Giménez-Roldán S, Mateo D, Dobato J L
Servicio de Neurología, Hospital General Universitario Gregorio Marañón, Madrid.
Neurologia. 1997 Mar;12(3):130-5.
A common observation in neurological practice is parkinsonism with concomitant cognitive decline, an association that usually arises from various underlying degenerative or vascular conditions, most of which are untreatable. An elderly woman with no history of psychiatric disease presented complaining of memory and cognitive impairment serious enough to interfere with daily life activities over the preceding year. She soon developed a predominantly left-sided tremor, rigidity and bradykinesia. She had had only 2 years of formal education. Neuropsychological assessment showed poor performance on Wechsler memory scale sub-items, as well as constructional apraxia, dyscalculia, reasoning difficulties and gross information deficits. A 3-month trial course of levodopa was followed by dramatic improvement in both parkinsonian symptoms and cognitive performance, including a 7-point gain in the Mini-Mental Status Examination score. At the same time, the Beck Depression Inventory score fell from 27 (baseline) to 18. Over the 10-year follow-up period the patient developed late levodopa syndrome and a persistent but mild dysthymic disorder, but never manifested dementia as defined by DSM-III-R criteria. This patient's case illustrates three important principles. First, although parkinsonism is known to be preceded by depressive episodes, particularly in a subgroup of younger patients, the symptoms of the elderly patient whose Parkinson's disease is foreshadowed by depression can mimic depressive pseudodementia, potentially leading to diagnostic confusion. Second, impaired motivation and disturbances in cognitive function are different from mood disorders, as the former involve the mesolimbic/mesocortical dopamine system, explaining the beneficial effect of levodopa on motivation and cognition in this patient even as mood was unaffected. Finally, depressive pseudodementia in Parkinson's disease does not necessarily herald the development of organic dementia in the long term.
神经科临床实践中的一个常见现象是帕金森综合征伴有认知功能下降,这种关联通常源于各种潜在的退行性或血管性疾病,其中大多数无法治疗。一位无精神疾病史的老年女性前来就诊,主诉在过去一年中出现严重的记忆和认知障碍,足以干扰日常生活活动。她很快出现了以左侧为主的震颤、僵硬和运动迟缓。她仅接受过两年正规教育。神经心理学评估显示,韦氏记忆量表子项目表现不佳,同时存在结构性失用、失算、推理困难和严重的信息缺失。左旋多巴治疗3个月后,帕金森症状和认知表现均有显著改善,包括简易精神状态检查表得分提高7分。同时,贝克抑郁量表得分从27(基线)降至18。在10年的随访期内,患者出现了晚期左旋多巴综合征和持续但轻度的心境恶劣障碍,但从未表现出符合DSM-III-R标准的痴呆。该患者的病例说明了三个重要原则。首先,虽然已知帕金森综合征之前会出现抑郁发作,尤其是在一部分年轻患者中,但抑郁症预示帕金森病的老年患者的症状可能类似抑郁性假性痴呆,可能导致诊断混淆。其次,动机受损和认知功能障碍与情绪障碍不同,因为前者涉及中脑边缘/中脑皮质多巴胺系统,这解释了左旋多巴对该患者动机和认知的有益作用,即使情绪未受影响。最后,帕金森病中的抑郁性假性痴呆不一定预示着长期会发展为器质性痴呆。