Spasticity is a term, which was introduced to describe the velocity-sensitive increased resistance of a limb to manipulation in subjects with lesions of descending motor pathways. This distinguishes spasticity from the changes in passive muscle properties, which are often seen in these patients, but are not velocity-sensitive. Increased excitability of the stretch reflex is thus a central component of the definition of spasticity. This review describes changes in cellular properties and transmission in a number of spinal reflex pathways, which may explain the increased stretch reflex excitability. The review focuses mainly on results derived from the use of non-invasive electrophysiological techniques, which have been developed during the past 20-30 years to investigate spinal neuronal networks in human subjects, but work from animal models is also considered. The reflex hyperexcitability develops over several months following the primary lesion and involves adaptation in the spinal neuronal circuitries caudal to the lesion. In animal models, changes in cellular properties (such as 'plateau potentials') have been reported, but the relevance of these changes to human spasticity has not been clarified. In humans, numerous studies have suggested that reduction of spinal inhibitory mechanisms (in particular that of disynaptic reciprocal inhibition) is involved. The inter-subject variability of these mechanisms and the lack of objective quantitative measures of spasticity have impeded disclosure of a clear causal relationship between the alterations in the inhibitory mechanisms and the stretch reflex hyperexcitability. Techniques which make such a quantitative measure possible as well as longitudinal studies where development of reflex excitability and changes in the inhibitory mechanisms are followed over time are in great demand.

2. TMS of low intensity (below threshold for a motor-evoked potential, MEP) produced a suppression of ongoing EMG activity during walking. The average latency for this suppression was 40·0 ± 1.0 ms. At slightly higher intensities of stimulation there was a facilitation of the EMG activity with an average latency of 29.5 ± 1.0 ms. As the intensity of the stimulation was increased the facilitation increased in size and eventually a MEP was clear in individual sweeps.3. In three subjects TMS was replaced by electrical stimulation over the motor cortex. Just below MEP threshold there was a clear facilitation at short latency (~28 ms). As the intensity of the electrical stimulation was reduced the size of the facilitation decreased until it eventually disappeared. We did not observe a suppression of the EMG activity similar to that produced by TMS in any of the subjects.4. The present study demonstrates that motoneuronal activity during walking can be suppressed by activation of intracortical inhibitory circuits. This illustrates for the first time that activity in the motor cortex is directly involved in the control of the muscles during human walking.

Study design: Review of the literature on the validity and reliability of assessment of spasticity and spasms. Objectives: Evaluate the most frequently used methods for assessment of spasticity and spasms, with particular focus on individuals with spinal cord lesions. Setting: Clinic for Spinal Cord Injuries, Rigshospitalet, University Hospital of Copenhagen, and Department of Medical Physiology, University of Copenhagen, Denmark. Methods: The assessment methods are grouped into clinical, biomechanical and electrophysiological, and the correlation between these is evaluated. Results: Clinical methods: For assessment of spasticity, the Ashworth and the modified Ashworth scales are commonly used. They provide a semiquantitative measure of the resistance to passive movement, but have limited interrater reliability. Guidelines for the testing procedures should be adhered to. Spasm frequency scales seem not to have been tested for reliability. Biomechanical methods such as isokinetic dynamometers are of value when an objective quantitative measure of the resistance to passive movement is necessary. They play a minor role in the daily clinical evaluation of spasticity. Electrophysiological methods: These techniques have provided valuable insight to the pathophysiological mechanisms involved in spasticity, but none of these techniques provide an easy and reliable assessment of spasticity for use in the daily clinic. Conclusion: A combination of electrophysiological and biomechanical techniques shows some promise for a full characterization of the spastic syndrome. There is a need of simple instruments, which provide a reliable quantitative measure with a low interrater variability.

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...

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The sensitivity of soleus H-reflexes, T-reflexes, and short-latency stretch reflexes (M1) to presynaptic inhibition evoked by a weak tap applied to the biceps femoris tendon or stimulation of the common peroneal nerve (CPN) was compared in 17 healthy human subjects. The H-reflex was strongly depressed for a period lasting up to 300-400 ms (depression to 48 +/- 23%, mean +/- SD, of control at a conditioning test interval of 70 ms) by the biceps femoris tendon tap. In contrast, the short-latency soleus stretch reflex elicited by a quick passive dorsiflexion of the ankle joint was not depressed. The soleus T-reflex elicited by an Achilles tendon tap was only weakly depressed (92 +/- 8%). The H-reflex was also significantly more depressed than the T-reflex at long intervals (>15 ms) after stimulation of CPN (H-reflex 63 +/- 14%, T-reflex 91 +/- 13%; P < 0. 01). However, the short-latency (2 ms) disynaptic reciprocal Ia inhibition evoked by stimulation of CPN was equally strong for H- and T-reflexes (H-reflex 72 +/- 10%, T-reflex 67 +/- 13%; P = 0.07). Peaks in the poststimulus time histogram (PSTH) of the discharge probability of single soleus motor units (n = 53) elicited by an Achilles tendon tap had a longer duration than peaks evoked by electrical stimulation of the tibial nerve (on average 5.0 ms as compared with 2.7 ms). All parts of the electrically evoked peaks were depressed by the conditioning biceps femoris tendon tap (average depression to 55 +/- 27% of control; P < 0.001). A similar depression was observed for the initial 2 ms of the peaks evoked by the Achilles tendon tap (69 +/- 48%; P < 0.001), but the last 2 ms were not depressed. Conditioning stimulation of the CPN at long intervals (>15 ms) also depressed all parts of the electrically evoked PSTH peaks (n = 34; average 65%; P < 0.001) but had only a significant effect on the initial 2 ms of the peaks evoked by the Achilles tendon tap (85%; P < 0.001). We suggest that the different sensitivity of mechanically and electrically evoked reflexes 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. We conclude that it is not straightforward to predict the modulation of stretch reflexes based on observations of H-reflex modulation.

Study design: Cross-sectional descriptive analysis of magnetic resonance imaging (MRI) and clinical outcome. Objectives: The aim of this study was to present anatomically consistent and independent spinal cord atrophy measures based on standard MRI material and analyze their specific relations to sensory and motor outcome in individuals with chronic incomplete spinal cord injury (SCI). Setting: Danish study on human SCI. Methods: We included 19 individuals with chronic incomplete SCI and 16 healthy controls. Participants underwent MRI and a neurological examination including sensory testing for light touch and pinprick, and muscle strength. Antero-posterior width (APW), left-right width (LRW) and crosssectional spinal cord area (SCA) were extracted from MRI at the spinal level of C2. The angular variation of the spinal cord radius over the full circle was also extracted and compared with the clinical scores. Results: The motor score was correlated to LRW and the sensory scores were correlated to APW. The scores correlated also well with decreases in spinal cord radius in oblique angles in coherent and non-overlapping sectors for the sensory and motor qualities respectively. Conclusion: APW and LRW can be used to assess sensory and motor function independently. The finding is corresponding well with the respective locations of the main sensory and motor pathways.