László Pálvölgyi

Impairment of post-movement beta synchronisation in parkinson's disease is related to laterality of tremor

OBJECTIVE Post-movement beta synchronisation (PMBS) is a physiological indicator of the activity of movement related neural networks. To investigate the pathophysiology of this phenomenon, we examined its characteristics in patients with unilateral tremor-dominant Parkinsons disease (PD). METHODS Movement duration and PMBS was measured after self-paced movement of the thumb at movement-reactive beta frequencies, over the supplementary motor area in 10 PD patients and 8 control subjects. RESULTS Movement duration in PD patients was longer than in controls. In left hand tremor patients, movement of the left hand was significantly longer compared to the right hand. When PD patients moved their non-affected hand, similarly to the controls, PMBS was higher contralateral to the movement. After movement of the tremulous hand, the contralateral PMBS decreased significantly and the contralateral preponderance disappeared. In the same hemisphere, PMBS was higher after contralateral to the non-affected hand movement, than after ipsilateral to the tremulous hand after movement. CONCLUSIONS PMBS in PD is affected by the activity of tremor related neural networks, suggesting that both cortical and subcortical sources are responsible for its generation. Examination of PMBS in various neurological diseases might provide further data on its physiological significance.

Delayed beta synchronization after movement of the more affected hand in essential tremor.

To investigate the pathomechanism of parkinsonian tremor (PT) and essential tremor (ET) by studying the correlation between tremor asymmetry and post-movement beta synchronization (PMBS) of the human EEG. We recorded the EEG of 10 patients with ET, 10 patients with Parkinsons disease and 10 controls. Subjects pressed an on-off switch in a self-paced manner with the thumb of their less (T+) and more (T++) tremulous hand. After digitalization of the EEG from the Cz, C3, C4 electrodes the movement reactive beta frequency, its maximum peak power value and its latency triggered to movement offset were determined. In ET tremor intensity did not influence the power of PMBS, however it was significantly delayed after the movement of the more tremulous hand. In Parkinsons disease after the movement of the more tremulous hand PMBS power was decreased, but it was not delayed. In controls the side of movement had no effect on the power and latency of the PMBS. The neuronal mechanisms underlying PMBS generation are differently affected in essential tremor and Parkinsons disease. The increase of PMBS latency after movement of the more affected hand in ET indicates possible cortical mechanisms in essential tremor generation.

Contralateral voluntary hand movement inhibits human parkinsonian tremor and variably influences essential tremor

While voluntary movement blocks Parkinsonian rest tremor (PT), essential tremor (ET) is enforced by postural and/or kinetic action. We studied the effect of contralateral externally- and internally triggered hand movement on PT and ET to investigate the transhemispheric influences on tremor genesis. We measured the changes of tremor peak frequency power after flash signal (F), flash triggered (FM) and self-paced (SPM) movement of the contralateral hand in nine PT and seven ET patients using accelerometer. PT significantly decreased both during FM and SPM tasks, suggesting that it is generated by a constant subcortico-cortical network, which includes higher order motor areas. Intensity of ET showed a remarkable intra- and interindividual variability both during FM and SPM reflecting a different generator circuitry with variable functional connections.

EEG correlates of subcortical optokinetic nystagmus.

OBJECTIVE Our aim was to reveal the changes of concomitant scalp EEG activity during subcortical (stare-) optokinetic nystagmus (OKN). METHODS Stare-OKN of 10 subjects was evoked and recorded simultaneously with the EEG. Frequency distribution of OKN-beats was determined in each subject. Power changes of alpha and beta frequency bands of the EEG during OKN stimulation were statistically analysed. RESULTS During continuous subcortical OKN-the EEG alpha power decreased significantly while beta power increase was not significant. A significant transient alpha power enhancement around the onset of subcortical OKN-clusters was detected. CONCLUSIONS We found significant changes in the parieto-occipital alpha EEG activity during subcortical OKN. The transient alpha synchronisation at the beginning of each OKN-cluster is a paradox phenomenon which might indicate increased visual attention. SIGNIFICANCE The present study is the first report investigating EEG changes related to subcortical OKN. Our findings suggest the involvement of cortical mechanisms in the generation of stare-OKN. The results might help in the elucidation of cortico-genicular mechanisms of ocular movements under physiological and pathological conditions.

P31.13 Correlation between EEG central frequency (CF), flow and hemodynamic parameters during cognitive efforts

Background: Decreased power in delta-theta bands of EEG/MEG has been associated to depression, drug and alcohol abuse, and other psychiatric conditions. In a previous work, we found decreased slow activity in alcoholic patients, associated to cortical atrophy and chronicity of alcohol consumption. However, we failed in reveal a significant association of this QEEG feature with depression, in spite of previous MEG data who pointed to a focal decrease of delta power in frontobasal areas. Objective: To assess differences in intracranial distribution of decreased surface QEEG delta power between depressed and non-depressed alcoholic patients in order to find any symptom-related topographic feature of physiopathological relevance. Methods: Low-Resolution Electric Tomography (LORETA) for the delta (1–3 Hz) band of EEG spectra was estimated from 25 normal control subjects and 28 alcoholic patients, 15 with and 13 without clinical depression according to Beck depression inventory (BDI), whose QEEG showed diffusely decreased delta power. Statistical non-parametric mapping was used to compare depressed and non-depressed groups. Measures of intracranial current source density in individual patients at areas of significant differences were correlated with BDI scores. Results: Depressed alcoholics had significantly less delta activity than non-depressed alcoholics at left temporal pole, left midtemporal cortex and frontobasal areas. Intracranial current source density at anterior cingulate, left orbitofrontal cortex and left parahippocampal cortex was negatively correlated with BDI score, but no correlation was found at right parahippocampal cortex. Conclusion: LORETA localized discrete areas of diffusely decreased delta activity in alcoholics, with a differential distribution linked to the presence of clinical depression, that seems to reveal a dysfunctional neuronal state at several specific limbic and other cortical locations that have been related to a specific clini.