: To assess cognitive and affective functioning in patients with essential tremor (ET). BACKGROUND: ET is traditionally thought to occur in isolation, without other neurologic abnormalities or cognitive changes. Recent evidence of gait disturbance and bradykinesia in these patients suggests that the neurologic abnormalities in ET may be more widespread than was once thought. Cognitive function in these patients has not been the subject of in-depth study. METHODS: Cognitive performance and mood were assessed in 18 consecutive patients with ET and 18 consecutive patients with PD who visited the neurosurgical clinic for surgical treatment of their symptoms. RESULTS: The patients with ET were found to have deficits on tests of verbal fluency, naming, mental set-shifting, verbal memory, and working memory, as well as higher levels of depression. In contrast to these areas of deficit, their performance was better than that of the normative sample on several tests of verbal and nonverbal conceptualization and reasoning. Tremor severity was not correlated with cognitive deficits. Patients with PD had deficits on the same tests that were impaired in the ET group and on tests of visuospatial processes. Direct comparison of the ET and PD groups showed greater impairment in facial perception in the PD group and greater impairment in verbal fluency and working memory in the ET group. CONCLUSION: Patients with ET have deficits in specific aspects of neuropsychological functioning, particularly those thought to rely on the integrity of the prefrontal cortex, which suggests involvement of frontocerebellar circuits in this disease.     

Depressed mood and executive dysfunction in early Parkinson's disease

OBJECTIVES: Studies on neuropsychological functions in early Parkinson's disease (PD) have reported changes with respect to memory and executive control related to dysfunction of fronto-striatal circuitry. The question has been raised, however, whether these findings are at least partly influenced by depression, which as such can also lead to cognitive impairments that depend on the functional integrity of the prefrontal cortex. MATERIAL AND METHODS: In the present investigation early non-depressed PD patients (NPD), early PD patients with mild depressive symptoms (DPD), patients with primary depression (DEP) and healthy controls (HC) completed a range of neuropsychological tests. RESULTS: Group comparisons revealed impairments of DPD patients in comparison with HC with respect to verbal fluency, short-term memory and concept formation. In addition they showed mild working-memory deficits. CONCLUSIONS: In summary the present results indicate that depressed mood in early PD may exacerbate cognitive impairments. Thus careful assessment of affective variables in PD should be an integral part of the treatment of PD.