Transition Phase

The recovery from spinal shock is reflected by an increase in the excitability of tendon tap reflexes and in muscle tone (assessed by the Ashworth scale) as well as more frequently occurring muscle spasms (assessed by the Penn spasm frequency scale).7 These clinical changes were associated in the electrophysiological recordings by an increase of F-wave persistence and flexor reflex activity.6 There was only a minor change in H-reflex excitability during this time period. It may be suggested that the increase in tendon tap reflex excitability is at least partially due to a recovery of alpha-MN and probably also of gamma-MN function mediating this reflex.

The increase in flexor reflex activity should be due not only to a recovery of alpha-MN excitability, but also to the function of spinal interneuronal circuits (see spinal shock). The fact that the flexor reflex is more difficult to elicit in healthy subjects than in paraplegic/tetraplegic patients28 indicates an increased excitability of interneuronal circuits some weeks after SCI. The pathway underlying the flexor reflex is a polysynaptic spinal one and allows the integration of inputs from muscles, joints and cutaneous afferents on common interneurons (review: Kiehn19).

The changes in flexor reflex excitability may at least partly be reflected in the appearance of muscle spasms. The increase in muscle tone may be due to a more general recovery of spinal neuronal (alpha-MN

and IN) activity. Nevertheless, for both clinical parameters reflecting recovery from spinal shock (Penn spasm frequency and Ashworth scale), it cannot be ruled out that other factors than the neuronal activity recorded here, as well as changes in muscle biomechanics, contribute to the development of spasticity.

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