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.

The central nervous system (CNS) takes advantage of a network of complex neural pathways and mechanisms in the control of normal human gait. One such mechanism is the use of afferent feedback from muscle, cutaneous and joint receptors. Our knowledge of the contribution of afferent information in human gait is still limited, although this has been an area of active research for many years (e.g. Dietz et al. 1985;Yang et al. 1991;Sinkjaer et al. 1996). Yang et al. (1991) and Sinkjaer et al. (1996) have shown that afferent-mediated feedback is used by the CNS in the control of gait when an unexpected stretch of the ankle extensors is imposed. More recently, Sinkjaer et al. (2000) provided evidence that during walking, up to 50 % of the background EMG from the soleus muscle can be attributed to afferent feedback. However, the relative importance of the separate afferent pathways may differ for the background locomotor EMG and the EMG that results from an imposed stretch.When the human soleus muscle is stretched in a seated subject, two distinct bursts, with average peak latencies of 59 and 86 ms are evident in the EMG (Toft et al. 1989). These bursts are often referred to as the short (SLR) and medium (MLR) reflex responses, respectively, and have also been labelled the M1 and M2 stretch reflex responses, respectively. The short latency response has an onset latency of approximately 40 ms and is attributed to monosynaptic excitation of spinal motoneurones from the large diameter group Ia afferent fibres (Taylor et al.Group II muscle afferents probably contribute to the medium latency soleus stretch reflex during walking in humans 1. The objective of this study was to determine which afferents contribute to the medium latency response of the soleus stretch reflex resulting from an unexpected perturbation during human walking.2. Fourteen healthy subjects walked on a treadmill at approximately 3.5 km h _1 with the left ankle attached to a portable stretching device. The soleus stretch reflex was elicited by applying small amplitude (~8 deg) dorsiflexion perturbations 200 ms after heel contact.3. Short and medium latency responses were observed with latencies of 55 ± 5 and 78 ± 6 ms, respectively. The short latency response was velocity sensitive (P < 0.001), while the medium latency response was not (P = 0.725).4. Nerve cooling increased the delay of the medium latency component to a greater extent than that of the short latency component (P < 0.005).5. Ischaemia strongly decreased the short latency component (P = 0.004), whereas the medium latency component was unchanged (P = 0.437).6. Two hours after the ingestion of tizanidine, an a 2 -adrenergic receptor agonist known to selectively depress the transmission in the group II afferent pathway, the medium latency reflex was strongly depressed (P = 0.007), whereas the short latency component was unchanged (P = 0.653).7. An ankle block with lidocaine hydrochloride was performed to suppress the cutaneous afferents of the foot and ankle. Neither the short (P = 0.453) nor m...

The total mechanical response to a stretch in a contracting muscle is the sum of the response from the properties of the fibres contracting prior to the stretch (intrinsic properties), the response from the passive tissues and the response from the stretch reflex-mediated contraction of the muscle fibres. The passive, the intrinsic and the reflex-mediated mechanical response to a 4 degrees stretch of the ankle extensors in both legs of nine spastic hemiparetic patients and, as control, the left ankle extensors in eight healthy subjects were measured. The stretch was imposed at the top of a maintained contraction, which was varied from zero to maximal contraction. The torque increments, measured 200 ms after stretch, were converted into stiffness by dividing by the amplitude of the stretch. We found that the reflex stiffness of the spastic and contralateral leg was within the normal range of the reflex stiffness in healthy subjects, and that the passive stiffness of the spastic and the contralateral leg is larger than the passive stiffness in healthy subjects, whereas the intrinsic stiffness is unchanged in the spastic extensor muscles.

The cerebral activation during bicycle movements was investigated by oxygen-15-labelled H2O positron emission tomography (PET) in seven healthy human subjects. Compared to rest active bicycling significantly activated sites bilaterally in the primary sensory cortex, primary motor cortex (M1) and supplementary motor cortex (SMA) as well as the anterior part of cerebellum. Comparing passive bicycling movements with rest, an almost equal activation was observed. Subtracting passive from active bicycle movements, significant activation was only observed in the leg area of the primary motor cortex and the precuneus, but not in the primary sensory cortex (S1). The M1 activation was positively correlated (alpha=0.75-0.85, t=6.4, P<10(-5)) with the rate of the active bicycle movements. Imagination of bicycle movements compared to rest activated bilaterally sites in the SMA. It is suggested that the higher motor centres, including the primary and supplementary motor cortices as well as the cerebellum, take an active part in the generation and control of rhythmic motor tasks such as bicycling.