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PubMed2001

[Early pain reduction in the treatment of spasticity after a single injection of botulinum A toxin].

UNLABELLED: HISTORY, ADMISSION FINDINGS AND DIAGNOSIS: After stem-cell transplantation a 45-year-old woman (case 1) had an attack of general hypoxia requiring resuscitation. She then developed a quadriplegia and spasticity of all limbs notably of the right arm and a severe pain syndrome which had to be treated by oral and intravenous analgesics. Immobilisation and secondary complications aggravated the already difficult situation. In the 2nd case a 66-year-old woman was admitted to our outpatient clinic with long-standing left-sided spastic hemiparesis after territorial infarction of the right middle cerebral artery. Beside the spasticity she also suffered from a distinct pain syndrome which did not respond to any oral analgesics. TREATMENT AND COURSE: For the treatment of the main symptoms, both patients received intramuscular injections of 1000 MU botulinum toxin A (Dysport(R) Ipsen Pharma). Astonishingly, both patients experienced pain relief the next day, whereas spasticity started to respond only 5-6 days later. CONCLUSIONS: In our experience pain relief after botulinum toxin A injections occurs not only due to reduced muscle hyperactivity, especially when such a temporal dissociation between pain relief and muscle relaxation appears as in the two cases reported above. Rather, we believe that botulinum toxin A interferes with the release of other neurotransmitters e. g. substance P (SP) and calcitonine-gene-related-peptide (CGRP) having a key function in the nociceptive cascade.

Aged↗
PubMed2006

Further clinical and genetic characterization of SPG11: hereditary spastic paraplegia with thin corpus callosum.

Hereditary spastic paraplegias (HSPs) are a heterogeneous group of neurodegenerative disorders leading to progressive spasticity of the lower limbs. Clinically, HSPs are divided into "pure" and "complicated" forms. In pure HSP, the spasticity of the lower limbs is the sole symptom, whereas in complicated forms additional neurological and non-neurological features are observed. Genetically, HSPs are divided into autosomal dominant (AD), autosomal recessive (AR) and X-linked (XL) forms. Up to date, 30 different HSPs are linked to different chromosomal loci and 11 genes could be defined for AR-HSP, AD-HSP and XL-HSP. SPG11, an AR-HSP (synonym: HSP11), is a complicated HSP associated with a slowly progressive spastic paraparesis, mental impairment and the development of a thin corpus callosum (TCC) during the course of the disease. SPG11 has been previously linked to chromosomal region 15q13 - 15. First, we applied rigid diagnostic criteria to systematically examine 20 Turkish families with autosomal recessive HSP for characteristic features of SPG11. We detected four large Turkish families with AR-HSP and TCC consistent with SPG11. Subsequent genetic linkage analysis of those 4 families refines the SPG11 locus further down to a small region of 2.93 cM with a maximum lod score of 11.84 at marker D15S659 and will guide further candidate gene analysis.

Adolescent↗
PubMed1997

Interventional neuropediatrics: treatment of dystonic and spastic muscular hyperactivity with botulinum toxin A.

Therapeutic effect of botulinum toxin A was studied in a group of pediatric patients (n = 28) aged between 6 months and 18 years. The patients were diagnosed with cervical dystonia (n = 6), adductor spasm of the hip (n = 8), spastic drop foot (n = 7) and various other focal motor problems associated with spastic muscular hyperactivity (n = 7). The mean dose of botulinum toxin A (Dysport) used to inject into the affected muscle was 22 U/kg body weight. Reduced muscular hyperactivity with a significant increase in joint mobility was achieved for dystonic (p < 0.0001) as well as for spastic conditions in patients with adductor spasm (p < 0.0002). For these patients the improved joint mobility represented a significant benefit for both daily activities and nursing care. Local paresis and local hematoma were observed in 1/28 and 1/28 patients, respectively; 1/28 patients developed a secondary non-response. However, apart from these side effects, no other adverse reactions to botulinum toxin A treatment were recorded during the treatment and observation period (12-64 months). Our results suggest that botulinum toxin A represents an effective and safe therapeutic substance for the treatment of pediatric patients suffering of focal motor problems due to dystonic or spastic muscular hyperactivity.

Adolescent↗
PubMed1981

Spinal surgery for spasticity (46 cases).

The authors report their experiences in the surgical treatment of spastic syndromes by operations on the spinal cord and nerve roots. In the authors' neurosurgical department 20 lumbar myelotomies, 19 posterior selective lumbar rhizotomies, 2 complete posterior lumbar rhizotomies, 4 anterior lumbar rhizotomies and five posterior cervical rhizotomies were performed. Clinical results can be considered good on the whole. There was no mortality and no major complication in the entire series. The effect of selective posterior lumbar rhizotomy on the evolution of cerebropathic spastic paraparesis was particularly impressive. Six of 46 patients experienced a late recurrence of spasticity, but they all had good results after a further operation. The particular criteria for selection of each surgical procedure are discussed and related to the aetiology and clinical picture of the spastic syndrome.

Adolescent↗
PubMed2004

Functional outcome following Botulinum toxin A injection to reduce spastic equinus in adults with traumatic brain injury.

PRIMARY OBJECTIVE: The aim of this study was to assess the effect of Botulinum toxin A in the management of spastic equinus resulting from traumatic brain injury. RESEARCH DESIGN: A before-after intervention design was used without controls. METHODS AND PROCEDURES: Subjects were seven patients suffering from traumatic brain injury of average duration 14 (4-38) months as a result of motor vehicle trauma, who had spastic equinus interfering with gait. EXPERIMENTAL INTERVENTION: The patients were treated with injections of Botulinum toxin A into the spastic calf muscles: gastrocnemius, soleus and tibialis posterior. Assessments were made pre-injection and at 2 weeks and 3 months post-injection. MAIN OUTCOME AND RESULTS: At the end of the 3-month period, all patients showed a significant improvement in gait velocity, cadence and stride length. CONCLUSIONS: The findings suggest that Botulinum toxin A may be useful in the management of spastic equinus following traumatic brain injury.

Adult↗
PubMed2001

The effect of cooling on muscle co-ordination in spasticity: assessment with the repetitive movement test.

PURPOSE: Cooling muscles might produce a temporary reduction of spasticity. This study investigated muscle co-ordination in spasticity under the influence of cooling. METHODS: A repetitive movement (RM-) test of the ankle was used, while measuring the angle and surface-electromyography (EMG) of the m. tibialis anterior and m. triceps surae. Ensemble averaging provided quantified measures of muscle activation. Sixteen patients with spasticity in their lower extremity due to stroke or spinal cord injury participated in the study. Physical examination and the RM-test was done before and after cooling the m. triceps surae for 20 minutes by coldpacks. RESULTS: The results show that Achilles hyperreflexia and clonus were abolished in all, and all but one patient, respectively. The EMG of the m. triceps surae, acting as a prime mover, was increased (p = 0.028). However, this improved muscle co-ordination resulted in just a slightly increased active range of motion (less than 2 degrees at p = 0.049). CONCLUSION: Apparently, the increase in excitability of the alpha motoneuron pool in voluntary movements of patients with spasticity is not followed by an improvement in the ability to move.

Ankle Joint↗
PubMedDate not supplied

Neurophysiological methods for the assessment of spasticity: the Hoffmann reflex, the tendon reflex, and the stretch reflex.

PURPOSE: To review the literature concerning neurophysiological methods to assess spasticity with respect to mechanisms and methodology, and to describe the three most commonly used methods: the Hoffmann reflex (H-reflex), the Tendon reflex (T-reflex), and the Stretch Reflex (SR). METHOD: A systematic internet database search was performed to identify neurophysiological measurement methods of spasticity. A systematic exclusion procedure resulted in 185 included references, completed by additional informal search. For this paper, information about the H-, T- and stretch reflexes was extracted from these references. RESULTS: Although the reflexes are basically monosynaptic, there are many supraspinal pathways which modulate the responses in terms of their amplitude and latency. As a consequence the methods are sensitive to a considerable number of experimental conditions and are characterized by a moderate reliability and sensitivity. Correlations with other (i.e. biomechanical, neurophysiological or clinical) spasticity assessment parameters are moderate to poor. Standardised and broadly accepted protocols are still largely lacking preventing an effective exchange of knowledge. CONCLUSIONS: The clinical and experimental use of the three methods is restricted due to moderate reliability and sensitivity. It is recommended to perform combined neurophysiological-biomechanical assessment of spasticity during active, functional movement.

Electromyography↗
PubMedDate not supplied

Biomechanical approaches applied to the lower and upper limb for the measurement of spasticity: a systematic review of the literature.

PURPOSE: To review and characterise biomechanical approaches for the measurement of spasticity as one component of the upper motor neurone syndrome. METHOD: Systematic literature searches based on defined constructs and a four-step review process of approaches used or described to measure spasticity, its association with function or associated phenomena. Most approaches were limited to individual joints and therefore, to reflect this trend, references were grouped according to which body joint(s) were investigated or whether it addressed a functional activity. For each joint, references were further sub-divided into the types of measurement method described. RESULTS: A database of 335 references was established for the review process. The knee, ankle and elbow joints were the most popular, perhaps reflecting the assumption that they are mono-planar in movement and therefore simpler to assess. Seven measurement methods were identified: five involving passive movement (manual, controlled displacement, controlled torque, gravitational and tendon tap) and two involving active movement (voluntary and functional). Generally, the equipment described was in an experimental stage and there was a lack of information on system properties, such as accuracy or reliability. Patient testing was either by cohort or case studies. The review also conveyed the myriad of interpretations of the concept of spasticity. CONCLUSIONS: Though biomechanical approaches provide quantitative data, the review highlighted several limitations that have prevented them being established as an appropriate method for clinical application to measure spasticity.

Arm↗
PubMed2003

Botulinum toxin--mechanisms of action and clinical use in spasticity.

Botulinum toxin is a potent neurotoxin produced by the bacterium Clostridium botulinum. There are seven serotypes, all of which block the release of acetylcholine from nerve endings, which gives the compound its theoretical base for reducing spasticity. Initial studies of the use of botulinum toxin in the management of spasticity were promising and now there are a number of well-designed, double-blind, placebo-controlled studies that confirm the place of botulinum toxin in our treatment armoury against focal spasticity. The studies have demonstrated both efficacy and safety. There is still more work to be done in terms of disability although early reports confirm functional improvements, particularly reduction of pain as well as improvements in nursing care, hygiene and carer burden. Further studies also need to be done to confirm the place of botulinum toxin in the overall context of other treatment possibilities in the management of spasticity.

Adult↗
PubMed2003

Long-term modification of spasticity.

This review of the long-term management of spasticity addresses some of the clinical dilemmas in the management of patients with chronic disability. As it is important for clinicians to have clear objectives in patient treatment, the available treatment strategies are set out. Why is it important to treat spastic patients and what treatment does one use? When should one consider a change in the strategy and why is it necessary to have a clear discharge policy from the service to avoid serious logistic problems? The review reiterates the role of physical treatment in the management and thereafter the maintenance of patients with spasticity. There are now a number of good papers on the use of botulinum toxin in spasticity, but this review sets out their context in clinical management and briefly mentions the use of phenol nerve blockade and intrathecal baclofen in clinical practice. Finally, how does one justify the use of an agent regarded as expensive? It is important to use outcome measures that are valid and sensitive to change, and an example is given of ways of demonstrating benefit.

Algorithms↗
PubMed2002

Infantile-onset ascending hereditary spastic paralysis is associated with mutations in the alsin gene.

We studied 15 patients, from 10 families, who presented with severe spastic paralysis with an infantile onset and an ascending progression. Spastic paraplegia began during the first 2 years of life and extended to upper limbs within the next few years. During the first decade of life, the disease progressed to tetraplegia, anarthria, dysphagia, and slow eye movements. Overall, the disease was compatible with long survival. Signs of lower motor-neuron involvement were never observed, whereas motor-evoked potentials and magnetic resonance imaging demonstrated a primitive, pure degeneration of the upper motor neurons. Genotyping and linkage analyses demonstrated that this infantile-onset ascending hereditary spastic paralysis (IAHSP) is allelic to the condition previously reported as juvenile amyotrophic lateral sclerosis at the ALS2 locus on chromosome 2q33-35 (LOD score 6.66 at recombination fraction 0). We analyzed ALS2, recently found mutated in consanguineous Arabic families presenting either an ALS2 phenotype or juvenile-onset primary lateral sclerosis (JPLS), as a candidate gene. In 4 of the 10 families, we found abnormalities: three deletions and one splice-site mutation. All the mutations lead to a truncated alsin protein. In one case, the mutation affected both the short and the long alsin transcript. In the six remaining families, absence of cDNA ALS2 mutations suggests either mutations in regulatory ALS2 regions or genetic heterogeneity, as already reported in JPLS. Alsin mutations are responsible for a primitive, retrograde degeneration of the upper motor neurons of the pyramidal tracts, leading to a clinical continuum from infantile (IAHSP) to juvenile forms with (ALS2) or without (JPLS) lower motor-neuron involvement. Further analyses will determine whether other hereditary disorders with primitive involvement of the central motor pathways, as pure forms of spastic paraplegia, could be due to alsin dysfunction.

Adolescent↗
PubMed2006

Biomechanical measurement of post-stroke spasticity.

BACKGROUND: spasticity following stroke is common, but clinical measurement is difficult and inaccurate. The most common measure is the modified Ashworth scale (MAS) which grades resistance to passive movement (RPM), but its validity is unclear. AIM: to assess the validity of the MAS. METHODS: spasticity was clinically graded using MAS and RPM measured biomechanically in the impaired arm of 111 patients following stroke. The biomechanical device measured RPM, applied force, angular displacement, mean velocity, passive range of movement (PROM) and time required. RESULTS: the median age was 72 years, and 66 subjects were male. The clinical grading by MAS was '0' in 15, '1' in 15, '1+' in 14, '2' in 13, '3' in 43 and '4' in 11. There was no difference in RPM among '0', '1', '1+' and '2' (P > 0.1). However, grade'4' was higher than '3' and below (P < 0.05). The force required increased with the increasing MAS while velocity and PROM decreased (P < 0.01). We regrouped the data using the algorithm: no stiffness = '0'; mild = '1' and '1+' and '2'; moderate = '3'; severe = '4'. There was no difference between 'no stiffness' and 'mild ' (P > 0.10), but 'mild' and moderate' as well as 'moderate' and 'severe' were different (P < 0.01). CONCLUSION: the MAS is not a valid ordinal level measure of RPM or spasticity. Objective measurement of RPM is possible in the clinical setting. However, additional measurements of muscle activity (electromyography) will be required to quantify spasticity.

Aged↗
PubMed1996

Interjoint coordination during pointing movements is disrupted in spastic hemiparesis.

Approaches to the rehabilitation of movement in spastic hemiparetic patients depend on knowledge of the underlying mechanisms of movement deficits. The goals of this study were to characterize end-point trajectories and interjoint coordination of arm pointing movements to different targets on a horizontal planar surface and to correlate disruptions in motor control in the affected arm of hemiparetic subjects with the level of spasticity and the degree of functional impairment measured clinically. Arm movements were studied in six normal and 10 hemiparetic subjects. Data from the affected arms of hemiparetic subjects were compared with those from their non-affected arms and to data from the arms of normal subjects. Subjects were seated in front of a horizontal surface adjusted to the height of the sternal notch with the trunk stabilized. They made planar arm reaching movements (20 and 40 cm) to four different targets located directly in front of them and in the ipsilateral and contralateral workspace. Kinematic data from the finger, wrist, elbow and shoulder were recorded with a three-dimensional optical tracking system. Results showed that movement amplitudes were lower and movement times were significantly prolonged in the affected arms. Although trajectories were marked by deviations from smooth straight lines and characterized by increased dispersion and segmentation, even those subjects with the most severe spasticity could reach into all parts of the workspace with both their affected and non-affected arms. This indicated that movement planning in terms of extrapersonal space was unaffected in these subjects. On the other hand, the interjoint coordination of movements made into or out of the typical extensor or flexor synergies was equally disrupted. These findings suggest a bi-level control organization of pointing movements in both normal and hemiparetic subjects: the level of trajectory planning in extrapersonal space and the level specifying interjoint coordination according to the trajectory plan. Deficits in motor performance in stroke patients may be associated with problems at the second control level. This implies some strategies for the rehabilitation of stroke patients with motor disorders. Treatment aimed at improving arm function should be oriented toward restoring the normal sensorimotor relationships between the joints. We also found that while clinical spasticity scores were correlated with some aspects of motor performance, they provided little information about the movement deficit itself.

Adult↗
PubMed1990

Spasticity in spinal cord injured persons: quantitative effects of baclofen and placebo treatments.

Spasticity commonly occurs after a spinal cord injury and is characterized by increased resistance to passive movement of peripheral joints. This study examined the effect of an antispasticity medication on stiffness from the myotatic reflex response generated by passive sinusoidal ankle motion. A repeated measures, multiple base-line, single-subject, double-blind design was employed. The independent variable was spasticity medication treatment, where the levels were 40 mg/day and 80 mg/day of baclofen v placebo treatment. Viscous and elastic stiffness measurements were taken at the ankle joint during a placebo base-line phase and during treatment with baclofen for five adult males with traumatic spinal cord injuries. Ankle sinusoidal oscillation frequencies were from 3 to 12 Hz during test sessions. Mean viscous and elastic stiffness scores for all frequencies were calculated for each phase of the study. Randomization tests of mean changes in stiffness measurements between each treatment phase of the study failed to provide any convincing evidence of a significant treatment effect for reduction of spasticity in the traumatic spinal cord injured subjects studied. Further testing is needed to exclude potential confounding factors before this conclusion can be confirmed. The results suggest that baclofen is not a universal treatment of choice for all individuals with spasticity resulting from traumatic spinal cord injury.

Adult↗
PubMed1993

Effect of transdermal clonidine on spinal spasticity. A case series.

Clonidine, a centrally acting alpha 2 receptor adrenergic agonist, has been successfully used as adjunctive therapy in patients with spinal cord injury with problematic spasticity not adequately controlled by recognized spasmolytic agents. A transdermal system providing approximately constant and continuous systemic delivery of clonidine has been recently introduced to enhance patient compliance. However, experience with transdermal clonidine in the management of spasticity is limited. Three cases are presented of patients with spasticity as the result of cervical spinal cord injury, inadequately managed by oral baclofen, in whom transdermal clonidine was administered. Significant improvement in spastic hypertonia was observed in all three cases. Transdermally delivered clonidine was well tolerated, with reported side effects limited to dryness of the mouth.

Administration, Cutaneous↗
PubMedDate not supplied

Quantitative measurement of improvement in sitting balance in children with spastic cerebral palsy after selective posterior rhizotomy.

Severe muscular spasticity encountered frequently in patients with spastic cerebral palsy not only affects patient locomotor function but also causes musculoskeletal complications. Significant reduction of spasticity over pelvis and lower limbs after selective posterior rhizotomy (SPR) results in improvement of trunk stability, locomotor function, and function of upper limbs also. The purpose of this study was to investigate the difference of sitting balance before and after SPR using a quantitative measurement in sitting stability represented as dispersion index provided by the Chattecx Balance System. Seventeen children with spastic cerebral palsy, ten boys and seven girls, with a mean age of 5.06 yr, underwent SPR. Their sitting stability under static and dynamic, visual and nonvisual testing conditions was assessed before SPR and three mo after SPR. Their sitting balance showed significant improvement at postoperative evaluation except for the static-nonvisual testing condition. Dispersion index under the dynamic testing condition was significantly higher than under the static testing condition, which implies that dynamic sitting balance was worse than static sitting balance in these patients. There was no statistical difference of sitting performance between visual and nonvisual condition both preoperatively and postoperatively. Quantitative measurement of dispersion index provided by the Chattecx Balance System offers an objective evidence of improvement in sitting balance for children after SPR.

Cerebral Palsy↗
PubMedDate not supplied

Therapeutic electrical stimulation for spasticity: quantitative gait analysis.

Improvement in motor function following electrical stimulation is related to strengthening of the stimulated spastic muscle and inhibition of the antagonist. A 26-year-old man with familial spastic paraparesis presented with gait dysfunction and bilateral lower limb spastic muscle tone. Clinically, muscle strength and sensation were normal. He was considered appropriate for a trial of therapeutic electrical stimulation following failed trials of physical therapy and baclofen. No other treatment was used concurrent with the electrical stimulation. Before treatment, quantitative gait analysis revealed 63% of normal velocity and a crouched gait pattern, associated with excessive electromyographic activity in the hamstrings and gastrocnemius muscles. Based on these findings, bilateral stimulation of the quadriceps and anterior compartment musculature was performed two to three times per week for three months. Repeat gait analysis was conducted three weeks after the cessation of stimulation treatment. A 27% increase in velocity was noted associated with an increase in both cadence and right step length. Right hip and bilateral knee stance motion returned to normal (rather than "crouched"). No change in the timing of dynamic electromyographic activity was seen. These findings suggest a role for the use of electrical stimulation for rehabilitation of spasticity. The specific mechanism of this improvement remains uncertain.

Adult↗
PubMed2002

Effect of intramuscular botulinum toxin injection on upper limb spasticity in stroke patients.

OBJECTIVE: To evaluate the therapeutic effect of intramuscular injection of botulinum toxin on spasticity of the upper limb, with emphasis on its influence over limb function. DESIGN: An open-label, noncontrolled trial with a duration of 12 wk was designed to determine the safety and efficacy of intramuscular botulinum toxin A injection in the treatment of 16 patients with stroke with spastic hemiparesis. Electromyographically guided intramuscular botulinum toxin A injections were applied to the spastic limbs. A detailed scale system was used for the evaluation of muscle tone and functional changes induced by botulinum toxin A treatment. RESULTS: No major side effect secondary to botulinum toxin A injection was reported. Statistically significant (P < 0.05) improvements of muscle tone, joint range of motion, hand muscle strength, and muscular pain were seen after the injection. The improvements lasted up to 8-12 wk after the treatment. However, there was no significant functional improvement except in two of the patients. CONCLUSIONS: Botulinum toxin A injection may help relieve upper limb spasticity and pain in patients with stroke. Its effect on function is probably determined by case selection.

Activities of Daily Living↗