Abnormal responses to paired magnetic transcramai stimuli in de novo Parkinson's Disease patients are reversed by Apomorphine

M. Pierantozzi, Lantomo Vy, A. Peppe, P. Stanzione

Research output: Contribution to journalArticlepeer-review


In Parkinson's Disease (PD) the excitability of the motor cortex may be modified because the cerebral cortex is a primary target for the output of the basal ganglia. In our study we investigated the changes of motor pathway excitability, induced by trancranial magnetic stimulation using paired stimuli (conditioning and test stimulus), in 19 de novo PD patients and 15 age-matched normal subjects. A circular magnetic coil was used to deliver paired magnetic stimuli over the scalp position for eliciting a motor evoked potentials (MEPs) in the controlateral abductor pollicis brevis (APB). We used selected interstimulus intervals (ISIs) between 250-20 msec. The stimulus intensit) was suprathreshold (120%). It has been calculated the amplitude of the MEP as a peak-to-peak measurement expressed as a percentage of an unconditioned control response. All results were analyzed using the two-way ANOVA. At ISIs between 60-80 msec the PD patients test responses were less inhibited compared with normal subjects. To evaluate the relationship between these neurophysiological data and the function of the dopamincrgic system, PD patients were recorded during administration of a dopamino-agonist drug, apomorphine, through an infusion pump (3 mg-h). Apomorphine induced an increased of motor cortical inhibition at ISI between 40 and 100 msec. The responsiveness of motor cortices to suprathreshold magnetic stimuli and the effects of apomorphine suggest that dopaminergic modulation of cortical activity, most probably at basal ganglia level, is involved in the modulation of excitability of the motor cortex.

Original languageEnglish
Pages (from-to)50
Number of pages1
JournalItalian Journal of Neurological Sciences
Issue number4
Publication statusPublished - 1997

ASJC Scopus subject areas

  • Neuroscience(all)
  • Clinical Neurology


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