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PubMed2000

[Optimized therapy of spastic syndrome by combination intrathecal baclofen with botulinum toxin].

Intrathecal administration of baclofen has proved to be an effective treatment of spasticity related to CNS damage. Especially patients with spinal spasticity due to traumatic spinal cord injury or transverse myelitis showed a dramatic reduction of spasticity and improvement of their Ashworth scores. The results are, however, often disappointing in patients with muscular hypertension of the extensor muscles, which is frequently found in patients with multiple sclerosis or cerebral hypoxia. In the latter, using intrathecal baclofen may be restricted by serious side effects. Botulinumtoxin A is widely used in patients with various forms of dystonia. It has also been studied in spastic disorders, where local injections were valuable in relieving focal spasticity in hemiparetic patients and in infantile cerebral palsy. It is used only cautiously in severe paraspasticity. The case reports of 4 patients with incomplete and complete paraparesis due to spinal cord injury, neurodegenerative pyramidal disorder, and cerebral hypoxia demonstrate that a combination of intrathecal baclofen and botulinumtoxin A can improve clinical benefits and reduce side effects.

Adult↗
PubMed2006

The tonic stretch reflex and spastic hypertonia after spinal cord injury.

The operational definition of spasticity is focused on increased resistance of joints to passive rotation and the possible origin of this increased resistance in the induced tonic stretch reflex (TSR). This term is applied in the context of both cerebral and spinal injury, implying that a similar reflex mechanism underlies the two disorders. From recent studies it is clear that increased passive joint resistance in resting limbs following stroke is highly correlated with the induced TSR, but this evidence is lacking in spinal injury. The contribution of the TSR to hypertonia in spinal cord injury (SCI) is unclear and it is possible that hypertonia has a different origin in SCI. The contribution of resting and activated TSR activity to joint stiffness was compared in SCI and normal subjects. The magnitude of the TSR in ankle dorsiflexors (DF) and plantarflexors (PF) and mechanical ankle resistive torque were measured at rest and over a range of contraction levels in normal subjects. Similar measures were made in 13 subjects with SCI to the limits of their range of voluntary contraction. Normals and SCI received a pseudo-sinusoidal stretch perturbation of maximum amplitude +/- 20 degrees and frequency band 0.1-3.5 Hz that was comparable to that used in manual clinical testing of muscle tone. Elastic resistance and resonant frequency of the ankle joint, after normalization for limb volume, were significantly lower in complete and incomplete SCI than normal subjects. No reflex response related to stretch velocity was observed. Resting DF and PF TSR gain, when averaged over the tested band of frequencies, were significantly lower in complete SCI than in resting normal subjects (<0.5 microV/deg). Linear regression analysis found no significant relationship between TSR gain and resting joint stiffness in SCI. Mean TSR gain of DFs and PFs at rest was not correlated with the subject variables: age, time since SCI, level of injury, Frankel score, number of spasms per day, Ashworth score or anti-spastic medication. DF and PF reflex gain were linearly related to voluntary contraction level and regression analysis produced similar slopes in incomplete SCI and normal subjects. Hence TSR loop gain was not significantly increased in SCI at any equivalent contraction level. Extrapolation of the regression lines to zero contraction level predicted that reflex threshold was not reduced in SCI. Low frequency passive stretches did not induce significant TSR activity in the resting limbs of any member of this SCI group. The TSR thus did not contribute to their clinical hypertonia. Other reflex mechanisms must contribute to hypertonia as assessed clinically. This result contrasts with our similar study of cerebral spasticity after stroke, where a comparable low frequency stretch perturbation produced clear evidence of increased TSR gain that was correlated with the hypertonia at rest. We conclude that a low frequency stretch perturbation clearly distinguished between spasticity after stroke and SCI. Spasticity in the two conditions is not equivalent and care should be taken in generalizing results between them.

Adult↗
PubMed2005

Long-term intrathecal baclofen therapy in ambulatory patients with spasticity.

BACKGROUND: Intrathecal baclofen (ITB) is an effective treatment for severe spasticity. In ambulatory patients with spasticity, it is possible that ITB treatment may compromise ambulatory function by unmasking underlying muscle weakness. This retrospective study is designed to determine the long-term ambulatory function in patients receiving ITB. METHODS: Thirty-six patients with severe spasticity previously screened for response to ITB were implanted with programmable pumps that allowed for continuous infusion of ITB. Patients were followed after implantation from 1 to 13 years. RESULTS: All 36 patients had decreased spasticity and retained ambulatory function. Three of the 36 patients eventually became paraplegic related to underlying disease progression. CONCLUSION: ITB therapy may be used in selected ambulatory patients with spasticity and is not associated with loss of ambulatory function.

Adult↗
PubMed2005

Short-term effects of thermotherapy for spasticity on tibial nerve F-waves in post-stroke patients.

Thermotherapy is generally considered appropriate for post-stroke patients with spasticity, yet its acute antispastic effects have not been comprehensively investigated. F-wave parameters have been used to demonstrate changes in motor neuron excitability in spasticity and pharmacological antispastic therapy. The present study aimed to confirm the efficacy of thermotherapy for spasticity by evaluating alterations in F-wave parameters in ten male post-stroke patients with spastic hemiparesis (mean age: 49.0+/-15.0 years) and ten healthy male controls (mean age: 48.7+/-4.4 years). The subjects were immersed in water at 41 degrees C for 10 min. Recordings were made over the abductor hallucis muscle, and antidromic stimulation was performed on the tibial nerve at the ankle. Twenty F-waves were recorded before, immediately after, and 30 min following thermotherapy for each subject. F-wave amplitude and F-wave/M-response ratio were determined. Changes in body temperature and surface-skin temperature were monitored simultaneously. The mean and maximum values of both F-wave parameters were higher on the affected side before thermotherapy. In the post-stroke patients, the mean and maximum values of both parameters were significantly reduced after thermotherapy (P<0.01). Hence, the antispastic effects of thermotherapy were indicated by decreased F-wave parameters. Body temperature was significantly increased both immediately after and 30 min after thermotherapy in all subjects. This appeared to play an important role in decreased spasticity. Surface-skin temperature increased immediately after thermotherapy in both groups and returned to baseline 30 min later. These findings demonstrate that thermotherapy is an effective nonpharmacological antispastic treatment that might facilitate stroke rehabilitation.

Adult↗
PubMed2005

A randomised, double-blind, dose-ranging study to evaluate efficacy and safety of three doses of botulinum toxin type A (Botox) for the treatment of spastic foot.

Botulinum toxin A (BTX) injections have been used successfully in the treatment of post-stroke foot spasticity, but the optimal dose-response relationship for selected muscles has yet to be established. The aim of this study was to outline beneficial and unwanted effects of three different doses of BTX in the treatment of spastic foot. In this randomised, double-blind, dose-ranging study, 45 spastic feet were randomly allocated to one of three groups, each of which was treated with a different dosage of BTX. The doses were decided on the basis of suggestions in the literature. Outcome measures (Modified Ashworth Scale, Medical Research Council Scale, gait assessment, presence of Achilles tendon clonus, Visual Analogue Scales for Gait Function and Pain, Adverse Effects scale) were applied at baseline, 4 weeks and 4 months after treatment. All the groups showed significant scales scores improvements after treatment with BTX. Group II (mean BTX total dose: 322 U) and Group III (mean BTX total dose: 540 U) showed a greater and more prolonged response than Group I (mean BTX total dose: 167 U). Group III showed the highest rate of adverse effects 4 weeks post-treatment. BTX injections constitute a useful and safe method of improving post-stroke foot spasticity, associated pain, gait speed and function. In particular, the medium BTX dosages (320 UI spread over 2-5 muscles) were found to be both safe and effective in producing long-lasting improvement of spastic foot dysfunction.

Aged↗
PubMed1990

Intrauterine growth and spastic cerebral palsy. I. Association with birth weight for gestational age.

Birth weight, gestational age at delivery, and other factors were collected for 171 white children with spastic cerebral palsy. Their birth weights were compared with the birth weight distribution expected for a population of the same race, gestation, sex, maternal height, and parity, born in the same geographic area, and during the same time period. Birth weights of children with spastic cerebral palsy tended to be significantly lower than the median birth weight of their comparison population. Analysis stratified by gestation at delivery suggested that if the reduced birth weight were causally associated with the spastic cerebral palsy, 22% of cases were attributable to being below the 10th percentile of the comparison population birth weight distribution. The risk of spastic cerebral palsy associated with poor intrauterine growth was dependent on gestation at delivery; poorly grown infants delivered between 34 and 37 weeks' gestation were at highest risk. Some probable pathways by which growth retardation could result in brain damage (intrapartum hypoxia, hypoglycemia, and hypothermia) were investigated. Only intrapartum hypoxia may have played a causal role but probably accounted for less than 2% of all cases. These data suggest that spastic cerebral palsy is associated with poor intrauterine growth in infants of more than 33 weeks' gestation, but no important causal mechanism has yet been identified.

Birth Weight↗
PubMed1982

Electrophysiological studies with the spastic mutant mouse.

Electromyographic (EMG) studies were carried out with the genetically spastic mouse (spa, autosomal recessive), obtained from matings of B6C3a/a, spa/+ heterozygotes. Spastic homozygotes exhibited high amplitude repetitive EMG bursts during spontaneous activity. Following an electrical stimulus to hindlimb or forelimb, high amplitude stereotyped EMG bursts were recorded from contralateral limbs in spastic mice, but were not observed in phenotypically unaffected littermates or normal C57BL/6J mice. The timing and latency of this stereotyped response to an electrical stimulus was consistent with the participation of spinal cord neuronal pathways. In normal C57BL/6J mice the administration of strychnine (0.65 mg/kg), but not picrotoxinin (up to convulsant doses), reproduced all of the behavioral and EMG features observed in spastic homozygotes. We hypothesize that the symptoms in the spastic mutant may result from a deficiency of strychnine-sensitive (presumably glycinergic) inhibition in the spinal cord.

Animals↗
PubMed1991

Correlative electrophysiological and behavioral evaluation following L5 lesions in the cat: a model of spasticity.

The present work developed an animal model of hindlimb spasticity by analyzing the electrophysiological and behavioral consequences of L5 spinal cord lesions in cats. In chronically lesioned animals (1 to 6 months), the L7-S1 dorsal roots were stimulated and evoked potentials were recorded from hindlimb flexor and extensor motor nerves. Following lateral hemisection, the monosynaptic responses were 2-5 times larger (for voltage-time integral and for amplitude) on the ipsilateral side than those from the contralateral side or from control animals. Half-widths, rise-times, and latencies of the monosynaptic responses were the same on both sides. Behavioral signs of spasticity, including hypertonia and increased deep tendon reflexes, were displayed from the ipsilateral hindlimb following lateral hemisection. With lateral hemisection or with extensive dorsal quadrant lesions, hopping and proprioceptive placing reflexes were abolished; these behavioral observations impart functional significance to physiological and anatomical studies of a mid-lumbar center considered to be important for movement control. The present model represents the first demonstration of a statistically significant correlation between electrophysiological and behavioral observations of spasticity for animals with a lateral hemisection. These correlations demonstrate the utility of behavioral screening of animals for subsequent neurophysiological analyses. This facilitates the investigation of cellular events underlying spasticity and of strategies for its relief with tissue repair techniques affecting local circuitry involved in spasticity.

Animals↗
PubMed1985

Modification of spastic gait through mechanical damping.

The effect of dissipative mechanical loads on spastic gait has been studied, to evaluate the feasibility of using mechanically damped orthoses to effect functional improvements in the gait of spastic patients. This concept is based on a hypothesis citing uninhibited, velocity-dependent stretch reflexes as a possible causal factor in spastic gait abnormalities, such as equinus and back-kneeing. In order to screen potential experimental subjects and to quantify velocity-dependent reflex behaviour, ankle rotation experiments and filmed gait analysis were performed. The results supported the existence of a velocity threshold. Orthosis simulation experiments were performed with one spastic subject, using a wearable, computer-controlled, electromechanical, below-knee orthosis simulator to apply a variety of damping loads to the ankle as the subject walked. Results indicated that appropriate damping can improve local joint kinematics. The damping causes a reduction in muscle stretch velocity which apparently results in reduced spastic reflex activity.

Adult↗
PubMed1996

Molecular genetics of familial spastic paraplegia: a multitude of responsible genes.

Familial spastic paraplegia (FSP or SPG) is a genetically heterogeneous group of upper motor neuron syndromes. To date, two distinct loci for X-linked recessive type (SPG1 and SPG2), three loci for autosomal dominant type (FSP1, FSP2 and FSP3), and one locus for autosomal recessive type have been reported. SPG1 and SPG2 have been mapped to Xq28 and Xq21-q22, respectively. SPG1 shows a mutation in the gene for neural cell adhesion molecule L1 (LICAM), which is an axonal glycoprotein involved in neuronal migration and differentiation. Different mutations of the same L1 gene also cause. MASA (mental retardation, aphasia, spastic paraplegia, adducted thumbs) syndrome and X-linked hydrocephalus. SPG2 shows mutations in one of the major myelin proteins, the proteolipid protein (PLP) gene, and is allelic to Pelizaeus-Merzbacher disease. Thus, mutations in two functionally distinct genes manifest the phenotype of X-linked spastic paraparesis. Three dominantly inherited spastic paraplegia genes have been genetically mapped to regions of chromosomes, yet no specific genes or mutations have been identified. FSP1 is mapped to a region of 7 cM on chromosome 14q12-q23 (approximately 20% of dominant FSP families) and FSP2 to 4 cM on chromosome 2p21-p24 (approximately 70% of dominant FSP families). Anticipation (increasing clinical severity in successive generations) has been observed in both FSP1 and FSP2 families. Another autosomal dominant FSP (FSP3) has been mapped in the centromeric region of chromosome 15q (< 10% of dominant FSP families). An autosomal recessive FSP has been mapped to chromosome 8q. The definite genetic heterogeneity in FSP indicates that a multitude of genes/proteins can cause spastic paraplegia. Clinical features of each of the loci which may permit differential diagnosis are discussed. We also present pedigrees of two new FSP families.

Chromosome Mapping↗
PubMed1984

Pendulum testing of spasticity.

Simple and inexpensive instrumentation required for pendulum testing of spasticity is described. It is based on the use of an electrogoniometer and tachometer. Eight parameters are extracted from the goniogram and the tachogram to evaluate the degree of spasticity. The correlation coefficients are calculated to determine the parameters relevant for the estimation of spasticity. Spasticity was assessed in the knee extensors of ten spinal cord injury patients and in five hemiplegics. The described instrumentation and evaluation of the pendulum test provide an effective spasticity testing in the clinical environment.

Adult↗
PubMed1981

Spastic cerebral palsy: changes in birthweight and gestational age.

The birthweight and gestational age frequency distributions for spastic cerebral palsy (CP) cases and their controls were obtained from the Western Australian CP register. Following the introduction of neonatal intensive care, spastic CP rates have fallen amongst heavier (greater than or equal to 2500 g) infants and remained steady or risen amongst low birthweight (LBW: less than 2500 g) infants. The expected bimodality of both the birthweight and gestational age distributions for spastic diplegia cases was obvious in these data. Marked peaks occurred at 1500 g and 31 weeks and 3000 g and 39 weeks. The numbers of heavier, term diplegics fell between 1961-1965 and 1971-1975, and thus there were proportionally more preterm LBW diplegics more recently. The reasons for the fall in the heavier diplegics need investigation. Spastic hemiplegic and quadriplegic cases were more like the controls but with distributions skewed to the left. More of these individuals were more recently small for gestational age (SGA: less than 2500 g and over 37 weeks gestation). This highlights the importance of intrauterine damage in these two groups of spastic CP individuals.

Australia↗
PubMed2005

[Peripheral neurolytic blocks and spasticity].

Peripheral nerve blockade is one of the therapeutic possibilities to treat spasticity of various muscles. Percutaneous nerve stimulation allows accurate location of nerves and neurolysis can be performed using intraneural injection of 65% ethanol or 5 to 12% phenol. Spastic contraction of various muscle groups is a common source of pain and disability which prevents from having efficient rehabilitation. Test-blocks as well as neurolytic blocks are possible in most of motor nerves of the upper and lower limbs and main indications are spastic sequelae of stroke and spinal trauma but also of multiple sclerosis, cerebral palsy and chronic coma. The use of percutaneous nerve stimulation allows accurate location and four nerves are more frequently treated: pectoral nerve loop, median, obturator and tibial nerves. In patients with spasticity of the adductor thigh muscles, nerve blocks are performed via a combined approach using fluoroscopy and nerve stimulation to identify the obturator nerve. No complications occurred and minor side effects are transient painful phenomena during injection. These approaches proved to be accurate, fast, simple, highly successful and reproducible. Percutaneous neurolytic procedures should be done as early as possible, as soon as spasticity becomes painful and disabling in patients with neurological sequelae of stroke, head trauma or any lesion of the motor neuron.

Animals↗
PubMed2004

[Treatment of focal upper limb spasticity with botulinum toxin after stroke. Interest of an individual approach].

INTRODUCTION: It is now demonstrated that botulinum toxin can improve upper limb spasticity after stroke. OBJECTIVES: This study was designed to assess the efficacy of botulinum toxin on upper limb spasticity with an individual approach. METHODS: Prospective study on 18 patients who had disabling spasticity of upper limb after stroke. For each patient, the treatment's target was fixed preliminary to botulinum toxin injection. Evaluation of efficacy (Ashworth scale and predefined targets) was performed at 1 month and treatment continuation was decided individually. RESULTS: A beneficial effect was reported by most patients when the treatment was aimed at improving comfort or quality of life. In one case, the treatment was designed to improve grasping. In that case, no effect was reported. For three patients, a neurotomy was performed in order to obtain a long lasting effect. For nine patients, repeated injections were decided. For the six other patients, no long-standing treatment was performed. DISCUSSION: This study confirms that botulinum toxin can improve comfort of patients with upper limb spasticity. On the base of our experience, we discussed contribution of botulinum toxin to enhance and optimise strategies for the treatment of focal upper limb spasticity with emphasis on the comparison with selective neurotomy.

Adult↗
PubMed2005

Reliability of biomechanical spasticity measurements at the elbow of people poststroke.

OBJECTIVE: To determine the minimum number of measurements required to obtain a reliable estimate of upper-extremity spasticity using biomechanic assessment across multiple testing trials and dates. DESIGN: Single-center, longitudinal study with repeated measurements of spastic upper-extremity torque measures taken 1 week apart. SETTING: A hospital-based laboratory with an isokinetic testing system. PARTICIPANTS: Sixteen subjects more than 6 months poststroke with upper-extremity spasticity. INTERVENTION: Elbow flexor hypertonia was assessed with a custom-made manipulandum attached to a 6-axis load cell and a Biodex System 3 isokinetic testing machine. Movements into extension were imposed at 4 speeds: 6 degrees /s, 30 degrees /s, 60 degrees /s, and 90 degrees /s. MAIN OUTCOME MEASURES: The resistive torque and electromyographic response to these imposed movements were measured. The torque response at the slowest speed (6 degrees /s) was attributed solely to the passive elements of the elbow and was subtracted from the torque response at the higher speeds (30 degrees /s, 60 degrees /s, 90 degrees /s), leaving only reflex torque. The reflex torques at 30 degrees /s, 60 degrees /s, and 90 degrees /s were used for further analysis. Peak torque, peak joint stiffness, and onset angle of reflex torque responses were found; repeatability and daily variability of these measures were statistically examined. The variabilities due to the subject, test day, and trial number were computed. The overall reliability of each parameter at the 3 higher test speeds using different testing schemes was also calculated. RESULTS: Ninety percent reliability in the measurement of all parameters was obtained after at least 2 days of testing during which 3 tests a day were performed. The variability in between-subjects measurements was at least 4 times greater than the intertrial variability when testing at the highest speeds; daily variability that was up to 50% of the intersubject variability was also observed. The biomechanic measures correlated well with the Ashworth Scale (Spearman rho=.84, P<.005), a clinical measure of hypertonia. CONCLUSIONS: We recommend at least 2 test dates to account for the daily variability in the spastic reflex response and to ensure reliable spasticity measurements.

Adult↗
PubMed2005

A clinical study of intrathecal baclofen using a programmable pump for intractable spasticity.

OBJECTIVE: To determine the impact of intrathecal baclofen (ITB) therapy on outcomes of functional independence, pain, subjective improvement, performance, and standard measures of spasticity. DESIGN: A noncomparative, multicenter, prospective cohort trial of patients with implanted pumps followed up over a 12-month period for the assessment of spasticity, pain, and function. SETTING: Twenty-four European centers of neurology or rehabilitation familiar with implantable pump technique participated. PARTICIPANTS: Patients with intractable spasticity (N=138) who responded positively to a trial dose of baclofen (n=133) and who began ITB therapy (n=129) were enrolled. INTERVENTION: Implantation of a Medtronic SynchroMed Infusion System with the administration of ITB therapy. MAIN OUTCOME MEASURES: Ashworth Scale assessment, Penn Spasm Frequency Scale scores, pain assessment, FIM instrument scores or WeeFIM scores for children, Canadian Occupational Performance Measure (COPM), and subjective ratings of overall relief were the tools administered. RESULTS: Muscle tone, spasm scores, and pain intensity reductions were observed. Overall FIM scores increased significantly in cognitive and motor function. COPM scores for both performance and satisfaction also improved significantly. Patients reported increased relief from pain and spasticity, supported by physician reports. Forty-three percent of patients reported adverse events, mostly related to patients' underlying conditions (20%), the device implant surgery (10%), or complications with the catheter (9%). CONCLUSIONS: ITB therapy using a programmable pump is clinically effective and well tolerated, despite a seemingly high level of adverse events, in patients with intractable spasticity of spinal or cerebral origin and may offer improvements in pain relief and function.

Adolescent↗
PubMed2005

Quantitative assessment of the velocity-dependent increase in resistance to passive stretch in spastic plantarflexors.

BACKGROUND: Although numerous studies revealed that isokinetic dynamometers were valuable tools for assessing spastic hypertonia, no standard methodology using such devices is currently widespread in clinical setting. The aim of this study was to standardize a protocol to assess spastic hypertonia in the triceps surae. METHODS: The passive resistance during dorsiflexions imposed from 10 to 300 degrees /s with an isokinetic dynamometer was measured at the neutral position in 15 patients with spastic hypertonia and 12 healthy subjects. The normalized passive resistance was obtained by expressing raw passive resistance as a percent of the values measured at the lowest velocity (10 degrees /s). EMG signals from plantar and dorsiflexors were also recorded. FINDINGS: While no significant difference between spastic patients and control subjects was observed in raw passive resistance values, the difference was significant for each tested velocity when considering the normalized values. Furthermore, the Ashworth score was significantly correlated with the normalized passive resistance for each velocity whereas no correlation was observed with the raw passive resistance. For the patients, except at the highest velocity, the normalized passive resistance was not affected by the fact that reflex responses in the triceps surae were elicited or not. INTERPRETATION: The normalized passive resistance, expressed with respect to the initial one, i.e., measured at very low velocity, seems a very effective parameter to quantify the velocity-dependent increase in resistance to passive stretch in spastic plantarflexors. However, while the simplicity of the isokinetic tests and the reduced time of data treatment seems to support the clinical use of this methodology, further investigations are required to definitely standardize the protocol.

Adult↗
PubMed2005

Functional outcome of intrathecal baclofen administration for severe spasticity.

PURPOSE: To estimate the functional benefit in patients with severe spasticity treated with intrathecal baclofen infusion through an implantable pump and to stress the need for functional assessment of these patients with a functional scale. PATIENTS AND METHODS: Between 1999 and 2003, 22 patients with a long history of severe and disabling pharmaceutically intractable spasticity, underwent implantation of a pump for continuous intrathecal baclofen infusion. The patients were subdivided into two categories according to the aetiology of spasticity: 15 had Multiple Sclerosis and seven had suffered a Spinal Cord Injury at different levels (from C4 to T11). Clinical status was assessed with the Ashworth and Penn spasm scales. Functional benefits were evaluated with the Barthel index score and pain relief with a self-reported visual analogue pain scale. RESULTS: Postoperatively, all patients presented improvement in spasticity, reduction of spasm frequency, significant improvement in functional status, enhancement of life comfort and reduction of pain. CONCLUSION: Reduction of spasticity and spasms achieved with intrathecally delivered baclofen, leads to functional improvement and pain relief.

Activities of Daily Living↗