Abstract

To elucidate the pathomechanism underlying persistent mirror movements (MM), we modelled the origin of electric brain activity associated with these movements. Movement-related cortical potentials (MRCP) in a group of subjects affected by persistent mirror movements were compared with those of a control group. The data of the normal subjects were best explained with two bilaterally active electric sources in the sensorimotor cortices with a clear preponderance of the hemisphere contralateral to the movement. In contrast, the MM subjects presented a fairly symmetric source activity in both hemispheres during unilateral intended movements. In the control group, the source representing the activity of the motor cortex ipsilateral to the moving finger reduced activity before the beginning of the movement; this was interpreted as an inhibition of the ipsilateral motor cortex during unilateral movement. In the MM group, however, this inhibition was not seen. Furthermore, while normal subjects demonstrated no relevant activity of an additional source placed near midline motor structures (supplementary motor area; SMA), subjects with MM showed considerable activity of this dipole source. These findings suggest that subjects with persistent MM have abnormal bilateral activation of the primary motor areas, probably together with an additional activation of mesial motor structures. This assumption fits well with the observation of an incomplete decussation of the pyramidal tract. The bilateral activation is then explained as a compensatory strategy in order to achieve sufficient force in the innervated target muscles.

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