Quantitative analysis of motor performance in epilepsy patients treated with valproate.

PURPOSE: The aim of our study was to detect objective signs of deterioration of motor performance in epilepsy patients treated with chronic valproate therapy. METHODS: We examined 14 controls and 15 epilepsy patients receiving chronic valproate monotherapy, who had no subjective complaints related to motor function. Regularity and maximum frequency of repetitive hand and finger movements, and simple reaction time were measured. Intensity and frequency characteristics of resting and postural tremor were assessed using accelerometry. Data were statistically evaluated. RESULTS: Repetitive hand and finger movements were significantly more irregular and the maximum frequency of repetitive movements was significantly lower in the valproate group than in controls. Resting tremor peak frequency and motor reaction time of the two cohorts did not differ. CONCLUSIONS: This is the first study, which quantitatively assesses motor performance of patients with epilepsy on chronic valproate therapy. The results suggest significant irregularity of repetitive hand movements and finger tapping even in patients with no motor complaints. Objective methods might help to recognize valproate-induced motor performance deterioration.

Post-movement beta synchronisation after complex prosaccade task.

OBJECTIVE: Post-movement beta synchronisation (PMBS) has been described as an induced, localised increase of beta activity over the contralateral sensorimotor cortex after termination of voluntary limb movement. The aim of our study was to investigate whether ocular saccades also evoke movement related EEG changes. METHODS: Complex saccades were recorded in six healthy volunteers using electro-oculography. EEG power changes in the beta frequency band were measured before, during and after saccades. RESULTS: Significant increase of beta-power was observed over the frontocentral region of both hemispheres after the offset of the complex saccade task. The latency of ocular PMBS was about 1100ms. CONCLUSIONS: Ocular PMBS evoked by complex saccade task is similar to that of recorded after limb movements. Its presence over both hemispheres irrespective of the direction of saccades indicates bilateral activation of cortical areas connected with the execution and planning of ocular movements. SIGNIFICANCE: The present paper is the first report on eye-movement related post-movement beta synchronisation. Investigation of ocular PMBS can be used both for research and clinical purposes for the functional assessment of neuronal networks controlling eye movements.

One-and-a-half syndrome--two cases.

One-and-a-half syndrome is characterized by combination of the clinical features of unilateral horizontal gaze palsy and internuclear ophthalmoplegia. The common symptoms are double vision and oscillopsia. The lesion is located in the paramedian pontine reticular formation, involving the centre of horizontal gaze and medial longitudinal fasciculus. More extensive brainstem damage may result in additional neurological signs. The most frequent underlying diseases are vascular insults, multiple sclerosis, and brainstem tumor. We present two cases of one-and-a-half syndrome. Both patients had lacunar infarction in the paramedian pontine tegmentum, revealed by MRI. The first patient had isolated eye movement disorder, while the second had additional nuclear-type facial paresis. In the first case brainstem evoked potentials indicated brainstem damage, in the second patient it was normal. Ocular symptoms improved within some days in both patients.

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.

[Complex eye movement disturbance in thalamic and mesencephalic infarcts]. / Osszetett szemmozgászavar thalamus- es mesencephaloninfarktusban.

A 36 year-old male patient developed sudden double vision and gait imbalance. Neurological examination revealed gaze paresis upward and on the left side downward (vertical "one-and-a-half"-syndrome), horizontal gaze nystagmus on the left bulbus directed to left. The MRI revealed bilateral thalamic and left midbrain ischemic lesions. The brainstem auditory and visual evoked responses were normally configured. Optokinetic nystagmus test found rightward, upward and downward hypometric saccades, convergence-retraction nystagmus--which was not visible at physical neurological examination--saccadic smooth pursuit eye movement and pseudoabducent palsy on both sides. The complex gaze disturbance was attributed to the lesions in the intralaminar nuclei of the thalamus and in the pretectal and rostromedial tegmentum of the mesencephalon. Infarcts may have been due to a variant artery: i.e. the thalamoperforant and the superior paramedian mesencephalic arteries originate with common branch from one of the communicant basilar artery. The authors discuss the mechanism of complex gaze palsy and call attention to the diagnostic value of optokinetic nystagmus examination.