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Management of spasticity.

The functional impairment due to spasticity must be carefully assessed before any treatment is considered. Therapeutic intervention is best individualized to a particular patient. Basic principles of treatment to ameliorate spastic hypertonia are: 1) avoid noxious stimuli and 2) provide frequent range of motion. Therapeutic exercise, cold or topical anesthesia may decrease reflex activity for short periods of time in order to facilitate minimal motor function. Casting and splinting techniques are extremely valuable to extend joint range diminished by hypertonicity. Baclofen, diazepam and dantrolene remain the three most commonly used pharmacologic agents in the treatment of spastic hypertonia. Baclofen is generally the drug of choice for spinal cord types of spasticity, while sodium dantrolene is the only agent which acts directly on muscle tissue. Phenytoin with chlorpromazine may be potentially useful if sedation does not limit their use. Tizanidine and ketazolam, not yet available in the United States, may be significant additions to the pharmacologic armamentarium. Intrathecal administration of antispastic medications allows high concentrations of drug near the site of action, which limits side effects. This form of treatment is the most exciting recent development in the treatment of spastic hypertonia. Peripheral electrical stimulation may have limited use in diminishing tone and facilitating paretic muscles. Dorsal column stimulation via electrodes within the spinal column was initially hailed as a therapeutic advance, but has subsequently been shown to be minimally effective. Phenol injections provide a valuable transition between short-term and long-term treatments and offer remediation of hypertonia in selected muscle groups. Tenotomies and tendon transfers offer significant benefit in carefully chosen patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Baclofen↗

Clonidine in the treatment of brainstem spasticity. Case report.

This report describes a patient who developed spasticity after a medullary infarct. No improvement in her spasticity was achieved by baclofen therapy and the side effects of the drug necessitated its gradual withdrawal. Recent reports of the success of clonidine in the management of spasticity due to spinal cord injury prompted an attempt at clonidine therapy. When clonidine therapy was initiated, the patient responded rapidly with both subjective and objective improvements in her spasticity. This case suggests a potential role for clonidine in the treatment of spasticity resulting from brainstem infarction.

Adult↗

Effects of surface spinal cord stimulation on spasticity and quantitative assessment of muscle tone in hemiplegic patients.

Spasticity after a stroke interferes with the normal function of a limb. Electric stimulation has been used in a variety of ways to decrease spasticity. The purposes of this study were (1) to quantify the effectiveness of electric stimulation on decreasing ankle spasticity and (2) to develop a quantitative assessment of muscle tone, which could be replicated in the clinic. Ten patients with hemiparesis resulting from ischemic stroke participated in the study according to the selection criteria. Their mean age was 57 yr, with a mean stroke interval of 12.5 months. Patients received electric stimulation for 45 min through surface electrodes applied to the skin in the 12th thoracic and 1st lumbar areas. All patients received five electric stimulation treatment sessions. The electrical pulses were amplitude modulated frequency beat with a carry frequency of 2500 Hz and a stimulation frequency of 20 Hz. The stimulation intensity was adjusted to each patient to produce a sensory stimulation. The pre- and posttreatment evaluation included surface electromyography activity during passive ankle dorsiflexion, passive ankle dorsiflexion resistance at different angular velocities, as measured by an isokinetic machine and the modified Ashworth scale. Our results indicate that the surface spinal cord stimulation with middle frequency modulated to low frequency for sensory stimulation on the skin of 12th thoracic and first lumbar area is effective in reducing calf muscle spasticity of hemiplegic patients. The isokinetic torque measures for spasticity are a sensitive tool to document the effects of the treatment.

Adult↗

Botulinum toxin treatment of lumbrical spasticity: a brief report.

Botulinum toxin A has been used to treat wrist and finger spasticity mainly through injection of the forearm flexor muscles. This case study describes its first reported use in managing spastic lumbricals of the hand. A 19-year-old male had significant flexion deformity and hypertonicity of the left wrist and hand, particularly the second through fifth metacarpophalangeal joints, after traumatic brain injury. By using the 0-4 Ashworth scale, spasticity of the lumbricals across the second to fourth metacarpophalangeal joints was rated 2, with persistent clonus of the finger flexors as confirmed by electromyography to the middle and ring fingers, even after botulinum toxin A injection of the flexor digitorum sublimis and profundus muscles. By using the electromyography-guided technique, botulinum toxin A was injected into the first lumbrical of the index finger (12 units), second and third lumbricals of the middle and ring fingers, respectively (15 units each), and fourth lumbrical of the little finger (10 units). At follow-up, clinical and electromyographic examination revealed a significant reduction in tone and clonus of the injected lumbricals. Ashworth scores of the lumbricals from the index to little finger improved to 1. Botulinum toxin A injection of the lumbricals can be beneficial in managing spasticity of these muscles. It is well tolerated and effective at doses of 10 to 15 units. Lumbrical injection of botulinum toxin A is a useful adjunct in our percutaneous armamentarium for managing the spastic hand.

Adult↗

Comparison of phenol block and botulinus toxin type A in the treatment of spastic foot after stroke: a randomized, double-blind trial.

Locally acting treatments for spasticity such as nerve and motor point blocks have the advantage of reducing harmful spasticity in one area, while preserving useful spasticity in another area. This randomized, double-blind study is the first trial that was designed to find out whether botulinus toxin Type A and phenol relieves the signs and symptoms of ankle plantar flexor and foot invertor spasticity after stroke and if either of these methods offers any advantages and disadvantages over the other. Twenty patients who were included in this preliminary study were randomly assigned to receive a single treatment of 400 mouse units of botulinus toxin Type A injected into the calf muscles or to receive a tibial nerve blockade with 3 ml of 5% phenol. A combination of subjective and objective measures were used to assess functional change at baseline and at Weeks 2, 4, 8, and 12. At follow-up, significant improvement (P < 0.05) in the Ashworth score for dorsiflexion was observed in both groups. The change in the Ashworth score for eversion was significant in the group that received botulinus toxin Type A (P < 0.05) but not in the group that received phenol (P > 0.05). When those variables were compared between the two groups, the change in the Ashworth score at Weeks 2 and 4 was significantly better in the group that received botulinus toxin Type A (P < 0.05) but there was not a significant difference between the two groups at Weeks 8 and 12 (P > 0.05). The decrease in clonus duration that was detected by electromyography was significant in both groups at all visits, but the decrease in the group that received botulinus toxin Type A was significantly better at Weeks 2 and 4 (P < 0.05). It is concluded that both motor point injections with botulinus toxin Type A and tibial nerve blockade with phenol are effective in plantar flexor spasticity, but the changes were more significant in the group that received botulinus toxin Type A at Weeks 2 and 4, whereas there was not a significant difference between the two groups at Weeks 8 and 12. Future research should explore the long-term effect of these two treatment modalities.

Adult↗

Performance of static standing balance in children with spastic diplegic cerebral palsy under altered sensory environments.

Seven children with spastic diplegic cerebral palsy and 14 age- and gender-matched nondisabled children participated in the present study for an investigation and comparison of their static standing balance under altered sensory environments. The type of visual input (full, occluded, or sway referenced vision) and the type of somatosensory input (fixed or compliant foot support) were varied factorially to give six sensory environments. Each participant was tested barefooted for 30 s under all six conditions. A force platform collected the ground reaction force, from which standing balance was calculated as the sway area of the center of pressure. The results showed that when somatosensory information was reliable (fixed foot support), there was no significant difference in stance stability between the children with spastic diplegic cerebral palsy and their matched controls, and both types of children were equally affected by the type of visual input. However, when somatosensory information was unreliable (compliant foot support), the difference in stance stability between the children with spastic diplegic cerebral palsy and their matched controls was significantly greater when the visual input was deprived (occluded) or unreliable (sway referenced) than when it was reliable. These results suggest that the children with spastic diplegic cerebral palsy may have difficulties in resolving intersensory conflicts for maintenance of standing balance, or the demands of motor control in sensory conflict conditions outweigh the motor ability of children with spastic diplegic cerebral palsy.

Cerebral Palsy↗

Mechanisms of action of phenol block and botulinus toxin Type A in relieving spasticity: electrophysiologic investigation and follow-up.

This preliminary study was designed to investigate the effects of botulinus toxin Type A and phenol treatments on electrophysiologic tests evaluating spinal afferent and efferent motor pathways involved in spasticity. The questions posed were whether different types of mechanisms act on reducing spasticity with these different treatment modalities and whether the tests are correlated with clinical recovery. Twenty patients with lower limb spasticity secondary to stroke were randomly assigned to receive 400 mouse units of botulinus toxin Type A injected into the calf muscles or to receive a tibial nerve blockade with 3 ml of 5% phenol. The amplitudes of the Achilles tendon response, M response, H reflex response, and maximum H:M ratio and Achilles tendon response to H response ratio were recorded from the soleus muscle at baseline and at Weeks 2, 4, and 12. The most obvious change was a reduction in the amplitude of the tendon response in the group that received botulinus toxin Type A, and it was a reduction in the M response amplitude in the group that received phenol. The decrease in the tendon response amplitude and tendon response to H ratio in the group that received botulinus toxin Type A and the decrease in the M response amplitude in the phenol group were found to be well correlated with clinical recovery as assessed by the Ashworth scale. The findings suggested that botulinus toxin Type A injection decreases spasticity primarily by affecting the fusimotor system and muscle spindle, and the involvement of the alpha-motor fibers within the tibial nerve is the most likely factor contributing to the reduction of spasticity after phenol blockade. The therapeutic effectiveness of these agents could be assessed and followed up by the changes in electrophysiologic responses matching their mechanisms of action. The findings should be supported by further electrophysiologic techniques.

Afferent Pathways↗

Effects of botulinum toxin A on upper limb spasticity in children with cerebral palsy.

OBJECTIVE: Botulinum toxin A inhibits presynaptic release of acetylcholine at the neuromuscular junction and has reportedly been successful in the treatment of spastic disorders. This prospective study attempted to determine whether botulinum toxin A injection resulted in clinically measurable gains for 4 mo. DESIGN: Measurements were obtained from 32 children (range, 1-18 yr; average age, 6.9 yr) with hemiplegic or quadriplegic cerebral palsy before and at 1, 3, and 4 mo after botulinum toxin A injections. Spasticity was measured using the Modified Ashworth Scale for 12 different joints. RESULTS: Results showed that spasticity as measured by Ashworth scores for elbow and wrist extension clearly declined (P < 0.02) by 1 mo after botulinum toxin A injection, and diminished spasticity continued for 3-4 mo. Caregivers reported improvement in subjectively rated management, appearance, and function. However, patient response to botulinum toxin A injection was not predictable. Age had no significant relationship to gains. CONCLUSIONS: Further research is needed on the use of botulinum toxin A to diminish spasticity and improve function.

Adolescent↗

Post-stroke spasticity management with repeated botulinum toxin injections in the upper limb.

OBJECTIVE: Although the botulinum toxin A (BTX-A) treatment has proved effective in spasticity management, no information is available with regard to the effects of repeated injections over time. DESIGN: To evaluate the effects of BTX-A on moderate or severe upper limb spasticity, an exploratory investigation was performed on 28 stroke patients treated for 2 yr or longer and observed for 3 yr. Every 3 to 5 mo, each patient received BTX-A injections in upper limb muscles. The assessment, performed before and 1 mo after each injection for a median of 28 mo, included technical and functional objectives and the burden of care. The former were evaluated by using the modified Ashworth Scale for spasticity and the goniometric measurement of rest position and range of motion; functional objectives were evaluated by means of the Frenchay Arm Test and a patient/caregiver goals assessment scale. RESULTS: BTX-A treatment was followed by an improvement in all technical outcome measures. Motor dexterity scores improved in only 8 of 28 patients, vs. daily living activities, which increased in all subjects. Although the average dosage injected per session did not change, intervals between injections became longer. No relationship between either spasticity onset or residual motoricity and response to treatment could be found. CONCLUSIONS: This investigation is relevant clinically because repeated BTX-A injections show unchanging effectiveness in the management of focal spasticity after stroke.

Activities of Daily Living↗

Spastic paretic stiff-legged gait: joint kinetics.

OBJECTIVE: The authors previously suggested that spastic paretic stiff-legged gait, defined as reduced knee flexion in swing associated with upper-motor neuron injury, can be attributed to multiple impairments besides spastic quadriceps activity. This study hypothesizes that subjects with spastic paretic stiff-legged gait have altered kinetics not only about the knee but also about the hip and ankle. DESIGN: Joint kinetic data of 20 subjects with spastic paretic stiff-legged gait caused by stroke were compared with data obtained from 20 able-bodied subjects. RESULTS: Significant reductions in the subject group were found in both peak knee-joint power absorption (0.42+/-0.34 vs. 0.99+/-0.27 W/(kg x m x m/sec)) and peak ankle-joint power generation (0.74+/-0.42 vs. 1.51+/-0.17 W/(kg x m x m/sec); both P < 0.0001). The authors observed increases in peak external-hip flexion torque in stance, hip-power generation in loading response, knee-extension torque in midstance, ankle-dorsiflexion torque, and ankle-power absorption in stance. There was substantial variability in most torque and power values among subjects, which was significantly greater than that observed in the control subjects. CONCLUSIONS: These findings, in conjunction with previous studies, support the likelihood of multiple mechanisms for reduced knee flexion in swing. Alternatively, some of the joint kinetic differences could be compensations for or associated with reduced knee flexion in swing. The substantial variability among subjects implies that despite a similar visual appearance of reduced knee flexion among subjects with a spastic paretic stiff-legged gait pattern, each individual has unique mechanisms associated with this observed gait pattern.

Ankle Joint↗

Botulinum toxin in upper limb spasticity after acquired brain injury: a randomized trial comparing dilution techniques.

OBJECTIVE: To compare the efficacy of two different volume preparations of the same dose of botulinum toxin-A in relieving spasticity in wrist and finger flexors secondary to acquired brain injury. DESIGN: Thirteen adult patients who had modified Ashworth scale scores of 3 for both wrist and finger flexors were included in this randomized, controlled trial. Wrist and finger flexors were each injected. Blinded modified Ashworth scale ratings of wrist and finger flexor spasticity were measured. RESULTS: Spasticity in both muscles decreased significantly in both treatment groups. However, the high-volume and low-volume groups did not differ significantly in spasticity reduction. CONCLUSIONS: Because this preliminary study found no difference in spasticity reduction between high- and low-volume preparations of a 60-unit dose of botulinum toxin-A, a larger-sample study seems warranted to compare the efficacy of high-volume and low-volume preparations.

Adult↗

Soleus neurotomy for treatment of the spastic equinus foot. Groupe d'Evaluation et de Traitement de la Spasticité et de la Dystonie.

OBJECTIVE: This prospective, nonrandomized, noncontrolled study was performed to evaluate the results of a new type of neurotomy, namely the soleus neurotomy, for treatment of the spastic equinus foot. METHODS: Between May 1996 and March 1998, 46 patients were treated for a spastic equinus foot. Clinical status, spasticity (Ashworth Scale score), and kinematic parameters of the gait were determined before and after surgery. The neurotomy was performed on the upper nerve of the soleus in all cases and was associated with other neurotomies (lower nerve of the soleus, 21 patients; gastrocnemius, 9 patients, tibialis posterior, 18 patients; flexor hallucis longus, 16 patients; and flexor digitorum longus, 17 patients). RESULTS: The mean follow-up period was 15 months (range, 8-28 mo). The equinus deformity disappeared clinically in all patients. Before the operation, all patients had an Ashworth Scale score of 2, with an inexhaustible clonus present on knee extension and persisting with knee flexion (Tardieu Scale score, 4), which was abolished in 95% of the patients after surgery. Two patients still had some clonus on knee extension; this did not interfere with their clinical improvement. Knee recurvatum disappeared in eight patients. Analysis of kinematic parameters demonstrated a statistically significant increase in joint motion of the second rocker (P = 0.0026) of the ankle during stance. The duration of the stance or swing phase, length of the walking cycle, and velocity or rate of spontaneous walking were not significantly modified. CONCLUSION: The study demonstrated that soleus neurotomy is effective for the treatment of spastic equinus foot, leading to abolition of spasticity and improvement in the range of ankle motion during the stance phase of gait.

Adolescent↗

Zolpidem for postanoxic spasticity.

A 28-year-old male sustained anoxic brain damage following aborted cardiac arrest, and subsequently developed severe muscular rigidity and spasticity involving all extremities. The spasticity was refractory to the standard regimens used for spastic hypertonia. Zolpidem dramatically inhibited muscular rigidity, spasticity, and dystonic posturing in a dose-dependent manner, resulting in a sustained improvement of his global performance over four years. The authors postulate a central mechanism of action by selective inhibition of GABAergic inhibitory neurons, and suggest a controlled clinical study to investigate the potential efficacy of zolpidem in relieving spasticity related to postanoxic brain injury.

Adult↗

Effect of botulinum toxin type A on cerebral palsy with upper limb spasticity.

OBJECTIVE: The objective of this study was to investigate the effects of botulinum toxin type A injections in reducing upper limb muscular spasticity and in improving motor function in children with cerebral palsy. DESIGN: Fifteen children with spastic cerebral palsy who were undergoing regular physical and occupational therapy were enrolled. Botulinum toxin type A injections in clinically indicated target muscle groups were administered after the children had received 3 mo of therapy. A follow-up study was carried out at 6 wk and 12 wk, respectively, after the botulinum toxin type A injections. The main outcome measurements included the Modified Ashworth Scale, the upper limb Physician's Rating Scale, the Bruininks-Oseretsky Test of Motor Proficiency, and the self-care domain of the Pediatric Evaluation of Disability Inventory. RESULTS: The reduction of spasticity in the treated muscle groups differed significantly between the control period and both study periods. Improvements on the Physician's Rating Scale score during the study period also differed significantly as compared with improvements during the control period. There was a significant difference in the improvement of fine motor skills, as measured with Bruininks-Oseretsky Test of Motor Proficiency, between the control period and both study periods. Improvements in self-care capability differed significantly between the control period and 12 wk after botulinum toxin type A treatment, but not between the control period and at 6 wk after treatment. Muscle strength of grasp and pinch did not differ significantly between the control and the study period. Distribution of body parts involvement, disease severity, and function in daily living activities had no significant correlation with functional improvement after the treatment. CONCLUSIONS: Our findings support the premise that botulinum toxin type A injections are effective in reducing upper limb spasticity and in improving movement pattern and fine motor function of patients with spastic cerebral palsy. A reduction in caregivers' burden and improved quality of life were demonstrated through the study period.

Adolescent↗

Assessment of the short-term effect of antispastic positioning on spasticity.

BACKGROUND: This study was performed in order to investigate the effect of antispastic positioning on spasticity by using different assessment methods. METHODS: A total of 16 patients (11 males [68.75%] and five females [31.25%]), diagnosed as spastic diplegic and referred to the School of Physical Therapy and Rehabilitation, Paediatric Rehabilitation Unit for treatment, were included in this study. The mean age of patients was 6.43 +/- 1.99 years (range, 4-13 years). Passive dorsi-flexion movement was measured by using goniometer and intensity of spasticity was determined by using Modified Ashworth Scale (MAS) and electromyography. For the objective measurement of severity of spasticity, Hoffman reflex (H) and Hoffman reflex/motor response (H/M) ratios were used. Children were placed in an antispastic position for 20 min. The patient was placed in a sitting position, by a physiotherapist, with hips abducted at a 45 degrees angle and externally rotated, knees extended, and ankles placed in a neutral position. RESULTS: The decrease in H responses, H/M ratios, MAS values and the increase in goniometric measurement values were found statistically significant after antispastic positioning (P < 0.05). CONCLUSION: Our study supports that antispastic positioning can be used with neurodevelopmental treatment approaches when it is required. Antispastic positioning may help exercises to be performed more easily, and also has importance in a home exercise program to prevent muscle contractures and joint limitation in children with long-term spastic diplegia.

Cerebral Palsy↗

The effects of isotonic and isokinetic muscle stretch on the excitability of the spinal alpha motor neurones in patients with muscle spasticity.

To examine the effect of isotonic (with and without weight bearing) and isokinetic muscle stretch on the excitability of the spinal alpha motor neurones (alphaMN) in patients with spasticity and to establish whether this effect is maintained for at least 24 h after the intervention. A single 20-min session of isotonic muscle stretch (with or without weight bearing) or isokinetic stretch was delivered to the ankle plantar flexors in patients with post-stroke lower limb spasticity and healthy control subjects. The effect of these types of muscle stretch on the excitability of alphaMN was assessed by measuring the latency of the Hoffmann reflex (H-reflex) and the ratio of the amplitude of the maximum H-reflex (H(max)) to that of the maximum action motor potential of the soleus muscle (M(max)). Sixty-six hemiplegic stroke patients and 21 healthy control subjects were recruited and completed the trial. The H(max):M(max) ratio was significantly higher in patients with spasticity than in healthy control subjects. However, there were no statistically significant differences in the H-reflex latency or the change in H(max):M(max) ratio between the baseline values and those recorded immediately after the therapy intervention or 24 h later for each type of muscle stretch. Similarly, there were no significant differences in these variables between the interventions. In the present study neither isotonic muscle stretch (with or without weight bearing) or isokinetic stretch had a statistically significant effect on the excitability of the alphaMN in patients with muscle spasticity. This suggests that the previously reported reduction in spasticity after muscle stretch is because of mechanisms other than the direct effect on alphaMN. However, the lack of a demonstrable benefit of treatment may be due the fact that we examined the effects of a single, rather than repeated treatment cycles.

Aged↗

Quantitative measurement of spasticity in children with cerebral palsy.

Spasticity was quantified in nine children with spastic diplegia, using a sinusoidal displacement of the foot at frequencies from 3 to 12Hz. Ankle-joint stiffness was separated into elastic (energy-storing) and viscous (energy-dissipating) components. 'Path length' was used to represent the variation in stiffness over this frequency range. Compared with 11 unaffected children, a significant difference in path lengths was demonstrated for the children with spasticity. An age-dependent effect was demonstrated when path lengths of unaffected children were compared with those of 10 unaffected adults. A modified path-length measure is proposed which minimizes age dependency, yet enables detection of spasticity. Passive stiffness properties of unaffected adults showed higher elastic stiffness, viscosity and friction than unaffected children. A method was developed to evade the need for temporary nerve blocks to calculate inerital properties of the foot in persons with spasticity.

Biomechanical Phenomena↗

Mechanisms of baclofen action on spasticity.

This investigation estimated the mechanisms of baclofen action on spasticity using a battery of electromyographic methods. Thirty patients with old post-stroke spastic hemiparesis took part in the investigation. They were treated with baclofen-mean daily dose 54.3 alpha 11.6 mg for a mean of 26.3 alpha 4.9 days. A questionnaire for assessment of subjective improvement after treatment used a 5-point scale. For standardization of the neurological examination 5-point scales were used to assess muscle tone, muscle force and tendon reflexes. A battery of electromyographic methods was used to analyse different mechanisms of spasticity: for alpha motoneurone activity--the F wave parameters; for gamma motoneurone activity--the T/H reflex amplitude ratio; for presynaptic inhibition--the ratio of H reflex amplitudes before and after vibration on the achilles tendon (Hvibr./Hmax); for common interneurone activity--the flexor reflex parameters. Our results revealed that baclofen reduces spastically increased muscle tone and Babinski sign. It has no influence on muscle force, tendon reflexes and ankle clonus. Baclofen acts by normalizing the altered interneurone activity and decreasing of alpha motoneurone activity. When spasticity has altered interneurone activity and increased motoneurone activity, it is better to treat with baclofen.

Baclofen↗