The prolonged TI suggests an abnormal activation of interhemispheric connections between the motor cortices and may be related to previously reported pathology of the corpus callosum in schizophrenic patients.
In a patient with a familial form of paroxysmal exertion induced dyskinesia (PED), the eYcacy of diVerent stimuli and manoeuvres in triggering dystonic attacks in the arm was studied. As a new approach, transcranial magnetic stimulation (TMS) of the motor cortex was used to trigger motor paroxysms and to monitor cortical excitability during attacks. Motor paroxysms could be provoked by muscle vibration, passive movements, TMS, magnetic stimulation of the brachial plexus, and electrical nerve stimulation. Sham stimulation over the motor cortex and thermal and tactile cutaneous stimuli were ineVective in triggering attacks. It is concluded that dystonic attacks are triggered by proprioceptive aVerents rather than cutaneous stimuli or the descending motor command itself. Outside the attacks, motor cortical excitatory and inhibitory neuronal mechanisms as assessed by TMS (response threshold and amplitudes, duration of the contralateral and ipsilateral silent period, corticocortical inhibition, and facilitation) were normal, which underlines the paroxysmal character of the disorder. (J Neurol Neurosurg Psychiatry 2001;70:247-251) Keywords: magnetic stimulation; dystonia; magnetic stimulationIn paroxysmal exertion induced 1 or excercise induced dystonia (PED), 2-4 which was formerly termed the intermediate form of paroxysmal dystonic choreoathetosis, 5 6 dystonic attacks are precipitated by prolonged muscular exertion and last for 5 to 30 minutes. To investigate the pathophysiology of the paroxysmal motor phenomena, diVerent stimuli and manoeuvres were studied in a patient with familial PED to investigate their eYcacy in triggering dystonic attacks. Besides conventional ways to produce cutaneous and proprioceptive aVerents such as touch, voluntary muscle contraction, passive limb movement, electrical nerve stimulation, and muscle vibration, also magnetic stimulation of the brachial plexus and motor cortex were performed as a new approach. Transcranial magnetic stimulation (TMS) was also used to monitor changes of cortical excitability during PED. In intervals between paroxysms the function of intracortical inhibitory and excitatory mechanisms was also investigated with the paired pulse stimulation technique 7 and by measuring the duration of the postexcitatory silent period and of the interhemispheric inhibition of tonic muscle contraction. 8 Results of gait analysis and perfusion SPECT of the patient have been published separately.
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Case reportThe 40 year old man and his son were the only members of a family with the same type of PED. PED of the legs and arms was present since the age of 7 and 14 respectively. In the legs, PED was elicited by walking about 1 km. In the arms, a dystonic contraction of the forearm muscles could be evoked by forceful manual work or prolonged writing. The attacks started with a feeling of stiVness in the hand and forearm, followed by abduction of the thumb, then of the fifth finger, and then by tonic cocontraction of the forearm flexors and extensors resulting in a slight wri...
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