Age and stage dependency of P300 latency alterations in non-demented Parkinson's disease patients without therapy

Abstract

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.