Abstract

 Introduction

 Materials
& Methods

 Results

 Discussion
& Conclusion

 References
 
 
 
 

Discussion
Board

Spastic hypertonia as a problem
Many insults to the central nervous system result in an upper motor neuron syndrome from which spastic hypertonia is a hallmark. Spastic hypertonia has been shown to be related to an increase in passive stiffness (Sinkjær & Magnussen, 1994) and decreased reflex threshold (Katz & Rymer, 1989).  Even though the effect of spastic hypertonia (impairment) has never been evaluated on the disability nor on the social and economical impact occurring with the upper motor neuron syndrome it is thought to be a chronic disabling situation with a major social and economical impact on the society and on the individual. Management of spastic hypertonia can be done by different modalities acting either exclusively on the joints (i.e. mechanical orthosis) to modalities acting only on the central nervous system (i.e. baclofen). Alternatives to pharmacological and surgical management of spastic hypertonia are desirable for several reasons: in pharmacological management an effective therapeutic dosage cannot always be reached because of side-effects, in surgical management the effect are permanent and may not be adapted to changes occurring in the clinical status of the patient and, in both cases, some patients refuse either kind of  treatment.

Mechanismes involved in spastic hypertonia
The decreased reflex threshold found with spastic hypertonia has been linked to an increase in motorneuronal excitability (Garcia-Mullin and Mayer, 1972; Magladery et al., 1952; Olsen and Diamantopoulos, 1967; Sax and Johnson, 1980, Takamori, 1967; Yap, 1967). This increased motorneuronal excitability seems to be related to a decreased presynaptic inhibition (Delwaide, 1973; Faist et al., 1994) and absent reciprocal inhibition (Crone et al., 1994). However, a recent study (Kagamihara et al.,1998) using a more controlled amplitude of the conditioning stimulus showed similar values of presynaptic inhibition for spastic and normals participants. Other changes occurring throughout the nervous system could influence this change in motorneuronal excitability as seen by the modifications of the brain motor output to hand muscles studied after a stroke by transcranial magnetic stimulation showing a higher excitability threshold in the affected hemisphere which decreased, in correlation with clinical measures, within the first 4 months post-stroke (Traversa et al, 1997; Cicinnelli et al, 1997). Furthermore, prolongation of the postexcitatory inhibition following transcranial magnetic stimulation can also be seen after a stroke (Braune and Fritz, 1995).

Inhibition of the SOL H-reflex 
By stimulating the deep peroneal nerve just below the motor threshold of the tibialis anterior, Crone et al. (1994) found that disynaptic reciprocal inhibition depressed the conditioned H-reflex by 15%. However, this disynaptic reciprocal inhibition was not found in a group of 39 spastic multiple sclerosis patients, except for four patients that were using a foot-drop stimulator daily. In contrast, a facilitation of the reflex was seen at conditioning-test intervals between 4 and 8 ms. Capaday et al. (1995) showed reciprocal inhibition by presynaptic inhibitory mechanisms of the soleus motor output in healthy subjects when stimulating the common peroneal nerve. The depression of soleus EMG as a response to the conditioning stimulation had a latency of approximately 40 ms. The inhibition increased with contraction level in the same way for standing and the stance phase of gait. Inhibition of the soleus H-reflex is not only possible by stimulation of Ia afferents, but can also be obtained when stimulating cutaneous nerves. Fung and Barbeau (1994) found significant inhibition of the soleus H-reflex in all phases of the gait cycle in healthy subjects, when stimulating the ipsilateral medial plantar arch at 2.5 - 3 times sensory threshold and a conditioning test delay of approximately 45 ms. At this stimulation site, mainly sensory nerve fibers are activated from cutaneous and mechanoreceptors of the sole. In moderately and severely impaired spastic paretic patients this conditioning stimulation restored a near normal phasic modulation of the H-reflex.Also, stimulation of the sural, posterial tibial and superficial peroneal nerves at the ankle during gait results in reflex responses in muscles in the ipsilatreal leg, which are dependent on the phase of the gait cycle and on the nerve which is stimulated (Van Wezel et al, 1997, Zehr et al, 1997).

The presynaptic inhibition of the SOL H-reflex and stretch reflex 
A previous study showed that the soleus stretch reflex cannot be inhibited by the usual techniques using presynaptic inhibition (Morita et al, 1998). In this study it was shown that an electrical stimulation to the deep peroneal nerve with an intensity of 0,9 times the motor threshold of the Tibialis Anterior inhibited the H-reflex and T-reflex of the soleus muscle but not the soleus stretch reflex evoked by an imposed ankle dorsiflexion. It was concluded that the modulation of the stretch reflexes could be different from the modulation of the H-reflex. It is suggested that this different sensitivity to presynaptic inhibition is caused by a difference in the shape and composition of the excitatory postsynaptic potentials underlying the two reflexes. This difference may be explained by a different composition and/or temporal dispersion of the afferent volleys evoked by electrical and mechanical stimuli.

Inhibition of the SOL stretch reflex
Apkarian and Naumann (1991) found that the soleus stretch reflex could be inhibited in healthy subjects by a conditioning stimulation applied to the deep peroneal nerve at a level which just caused a small twitch in the tibialis anterior. This inhibition was not consistently observed in six spastic patients with varying neuromuscular disorders. The optimal conditioning test interval was found to be 160 ms on average, which is much larger than found for disynaptic reciprocal inhibition in H-reflex studies (2 ms; Crone et al, 1987, 1994), as well as for presynaptic inhibition (25-60 ms).
Studies have shown the potentially beneficial antispastic effects of prolonged repetitive stimulation of peripheral nerves (Levin and Hui-Chan 1992, Hui-Chan and Levin 1993, Nielsen et al. 1995, 1996), but because of variations in patients, differences in stimuli protocols and stimulus location, and uncertainties regarding quantification of spastic hypertonia, no clear scientific effect of repetitive stimulation has been provided. Moreover, the neural mechanisms underlying the antispastic effects are completely unknown. More knowledge about the mechanisms could greatly accelerate the development of new or improved stimulation methods.

Mechanisms involved in the inhibition of the SOL stretch reflex
The neural mechanisms of the reduction in spastic hypertonia by electrical and magnetic stimulation are not known. Long term depression (LTP) of motoneuron excitability could induced by numerous mechanisms like changes in the propriospinal system resulting in a depression when cutaneous afferents are excited by electrical stimulation (Alstermark et al., 1984), or be mediated via primary afferents since recent studies have suggested that long-term synaptic plasticity mediated via primary afferents may help explaining the long-term reduction in stretch reflex responsiveness after cutaneous stimulation. Other results suggest that a presynaptic mechanism might be responsible for the decreased reflex after repetitive stimulation (Dewald et al. 1996, Nielsen and Sinkjær 1995). Besides mechanisms in the spinal cord, supraspinal mechanisms could be involved as well, which might be confirmed by the fact that no long term effects were found in spinal cord injured subjects (Robinson et al. 1988).
 

The objectives of this study were:
1. Explore the inhibition of the soleus stretch reflex caused by an electrical conditioning stimulus to different nerve of the lower limb.
2. Explore the characteritics of the conditioning of the soleus stretch reflex by an electrical stimulus to the common peroneal nerve.