未经治疗的非痴呆性帕金森病患者P300潜伏期改变的年龄和分期依赖性

P Stanzione , R Semprini , M Pierantozzi , A.M Santilli , L Fadda , R Traversa , A Peppe , G Bernardi
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引用次数: 36

摘要

通过“奇数球”模式记录44名非痴呆新生帕金森病患者(PD)或正在停药的PD患者以及31名年龄匹配的正常受试者的Fz, Cz和Pz的声学P300,以评估PD患者是否存在P300潜伏期增加。通过对PD患者按年龄(“年轻”或“年老”)和疾病分期(“早期”或“晚期”)进行亚组,依次验证年龄和疾病分期对潜伏期的影响。将PD患者的数据与正常受试者的数据进行比较,正常受试者分为“年轻”和“老年”两组,或者为了消除年龄相关的潜伏期变化,在所有被检查的受试者中,将后者调整为60岁。在使用两种方法的老年PD患者组(n=23)中,Fz和Cz的潜伏期显著增加,而在年轻PD患者组(n=21)中则没有。此外,在“晚期”PD患者组(n=8)中,Fz和Cz也存在显着的潜伏期增加,但在“早期”PD患者组(n=36)中没有使用年龄调整测量。将“早期”PD患者组分为“年轻”组(n=20)和“老年”组(n=16),与正常受试者相比,“早期老年”组的Fz潜伏期明显增加。通过分析原始数据,至少在一个电极上观察到异常的P300潜伏期,在5.0%的“早期年轻”患者中,43.7%的“早期老年”患者中,高达62.7%的“晚期”患者中。Fz代表最常观察到异常P300潜伏期的部位。此外,在整个PD患者组中,与正常受试者相比,P300延迟仅在额叶(Fz)部位显著。报告的发现被解释为PD对认知功能产生了一种“年龄的加速效应”,可能是由一种不同于产生运动损伤的机制产生的,因为P300潜伏期和运动评分之间没有明显的相关性。P300的额叶损伤与先前在这些患者中获得的神经心理学发现一致。考虑到约30%的PD患者在疾病进展过程中发生痴呆,在发病时观察到的边缘性或异常P300潜伏期可能是这一演变的预测标志。
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Age and stage dependency of P300 latency alterations in non-demented Parkinson's disease patients without therapy

Acoustic P300 was recorded from Fz, Cz and Pz by means of an `odd-ball' paradigm in 44 non-demented de novo Parkinson's disease patients (PD) or PD patients under treatment withdrawal, and in 31 age-matched normal subjects, to evaluate whether a P300 latency increase was present in PD patients. The influence of age and disease stage on latency was successively verified by subgrouping PD patients according to different age (`young' or `old') and disease stage (`early' or `advanced'). PD patient data were compared to data of normal subjects subgrouped into `young' and `old' or, to eliminate the age-dependent shift of latency, this latter was adjusted to 60 years in all the examined subjects. A significant increase of latency has been found in Fz and Cz in the `old' group of PD patients (n=23) but not in the `young' group (n=21) utilising both methods. Moreover, a significant latency increase was also present in Fz and Cz in the group of `advanced' PD patients (n=8), but not in the group of `early' PD patients (n=36) utilising age-adjusted measurements. When the `early' PD patient group was divided into `young' (n=20) and `old' (n=16), the `early old' group displayed significantly increased latencies in Fz compared with normal subjects. Abnormal P300 latencies were observed, at least in one electrode, by analysing the raw data, in 5.0% of the `early young', 43.7% of the `early old' and up to 62.7% of the `advanced' patients. Fz represented the site in which abnormal P300 latencies were most often observed. Moreover, in the total group of PD patients, the P300 delay was significant only on the frontal (Fz) site when compared with normal subjects. The reported findings were interpreted as if PD produces a sort of `accelerated effect of age' on the cognitive functions, presumably produced by a mechanism different from that producing motor impairment since no clear correlation could be detected between P300 latency and motor score. The frontal impairment of P300 is in line with previous neuropsychological findings obtained in these patients. Considering that about 30% of PD patients develop dementia during their disease progression, a border-line or abnormal P300 latency observed at disease onset may represent a predictive marker of this evolution.

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