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PubMed1993

Common gait abnormalities of the knee in cerebral palsy.

Gait abnormalities in children with cerebral palsy are the consequence of contractures across joints, muscle spasticity, and phasically inappropriate muscle action. Though abnormalities involving one of the major joints of the lower extremity will usually have consequences on the function of the other joints, it is possible to recognize certain primary disorders at each joint. The most common gait abnormalities of the knee in patients with cerebral palsy occur in the sagittal plane. Based on the experience gained from performing gait analysis on more than 588 patients with cerebral palsy, four primary gait abnormalities of the knee have been identified: jump knee, crouch knee, stiff knee, and recurvatum knee. In this review, each abnormality is described by its motion analysis laboratory profile (physical examination, motion parameters, electromyography [EMG] data, and force plate data). The most common etiologies and the consequences for gait of each disorder are also considered. Appreciation of the most common pathologic patterns of gait should facilitate accurate and detailed analysis of the individual patient with gait abnormalities.

Biomechanical Phenomena↗
PubMed2002

Cost-effectiveness comparison of tizanidine and baclofen in the management of spasticity.

OBJECTIVE: Baclofen and tizanidine are both used for the treatment of muscle spasticity of spinal origin. Their effectiveness, cost and adverse-effect profiles differ. This paper sets out to estimate the cost effectiveness of each drug, and the impact of changing from baclofen to tizanidine. DESIGN: A simplified but realistic model of physician behaviour and patient response was developed as a decision tree and populated with data derived from the available published clinical comparative trials. We considered patients with spasticity caused by multiple sclerosis or spinal cord injury. The outcome measure used was 'cost per successfully treated day' (STD). Costs were estimated from the perspective of the UK National Health Service at 2000 values. RESULTS: Expected cost for a cohort of 100 patients over 1 year was estimated to be pound 181 545 with baclofen and pound 211 930 with tizanidine. The estimated number of STDs was 20,192 with tizanidine and 17,289 with baclofen. The overall cost effectiveness of managing spasticity using baclofen and tizanidine was very similar ( pound 10.50 and pound 10.49 per STD respectively). The incremental cost effectiveness (ICE) of using tinzanidine as an alternative to baclofen for first-line treatment was pound 10.47 per STD. Sensitivity analysis found the model to be robust to changes in key parameters CONCLUSION: Drug cost should not be a determining factor in making this treatment choice, as the cost effectiveness ratios are similar for both products.

Baclofen↗
PubMed1980

Phenytoin and chlorpromazine in the treatment of spasticity.

The efficacy of phenytoin sodium and chlorpromazine hydrochloride in the reduction of spasticity was evaluated in both open and controlled studies. In each study, the majority of patients exhibited both objective and subjective signs of improvement. Reduction of motor tone in spastic muscles, as well as improvement in functiional status, was observed. Most patients experienced greater benefit from the combination of phenytoin and chlorpromazine than from either drug alone. The use of the drugs in combination permitted decreased chlorpromazine doses and reduced unwanted side effects such as lethargy and somnolence. These drugs may exert their action by suppressing fusimotor efferent as well as afferent discharged from muscle spindles. The results suggest that the fusimotor system is an important pharmacologic target in the treatment of spasticity.

Adult↗
PubMed2002

The role of botulinum toxin a in the management of lower limb spasticity in patients with cerebral palsy.

This study aimed to determine the effects of botulinum toxin-A (btA) on spasticity in children with cerebral palsy (CP). Thirty-five children with spastic CP were evaluated. The injection group consisted of 25 patients who were injected with btA and received conventional physical therapy. The control group consisted of 10 patients who were treated with conventional physical therapy only. In the injection group, btA was applied to the lower extremity spastic muscles at a total dose of 8-10 lU/kg. Spasticity was measured by the Ashworth scale. Gait function was evaluated by clinical gait assessment in all patients and temporal distance factors in 16 patients. All the parameters were recorded before treatment, after three days and after one month of therapy. Following injection of btA, significant improvement in all parameters was observed. No statistically significant progression was noted in the control group except clinical gait analysis scores. Comparing the three-day and one-month measurements of spasticity of the two groups, statistically significant results were obtained in favour of the injection group in all parameters except for clinical gait analysis scores. The findings of this study showed btA injection to be an effective treatment for reducing spasticity and improving gait function in patients with spastic CP

Adolescent↗
PubMed1994

The quantitative measurement of spasticity: effect of cutaneous electrical stimulation.

The goal of this research was to determine if cutaneous electrotherapy would temporarily reduce muscle spasticity. Five traumatically brain injured (TBI) and five spinal cord injured (SCI) subjects, all with clinically evident spasticity, received surface electrical stimulation over the tibialis anterior muscle. Using the Spasticity Measurement System, stiffness around the ankle was measured before, immediately after, and 24 hours after treatment. With stimulation, ipsilateral ankle viscoelastic stiffness immediately decreased in 9 of 10 subjects and remained significantly depressed for up to 24 hours. Contralateral ankle spasticity did not significantly change. Using the same subjects under sham conditions, no significant decrements in spasticity occurred. In a subjective survey, only SCI participants reported functionally evident spasticity reductions. Also within this subgroup, efficacy of treatment was directly proportional to the severity of pre-stimulation clonus. We conclude that (1) cutaneous electrotherapy transiently decreases both TBI and SCI related spasticity and (2) pre-stimulation clonus may function as a clinical indicator of SCI patients most likely to benefit from this process.

Adult↗
PubMed2001

[Selective fasicular neurotomy for spastic equinovarus foot deformity in cerebral palsy children].

Spasticity is usually treated by rehabilitation, orthosis, chemical denervations, orthopaedic surgery and neurosurgery. Selective fascicular neurotomy is a neurosurgical procedure consisting in partial section of selected motor nerves innervating spastic muscles. Neurotomy is indicated in cases of localised disabling spasticity without musculotendinous shortening, resistant to chemical denervation and for which a motor nerve block with anaesthetic has given a good functional result. Neurotomy includes division of the afferent Ia and Ib fibers, unable to recover, leading to permanent disappearance of the spasticity. Neurotomy also includes section of the motor efferent fibers with transient paresis as a result. In adults, neurotomy provides functional improvement in 81 to 97% of cases. In case of posterior tibial neurotomy, improved walking stability and a decrease in foot equinus and knee recurvatum is observed. In children, the risk of deformity recurrence seems higher because of motor axonal reinnervation: indications must therefore be carefully considered and rehabilitation provided after surgery.

Afferent Pathways↗
PubMed1987

Role of peripheral afferents and spinal reflexes in normal and impaired human locomotion.

For many years, electrophysiological investigations of locomotion were restricted to animals, largely the cat. They concentrated on and emphasized the role of spinal interneuronal networks responsible for the generation of the locomotor pattern. Following the introduction of perturbation impulses and electrical nerve stimulation during stance and gait, information became increasingly available concerning the role of the reflex systems involved in the regulation of gait, their afferent pathways and their control by supraspinal motor centres. During gait monosynaptic stretch reflexes are inhibited. From a knowledge of the behaviour of the cerebral potentials evoked during stance and gait, it can be deduced that during gait the signals of group I afferents are blocked at both segmental and supraspinal levels. Polysynaptic reflex responses are mainly responsible for the compensation of perturbations introduced during gait. They are most probably mediated by group II afferents via a spinal pathway closely connected with the spinal locomotor centres. The functioning of these responses depends on an intact supraspinal control. They are suggested to be incorporated in a more complex e.m.g. pattern mainly determined by central mechanisms. In contrast to the gait condition, segmental stretch reflex activity does contribute to activation of extensor muscles of the leg during fast movements, such as running and hopping. In children at an early stage in the development of gait (around 1 to 2 years of age), as well as in patients with spastic paresis, the polysynaptic reflex responses are reduced or absent, and isolated monosynaptic reflex potentials are present. This suggests a reciprocal modulation of mono- and polysynaptic reflex mechanisms, both being dependant on supraspinal control. When this control is either not yet matured (small children) or impaired (spastic paresis), inhibition of monosynaptic stretch reflexes is absent and associated with a reduced facilitation of polysynaptic spinal reflexes. In spastic muscle hypertonia, the tension developed at the Achilles tendon during gait cannot be explained by gastrocnemius activation alone. In patients with spastic hemiparesis gastrocnemius e.m.g. activity is reduced in the spastic leg as compared to the unaffected one. It can be concluded that the paretic muscle undergoes changes in its mechanical properties, secondary to the supraspinal lesion, which results in the development of spastic muscle hypertonia.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1998

[Botulinum toxin in spasticity treatment].

The author reviews the current opinions on the treatment of spasticity with special consideration given to the new method of treatment with local injections of botulinum toxin A into the spastic muscles. Botulinum toxin is the treatment of choice in focal dystonias and hemifacial spasm. The mechanism of action of the toxin is unique and is a result of dose-dependent and partial chemical denervation of the muscles, with preservation of tonus and thus its function. Recent reports have confirmed the safety and effectiveness of the method in spasticity, especially when it is focal, not diffuse or severe and without concomitant severe paresis. The author describes also the basic data of the pathophysiology of spasticity and reviews other therapeutic options and practical problems concerning the injections of botulinum toxin.

Botulinum Toxins, Type A↗
PubMed1993

Intrathecal baclofen for severe spasticity secondary to spinal cord injury.

OBJECTIVE: To evaluate the use of intrathecal baclofen for the treatment of muscle spasticity in patients with spinal cord injury. DATA SOURCES: A MEDLINE search was used to identify relevant and pertinent literature. Information was obtained from open-label clinical trials, abstracts, conference proceedings, and review articles. Index terms in the search included baclofen, spasticity, intrathecal drug infusion, spinal cord disease, and neurosurgery. DATA EXTRACTION: Studies were selected for review if they evaluated intrathecal baclofen in patients with spinal cord injury. Emphasis was placed on human studies published in the English language. Trials were reviewed by dosage regimen, therapeutic response, adverse effects, and complications. DATA SYNTHESIS: Thus far, intrathecal baclofen administration shows promise in the treatment of spasticity resulting from spinal cord trauma. Few complications and adverse effects have been reported. CONCLUSIONS: Muscle spasms and spasticity constitute a significant problem in spinal cord injuries, interfering with rehabilitation and leading to inconveniences and complications in these patients. Oral baclofen is the drug of choice for spasticity due to spinal cord trauma. It often is ineffective, however, because of the large dosages required to cross the blood-brain barrier and the subsequent appearance of central nervous system adverse effects. These adverse effects are not tolerated by many patients. Intrathecally administered baclofen has been approved by the Food and Drug Administration (FDA) for the treatment of spasticity in patients with spinal cord injury who are refractory to or cannot tolerate oral baclofen. It is intended for use only in implantable pumps approved by the FDA for the administration of baclofen into the intrathecal space. Intrathecal administration achieves high concentrations in the spinal cord with small dosages, thus reducing the incidence of central nervous system adverse effects. To date, approximately 350 patients with spinal cord injury have been treated with intrathecal baclofen. Reductions in spasticity have been demonstrated in both open-label and placebo-controlled trials. Patients also often make substantial gains in activities of daily living. Few adverse effects and complications have been reported. However, tolerance to the clinical effects of intrathecal baclofen has been reported. Further studies are needed to determine specific patient populations that may benefit most from intrathecal baclofen administration. Individual dosage ranges and follow-up care also need to be defined more completely. In addition, the question of whether tolerance detracts from long-term clinical benefits with intrathecal baclofen needs to be addressed.

Baclofen↗
PubMed2006

Comparison of the efficacies of botulinum toxin A and Johnstone pressure splints against hip adductor spasticity among patients with cerebral palsy: a randomized trial.

OBJECTIVE: The goal was to compare the efficacies of botulinum toxin A (BTX) treatment and Johnstone pressure splint (JPS) treatment against hip adductor muscle spasticity among children with spastic diplegic cerebral palsy. METHODS: For each patient in the BTX group, a total of 300 IU of BTX was injected into adductor and medial hamstring muscle groups. In the JPS group, long leg JPS were administered for 30 minutes 3 days per week. Bobath neurodevelopmental exercises were administered to both groups 3 days per week during the study period. All cases were assessed by using gross motor function measurements, passive hip abduction goniometric measurements, modified Ashworth Scale scores, and measurements of the distance between the knees as indicator variables. RESULTS: We found that there was statistically significant improvement in all indicators for both groups. BTX treatment was found to be superior to JPS treatment in terms of the indicator variables of our study.

Adolescent↗
PubMed1994

A double-blind, placebo-controlled trial of tizanidine in the treatment of spasticity caused by multiple sclerosis. United Kingdom Tizanidine Trial Group.

Tizanidine was evaluated in a prospective, double-blind, randomized, placebo-controlled trial in 187 patients with MS. Taken orally for 9 weeks and preceded by a titration phase for a period of 3 weeks starting at 2 mg daily, tizanidine produced a significant reduction in spastic muscle tone compared with placebo treatment. Within the effective dose range of 24 to 36 mg given daily in three doses, tizanidine achieved a 20% mean reduction in muscle tone. Approximately 75% of patients, with all degrees of spasticity, reported subjective improvement without an increase in muscle weakness, but there was no improvement in activities of daily living depending on movement. Tizanidine achieved its maximum effect on spasticity within 1 week of the start of treatment; the benefit was maintained for at least 1 week after discontinuation of therapy. A variety of adverse events was recorded by patients taking tizanidine, but these were minor and reversible, and rarely limited treatment. Tizanidine is a well-tolerated and effective drug for symptomatic treatment of spasticity.

Activities of Daily Living↗
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↗
PubMed2004

The beneficial antispasticity effect of botulinum toxin type A is maintained after repeated treatment cycles.

OBJECTIVE: To study the efficacy, safety, and incidence of BtxA antibody formation with repeated treatments with BtxA in post-stroke upper limb muscle spasticity. METHODS: The study was a prospective open label trial. Patients with established post-stroke upper limb spasticity received 1000 units of BtxA (Dysport) into five muscles of the affected arm on study entry. Treatment was repeated every 12, 16, or 20 weeks as clinically indicated. Each patient received a total of three treatment cycles. Efficacy of treatment was assessed using the Modified Ashworth Scale. Patients were assessed on study entry and on week 4 and 12 of each treatment cycle for all safety and efficacy parameters. Blood samples for BtxA antibody assay were taken at baseline and on completion of the trial. RESULTS: Fifty one patients were recruited and 41 of them completed the study. Improvement from the cycle one baseline was observed in all the outcome measures. Mild to moderately severe treatment related adverse events were reported in 24% of cases. There were no serious adverse events. No BtxA antibodies were detected. CONCLUSION: BtxA at a dose of 1000 units Dysport was efficacious in the symptomatic treatment of post-stroke upper limb spasticity. The study suggests that this effect can be maintained with repeated injections for up to at least three treatment cycles, with duration of effect per cycle of between 12 and 20 weeks. BtxA was safe in the dose used in this study and did not induce the formation of detectable levels of neutralising BtxA antibodies.

Adult↗
PubMed2005

Characterization of the mechanical and neural components of spastic hypertonia with modified H reflex.

As the H reflex remains unable to assess mechanical changes intrinsic to a muscle, the aim of this study was to modify the H reflex techniques and to characterize the neural and mechanical components of muscle spasticity, relating the two components to clinical observations. Thirty-four patients featuring either a spinal-cord lesion (n=15) or stroke (n=19) and 23 neurologically normal subjects were recruited. Soleus H reflex and maximal M response (M(max)) were measured with electromyography and mechanomyography (MMG). The motoneuronal excitability was represented with the adjusted ratio of the H reflex to the M(max) (H/M(max)) and the ratio of the paired H reflexes (H(2)/H(1)). Muscle mechanical properties were characterized by the amplitude and median frequency of maximal M response recorded with MMG (MMG(Mmax)). The results showed that spastic patients exhibited a larger H/M(max), H(2)/H(1) and amplitude of MMG(Mmax) than the control group. H/M(max) and amplitude of MMG(Mmax) accounted for 55.7% of the variance in the Modified Ashworth Scale, the clinical hypertonia assessment. The amplitude of MMG(Mmax) correlated with functional impairments, as assessed with the Barthel index and Fugl-Meyer motor-assessment scale. It was concluded that spastic hypertonia involved an atypical increase in motoneuronal excitability and muscle mechanical properties, while impairment of functional performance and daily activity was attributable primarily to altered mechanical properties of a spastic muscle.

Adult↗
PubMed2001

A dynamical model of locomotion in spastic hemiplegic cerebral palsy: influence of walking speed.

OBJECTIVE: The objective of this study was to assess the capability of an escapement-driven inverted pendulum with springs and damping model to estimate the effects of impairments (e.g. spasticity, muscle weakness) on the dynamics and patterns of locomotion of children with spastic cerebral palsy. METHODS: Kinematic data of six children with spastic hemiplegic cerebral palsy and six matched, typically developing children were collected at five different self-selected overground walking speeds ('very slow' to 'very fast'). Changes in forcing, stiffness and gravitational potentials were estimated during the stance phase of each leg according to the model's equation of motion. RESULTS: Significantly greater stiffness and decreased forcing was observed in the more affected limbs of children with spastic hemiplegic cerebral palsy and compared to typically developing peers. The forcing term of the non-affected limb was greater than that of the matched typically developing children. CONCLUSIONS: Results support the claim that disabled individuals with losses in dynamic resources (stiffness, muscle forcing capability) exploit and develop the remaining resources in their adapted gait patterns. It was suggested that clinical interventions aimed at normalizing a gait pattern may be contraindicated, and that rehabilitation might be more effective if focused at the level of dynamics. RELEVANCE: Pattern formation is seen as an optimal solution based on the individuals' action capabilities and dynamic properties under environmental and task demands. This perspective could lead to the development of interventions that address these dynamic variables with the objective of improving the functional capabilities of children with cerebral palsy.

Adolescent↗
PubMed1988

Spasticity and contracture. Physiologic aspects of formation.

Disruption of the upper motor neuron inhibitory pathways by stroke, brain trauma, or spinal cord injury leads to muscle spasticity. Spasticity is characterized by increased muscle tone, hyperactive reflexes, and possible clonus or rigidity. The increased muscle tone may result in loss of joint motion, leading to contractures. Treatment of established contractures is difficult. Prevention of contractures by joint mobilization is emphasized as a goal in the management of patients with spasticity.

Animals↗
PubMed1987

Treatment of spasticity with tizanidine in multiple sclerosis.

Spasticity is a frequent and often disabling symptom in MS patients. Current drugs used as antispastic agents include Dantrolene Sodium, Baclofen and Diazepam. Tizanidine (5-chloro-4-(2imidazolin-2 yl amino)-2,1,3-benzothialdiazole) is a new antispasticity agent that has purported central action. A double blind placebo controlled trial was performed to study the efficacy of this drug in MS patients. Sixty-six patients entered an eight week therapeutic trial and fifty-nine completed the trial. Patients were assessed at 0, 2, 3 and 8 weeks of therapy for clinical effects. Electrophysiologic tests were performed at 0 and 8 weeks. A statistically significant benefit was noted in spastic muscle groups in the legs with concomitant significant reduction in hyperactive stretch reflexes and ankle clonus. Side effects most frequently cited included dry mouth and drowsiness. Two patients developed elevated liver function test that decreased with cessation of therapy. Other clinical details, side effects and electrophysiologic data will be presented. Tizanidine appears to reduce clinical spasticity and hyperreflexia in MS patients although no change in functional status was detected. Tizanidine may well serve as an alternate antispastic agent, alone or in combination with other agents.

Adolescent↗