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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Modulation of electromyographic activity of wrist flexor and extensor muscles in patients with writer's cramp.

Patients with writer's cramp have two well-recognized neurophysiological abnormalities: reduced reciprocal inhibition of the wrist flexor motoneurons at rest, and increased cocontraction of antagonist muscles of the forearm during voluntary activity. In this article we present evidence for an impaired integration of sensory inputs into the voluntary motor activity during performance of a force-related task in patients with writer's cramp. Normal (control) subjects and patients activated wrist flexor and extensor muscles to maintain a predetermined level of force. Electrical stimuli were applied to median and radial nerve afferents and the modulatory effects induced in the electromyographic (EMG) activity were measured. For each muscle studied and nerve stimulated, we defined a characteristic sequence of excitatory (E) and inhibitory (I) phases of modulation of the averaged rectified EMG activity in control subjects. E and I phases were thought to represent excitation and inhibition, respectively, of the corresponding motoneuronal pool to homonymous or reciprocal afferent inputs. There were no differences between control subjects and patients regarding the level of background EMG activity in the agonist muscles during wrist flexion or wrist extension. In the agonist wrist flexors, patients had reduced homonymous and reciprocal inhibition. In the agonist wrist extensors, patients had reduced reciprocal excitation and reciprocal inhibition. These results are compatible with an abnormal CNS processing of the inputs generated by external stimuli during voluntary contraction of wrist flexor and extensor muscles. Defective integration of inputs from peripheral nerve afferents into the command for voluntary movement may partly underlie the pathophysiology of the motor dysfunction in patients with writer's cramp.[1]


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