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PubMed1997

Muscle, reflex and central components in the control of the ankle joint in healthy and spastic man.

In understanding the control of the ankle joint during different motor tasks, we have to investigate at least three components, namely the influence of i) the passive and intrinsic properties of the intact and active muscle system around the joint (termed the non-reflex component), ii) the mechanical importance of the stretch reflex in the stretched and unloaded muscles, and iii) the supraspinal control of the stretch reflex. This thesis is dealing with the importance of the three components in healthy and spastic persons during sitting, standing, and walking. The results are based on stretch reflex and H-reflex measurements from the ankle extensor muscles. During stretch reflex experiments the foot was mounted to a platform (portable during walking) from which the ankle joint torque and the position were measured. To elicit a stretch reflex, the ankle joint was rotated by a strong motor connected to the platform. The mechanical importance of the stretch reflex was investigated by measuring the changes in joint torque. Electrically, the stretch reflex was recorded as the compound muscle action potential through bipolar surface EMG electrodes placed over the soleus muscle. During H-reflex experiments, the tibial nerve was stimulated at the popliteal fossa and the H-reflex recorded over the soleus muscle as during stretch reflex experiments. To investigate how the contractile properties of a muscle in humans depend on the history of activation, we investigated the intrinsic stiffness of the ankle extensors in healthy subjects. At matched background contraction in sitting subjects, a prolonged contraction increased the intrinsic muscle stiffness by 49%. Muscle yielding has been considered especially important for understanding the reflex compensation. We found a general lack of muscle yield and a mechanically important non-reflex stiffness of the ankle extensors showing that non-reflex stiffness is a prominent factor in normal movements of the ankle joint. In both healthy and spastic persons, we found a mechanically strong stretch reflex in the isometric, contracted muscles during sitting. This posed the question; how is the reflex regulated during more functional motor tasks. This was dealt with by studying the H-reflex during isometric ramp contractions and during walking in healthy and spastic persons. In the healthy subjects the H-reflex was modulated in consistency with a task dependent control. In the spastic patients the H-reflex lacked a task dependent modulation. In consistency with earlier findings it was suggested that the decreased modulation could have been caused by decreased control of the pre-synaptic inhibition of the Ia terminals or a change in recruitment gain. To test if the stretch reflex behaved as the H-reflex, the short latency stretch reflex was investigated during walking. Here we found that the stretch reflex was strongly modulated during a step in healthy subjects as seen for the H-reflex, but when comparing the stretch reflex at matched excitation levels (same background EMGs) during standing and walking, no task-specific reflex modulation was found except the one relating to the excitation level. Therefore, the results emphasise that at least during walking and standing it is not always possible to draw conclusions about the stretch reflex based on observations of the H-reflex. When investigating the modulation of the short latency stretch reflex during walking in spastic patients, we found that the stretch reflex modulation was impaired in spastic patients at least to the extent demonstrated earlier for the H-reflex. The passive stiffness of the ankle joint was at the same time increased in the patients. At matched ankle extensor contraction levels, stretch responses were compared before and after reversible block of the common peroneal nerve and during an attempted, voluntary, fictive dorsiflexion after common peroneal nerve block. (ABSTRACT TRUNCATED)

Afferent Pathways↗
PubMed2026

Safety and efficacy of recombinant botulinum toxin type A (Eveotox®) in patients with post-stroke upper limb spasticity: Results from a Phase Ib/II clinical trial.

Upper limb spasticity is a common and disabling complication of stroke. Botulinum toxin type A (BoNT-A) is widely used for focal spasticity treatment, but naturally derived products may present limitations related to immunogenicity and manufacturing variability. Recombinant botulinum toxin type A, produced by genetic engineering without complexing proteins, may provide improved product consistency. This Ib/II study evaluated the safety, tolerability, and preliminary efficacy of recombinant botulinum toxin type A in adults with post-stroke upper limb spasticity. This multicenter, seamless Ib/II clinical study included an open-label dose-escalation Ib phase and a randomized, double-blind, placebo-controlled II phase. Adult patients with post-stroke upper limb spasticity received a single intramuscular injection of recombinant botulinum toxin type A or placebo. The primary endpoint in Phase II was the change from baseline in the Modified Ashworth Scale (MAS) score of the primary target muscle group at Week 4. Secondary endpoints included MAS and Tardieu scale changes in individual muscle groups, Disability Assessment Scale (DAS), Physician's Global Assessment (PGA), and immunogenicity. The Ib phase showed improvements in MAS, DAS, and PGA, indicating an early efficacy signal. In Phase II, recombinant botulinum toxin type A produced a significant reduction in MAS score of the primary target muscle group at Week 4 compared with placebo, with effects sustained through Week 12. At Week 4, the PGA score in the Eveotox® group showed a statistically significant improvement compared with the placebo group. While MAS and PGA scores showed significant improvement, DAS functional scores did not differ statistically from the placebo group at week 4. The treatment was generally well tolerated, and low incidence of antibodies were observed. Recombinant botulinum toxin type A was safe and effective in reducing post-stroke upper limb spasticity after a single administration. These results support further Phase III clinical evaluation.

Humans↗
PubMed1993

Continuous intrathecal baclofen infusion for spasticity of cerebral origin.

OBJECTIVE: To determine if continuous intrathecal baclofen infusion (CIBI) would provide continuous relief of spasticity in patients with spasticity of cerebral origin, especially children with cerebral palsy. DESIGN: Prospective, unblinded trial, before and after CIBI. SETTING: Children's Hospital of Pittsburgh (Pa). PATIENTS: Thirty-seven patients, 5 to 27 years of age, with spasticity of cerebral origin. INTERVENTION: Continuous intrathecal baclofen infusion for 3 to 48 months. MAIN OUTCOME MEASURES: Muscle tone, range of motion, upper extremity timed tasks, activities of daily living (ADLs). RESULTS: Six and 12 months after CIBI, muscle tone was significantly decreased in the upper (P = .04) and lower (P = .001) extremities. There was a significant relationship between baclofen dosage and muscle tone in the upper (P = .02) and lower (P = .001) extremities. Hamstring motion, upper extremity function, and ADLs were significantly improved in 25 patients who were capable of self-care. CONCLUSION: Spasticity of cerebral origin can be effectively treated with CIBI. Because baclofen dosages can be titrated for the desired clinical response, CIBI is particularly useful for patients who need some spasticity to stand and ambulate.

Adolescent↗
PubMed1996

[Effect of the Nucleus CMP forte in 46 patients with progressive spastic paraparesis. Randomized and blind study].

BACKGROUND: Idiopatic or HTLV-1 associated progressive spastic paraparesis does not have a clear etiology or treatment. AIM: To assess the effects of a medication containing cytidinmonophosphate, uridintriphosphate and vitamin B 12 in the treatment of progressive spastic. PATIENTS AND METHODS: Patients with the disease were randomly assigned to receive the Nucleus CMP forte (containing dysodic cytidinmonophosphate 5 mg, trisodic uridintriphosphate 3 mg and hydroxicobalamin 2 Mg) tid or placebo during six months. Gait, spasticity, degree of neurogenic bladder and somatosensitive evoked potentials were assessed during treatment. RESULTS: Forty six patients aged 25 to 79 years old were studied, 24 were female and 29 HTLV-1 positive. Twenty two were treated with the drug and the rest with placebo. Gait and spasticity improved in 7 of 22 patients receiving the drug and 1 of 24 receiving placebo (p < 0.05). Neurogenic bladder improved in 10 of 22 receiving the drug and 4 of 24 receiving placebo (NS) Somatosensitive evoked potentials improved in four of seven patients treated with the drug and in two of seven treated with placebo. CONCLUSIONS: The medication caused a modest improvement in patients with progressive spastic paraparesis and was free of side effects.

Adult↗
PubMed2026

Treatment of spinal injury muscle spasticity by spinal subpial AAV9-GAD65/VGAT delivery: An efficacy and safety study in rat, pig, and NHP.

The loss in segmental inhibitory GABAergic tone plays the key role in the development of spinal injury-induced muscle spasticity. We use a subpial segment-targeted delivery of adeno-associated virus vector(s) expressing GAD65 (glutamic acid decarboxylase-65) and VGAT (vesicular GABA transporter) transgenes in rats with spinal transection-induced spasticity. In treated animals, a significant suppression in spasticity was seen at 5-8 weeks after treatment. Naive rats, pigs, and non-human primates (NHPs) injected with human equivalent dose of treatment vectors and surviving for 3 weeks to 4.5 years showed normal motor function and pinch-evoked response. A significant increase in the number of VGLUT2 terminals co-expressing GAD65 and VGAT protein in vector-injected segment was seen. This corresponded with the presence of transgene-specific rat Gad2 or human GAD2 and rat Slc32a1 or human SLC32A1 mRNA signal. No spinal toxicity was noted in NHPs at 4.5 years post vector delivery. Analysis of peripheral organs (liver, spleen, and skeletal muscle) showed minimal or no detectable transgenes in pigs and NHPs. These data demonstrate that a single-time-point spinal-segment-targeted subpial delivery of GAD65/VGAT transgenes is effective in suppressing spinal injury-induced spasticity and has a favorable long-term safety profile as defined by normal neurological function and histopathology in naive pigs and NHPs.

Animals↗
PubMed2004

Three novel mutations of the spastin gene in Chinese patients with hereditary spastic paraplegia.

BACKGROUND: Hereditary spastic paraplegia is a group of genetically heterogeneous neurodegenerative disorders characterized by progressive spasticity of the lower limbs. The most common form of hereditary spastic paraplegia is caused by mutations in the spastin gene (SPG4), which encodes spastin, an adenosine triphosphatase associated with various cellular activities protein. OBJECTIVE: To investigate the Chinese patients with hereditary spastic paraplegia for mutations in SPG4. METHODS: DNA samples from 31 unrelated patients were analyzed for mutations in SPG4 by single-strand conformation polymorphism analysis and direct sequencing. All DNA samples were screened for mutations by the polymerase chain reaction, followed by electrophoresis and silver staining. Each new variant identified was analyzed in 50 control subjects to determine whether it is a polymorphism or a mutation. RESULTS: Three novel mutations were detected in 4 affected individuals, including 2 missense mutations (T1258A and A1293G) and 1 deletion mutation (1668-1670delCTA). CONCLUSIONS: To our knowledge, this is the first report of SPG4 mutations in the People's Republic of China. The percentage of involved Chinese families with autosomal dominant hereditary spastic paraplegia with an SPG4 mutation is 18% (4/22), lower than the estimated 40% linked to this locus.

Adenosine Triphosphatases↗
PubMed2000

The surgical treatment of spasticity.

Many neurosurgical procedures have been designed for or applied to the treatment of spasticity arising from different disorders, including cerebral palsy; traumatic, ischemic, or hypoxic brain injury, multiple sclerosis, and spinal cord injury. Neurosurgical procedures are primarily aimed at reducing spasticity by interrupting the stretch reflex at various sites along the spinal reflex arc or attempting to increase the centrally mediated inhibitory influence on the pool of motor neurons in the anterior horn. Surgical interventions for spasticity can be classified into peripheral ablative procedures, such as rhizotomy or peripheral neurectomy, and central ablative procedures, such as cordectomy, myelotomy, or stereotactic procedures. Non-ablative procedures include peripheral nerve or motor point blocks, the implantation of cerebellar or spinal stimulators, and the implantation of subdural catheters for infusion of pharmacologic agents to increase inhibitory activity. Several proposed mechanisms for spasticity are reviewed so that the rationale for the various surgical interventions for spasticity described may be better understood.

Efferent Pathways↗
PubMed2004

Botulinum toxin A as an adjunct to treatment in the management of the upper limb in children with spastic cerebral palsy.

BACKGROUND: Cerebral palsy (CP) is a central nervous system deficit resulting from a non-progressive lesion in the developing brain. Although the brain lesions are static, the movement disorders that arise are not unchanging and are characterised by atypical muscle tone, posture and movement (Rang 1990). The spastic motor type is the most common form of CP and its conventional therapeutic management may include splinting/casting, passive stretching, facilitation of posture and movement, spasticity-reducing medication and surgery. More recently, health care professionals have begun to use botulinum toxin A (BtA) as an adjunct to interventions in an attempt to reduce muscle tone and spasticity to improve function OBJECTIVES: To assess the effectiveness of intramuscular BtA injections as an adjunct to managing the upper limb in children with spastic CP. SEARCH STRATEGY: We searched the Cochrane Central Register of Controlled Trials (The Cochrane Library, Issue 4, 2003), MEDLINE (1966 to March Week 3 2004), EMBASE (1980 to 2003 Week 16) and CINAHL (1982 to Week 3 March 2004). SELECTION CRITERIA: All randomised controlled trials (RCTs) comparing intramuscular BtA injections into any muscle group of the upper limb with placebo, no treatment or other interventions. DATA COLLECTION AND ANALYSIS: Two authors using standardised forms extracted the data independently. Each trial was assessed for internal validity with differences resolved by discussion. Data was extracted and entered into RevMan 4.2.3. MAIN RESULTS: Two trials met the inclusion criteria, each having short-term follow up, a small number of subjects and using a single set of injections. The study by Corry 1997 compared BtA with an injection of normal saline and found promising results in elbow extension, elbow and wrist muscle tone. At three months, encouraging results for wrist muscle tone and grasp and release were noted. The trial reported median change, range of changes and the difference in these measures between groups. The study by Fehlings 2000 compared BtA with no intervention. When data were analysed no treatment effect was found for quality of upper limb function, passive range of motion, muscle tone, grip strength or self-care ability. REVIEWERS' CONCLUSIONS: This systematic review has not found sufficient evidence to support or refute the use of intramuscular injections of BtA as an adjunct to managing the upper limb in children with spastic cerebral palsy. Only one of the two identified RCTs reported some promising results in support of reduced muscle tone following BtA injections. Further research incorporating larger sample sizes, rigorous methodology, measurement of upper limb function and functional outcomes is essential.

Adolescent↗
PubMed2006

Treatment for spasticity in amyotrophic lateral sclerosis/motor neuron disease.

BACKGROUND: Spasticity commonly affects patients with motor neuron disease. It is likely to contribute to worsening muscle dysfunction, increased difficulty with activities of daily living and deteriorating quality of life. OBJECTIVES: The objective of this review is to systematically review treatments for spasticity in amyotrophic lateral sclerosis, also known as motor neuron disease. SEARCH STRATEGY: We searched the Cochrane Neuromuscular Disease Group trials register (January 2003 and January 2005), MEDLINE (January 1966 to February 2005), EMBASE (January 1980 to February 2005), CINAHL (January 1982 to February 2005), AMED (January 1985 to February 2005) and LILACS (January 1982 to January 2003). We reviewed the bibliographies of the randomized controlled trials identified, and contacted authors and experts in the field. SELECTION CRITERIA: We included quasi-randomized or randomized controlled trials of participants with probable or definite amyotrophic lateral sclerosis according to the El Escorial diagnostic criteria (or a revised version) or the Airlie House revision. We would have included trials of physical therapy, modalities, prescription medications, non-prescription medications, chemical neurolysis, surgical interventions, and alternative therapies. Our primary outcome measure was reduction in spasticity at three months or greater as measured by the Ashworth (or modified Ashworth) spasticity scale. Our secondary outcome measures were: validated measures based on history, physical examination, physiological measures, measures of function, measures of quality of life, serious adverse events, and measures of cost. DATA COLLECTION AND ANALYSIS: We identified only one randomized controlled trial that met our inclusion criteria. Two authors extracted the data. We also contacted the author of the paper and obtained information not available in the published article. MAIN RESULTS: The included study was a trial of moderate intensity, endurance type exercise versus 'usual activities' in 25 patients with amyotrophic lateral sclerosis. At three months patients performing the 15 minute twice daily exercises had significantly less spasticity overall (mean reduction of -0.43, 95% CI -1.03 to +0.17 in the treatment group versus an increase of +0.25, 95% CI -0.46 to +0.96 in control) but the mean change between groups was not significant (-0.68, 95% CI -1.62 to +0.26), as measured by the Ashworth scale. AUTHORS' CONCLUSIONS: The single trial performed was too small to determine whether individualised moderate intensity endurance type exercises for the trunk and limbs are beneficial or harmful. No other medical, surgical or alternative treatment and therapy has been evaluated in a randomized fashion in this patient population. More research is needed.

Amyotrophic Lateral Sclerosis↗
PubMed1988

Quantitative relations between hypertonia and stretch reflex threshold in spastic hemiparesis.

The relative contributions of variations in stretch reflex threshold and total joint stiffness to changes in stretch-evoked torque were assessed in the spastic elbow muscles of 14 hemiparetic spastic subjects. For a given subject, variations in torque, measured after a constant angular deflection, were mediated largely by changes in stretch reflex threshold, rather than by changes in reflex stiffness. Between-subject comparisons were sensitive to stiffness differences between limbs, but reflex thresholds were still broadly correlated with torque magnitude, suggesting that reductions in stretch reflex threshold are uniformly present in spastic muscles. These findings, coupled with the apparent similarity of reflex stiffness estimates in voluntarily activated spastic and normal muscles, suggest that the central disturbance in spasticity is a reduction in the threshold of the stretch reflex, without a significant enhancement of reflex gain.

Adult↗
PubMed1989

Stretch reflex dynamics in spastic elbow flexor muscles.

Previous studies of stretch reflexes in patients with spastic hypertonia have emphasized the dynamic character of stretch reflex output. In contrast, our own studies of stretch reflex dynamics in spastic elbow flexor muscles of 14 hemiparetic human subjects have shown that stretch-evoked torque displays a relatively weak dependence on stretch velocity, and there is generally no preferential enhancement of dynamic as compared with static reflex output. Moreover, stretch reflex dynamics are broadly similar in voluntarily activated spastic and normal elbow flexor muscles. These findings support our hypothesis that spastic hypertonia results primarily from a decrease in stretch reflex threshold. The strong velocity dependence of stretch-evoked electromyographic activity in initially inactive spastic muscles could be due to a decrease in reflex threshold with increasing stretch velocity, rather than an abnormal velocity-dependent increase in stretch reflex responsiveness.

Adult↗
PubMedDate not supplied

Treatment of human spasticity with delta 9-tetrahydrocannabinol.

Spasticity is a common neurologic condition in patients with multiple sclerosis, stroke, cerebral palsy or an injured spinal cord. Animal studies suggest that THC has an inhibitory effect on polysynaptic reflexes. Some spastic patients claim improvement after inhaling cannabis. We tested muscle tone, reflexes, strength and performed EMGs before and after double-blinded oral administration of either 10 or 5 mg THC or placebo. The blinded examiner correctly identified the trials in which the patients received THC in seven of nine cases. For the group, 10 mg THC significantly reduced spasticity by clinical measurement (P less than 0.01). Quadriceps EMG interference pattern was reduced in those four patients with primarily extensor spasticity. THC was administered to eight other patients with spasticity and other CNS lesions. Responses varied, but benefit was seen in three of three patients with "tonic spasms." No benefit was noted in patients with cerebellar disease.

Clinical Trials as Topic↗
PubMedDate not supplied

Intrathecal baclofen infusion: an innovative approach for controlling spinal spasticity.

Severe and disabling spasticity frequently occurs in people with multiple sclerosis and spinal cord injury. Approximately 30% of these people are treated with oral antispasmodic medications that do not provide adequate relief from spasticity (Hattab, 1980). Clinical trials with spinal stimulation and ablative neurosurgical procedures have not been as uniformly successful for controlling spasticity as has intrathecal baclofen injection (Kasdon, 1986). Delivered by an implantable programmable drug pump, intrathecal baclofen injection has proven to be successful in treating individuals with intractable spasticity. Significant reduction in muscle tone and frequency of spasms have contributed to improved function with activities of daily living, bladder management, overall comfort, and quality of sleep (Penn et al., 1989; Parke, Penn, Savoy, & Corcos, 1989). This article introduces an innovative therapy for controlling spasticity and discusses the nurse's role in patient selection and management.

Activities of Daily Living↗
PubMed2004

Structural and functional changes in spastic skeletal muscle.

This review summarizes current information regarding the changes in structure or function that occur in skeletal muscle secondary to spasticity. Most published studies have reported an increase in fiber size variability in spastic muscle. There is no general agreement regarding any shift in fiber type distribution secondary to spasticity. Mechanical studies in whole limbs as well as in isolated single cells support the notion of an intrinsic change in the passive mechanical properties of muscle after spasticity in addition to the more widely reported neural changes that occur. Evidence is presented for changes within both the muscle cell and extracellular matrix that contribute to the overall changes in the tissue. Taken together, the literature supports the notion that, although spasticity is multifactorial and neural in origin, significant structural alterations in muscle also occur. An understanding of the specific changes that occur in the muscle and extracellular matrix may facilitate the development of new conservative or surgical therapies for this problem.

Animals↗
PubMed2002

Combined intrathecal baclofen and morphine infusion for the treatment of spasticity related pain and central deafferentiation pain.

OBJECTIVES: Complex pain syndromes due to spasticity and central deafferentation often fail to respond to medical therapy and create challenging problems in the pain management. So far, only spasticity associated musculosceletal pain has been reported to respond to intrathecal baclofen application [1, 2]. METHODS: We report the treatment of severe neuropathic pain in a patient with ED and the combined intrathecal application of baclofen and morphine in 5 patients with severe spasticity related pain. RESULTS: Continuous intrathecal baclofen infusion resulted in a pain free period of 20 months in the patient with ED. Patients with spasticity treated with intrathecal application of baclofen and morphine were pain free for a mean period of 2 years. CONCLUSION: Intrathecal baclofen and morphine application proved to be effective in spasticity related and central deafferentation pain and should therefore be considered in the management of these patients.

Afferent Pathways↗
PubMed1977

Long-term assessment of stereotactic dentatotomy for spasticity and other disorders.

In the 60's stereotactic electrocoagulation of the dentate nucleus became a promising approach in the neurosurgical treatment of muscular hypertonicity, particularly when spasticity was evident. A relatively satisfactory improvement of spasticity has been reported earlier as a result and the authors were supporting these clinical results in previous publications. A long-term assessment of the results obtained in a large series of patients would permit a better evaluation of the effect of the operation. Analysing 109 stereotactic electrocoagulations of the dentate nucleus on 50 patients mainly in cases of cerebral palsy over a period of more than 10 years (most patients underwent a bilateral dentatotomy), the authors give a more realistic appreciation of the results, which depend on the criteria chosen. In 30% of the cases a clear improvement in the spasticity was obtained, and in 50% of all cases, nursing and rehabilitation were facilitated. The stereotactic dentatotomy never completely cured the spasticity and spectacular results were never observed, but the operation can be performed without complications and an unexpected neurological deficit did not occur. The role of the stereotactic dentatotomy and other neurosurgical methods in the treatment of spasticity has to be evaluated more critically.

Adolescent↗
PubMed1988

Implanted pump systems for treatment of spasticity.

In about one third of patients with violent spasticity due to spinal trauma, multiple sclerosis, and diffuse brain injury adequate control with oral antispastic medication cannot be achieved and successful rehabilitation is severely handicapped. In the past these patients were subjected to destructive chemical procedures or extensive surgery. The authors present the results of management of uncontrollable spasticity by means of continuous intrathecal administration of baclofen with a totally implantable gas driven pump system (Infusaid). 30 patients were treated between June 1985 and January. 1987. The main indication was incapacitating spasticity resistant to oral treatment with baclofen and caused by spinal cord injury or lesion (11 patients), multiple sclerosis (11 patients), infantile cerebral palsy (3 patients) and cerebral injury, hypoxia or ischaemia (5 patients). Clinical assessment included spasticity scores, integrated electromyography (Iemg) and motography. Effective control for spasticity with mean reduction of Iemg by 55%, decrease of Ashworth's score from 3 to 0 and improvement of life quality was obtained in all patients with daily dose of 10-800 micrograms of Baclofen. Voluntary resting motoricity was not impaired and there were no untoward central side effects. The excellent effect of intrathecal baclofen in comparison with oral therapy is explained by local, spinal GABAergic inhibitory action of the drug which is delivered directly into spinal subarachnoid space. Dose finding and dose adjustment is performed prior to pump implantation by intermittent injections into a subcutaneous port. The complications of the procedure were minor (catheter displacement, disconnection) and easily correctable.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1995

The influence of glycine and related compounds on spinal cord injury-induced spasticity.

Spasticity is a frequent and complex sequel to spinal cord injury. The neurochemical basis for the origin of spasticity is largely unknown. Glycine is among the most abundant neurotransmitters in the spinal cord. However, the role of glycine and related compounds in spasticity have received little attention. An ischemic spinal cord injury was created in rabbits, by an intraaortic balloon occlusion technique, which produced lower limb spasticity. A catheter was inserted into the cisterna magna and the spinal cord was bathed with 100 microM solutions of glycine, strychnine, D-serine, beta-alanine, MK-801, or artificial CSF for 4 hours at a rate of 10 microliters/min. H-reflexes were monitored before and during infusion by stimulating the posterior tibial nerve and recording from the plantar surface of the foot. Glycine, D-serine, and MK-801 depressed the H wave, strychnine produced a heightened H wave, and beta-alanine caused no significant changes. These results indicate that glycine and related compounds may influence spasticity.

Animals↗