COGNITIVE IMPAIRMENT IN EARLY, UNTREATED PARKINSONS-DISEASE AND ITS RELATIONSHIP TO MOTOR DISABILITY

COGNITIVE IMPAIRMENT IN EARLY, UNTREATED PARKINSONS-DISEASE AND ITS RELATIONSHIP TO MOTOR DISABILITY
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DOI:
10.1093/brain/114.5.2095
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发表时间:
1991-10-01
期刊:
影响因子:
14.5
通讯作者:
SULLIVAN, EV
SULLIVAN, EV
中科院分区:
医学1区
文献类型:
--
作者:
COOPER, JA;SAGAR, HJ;SULLIVAN, EV

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目前对帕金森病(PD)认知功能障碍的认识主要来自长期治疗患者的研究,其中疾病慢性化、治疗、抑郁和痴呆是混杂因素。未经治疗的患者的研究已经检查了几个认知领域和认知,抑郁症和运动障碍之间的关系已经不完全探索。因此,我们研究了60例新诊断的、未经治疗的特发性PD患者和37例匹配的健康对照受试者;没有受试者患有临床痴呆或抑郁症。所有受试者都接受了记忆和认知的特定过程的测试,包括工作记忆、语言和非语言的短期和长期记忆、语言、视觉空间能力、集合形成和转移以及排序。患者还接受了痴呆、抑郁和运动残疾严重程度的定量全球临床测量。PD组作为一个整体表现出缺陷的即时回忆的口头材料,语言生产和语义流畅性,集形成,认知排序和工作记忆和视觉运动的建设。然而,这一组在即时记忆广度、长期遗忘、命名、理解和视觉感知方面没有受损。语言缺陷和更严重的额叶损伤仅限于那些在简易精神状态检查中得分异常的PD患者。运动功能障碍与抑郁严重程度相关性强,与认知功能障碍相关性弱。认知顺序、定势形成和定势转换缺陷倾向于与抑郁症相关,但认知与抑郁症之间没有关联。结果表明,分离的认知和运动控制早期PD这表明,认知功能障碍在很大程度上是独立的额纹状体多巴胺缺乏症潜在的运动障碍。一些,但不是所有的,额叶缺陷的慢性疾病是可检测的早期,未经治疗的PD。此处显示的认知缺陷的发病机制似乎涉及纹状体外多巴胺系统或非多巴胺能病理学。纵向研究是必要的,以确定是否增加疾病的持续时间加剧了早期的认知缺陷,并影响新的认知领域,除了产生增加运动障碍。
Current knowledge of cognitive dysfunction in Parkinson's disease (PD) has largely been obtained from studies of chronically treated patients in whom effects of disease chronicity, treatment, depression and dementia are confounding factors. Studies of untreated patients have examined few cognitive domains and relationships between cognition, depression and motor disability have been incompletely explored. Accordingly, we studied 60 consecutive patients with newly diagnosed, untreated, idiopathic PD and 37 matched, healthy control subjects; no subject had clinical dementia or depression. All subjects received tests of specific processes of memory and cognition, including working memory, verbal and non-verbal short- and long-term memory, language, visuospatial capacity, set-formation and shifting and sequencing. Patients also received quantitative global clinical measures of severity of dementia, depression and motor disability. The PD group as a whole showed deficits in immediate recall of verbal material, language production and semantic fluency, set-formation, cognitive sequencing and working memory and visumotor construction. However, this group was unimpaired in immediate memory span, long-term forgetting, naming, comprehension and visual perception. Language deficits and more severe frontal lobe impairments were confined to those PD patients scoring abnormally on a Mini Mental State examination. Motor disability correlated strongly with severity of depression but weakly with cognitive impairment. Cognitive sequencing, set-formation and set-shifting deficits tended to associate with depression, but otherwise there was no association between cognition and depression. The results indicate dissociation of cognition and motor control in early PD which suggests that cognitive dysfunction is largely independent of frontostriatal dopamine deficiency underlying motor disability. Some, but not all, of the frontal lobe deficits of chronic disease are detectable in early, untreated PD. The pathogenesis of the cognitive deficits shown here appears to involve extrastriatal dopamine systems or non-dopaminergic pathology. Longitudinal study is necessary to determine whether increasing disease duration exacerbates the early cognitive deficits and affects new cognitive domains, in addition to producing increasing motor disability.