Motoric disorders in spinel lesions

A spinal cord lesion is experienced by the patient as a movement disorder o f the legs, for example as a gait disorder. The neurological examination in dicates on the basis of exaggerated tendon top reflexes an enhanced resista nce of the non-activated leg muscles to stretch by the examiner, that the m ovement disorder underlies a spastic paresis. This combination of symptoms and clinical (physical) signs suggests that the exaggerated tendon tap refl exes are responsible for muscle hypertonia and the latter causes the moveme nt disorder. However, electromyographic examinations during the movement sh ow that the exaggerated short latency reflexes are associated with a loss o r attenuation of the functionally essential polysynaptic spinal reflexes. I n the case of an impaired (spasticity) or immature (small children) suprasp inal control, a loss of inhibition of monosynaptic stretch reflexes takes p lace in combination with a reduced facilitation of polysynaptic spinal refl exes. The development of tension at the tonically active calf muscles in pa tients with spastic paresis during gait occurs independently of spinal refl ex activity. According to electrophysiological and histological observation s one can assume that a transformation of motor units with the consequence of simpler and less adapted regulation of muscle tone allows for movements with body support, such as gait. The reduction of muscle tone achieved by a nti-spastic drugs is usually associated with paresis and may therefore hamp er locomotion. The locomotor training represents a new attempt to improve t he mobility of patients with incomplete paraplegia. It includes an activati on of neuronal circuits within the spinal cord below the level of lesion. I n incompletely paraplegic patients a coordinated leg muscle activation patt ern and corresponding leg movements can be released and can be trained with the patient standing on a treadmill with partial body weight support. An i mprovement of this training of spinal cord locomotor centres can be expecte d from the release of spinal reflexes and the local application of noradren ergic substances.