The effect of transcranial magnetic stimulation (TMS) on reaction time (RT) and motor cortex excitability in the premovement period was investigated. Single and paired-pulse TMS with 3 and 13 ms interstimulus intervals (ISI) were applied to the left motor cortex at different delays after a visual command for isometric right hand index finger abduction. Motor evoked potentials (MEPs) recorded from the right first dorsal interosseous (FDI) were analysed to assess cortex excitability. The MEPs in response to single pulse TMS were gradually increased in the premovement period in general, but strongly augmented in a period of 90-100 ms before the voluntary myoelectrical activity (EMG) onset. In paired-pulse TMS (13 ms ISI), the MEP augmentation was smaller but started earlier before the EMG burst, and a gradual increase of MEP amplitudes was not evident. In case of 3 ms ISI, the expected intracortical inhibition (ICI) was evident only when TMS preceded the voluntary EMG by an interval of more than 60 ms, but at shorter intervals, rather some MEP augmentation was observed. Generally, the augmentation of MEPs in the premovement period was more pronounced in single pulse TMS. Most strikingly, a dead band period without MEP occurrences was observed within an interval of 30-50 ms before the voluntary EMG. In conclusion, parallel action of intracortical facilitation (ICF) and ICI as well as different dynamic behaviour of ICF and pre movement facilitation may explain the earlier mentioned effects. Moreover, this leads to an extended description of the rather subtle TMS influence on RT.

We studied the postural stability of 23 canoeing and kayaking young athletes and 15 healthy untrained age matched subjects during quiet and sensory conflicted stance (standing on stable and foam support with open and closed eyes). We measured with a force platform the center of pressure excursions and applied mean sway amplitude (MA), mean sway velocity (SV) and their Romberg ratios, and sway dispersion index to evaluate standing balance. During standing with eyes open, the athletes in comparison to non-athletes showed in sagittal and frontal plane greater MA and SV when the support was stable and smaller MA and SV when it was unstable. During standing with eyes closed, there were no differences between groups when the support was stable, however, the athletes sway faster and have smaller MA than controls while standing on the foam support. During standing on stable support, Romberg ratios for MA and SV revealed that unlike non-athletes the athletes' MA and SV were vision independent. However, while standing on unstable support the athletes' MA and SV became vision dependent and even greater for the medio-lateral sway. Canoeists' SV vision dependency in both planes was greater than for other groups. These results are in line with our hypothesis that young kayaking and canoeing athletes have a different from non-athletes model of sensory integration due to their specific sporting activity. One possible mechanism of this model may be a subtle re-adaptation deficit after disembarking to stable ground with diminished sensitivity of vision and vestibular apparatus.

The relative distribution of gangliosides was determined in the serum of 37 patients with multiple sclerosis (MS) and of 30 healthy subjects. There was a significant increase of GM1 and GD1a, and a decrease of GM3 proportion in the serum of relapsing-remitting MS patients (RRMS) during their first MS attack. The RRMS patients in relapse with a long duration of the disease had a significant decrease of GM1 and an increase of GD1a portion in the serum. An increase of GD1a, one of the major brain neuron ganglioside fraction, suggested the neuron injury in the early and with a long duration RRMS. The finding of an increase of GM1, the main human myelin ganglioside, during the first MS attack in RRMS patients confirms previous evidence for the possible involvement of gangliosides in the early pathological course of demyelination in MS.