Motoneurone Dysfunction in Patients with Hemiplegie Atrophy

THE nature of the mechanism responsible for the wasting of muscles in patients after lesions of the upper moto-neurone has been the subject of many studies^1,2 and various possibilities are summarized in Fig. 1. The simplest mechanism would be disuse alone; but atrophy might also result from disturbed blood flow in muscles of paralysed limbs or from a secondary arthritis. Another possibility is that an upper moto-neurone lesion deprives muscle of a trophic influence which is normally exerted, through an unspecified route, by the pre-central or postcentral gyrus. Finally, the upper motoneurone lesion may cause secondary changes in lower motoneurones which, in turn, affect muscles. The most widely held opinion is that wasting results from disuse only³, but we have findings which demonstrate that this supposition is incorrect. Instead it seems probable that the most important single factor in the genesis of atrophy is denervation of muscle fibres secondary to disturbed lower motoneurone function.