It was demonstrated that the soleus H-reflex was depressed for more than 10 s following a preceding passive dorsiflexion of the ankle joint. This depression was caused by activation of large-diameter afferents with receptors located in the leg muscles, as an ischaemic block of large-diameter fibres just below the knee joint abolished the depression, whereas a similar block just proximal to the ankle joint was ineffective. The depression of the H-reflex was not caused by changes in motoneuronal excitability, as motor-evoked potentials by magnetic brain stimulation were not depressed by the same passive dorsiflexion. Therefore it was concluded that the long-lasting depression is due to mechanisms acting at presynaptic level. The transmission of the monosynaptic Ia excitation from the femoral nerve to soleus motoneurones was not depressed by the ankle dorsiflexion. The depression thus seems to be confined to those afferents that were activated by the conditioning dorsiflexion. In parallel experiments on decerebrate cats, more invasive methods have complemented the indirect techniques used in the experiments on human subjects. A similar long-lasting depression of triceps surae monosynaptic reflexes was evoked by a preceding conditioning stimulation of the triceps surae Ia afferents. This depression was accompanied by a reduction of the monosynaptic Ia excitatory postsynaptic potential recorded intracellularly in triceps surae motoneurones, but not by changes in the input resistance or membrane potential in the motoneurones. Stimulation of separate branches within the triceps surae nerve demonstrated that the depression is confined to those afferents that were activated by the conditioning stimulus. This long-lasting depression was not accompanied by a dorsal root potential. It is concluded that the long-lasting depression is probably caused by a presynaptic effect, but different from the “classical” GABAergic presynaptic inhibition which is widely distributed among afferent fibres and accompanied by dorsal root potentials. It is more probably related to the phenomenon of a reduced transmitter release from previously activated fibres, i.e. a homosynaptic post-activation depression. The consequences of this post-activation depression for the interpretation of results on spinal mechanisms during voluntary movements in man are discussed.

On the mechanism of the post-activation depression of the H-reflex in human subjects

The pathophysiology of spasticity is a complex subject and one frequently avoided by clinicians. Spasticity and the other features, positive and negative, of the upper motor neurone (UMN) syndrome arise from disruption of certain descending pathways involved in motor control. Hyperexcitability of spinal reflexes forms the basis of most of the positive clinical signs of the UMN syndrome, which have in common excessive muscle activity. These spinal reflexes may be divided into two groups, proprioceptive reflexes and nociceptive/cutaneous reflexes. The clasp-knife phenomenon combines features of both groups, at least in the lower limbs. Contractures are a well known and feared complication of the UMN syndrome, reducing the range of motion of a joint. There has been a recent investigation of the relationship between the stretch reflex hyper excitability of spasticity and contractures. Spasticity does not appear to exist in contracting agonists and would not really interfere with movement.

Upper Motor Neurone Syndrome and Spasticity: Neurophysiology of spasticity

Clonus in man: a rhythmic oscillation maintained by a reflex mechanism

Neural modulation of muscle contractile properties during fatigue: afferent feedback dependence

We conducted two types of experiments to assess the validity of the H-reflex recovery test, using double stimulation to test soleus motoneuron pool excitability in healthy and spastic subjects. One type dealt with the mechanical effect of the conditioning H reflex on the ankle joint; the other type with the effect of change in reflex size. The mechanical effect was tested both with the ankle joint fixed (FX) and free to move (FR). Differences between FX and FR conditions commenced with relaxation of soleus muscle contraction by the conditioning H reflex. In the FR condition, abrupt facilitation occurred, and changed to marked depression. We conclude that specific facilitation and inhibition in the FR condition were secondary effects of group Ia inflows caused by the ankle extensor muscle stretching on relaxation. In some spastic patients as well as in controls, facilitation due to the mechanical effect in the FR condition was observed despite the FX condition. The effects of systematic changes on soleus H-reflex size were investigated at conditioning-test intervals of 80 ms, so as to avoid mechanical effects. When conditioning and test reflexes were the same size, the amount of recovery increased as the H-reflex size increased. Comparison of the relation between amount of recovery and H-reflex size, expressed as a percentage of Mmax, showed no significant difference between the two groups. We speculate that the stronger recovery of spasticity mentioned in previous literature may have resulted from the fact that relatively greater H reflexes were tested in those studies. In conclusion, the present study indicates that double stimulation is not appropriate for assessing spinal motoneuron pool "excitability increase" in spasticity.

Reassessment of H-reflex recovery curve using the double stimulation procedure.

The recovery curve of the soleus H reflex, evoked by stimulation of the tibial nerve in the popliteal fossa, was studied by applying an electrical conditioning stimulus to the inferior soleus nerve. Under these conditions a long-latency facilitatory phase could be superimposed on a long-lasting inhibition, the excitability cycle being therefore similar to that obtained by means of a paired shock to the tibial nerve. In order to identify the afferent fibres responsible for the effects observed, various conditioning stimulus strengths and nerve compression were used. A low-intensity stimulus induced only a facilitatory phase, while the inhibition promptly ensued on increasing stimulus strength, which remained however subliminal for activation of group II fibres. During calf compression exerted by a sphygmomanometer cuff placed between the conditioning and test stimuli, the facilitatory effects disappeared within 10 to 15 min, and the inhibitory ones disappeared within 25 to 30 min from the onset of compression. Tonic voluntary contraction enhanced both the inhibition and the facilitation. In a subject with complete spinal section, both inhibitory and facilitatory phases could be demonstrated on low-intensity stimulation. The present data, and previous results of ours, allow the following conclusions. (1) Facilitation and inhibition are produced by fibres likely belonging to group Ia spindle afferents. (2) Both effects are of spinal origin. (3) The spinal circuits mediating the effects may be modulated by descending commands. (4) The facilitation is sustained by tonic supraspinal influences while the inhibition is independent of it. Arguments are proposed against the hypotheses that the inhibition be due to transmitter depletion or to presynaptic mechanisms.

The H reflex recovery curve reinvestigated: low-intensity conditioning stimulation and nerve compression disclose differential effects of presumed group Ia fibres in man.

Rossi A

Papers

The H reflex recovery curve reinvestigated: low-intensity conditioning stimulation and nerve compression disclose differential effects of presumed group Ia fibres in man.