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Although synaptic plasticity in the human cerebral cortex is governed by metaplasticity, whether a similar mechanism operates at brainstem level is unknown. In this study in healthy humans we examined the effects and interactions induced by pairing supraorbital nerve high-frequency electrical stimulation (HFS) protocols on the R2 component of the trigeminal blink reflex [Mao, J.B. & Evinger, C (2001) J Neurosci., 21:RC151(1-4)]. Changes in the R2 component were tested by pairing three different priming stimulation protocols inducing long-term potentiation (LTP)-like or long-term depression (LTD)-like effects (LTP-HFS and LTD-HFS), or no change (CONTROL-HFS) with a subsequent test LTP-HFS. Additionally, to examine changes in the R2 component induced by nonspecific factors, two CONTROL-HFS sessions were paired. Priming LTP-, LTD- or CONTROL-HFS potentiated, inhibited or left unchanged the area of the R2 component. Regardless of the type of priming LTP-, LTD- or CONTROL-HFS, the test LTP-HFS induced negligible differences in the R2 component. When two CONTROL-HFS sessions were paired, the test CONTROL-HFS increased the latency and markedly reduced the duration and area of the R2 component. The analysis of the normalized data across the first three experimental sessions, corrected for the inhibitory effects found in the fourth experiment, showed that the test LTP-HFS potentiated the R2 component area of the trigeminal blink reflex only when preceded by a priming LTD-HFS. We propose that homosynaptic metaplasticity might operate in the brainstem circuitry of the blink reflex.

Theta-burst stimulation (TBS) is currently used for inducing long-lasting changes in primary motor cortex (M1) excitability. More information is needed on how M1 is involved in early motor learning (practice-related improvement in motor performance, motor retention and motor consolidation). We investigated whether inhibitory continuous TBS (cTBS) is an effective experimental approach for modulating early motor learning of a simple finger movement in healthy humans. In a short task, 11 subjects practised 160 movements, and in a longer task also testing motor consolidation ten subjects practised 600 movements. During both experiments subjects randomly received real or sham cTBS over the left M1. Motor evoked potentials were tested at baseline and 7 min after cTBS. In the 160-movement experiment to test motor retention, 20 movements were repeated 30 min after motor practice ended. In the 600-movement experiment motor retention was assessed 15 and 30 min after motor practice ended, motor consolidation was tested by performing 20 movements 24 h after motor practice ended. Kinematic variables - movement amplitude, peak velocity and peak acceleration - were measured. cTBS significantly reduced the practice-related improvement in motor performance of finger movements in the experiment involving 160 movements and in the first part of the experiment involving 600 movements. After cTBS, peak velocity and peak acceleration of the 20 movements testing motor retention decreased whereas those testing motor consolidation remained unchanged. cTBS over M1 degrades practice-related improvement in motor performance and motor retention, but not motor consolidation of a voluntary finger movement.

We investigated finger movements in patients with hand dystonia to compare the kinematics of repetitive individual and non-individual finger oppositions. We used an optoelectronic motion analysis system to record movements in 3-D space, and recorded three 5-second trials for each task, counting how many finger oppositions subjects carried out during each trial, and measured the duration and amplitude of flexions, extensions, and pauses. During tasks, normal subjects and patients carried out finger flexions faster than extensions, and invariably they paused longer before extension than before flexion. Patients were slower and paused longer than controls during both individual and non-individual oppositions. During individual finger movements, patients were disproportionately slow during extension and pause before extension. Patients with hand dystonia perform finger movements abnormally; they are affected predominantly during individual oppositions. This finding reflects the finer cortical control needed to promote and sustain this highly fractionated type of motor output, and points toward underactivity of the primary motor cortex in dystonia.

A retrospective analysis was performed on the records of 33 off-therapy parkinsonian patients. We analyzed the clinical score of three sequential upper limb movements: finger tapping, hand opening and closing, and forearm pronation and supination. The records showed that nearly all patients had difficulty in performing all three motor tasks, but movement scores showed that they found the sequential finger-tapping task significantly more difficult than the other two tasks. We suggest that parkinsonian patients find individual finger movements more difficult to execute than gross hand movements because--owing to their abnormal basal ganglia output--they lack the finer cortical control and greater facilitation that the finger task demands.

We examined the motor performance of Parkinson's disease patients and normal subjects during nonrepetitive and repetitive sequential tasks. Parkinson's disease patients took longer than normal subjects to complete the nonrepetitive task, the sequential drawing of a pentagon. In patients, movement times lengthened as the sequence neared completion. The amount of lengthening was similar in nonrepetitive and repetitive tasks (sequential alternating drawing of each side of the pentagon). In parkinsonian patients the slowing at the end of the sequential tasks does not appear to be influenced by whether the sequential task involves nonrepetitive or repetitive movements.

Blink and corneal reflexes were studied in 11 patients with Huntington's chorea and the results compared with the severity of the disease. The latency of the R2 component of the blink reflex was delayed and the duration of R2 and of the corneal reflex (CR) prolonged. A greater habituation of the R2 component was found in the patients with involuntary movements in the face, and in some patients a long-lasting depression of R2 was present. A correlation was found between: (a) severity of involuntary face movements and R2 and CR latency and (b) severity of involuntary movements in the neck and latency of R2.