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PubMed1986

Motor unit involvement in spastic paresis. Relationship between leg muscle activation and histochemistry.

In 4 patients with spastic hemiparesis the electromyograms (EMG) of leg muscles were recorded during walking and the gastrocnemius medialis on both sides was investigated by histochemistry and morphometry. During walking a reciprocal mode of muscle activation was preserved on the spastic side, but the EMG amplitude was reduced. In one patient the discharge behaviour of single motor units was investigated during stance. The mean discharge rate on both the spastic and the unaffected side amounted to about 5.5 Hz. Modification of this rate over a wider range by manoeuvres of the trunk was only observed on the unaffected side. Histochemistry and morphometry of the spastic muscle revealed: Increased levels of muscle fibre atrophy (especially type II); A predominance of type I fibres during later stages, when spasticity was established; Structural changes, such as the appearance of target fibres, mainly in type I fibres. These results suggest that the low level of tonic activation in spastic muscle develops tension enough during the stance phase of gait to support the body. The histopathological profile of the spastic gastrocnemius muscle is considered to be indicative of denervation, due to the combined effects of an impaired supraspinal control of the lower motoneurone and a concurrent transsynaptic muscle membrane dysfunction, muscle cell atrophy and fibre type transformation.

Adult↗
PubMed2005

The use of a portable muscle tone measurement device to measure the effects of botulinum toxin type a on elbow flexor spasticity.

OBJECTIVE: To use a portable muscle tone assessment device to measure spasticity after a botulinum toxin type A (BTX-A) injection. DESIGN: Before-after trial. SETTING: Hospital. PARTICIPANTS: Ten chronic stroke patients with upper-limb spasticity. INTERVENTION: BTX-A was injected in the biceps brachii. MAIN OUTCOME MEASURES: The biomechanic parameters, viscous component, and averaged viscosity derived from the acquired reactive resistance and angular displacements, as well as the reflex electromyographic threshold of biceps brachii, were used for spasticity evaluation. RESULTS: A statistically significant decrease in averaged viscosity and a significant increase in reflex electromyographic threshold (P<.05) both indicated reduction in spasticity owing to BTX-A intervention. There was no clear reflex electromyographic activity detected at lower stretch frequencies. CONCLUSIONS: Our portable design allows for the convenient use of the device for quantifying spasticity in clinics. All quantitative measurements suggest that BTX-A decreases spasticity within 2 weeks of injection. Our portable muscle tone measurement device may be useful for the clinical assessment of elbow flexor spasticity.

Adult↗
PubMed2005

Alteration in axial motoneuronal morphology in the spinal cord injured spastic rat.

Following spinal cord injury (SCI), exaggerated reflexes and muscle tone emerge that contribute to a general spastic syndrome in humans. At present, the underlying mechanisms involved with the development of spasticity following traumatic spinal cord injury, especially with regard to axial musculature, remains unclear. The purpose of the present study was to examine the temporal changes in sacrocaudal motoneuronal morphology following complete transection of the sacral spinal cord and to correlate these changes with the onset and progression of spasticity within the tail musculature. The spinal cords of rats were transected at the upper sacral (S(2)) level. Animals were behaviorally tested for the onset and progression of spasticity in the tail and at 1, 2, 4, or 12 weeks postinjury were sacrificed. At these time points, the animals demonstrated stage 1, 2, 3, or 4 spastic behavior, respectively. Sacrocaudal motoneurons innervating selected flexor muscles within the tail were retrogradely labeled with cholera toxin beta-subunit and neuronal morphology was analyzed using a combination of immunocytochemistry and standard microscopy. Initially over the first 2 weeks postinjury, a transient increase in the lengths of primary and secondary dendrites occurred. However, a progressive decrease in the overall number of dendritic branches was observed between 2 and 12 weeks postinjury, which parallels the time frame for the progressive increase in spastic behavior in the tail musculature. Following spinal cord injury, there is an alteration in the morphology of tail flexor motoneurons, which may be relevant to the development of spasticity within the tail.

Animals↗
PubMed2006

Development of GABA-sensitive spasticity and rigidity in rats after transient spinal cord ischemia: a qualitative and quantitative electrophysiological and histopathological study.

Transient spinal cord ischemia may lead to a progressive degeneration of spinal interneurons and subsequently to increased hind limb motor tone. In the present work we sought to characterize the rigidity and spasticity components of this altered motor function by: i) tonic electromyographic activity measured in gastrocnemius muscle before and after ischemia, ii) measurement of muscle resistance during the period of ankle flexion and corresponding changes in electromyographic activity, iii) changes in Hoffmann reflex, and, iv) motor evoked potentials. In addition the effect of intrathecal treatment with baclofen (GABAB receptor agonist; 1 microg), nipecotic acid (GABA uptake inhibitor; 300 microg) and dorsal L2-L5 rhizotomy on spasticity and rigidity was studied. Finally, the changes in spinal choline acetyltransferase (ChAT) and vesicular glutamate transporter 2 and 1 (VGLUT2 and VGLUT1) expression were characterized using immunofluorescence and confocal microscopy. At 3-7 days after ischemia an increase in tonic electromyographic activity with a variable degree of rigidity was seen. In animals with modest rigidity a velocity-dependent increase in muscle resistance and corresponding appearance in electromyographic activity (consistent with the presence of spasticity) was measured during ankle rotation (4-612 degrees /s rotation). Measurement of the H-reflex revealed a significant increase in Hmax/Mmax ratio and a significant loss of rate-dependent inhibition. In the same animals a potent increase in motor evoked potential amplitudes was measured and this change correlated positively with the increased H-reflex responses. Spasticity and rigidity were consistently present for a minimum of 3 months after ischemia. Intrathecal treatment with baclofen (GABA B receptor agonist) and nipecotic acid (GABA uptake inhibitor) provided a significant suppression of spasticity, rigidity, H-reflex or motor evoked potentials. Dorsal L2-L5 rhizotomy significantly decreased muscle resistance but had no effect on increased amplitudes of motor evoked potentials. Confocal analysis of spinal cord sections at 8 weeks-12 months after ischemia revealed a continuing presence of ChAT positive alpha-motoneurons, Ia afferents and VGLUT2 and VGLUT1-positive terminals but a selective loss of small presumably inhibitory interneurons between laminae V-VII. These data demonstrate that brief transient spinal cord ischemia in rat leads to a consistent development of spasticity and rigidity. The lack of significant suppressive effect of dorsal L2-L5 rhizotomy on motor evoked potentials response indicates that descending motor input into alpha-motoneurons is independent on Ia afferent couplings and can independently contribute to increased alpha-motoneuronal excitability. The pharmacology of this effect emphasizes the potent role of GABAergic type B receptors in regulating both the spasticity and rigidity.

Acetyltransferases↗
PubMed1995

Reduction of spastic hypertonia in patients with spinal cord injury: a double-blind comparison of intravenous orphenadrine citrate and placebo.

Spasticity is one of the major problems affecting the outcome of rehabilitation in paraplegic patients. Orphenadrine citrate possesses an effective muscle relaxant action in many pathologies. Nevertheless, despite a recognized central site of action, no controlled data are available on its use in the treatment of spastic hypertonia in patients with spinal cord injuries. Therefore, the effect of intravenous administration of 60mg of orphenadrine citrate versus placebo on spastic hypertonia after spinal cord injury was studied in 11 patients. The threshold of the flexion reflex of the lower limb was studied as a neurophysiological correlate of spastic hypertonia. Clinical assessment was made using the Ashworth Spasticity Scale. The threshold, expressed in mAmp, was studied for 60 minutes after the treatment. A significant difference was found using the active drug compared with placebo (p < 0.0001). In 9 patients, the reduction of the abnormal flexion responses after orphenadrine appeared to begin only after 30 minutes. In one patient the onset of the therapeutic effect was early but weak. One patient with severe spastic hypertonia leading to triple flexion when the limb was manipulated did not gain any relief with orphenadrine. The clinical and neurophysiological results suggest an efficacy of orphenadrine citrate in the control of spastic hypertonia in paraplegics. This could be relevant in the rehabilitation strategy, although further studies are needed on the duration of its action.

Adult↗
PubMed2001

[Effect of spasticity on functional capacity in spinal cord injuries: value of visual analogue scale (preliminary study)].

OBJECTIVES: Assessment of the influence of spasticity on activities of daily living in spinal cord injuries. MATERIAL AND METHODS: Fifteen patients with spinal cord injuries have been submitted to a clinical examination and functional assessment by FIM. They answer to a questionnaire on the influence of spasticity on 11 activities of daily living (response by visual analogic scale). RESULTS: The impact of spasticity in daily life is weak (evaluation of difficulties less than 3 on 10 for 7 of the 11 activities of daily living), except for transfers and precision motions when it is on superior limbs. Spasticity has never been considered as useful by patients (VAS less than 3 for 13 persons). DISCUSSION: This study discusses about the real functional influence of spasticity in daily life. It shows the insufficiency of currently used scales and their lack of sensibility to detect the effects of spasticity in daily life's activities. CONCLUSION: Further outcome studies are required to assess the functional role of spasticity in neurologic patients and the real interest of treatments.

Humans↗
PubMed1999

Passive dynamics of the knee joint in healthy children and children affected by spastic paresis.

OBJECTIVE: The purposes of this study were (1) to evaluate how changes in biomechanical parameters affect segment dynamics in children and (2) to determine whether the biomechanical parameters were changed in children with spastic paresis. DESIGN: In vivo measurements were collected of knee viscoelastic properties. Background. It is unknown if the inertial and viscoelastic properties of a human growing limb should be considered in motor performance. Also unclear are whether changes in passive dynamics might be responsible for abnormal control in human spastic paresis. METHOD: Small oscillation techniques were used to measure moment of inertia of lower leg, stiffness and viscous damping of the knee joint. Eighty seven healthy children and 32 children with spastic paresis participated. RESULTS: Moment of inertia, stiffness and the damping changed with the fifth power of child's height. Dynamic equation of motion parameters were a constant, independent of the child's height. Passive viscoelastic parameters were not changed in spastic patients. CONCLUSIONS: Inertial and viscoelastic properties of a growing limb segment should not be considered in motor performance. Passive viscoelastic properties were not changed in patients with spastic paresis and, therefore, cannot be responsible for abnormal control in human spastic paresis. RELEVANCE: There is no need to adapt control patterns in children (ages 6-18). Passive viscoelastic parameters cannot be used as a descriptor of spasticity.

Adolescent↗
PubMed1997

Effectiveness of gabapentin in controlling spasticity: a quantitative study.

The purpose of this investigation was to study the effectiveness of gabapentin in controlling spasticity in persons with spinal cord injury (SCI) using a surface EMG-based quantitative assessment technique called the brain motor control assessment (BMCA). Six men from a Veterans Affairs Medical Center with spasticity due to traumatic SCI were studied as part of a multi-center, placebo-controlled, cross-over, clinical trial of gabapentin. Spasticity was evaluated using multi-channel surface EMG recordings of muscles in the lower extremities, abdomen and low back before and during treatment with oral gabapentin or placebo. Gabapentin or placebo was given orally in doses 400 mg three times daily for 48 h. Following a 10 day wash-out period subjects were crossed-over to receive the medication not received the first time. This was followed by an elective open-label extension. Group results during the controlled trial did not reach statistical significance at the dosage used. One subject demonstrated a dramatic improvement in spasticity that was apparent both clinically and with the BMCA. Other subjects demonstrated modest improvements which were seen in the BMCA but not recognized clinically. During the open label extension, the four subjects who participated experienced important clinical improvements with higher doses (to 3600 mg/day). These improvements were often in components of spasticity in which the BMCA had detected subclinical changes during the cross-over trial. A seventh subject was studied using the BMCA at doses of 1200 mg T.I.D. gabapentin, off gabapentin and 800 mg T.I.D. gabapentin and demonstrated quantitatively a dose-related effect with higher doses of gabapentin which matched clinical observations. Gabapentin at doses of 400 mg T.I.D. may be effective in controlling some features of spasticity in persons with SCI. Higher doses provide greater control of spasticity, and controlled studies using higher doses are needed to evaluate gabapentin's efficacy.

Acetates↗
PubMed1997

Gabapentin for the treatment of spasticity in patients with spinal cord injury.

Our serendipitous observations suggested that some patients with spasticity appeared to have improved following the administration of the anticonvulsant drug gabapentin. As some patients with spasticity are either refractory to or intolerant of established medical treatments, we conducted this study to investigate the effect of gabapentin on spasticity in patients with spinal cord injury. Twenty-five patients with spinal cord injury and spasticity received oral gabapentin (2400 mg over 48 h) in a randomized, double blind, placebo-controlled crossover study. We assessed responses by measuring the Ashworth spasticity scale, muscle stretch reflexes, presence of clonus and reflex response to noxious stimuli. Patient ratings were obtained using a Likert Scale. Administration of gabapentin, but not placebo, was associated with an 11% reduction in spasticity as measured by the Ashworth Scale (P = 0.04) and by a 20% reduction in the Likert Scale (P = 0.0013). Significant changes were not obtained for the other measures. The data obtained suggest that gabapentin may be useful in the management of spasticity associated with spinal cord injury.

Acetates↗
PubMed2005

The effect of passive cycling movements on spasticity after spinal cord injury: preliminary results.

OBJECTIVE: To investigate the influence of rhythmic passive movements of the legs on the reduction of spasticity after spinal cord injury (SCI). SETTING: Swiss Paraplegic Centre Nottwil, Switzerland. METHODS: A total of 10 subjects with motor complete SCI were treated with a cycling device for half an hour. Before and after cycling their spasticity was tested with an isokinetic dynamometer. The subjects were tested one week later by exactly the same procedure with a half an hour break instead of the cycling. Subjects were asked about their spasticity before and after the cycling and break. RESULTS: There was no significant difference in elicited peak torque either before and after the cycling, or before and after the break (MANOVA, P<0.05). Six out of 10 subjects estimated their spasticity as less after the cycling. CONCLUSION: With the isokinetic dynamometer, it was not possible to show an effect of passive cycling on spasticity reduction. However, six out of 10 of the subjects estimated their spasticity to be less after cycling. This positive effect might be attributed to a reduced spasticity in the trunk and/or to the attention the subjects perceived during the intervention.

Adult↗
PubMed2006

Spasticity-assessment: a review.

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.

Biomechanical Phenomena↗
PubMed2002

Outcome measures of spasticity.

Spasticity is characterized by a velocity-dependent increase in muscle resistance, in response to a passive stretch. Whilst clinical scales probably represent the most common approach to its measurement, these are limited by poor reliability and difficulties with some definitions. However, recently, a simple system has been used to provide the clinician with a measure of the force applied during the Ashworth Test. The Wartenberg Pendulum Test has been devised for measuring spasticity at the knee, but has been shown to be unsuitable for measuring more severe spasticity. Powered systems have been used in research studies, but are rarely considered suitable for routine clinical use. However, one method of interest, using a low inertia torque motor to measuring stiffness at the wrist, has been shown to provide rapid measurements which correspond to the degree of spasticity defined by other scales. Clinical gait analysis may have an important role to play in assessing spasticity - since there are clear associations between lower limb spasticity and gait problems - but it does not provide a true measure of the condition. In summary, while scales remain the most common method of measuring spasticity, there is considerable potential in instrumented techniques that can provide greater reliability and precision of measurement.

Biomechanical Phenomena↗
PubMed2000

Electromechanical delay and reflex response in spastic cerebral palsy.

OBJECTIVE: Electromechanical delay (EMD) and reflex response in patients with spastic cerebral palsy (CP) were quantified and compared with those in normally developing individuals. It was hypothesized that the increased muscle stiffness associated with spasticity must make EMD shorter than the EMD of normally functioning muscles. DESIGN: Electromechanical reflex behavior was assessed in a case-control study. SETTING: Motion Analysis and Motor Performance Laboratory, University of Virginia, a tertiary clinical referral center and research facility. PARTICIPANTS: A volunteer sample of 12 children diagnosed with spastic CP and 12 age-matched, normally developing children recruited from the local community and clinical services. RESULTS: EMD in the patients with spasticity was significantly shorter than in the normally developing subjects, 40.5 msec and 54.7 msec, respectively. The spastic group also had greater reflex activity, rate of force development, and antagonistic muscle activation. Knee flexion angle did not influence EMD in either group. CONCLUSIONS: Increased biomechanical stiffness in spastic muscle results in abnormally reduced EMD. Reciprocal excitation of antagonistic cocontraction was uniquely observed in the spastic group, but did not explain the reduced EMD.

Adolescent↗
PubMed2001

Locomotor-specific measure of spasticity of plantarflexor muscles after stroke.

OBJECTIVES: To study the stretch reflex excitability (spasticity) of the plantarflexor muscles during gait in patients with hemiparesis and to study the relationships of spasticity during gait with spasticity at rest and gait speed. DESIGN: Cross-sectional, descriptive. SETTING: Rehabilitation center. PARTICIPANTS: Convenience sample of 30 patients (58 +/- 11yr) with hemiparesis (<6mo poststroke) and 15 healthy controls (59 +/- 8yr). INTERVENTIONS: Patients walked at natural speed, healthy subjects at very slow speed for 10 gait cycles. Electromyographic activation of the medial gastrocremius was recorded by using surface electrodes. A 2-dimensional video camera system with reflective markers was used to acquire kinematics of the lower limbs. MAIN OUTCOME MEASURES: Electromyography-lengthening velocity slopes, calculated from measures obtained during the lengthening periods of the medial gastrocnemius muscle during the stance and the swing phases. Measured spatisticity (Modified Ashworth Scale [MAS]), static strength (ankle clonus), and motor control (Fugl-Meyer test). RESULTS: Velocity-sensitive electromyographic responses, indicative of hyperactive stretch reflexes, were found on the paretic side during the stance phase of gait (in 66% of the patients), but not on the nonparetic side or in controls. In many patients, velocity-sensitive responses coexisted with low plantarflexor activation levels during the stance phase. No clear patterns of response were measured during the swing phase in either group. Spasticity during gait in the patients was found to be positively related (r = .47, p < .01; r = .57, p < .001) to spasticity at rest (MAS; ankle clonus), whereas it was found to be negatively related to gait speed (r = -.47 to -.53, p < .01). CONCLUSIONS: The validity of the present method is supported by the fact that it is locomotor-specific and that it allowed for a good discrimination between spastic and nonspastic limbs, as well as between stance and swing phases of the gait cycle. The results also support plantarflexor spasticity as a factor contributing to the poor locomotor performance after stroke.

Adult↗
PubMedDate not supplied

Clinical scales for the assessment of spasticity, associated phenomena, and function: a systematic review of the literature.

PURPOSE: To characterise clinical assessment methods for spasticity and/or its functional consequences in clinical patient populations at risk to suffer from spasticity. METHOD: Systematic literature search and manual-based two-step review process of psychometric properties of clinical assessment scales for spasticity and associated phenomena, as well as of functional scales with an association with spasticity. Reviewed psychometric properties included internal consistency, interrater, intrarater as well as retest reliability, construct validity, ecological validity, and responsiveness. RESULTS: Until May 2003 electronic database searches established a reference pool of 4151 references of which 90 references contributed to the review objectives. An additional 20 references were identified by an informal reference search. Twenty-four clinical scales that assess spasticity and/or related phenomena as well as 10 scales for 'active function' and three scales for 'passive function' with an association with spasticity could be identified. Some evidence signals that a high interrater reliability of the Ashworth and modified Ashworth scales can be achieved, however not in all circumstances. For many scales, reliability data is, however, missing. This is especially true for test retest reliability. Information about construct validity can promote our understanding of what individual scales are likely to assess. Many scales have been able to document changes after therapeutic intervention. CONCLUSIONS: The collated evidence can guide our clinical decision about when to use which scale and can promote evidence-based assessment of spasticity and related clinical phenomena.

Adult↗
PubMed1987

Stretch and vibration reflexes of wrist flexor muscles in spasticity.

The surface electromyographic (EMG) reflex responses of the voluntarily contracting flexor carpi radialis evoked by 'stretch' and by tendon vibration have been compared in patients with spasticity of the upper limb, arising from upper motor neuron lesions, and normal subjects. Reflex responses to 'stretch' comprised increases in EMG activity lasting up to 100 ms which were often divided into 'short' and 'long'-latency peaks. The short-latency responses of spastic patients were increased in size compared with those of normal subjects whereas later activity was commonly reduced or absent. In both groups vibration elicited short-latency, essentially phasic responses with activity falling back to or below the background level within 50 ms despite continuing stimulation. These initial reflex responses were exaggerated in the spastics as compared with the normals. In the relaxed state 'stretch' and vibration either failed to elicit reflex responses in normal subjects or reflexes were of small amplitude; in spastic patients both modes of stimulation regularly evoked well developed responses. These findings with 'stretch' and vibration, both of which forms of stimulation powerfully excite primary endings of muscle spindles, support the view that group Ia afferent-mediated reflex action is enhanced in spasticity. The observation that the normal long-latency responses evoked by stretch, which have been attributed to the action of spindle group II afferents (Matthews, 1984a) additionally excited with this stimulus, are depressed in many spastic patients is consistent with reduced group II effects. Observed abnormalities of stretch reflex behaviour did not readily explain the severity of accompanying spasticity of individual patients.

Adult↗
PubMed1993

Stretch-induced electromyographic activity and torque in spastic elbow muscles. Differential modulation of reflex activity in passive and active motor tasks.

Stretch-evoked electromyographic (EMG) activity and torque signals have been studied in elbow joint muscles of both sides of patients with spastic hemiparesis and healthy subjects. In order to reveal differences in the generation of muscle tone between clinical assessment and functional movement, stretches of different velocities and amplitudes were applied during passive and quasi-functional active motor tasks. In spastic patients the strength and duration of the EMG responses following stretching of flexor and extensor muscles during both passive and active tasks were dependent on the stretch velocity and duration, respectively. This effect was seen on both the spastic and unaffected side. Under passive conditions EMG activity after stretching was negligible in the limb muscles of healthy subjects, of small amplitude in unaffected limbs of the patients, but was strong in affected muscles. Under active conditions, the amplitude of the early (M1) component of the EMG signal was larger, while the later components (M2 and M3) were smaller. These differences were due more to a change in reflex gain than to a change in reflex threshold when the stretch velocity signal was the basis for calculation. It is suggested that in spastic paresis, modulation of stretch-induced EMG activity in the spastic limb becomes restricted to a smaller range with a poor ability to switch off under passive conditions. Furthermore, the reflex EMG activity suffers a reduced facilitation under active conditions. In comparison with unaffected limbs the stretch-evoked torque on the affected side was increased under passive conditions (due to the extra EMG activity) and decreased under active conditions (due to a reduced EMG activity). An increased torque to EMG ratio was found in spastic flexor and extensor muscles during active tasks. This is thought to be due to changes in mechanical muscle fibre properties suffered as a consequence of defective muscle activation following cerebral lesions. The consequences for clinical assessment of muscle tone and therapy of spastic movement disorder are discussed.

Adult↗
PubMed1995

Changes in transmission across synapses of Ia afferents in spastic patients.

The transmission across synapses of Ia afferents on spinal motor neurons was investigated in 30 healthy subjects and 25 spastic multiple sclerosis patients. Slow passive stretch (17 degrees/s of the soleus muscle evoked a pronounced depression of the soleus Hoffmann reflex (H-reflex) lasting for more than 10 s in the healthy subjects. This depression was less pronounced and had a shorter duration in the spastic patients. A tap applied to the biceps femoris tendon also produced an inhibition of the soleus H-reflex, which was larger in the healthy subjects than in the spastic patients. This inhibition only lasted for 300-400 ms. Finally, stimulation of the femoral nerve (FN) produced a facilitation of the soleus H-reflex, which was larger in the spastic patients than in the healthy subjects. The inhibition of the H-reflex evoked by the biceps femoris tendon tap is known to be caused by presynaptic inhibition of the Ia afferents, which mediate the reflex. The facilitation of the soleus H-reflex produced by FN stimulation has also been shown to be influenced by changes in presynaptic inhibition. The increased facilitation from the FN and the decreased inhibition from the biceps femoris tendon tap onto the soleus H-reflex in spastic patients are thus both compatible with a deficient presynaptic inhibition in these subjects. The long lasting depression of the reflex evoked by a previous slow stretch of the soleus muscle is most likely caused by a decrease of the probability of transmitter release from the Ia afferents. The decrease of this depression in spastic patients suggests that mechanisms other than presynaptic inhibition may contribute to changes in the efficiency of transmission across the synapses of Ia afferents in spastic patients and thus contribute to the exaggeration of stretch reflexes seen in these patients.

Adult↗