Computerised brain electrical activity findings of parkinson patients suffering from hyperkinetic side effects (hypersensitive dopamine syndrome) and a review of possible sources.

Among 2,000 Park. pat. hospitalised during the years 1988 till 1990 we found 61 pat. with hyperkinetic side-effects in the sequence of a long-term L-dopa treatment. 43 (mean age 64y.) had a complete clinical data set and hyperkinesia ratings (AIMS scale). Compared to the system's data base--none of these patients showed a strickly normal CEEG. Our standard parkinson treatment was established in 1986: L-dopa as low as possible, dopamine agonists low, amantadines as high as necessary, L-deprenyl till 10 mg and anticholinergics--no, if possible. Our pat. group got initially a mean of 508 mg L-dopa, at the end of the study 296 mg. Conventional EEG (Picker-Schwarzer) and CEEG data were recorded (Dynamic Brain Mapping, Itil). Clinical and CEEG follow-up investigations were done after 2 weeks and 2 years. At follow-up, a reduction of the hyperkinesias was found in 43 patients (AIMS scale). 28 pat. received an additional treatment with nootropic drugs, 15 pat. were without this additional therapy. The visually evaluated CEEG at the latter group showed an acceleration ("response") in 33%, but among the patients with nootropic drugs the acceleration was seen in 66%. In patients without nootropics the mean delta power increased, patients additionally treated showed a reduction of delta. In cases of high L-dopa dosage--associated with severe hyperkinetic side effects--more slow waves were registered. The non-nootropic treated patients were divided into two groups--non-responders and the responders: a) Non-responders (n = 10) showed a significant reduction of alpha and a significant increase of delta and theta, b) Responders (5 pat.) without nootropics had a significant reduction of theta and a increase of alpha, but the acceleration is less pronounced than in the responder group with nootropics. Without co-medication a high L-dopa dosage may provoke/facilitate an organic cerebral dysfunction. The nootropic-treated but non-responder group showed no significant changes (n = 13). The best results were seen in the nootropic-treated responder group (n = 15): a significant diminution of delta and theta and an increase of alpha and beta. Summing-up documented by CEEG methods--high L-dopa dosages seemed to be one of the causes of cerebral dysfunctions. Nootropic drugs were able to ameliorate the pathological CEEG patterns.