Abstract
Patients with an acute complete spinal cord injury (SCI) present a syndrome called "spinal shock". During spinal shock the loss of tendon reflexes and flaccid muscle tone is associated with a low persistence of F-waves and loss of flexor reflexes while H-reflexes are well elicitable. When clinical signs of spasticity become established, the electrophysiological parameters show little change. The divergent course of clinical signs of spasticity in their possible neuronal correlates indicate the occurrence of non-neuronal changes contributing to spasticity. - When signs of spinal shock had disappeared in patients with incomplete and complete paraplegia a locomotor pattern can be induced and trained under conditions of body unlaoding using a moving treadmill. In complete and incomplete paraplegic patients an increase of gastrocnemius electromyographic activity occurs during the stance phase of a step cycle with a daily locomotor training, coincident with a significant decrease of body unloading. In contrast to this, neither clinical nor electrophysiological examination scores improve. The locomotor pattern depends on the level of lesion: the higher the level of spinal cord lesion the more 'normal' is the locomotor pattern. This suggests that neuronal circuits underlying 'locomotor pattern generation' in man is not restricted to any specific level of the spinal cord, but extends from thoraco-lumbal to cervical levels.
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