An important basis of skilled human behaviour is the appropriate retrieval of acquired and memorized motor programmes ('motor memory traces'). Appropriate retrieval is warranted if motor programmes are only activated if necessary and are, probably more often, inhibited if required by the context of a given situation. It is unknown how this type of inhibition is accomplished in the brain. We studied context-dependent modulation of motor memory traces in 18 volunteers and six patients with focal dystonia. Cortical function was assessed with transcranial magnetic stimulation over the primary motor cortex (M1) and with task-related analysis of oscillatory EEG activity. An activation (ACT) and inhibition (INH) condition were compared. In both, visual cues were presented at 1/s. In ACT, subjects had to respond to these cues with individual finger movements as learned in a preceding training session. In INH, subjects had to observe the cues without retrieval of motor responses. During INH, inhibitory control of the motor memory trace was confirmed by significant amplitude reduction of motor evoked potentials (MEPs) compared with baseline. This was accompanied by a significant increase of 11-13 Hz oscillatory activity over the sensorimotor areas during INH. During active retrieval of the motor memory traces, the reverse was true (increased MEP amplitudes, decreased oscillatory 11-13 Hz activity). In a small sample of dystonic patients (n = 6), the increase of 11-13 Hz oscillatory activity during INH was consistently absent. The present data demonstrate for the first time cortical correlates of appropriate, context-dependent inhibition of motor memory traces. We propose that focal increases of oscillatory activity are instrumental for inhibitory control at the cortical level. This concept is supported by the preliminary observations in dystonic patients who are known to have deficits of inhibitory motor control and in whom these context-dependent focal increases of oscillatory activity were absent.
Bimanual co-ordination of skilled finger movements is a high-level capability of the human motor system and virtually always requires training. Little is known about the physiological processes underlying successful bimanual performance and skill acquisition. In the present study, we used task-related coherence (TRCoh) and task-related power (TRPow) analysis of multichannel surface EEG to investigate the functional coupling and regional activation of human sensorimotor regions during bimanual skill acquisition. We focused on changes in interhemispheric coupling associated with bimanual learning. TRCoh and TRPow were estimated during the fusion of two overlearned unimanual finger-tapping sequences into one novel bimanual sequence, before and after a 30-min training period in 18 normal volunteers. Control experiments included learning and repetition of complex and simple unimanual finger sequences. The main finding was a significant increase in interhemispheric TRCoh selectively in the early learning stage (P < 0.0001). Interhemispheric TRCoh was also present during the unimanual control tasks, but with lower magnitude, even if learning was involved. Training improved bimanual sequence performance (from 58.3+/-24.1 to 83.7+/-15.3% correct sequences). After training, interhemispheric (bimanual) TRCoh decreased again, thereby approaching levels similar to those in the unimanual controls. We propose that the initial increase in TRCoh reflects changes in interhemispheric communication that are specifically related to bimanual learning and may be relayed through the corpus callosum. The present data might also offer a neurophysiological explanation for the clinical observation that patients with lesions of the corpus callosum may show deficits in the acquisition of novel bimanual tasks but not necessarily in the execution of previously learned bimanual activities.
Forty-one patients suffering from autosomal dominant cerebellar ataxia type I (ADCA-I) were subjected to a genotype-phenotype correlation analysis using molecular genetic assignment to the spinocerebellar ataxia type 1, 2 or 3 (SCA1, -2 or -3) genetic locus, clinical examination and nerve conduction as well as evoked potential studies. Pyramidal tract signs, pale discs, and dysphagia were more frequent in SCA1 compared with SCA2 and SCA3 patients, while double vision occurred less frequently. Visual evoked potentials and motor evoked potentials following transcranial magnetic stimulation were abnormal in almost all SCA1 patients, but only in a minority of SCA2 and SCA3 patients. In contrast, somatosensory evoked potentials were delayed or absent in the majority of patients with no significant differences between the mutations. Abnormalities of brainstem auditory evoked potentials were found in about half of the patients irrespective of the underlying mutation. In addition, reduced sensory nerve action potentials, suggesting sensory axonal neuropathy were found in all three mutations. These findings provide electrophysiological evidence that pyramidal and visual pathways are differentially affected in SCA1, SCA2 and SCA3 patients.
We investigated changes in the activation and functional coupling of bilateral primary sensorimotor (SM1) and supplementary motor (SMA) areas with different movement rates in eight normal volunteers. An auditory-cued repetitive right-thumb movement was performed at rates of 0.5, 0.75, 1, 2, 3, and 4 Hz. As a control condition, subjects listened to pacing tones with no movements. Electroencephalogram (EEG) was recorded from 28 scalp electrodes and electromyogram was obtained from the hand muscles. The event-related changes in EEG band-power (ERpow: activation of each area) and correlation (ERcor: functional coupling between each pair of cortical areas) were computed every 32 ms. Modulations of ERpow and ERcor were inspected in alpha (8-12 Hz) and beta (16-20 Hz) bands. Motor cortical activation and coupling was greater for faster movements. With increasing movement rate, the timing relationship between movement and tone switched from synchronization (for 0.5-1 Hz) to syncopation (for 3-4 Hz). The results suggested that for slow repetitive movements (0.5-1 Hz), each individual movement is separately controlled, and EEG activation and coupling of the motor cortical areas were immediately followed by transient deactivation and decoupling, having clear temporal modulation locked to each movement. In contrast, for fast repetitive movements (3-4 Hz), it appears that the rhythm is controlled and the motor cortices showed sustained EEG activation and continuous coupling.
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