In clinical practice the dominant view is that the signs of exaggerated tendon tap reflexes associated with muscle hypertonia are responsible for the spastic movement disorder. Consequently, most anti-spastic treatments are directed at reducing reflex activity. During the last years an increasing body of evidence suggests a discrepancy between clinical spasticity and spastic movement disorder.This is primarily due to the different role reflexes play in the passive and active condition, respectively. Today we know that a central motor lesion is associated with a loss of supraspinal drive and a defective utilization of afferent input with an impaired behaviour of short-and longlatency reflexes. This leads to a paresis and a mal-adaptation of the movement pattern.Secondary changes in mechanical muscle fibre, collagen tissue and tendon properties (e.g. loss of sarcomers; sub-clinical contractures) result in spastic muscle tone, which at part compensates for paresis. This allows functional movements on a simpler level of organisation. Anti-spastic drugs can accentuate paresis and therefore should be applied with caution in mobile subjects.

1. The purpose of this study was to evaluate the mechanical response to stretch in normal human ankle dorsiflexors at different levels of voluntary contraction. In an active muscle, the total mechanical response is the sum of the intrinsic response from the contractile apparatus, the response from passive tissues, and the reflex mediated response. Each of these components was investigated. 2. The total incremental stiffness was defined as the ratio between the torque increment and the amplitude of the stretch. In 14 subjects the total stiffness increased from approximately 0.6 N.m/deg to approximately 2.5 N.m/deg at 50% of MVC and remained constant (+/- 10%) from 30 to 80% of MVC. 3. The contribution to incremental stiffness from intrinsic muscle properties was measured during electrical stimulation of the deep peroneal nerve at 7-50 Hz. Intrinsic stiffness increased linearly with torque from approximately 0.5 N.m/deg to approximately 2.5 N.m/deg at 80% of MVC. 4. The reflex component (total minus intrinsic stiffness) had a maximum of 0.5-1.5 N.m/deg at 30-50% of MVC and was approximately zero at no and maximal contraction. For intermediate levels of contraction the reflex increased the stiffness with 40-100% of the intrinsic stiffness in this flexor muscle. 5. The reflex contribution to total stiffness began approximately 50 ms after onset of stretch and peaked 150-300 ms after onset of stretch. 6. Total, intrinsic, and reflex mediated stiffness were all nearly independent of the amplitude of stretch in the range from 2 to 7 degrees. The higher stiffness observed for 1 degree stretches could be due to "short range stiffness" of the cross bridges. 7. Stretching of a contracting muscle generates large force increments even for moderate amplitudes of stretch. Approximately half of this force increment is due to the stretch reflex, which makes the muscle stiffer than predicted from the intrinsic stiffness. These findings in human flexor muscles are surprisingly similar to previous findings in extensor muscles of the decerebrate cat.

Sensory feedback plays a major role in the regulation of the spinal neural locomotor circuitry in cats. The present study investigated whether sensory feedback also plays an important role during walking in 20 healthy human subjects, by arresting or unloading the ankle extensors 6 deg for 210 ms in the stance phase of gait. During the stance phase of walking, unloading of the ankle extensors significantly (P < 0·05) reduced the soleus activity by 50 % in early and mid‐stance at an average onset latency of 64 ms. The onset and amplitude of the decrease in soleus activity produced by the unloading were unchanged when the common peroneal nerve, which innervates the ankle dorsiflexors, was reversibly blocked by local injection of lidocaine (n= 3). This demonstrated that the effect could not be caused by a peripherally mediated reciprocal inhibition from afferents in the antagonist nerves. The onset and amplitude of the decrease in soleus activity produced by the unloading were also unchanged when ischaemia was induced in the leg by inflating a cuff placed around the thigh. At the same time, the group Ia‐mediated short latency stretch reflex was completely abolished. This demonstrated that group Ia afferents were probably not responsible for the decrease of soleus activity produced by the unloading. The findings demonstrate that afferent feedback from ankle extensors is of significant importance for the activation of these muscles in the stance phase of human walking. Group II and/or group Ib afferents are suggested to constitute an important part of this sensory feedback.

In human subjects, stretch applied to ankle dorsiflexors elicited three bursts of reflex activity in the tibialis anterior (TA) muscle (labelled M1, M2 and M3) at mean onset latencies of 44, 69 and 95 ms, respectively. The possibility that the later of these reflex bursts is mediated by a transcortical pathway was investigated. The stretch evoked a cerebral potential recorded from the somatosensory cortex at a mean onset latency of 47 ms in nine subjects. In the same subjects a compound motor‐evoked potential (MEP) in the TA muscle, evoked by magnetic stimulation of the motor cortex, had a mean onset latency of 32 ms. The M1 and the M2 reflexes thus had too short a latency to be caused by a transcortical pathway (minimum latency, 79 ms (47 + 32)), whereas the later part of the M2 and all of the M3 reflex had a sufficiently long latency. When the transcranial magnetic stimulation was timed so that the MEP arrived in the TA muscle at the same time as the M1 or M2 reflexes, no extra increase in the potential was observed. However, when the MEP arrived at the same time as the M3 reflex a significant (P < 0.01) extra‐facilitation was observed in all twelve subjects investigated. Peaks evoked by transcranial magnetic stimulation in the post‐stimulus time histogram of the discharge probability of single TA motor units (n= 28) were strongly facilitated when they occurred at the same time as the M3 response. This was not the case for the first peaks evoked by electrical transcranial stimulation in any of nine units investigated. We suggest that these findings are explained by an increased cortical excitability following TA stretch and that this supports the hypothesis that the M3 response in the TA muscle is ‐ at least partly ‐ mediated by a transcortical reflex.

1. The modulation of the short-latency stretch reflex during walking at different walking speeds was investigated and compared with the stretch reflex during standing in healthy human subjects. 2. Ankle joint stretches were applied by a system able to rotate the human ankle joint during treadmill walking in any phase of the step cycle. The system consisted of a mechanical joint attached to the subject's ankle joint and connected to a motor placed beside the treadmill by means of bowden wires. The weight of the total system attached to the leg of the subject was 900 g. 3. The short-latency soleus stretch reflex was modulated during a step. In the stance phase, the amplitude equaled that found during standing at matched soleus background electromyogram (EMG). In the transition from stance to swing, the amplitude was 0 in all subjects. In late swing, the stretch reflex amplitude increased to 45 +/- 27% (mean +/- SD) of the maximal amplitude in the stance phase (stretch amplitude 8 degrees, stretch velocity 250 degrees/s). 4. The onset (42 +/- 3.2 ms) and peak latencies (59 +/- 2.5 ms) of the stretch reflex did not depend on the phase in the step cycle at which the reflex was elicited. 5. When the ankle joint is rotated, a change in torque can be measured. The torque measured over the first 35 ms after stretch onset (nonreflex torque) was at a maximum during late stance, when the leg supported a large part of the body's weight, and at a minimum during the swing phase. At heel contact the nonreflex torque was 50% of its maximal value. 6. During the stance phase the maximal EMG stretch reflex had a phase lead of approximately 120 ms with respect to the maximal background EMG and a phase lead of approximately 250 ms with respect to the maximal nonreflex torque. 7. The constant latency of the stretch reflex during a step implied that the ankle extensor muscle spindles are always taut during walking. 8. The relatively high amplitude of the stretch reflex in late swing and at heel contact made it likely that the stretch reflex contributed to the activation of the ankle extensor muscles in early stance phase.