Spastic State

Clinically, the development of the spastic syndrome is characterized by exaggerated muscle tendon tap reflexes, increased muscle tone and involuntary muscle contractions. The onset of spastic signs is difficult to determine because there is a smooth transition to a clearly established spasticity.

During this stage, both M-wave and flexor reflex amplitudes remained approximately stable in tetraplegic or decreased in amplitude in paraplegic patients, i.e. developed opposite to the clinical signs.6 The latter observation was not due to a change in threshold, as the decrease in flexor reflex amplitude was the same with higher stimulation intensity (3 X instead of 2 X MT). The slight increase of H/M ratio, which is in line with an earlier study,23 might contribute to exaggerated tendon tap reflexes. However, this increase, which was thought to be well correlated with the spastic state, must be considered cautiously: (1) the high H/M ratio can represent a decrease of M-wave (as found here) rather than an increase in reflex excitability; (2) short latency reflex hyperexcitability was shown to be little related to spastic muscle tone.29

The fact that the decrease of M-wave and flexor reflex amplitude was more pronounced in paraplegic than in tetraplegic patients indicates that several weeks after a SCI secondary degenerations of spinal tracts occur, including pre-motoneu-ronal circuits and alpha-MN. One may argue that some of the tetraplegic patients were sensory incomplete. However, there was no difference in flexor reflex amplitudes between sensory complete and incomplete, and chronic complete tetraplegic patients.

The decline of M-wave amplitude (i.e. loss of alpha-MN) was about equally distributed over all paraplegics, i.e. was little related to the decrease in flexor reflex excitability. Also, direct damage of alpha-MN as an underlying cause is rather unlikely, because M-wave amplitude increased up to the fourth week after SCI. Furthermore, entrapment of peripheral nerves could largely be excluded by electrophysiological examinations. Therefore, secondary degenerations are likely to depend on the level of the lesion, i.e. are less pronounced with a higher level of lesion.

On the basis of the observations made in the study of Hiersemenzel et al,6 clinical signs of increasing spasticity, such as muscle tone and spasms, can hardly be related to the electrophysiological recordings. Secondary changes of motor units might contribute to the syndrome of spasticity, especially in respect of muscle tone and spasms.

Several studies claim that 'peripheral changes' (e.g. chronic transformation of muscle in spasticity) contribute to the increased muscle tone.30,31 A decrease of M-wave in patients with a SCI32 or those with a cerebral lesion33 indicates an affection of spinal MN in the case of a disconnection from supraspinal input. Furthermore, signs of denerva-tion are reported to occur during the first 2 months after SCI.34 It has become obvious during recent years that, following a central motor lesion, changes in mechanical muscle fiber properties occur starting early after a lesion with the consequence of a significant contribution to muscle tone in the active (review: Dietz35) and passive muscles36 (review: O'Dwyer and Ada29).

This study can only give a limited view of the neuronal adaptations occurring after a SCI. Spinal neuronal networks and reflex mechanisms may remain which were not assessed by our electro-physiological recordings. Therefore, the correlations made with the clinical signs have to remain to some extent speculative. Nevertheless, some of the results may be helpful for a better understanding of patho-physiological changes underlying spinal shock and the transition to the spastic syndrome with consequences for appropriate treatment.

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