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PubMed2004

Prevalence and treatment of spasticity reported by multiple sclerosis patients.

The objective of this study was to characterize the population of multiple sclerosis (MS) patients suffering from spasticity and to evaluate treatment patterns, including intrathecal baclofen (ITB) delivery, related to patient quality of life (QOL). We conducted a cross-sectional, two-level study using data from the Patient Registry of the North American Research Committee on MS (NARCOMS). In addition, we surveyed a subgroup of 198 preselected patients who are using ITB (ITBG) and a random sample of 315 oral drug users (ORALG). Among the registrants, 16% reported no spasticity, 31% minimal, 19% mild, 17% moderate (frequently affects activities), 13% severe (daily forced to modify activities) and 4% total (prevents daily activities). Patients experiencing greater severity included by proportion males, and those older and with longer duration of MS. QOL scores decreased inversely with severity. In the focused survey, ITBG reported lower levels of spasticity than ORALG, less stiffness in the legs, less pain and fewer spasms at any time. They scored significantly lower in the SF-36 physical component, yet reported less fatigue on the MFIS scale. Prevalence data reveal that one third of MS patients modify or eliminate daily activities as a result of spasticity. Treatment of spasticity can significantly impact QOL parameters by reducing spasms, pain and fatigue.

Administration, Oral↗
PubMed2006

Lack of modulation of Ib inhibition during antagonist contraction in spasticity.

OBJECTIVE: To examine the modulation of non-reciprocal group I (Ib) inhibition during tonic contraction of antagonist muscles in patients with spasticity vs normal subjects. METHODS: The authors studied 10 patients with spastic paraplegia due to cervical compression myelopathy and 16 age-matched normal subjects. Ib inhibition to soleus motoneurons was recorded as the change in size of the H-reflex of the soleus, evoked by conditioning stimulus to the nerve innervating the medial gastrocnemius muscle. The extent of inhibition was studied at rest and during tonic contraction of the pretibial muscles of variable strength. RESULTS: In the resting state, the extent of inhibition in the patients did not differ from normal controls. During antagonist contraction, the extent of inhibition increased both in the normal subjects and patients. The increment was smaller in the patients, especially in those with severe spastic gait. The smaller increment in the inhibition was correlated with the time required to walk 10 m in the patients. CONCLUSION: The authors observed a lack of modulation of Ib inhibition during tonic antagonist contraction in patients with spasticity, especially those with gait disturbance. Disturbed central modulation of non-reciprocal (Ib) interneurons may be responsible for spasticity.

Aged↗
PubMed1999

Quantitative assessment of subclinical spasticity in human T-cell lymphotropic virus type I infection.

OBJECTIVE: To compare human T-cell lymphotrophic virus type I (HTLV-I) seropositive and seronegative women for symptoms and signs of spasticity. BACKGROUND: Infection with HTLV-I causes tropical spastic paraparesis/ HTLV-I-associated myelopathy (TSP/HAM). Certain populations, including female commercial sex workers (FSW), are at increased risk of developing this infection. Fewer than 5% of HTLV-I-seropositive persons develop TSP/HAM, which is typically associated with spasticity. METHODS: Cross-sectional study of 255 registered FSW in Callao, Perú, involving a questionnaire detailing demographics and neurologic symptoms, standard neurologic examination, quantitative assessment of spasticity (QSA) of muscle tone, and serologic testing for HTLV-I. Participants and examiners were blinded to serology results. RESULTS: On the questionnaire and neurologic examination, none of the 32 HTLV-I-seropositive or 223 seronegative women had signs or symptoms of spasticity. However, mean values on QSA were significantly higher among seropositive women (27.1 Newton-meters/radian [N-m/r]) than among seronegative women (21.6 N-m/r, p = 0.01), indicating a subclinical increase in lower extremity tone. With values of QSA divided into tertiles, and the first tertile serving as the comparison group, the odds ratio for seropositivity was 1.4 (95% confidence interval [CI] 1.0 to 2.0) in the second and 3.1 (95% CI 2.2 to 4.3) in the third tertile, after adjusting for age and place of birth. CONCLUSIONS: Although a standard neurologic evaluation could not distinguish between women with and without HTLV-I infection, QSA indicated significantly increased lower extremity tone in those with infection. Long-term follow-up will determine whether these subclinical findings in asymptomatic women progress to overt TSP/HAM.

Adult↗
PubMed2000

From spinal shock to spasticity: neuronal adaptations to a spinal cord injury.

OBJECTIVE: To investigate the adaptational changes in excitability of spinal neuronal circuits below the level of lesion from spinal shock to spasticity in patients with spinal cord injury (SCI). METHODS: More than 6 months after an acute SCI, clinical follow-up examinations were paralleled by electrophysiologic recordings with tibial nerve stimulation (M-wave, F-wave, H-reflex, and flexor reflex). RESULTS: During spinal shock, the loss of tendon tap reflexes and flaccid muscle tone were associated with low persistence of F-waves and loss of flexor reflexes, whereas H-reflexes were already elicitable. During the transition to spasticity, the reappearance of tendon tap reflexes and muscle tone and the occurrence of spasms was associated with the recovery of F-waves and flexor reflex excitability, whereas the H-to-M ratio remained about stable over months. At later stages (2 to 6 months after SCI) when clinical signs of spasticity became established, the electrophysiologic measures showed little change. In paraplegic patients, in contrast to tetraplegic patients, M-wave and flexor reflex amplitudes even decreased. CONCLUSIONS: The late decrease in M-wave and flexor reflex amplitude in paraplegic patients suggests a secondary impairment/degeneration of premotoneuronal circuits and of motoneurons. The divergent course of clinical signs of spasticity and their probable neuronal correlates indicates the occurrence of non-neuronal changes contributing to spasticity.

Adaptation, Physiological↗
PubMed1988

Selective neurotomy of the tibial nerve for treatment of the spastic foot.

One of the most frequent neurological sequelae seen by the specialist in rehabilitation is the spastic foot. Spasticity in the foot may be responsible for abnormal posture and painful or trophic disturbances impairing standing and walking. This disability can be corrected by a simple neurosurgical procedure, the selective tibial neurotomy. In this procedure, one sections the tibial nerve branches to the muscles sustaining spasticity, i.e., the soleus and/or the gastrocnemius nerves for equinus and ankle clonus or the posterior tibialis branch for varus and the flexor fascicles for tonic flexion of the toes. After microsurgical dissection of each tibial nerve branch at the lower part of the popliteal region and their identification with bipolar electrostimulation, the selected branches are partially sectioned under the operating microscope. The present series consists of 62 operations performed in 53 patients, 9 bilaterally and 44 unilaterally. Operation obtained complete suppression of the disabling spasticity that had been present for 2 to 17 years (4 on average), total pain relief, and consequently improvement of the residual voluntary movements (by achieving a better balance between agonist and antagonist muscles) in 51 of the 62 spastic feet (i.e., 82% of the cases). For all of these patients, the beneficial effects were long-lasting over the 1- to 10-year follow-up (3 years on average). Selective neurotomy of the tibial nerve should be considered only after failure of intensive prolonged kinestherapy and of all available medical treatment. It must take place, however, before the onset of irreversible articular disturbances and musculotendinous retractions, which require complementary orthopedic corrections.

Adolescent↗
PubMed2000

Management of spasticity in stroke.

Spasticity treatment must be considered in relation to other impairments with functional goals defined prior to intervention. The effects of muscle co-contraction and involuntary limb movement associated with exaggerated cutaneous reflexes or effort as well as stretch reflex hyperexcitability need to be considered. Exacerbating factors such as pain must be identified. Physical therapy and conventional orthoses are the mainstays of spasticity management during acute rehabilitation. Botulinum toxin shows promise but needs further evaluation in the context of acute rehabilitation. Phenol chemodenervation can produce good results in spasticity refractory to standard treatments. Muscle strengthening exercises may be appropriate in chronic hemiparesis without adversely affecting tone. Electrical stimulation may be a useful adjunct to other spasticity treatments. Difficulty demonstrating functional benefit from antispasticity treatment may imply that interventions directed at single motor impairments whether weakness or spasticity are not likely to result in functional benefit, but it is their combination that is important.

Humans↗
PubMed1987

Delta-9-THC in the treatment of spasticity associated with multiple sclerosis.

Marijuana is reported to decrease spasticity in patients with multiple sclerosis. This is a double blind, placebo controlled, crossover clinical trial of delta-9-THC in 13 subjects with clinical multiple sclerosis and spasticity. Subjects received escalating doses of THC in the range of 2.5-15 mg., five days of THC and five days of placebo in randomized order, divided by a two-day washout period. Subjective ratings of spasticity and side effects were completed and semiquantitative neurological examinations were performed. At doses greater than 7.5 mg there was significant improvement in patient ratings of spasticity compared to placebo. These positive findings in a treatment failure population suggest a role for THC in the treatment of spasticity in multiple sclerosis.

Administration, Oral↗
PubMed2000

Drugs used to treat spasticity.

Spasticity is a common and disabling symptom for many patients with upper motor neuron dysfunction. It results from interruption of inhibitory descending spinal motor pathways, and although the pathophysiology of spasticity is poorly understood, the final common pathway is overactivity of the alpha motor neuron. Therapy for spasticity is symptomatic with the aim of increasing functional capacity and relieving discomfort. Any approach to treatment should be multidisciplinary, including physical therapy, and possibly surgery, as well as pharmacotherapy. It is important that treatment be tailored to the individual patient, and that both patient and care giver have realistic expectations. Pharmacotherapy is generally initiated at low dosages and then gradually increased in an attempt to avoid adverse effects. Optimal therapy is the lowest effective dosage. Baclofen, diazepam, tizanidine and dantrolene are currently approved for use in patients with spasticity. In addition, clonidine (usually as combination therapy), gabapentin and botulinum toxin have shown efficacy, however, more studies are required to confirm their place in therapy. Intrathecal baclofen, via a surgically implanted pump and reservoir, may provide relief in patients with refractory severe spasticity.

Baclofen↗
PubMed1980

Treatment of spasticity by dorsal cord stimulation.

Two types of operations can be proposed today in the neurosurgical treatment of spasticity; the destruction of a brain target, a medullary pathway or a nerve root, and electrical stimulation of nervous structures. Striking improvements in voluntary motor control and sensory appreciation were first reported by Cook and Weinstein (1) in 1973, after implantation of a dorsal cord stimulator for intractable back pain in a case of muiltiple scleroris. The favourable effect on spasticity was confirmed later by other groups. Our own experience, with 26 cases tested for a few days with floating electrodes and 11 cases operated on and followed up for more than 3 years, shows that the best results are obtained in cases of medullary spasticity, without complete section of the cord, occurring mainly in multiple sclerosis. Cerebral spasticity did not respond as well. The objective data, measurement of stretch and H-reflexes, support the clinical results. The physiological mechanisms of dorsal cord stimulation on spasticity have not yet been elucidated.

Electric Stimulation Therapy↗
PubMed1983

Selective posterior rhizotomy for treatment of spasticity.

In 1976, Fasano, et al., described a new technique of posterior rhizotomy for treatment of spasticity. They stimulated electrically fascicles of the posterior roots in spastic patients and found that some fascicles responded to stimulation with tonic muscle contractions. They cut these fascicles, preserving those with a weaker or no reaction. The present authors have used a fairly similar technique in the treatment of eight patients with spasticity of the legs and one patient with spasticity of the arm: all fascicles of the posterior roots T12-Sl and C6-8, respectively, were stimulated electrically during surgery under general anesthesia. Approximately 60% to 80% of the fascicles responded to stimulation with tonic muscle jerks, and only these fascicles were cut. All nine patients showed a good reduction of spasticity. The residual cutaneous and joint sensation remained unchanged. Motility of the limbs usually improved.

Adult↗
PubMed2006

Long-term functional results of selective peripheral neurotomy for the treatment of spastic upper limb: prospective study in 31 patients.

OBJECT: To manage refractory upper-limb spasticity, selective peripheral neurotomy (SPN) is proposed when the spastic muscles to be treated are under the control of a single or a few peripheral nerves. The aim of this study was to assess prospectively the long-term effects of SPN. METHODS: Thirty-one patients with disabling upper-limb spasticity were selected by a multidisciplinary team using clinical, analytical, and functional scales as well as nerve block tests for assessment. Sixty-four SPNs were performed at the level of the musculocutaneous (15 SPNs), the median (25 SPNs), and the ulnar (24 SPNs) nerves. Results of a long-term follow up (mean 4.5 years) showed statistically significant improvement on 1) analytical assessment (p < 0.01): resting position, active amplitude, and motor strength; 2) Ashworth Scale scoring (p < 0.01); 3) hand function assessment (p < 0.01); and 4) rating of daily activities. Four patients with severe painful spasticity experienced complete pain relief after surgery. On the basis of a Visual Analog Scale ranging from 0 to 100, the mean degree of patient satisfaction was 61.5. Complications occurred in five patients (15%): two postoperative hematomas, one (temporary) hypesthesia, and one transient paresia of the wrist and finger flexors. CONCLUSIONS: Selective peripheral neurotomy leads to long-term satisfactory improvement in function and/or comfort with a low morbidity rate in appropriately selected patients suffering from severe harmful spasticity of the upper limb that has been refractory to conservative therapy. Patients must be selected after complete assessment by a multidisciplinary team.

Adolescent↗
PubMed1995

Treatment of acquired muscle spasticity using phenol peripheral nerve blocks.

The use of phenol motor nerve blocks is advantageous in the early period of acquired spasticity (ie, that occurring following traumatic brain injury or incomplete spinal cord injury), when increased muscle tone is often the most severe. Because acquired spasticity is dynamic and usually improves slowly, a temporary treatment method used to ameliorate increased muscle tone is desirable. Phenol nerve infiltration provides a temporary motor nerve block that lasts for weeks or months. It allows passive limb mobilization in a comprehensive rehabilitation program that attempts to prevent fixed soft tissue contractures. Permanent or irreversible methods such as operative tendon lengthening, muscle release or recession, or neurectomy are usually best delayed until the spasticity has become static, when the need for surgical correction becomes more firmly indicated, and outcomes of operative intervention are more predictable. Although phenol nerve blocks were initially administered at the spinal cord level to control spasticity, the potential side effects have caused a loss of popularity of this method of administration. The safer and more common use of phenol infiltration at the peripheral nerve level is now more accepted for brain injury and spinal cord injury patients. This report reviews the indications, current concepts, and development of the different methods used to administer phenol nerve blocks. Comparisons to other methods to control spasticity are discussed.

Animals↗
PubMed2000

Utility of brainstem auditory evoked potentials in children with spastic cerebral palsy.

In a retrospective study of 75 children with spastic cerebral palsy (CP), brainstem auditory evoked potentials (BAEP) were recorded and subsequently correlated with birthweight, gestational age, aetiology and type of CP, neuroradiological findings, additional impairments and disabilities (including the inability to walk independently). Seventeen patients (22.7%) had abnormal BAEP recordings. Thirteen of these 17 patients (76.5%) had spastic tetraplegia, 16 patients (94.1%) were full-term infants, 12 patients (70.6%) had myoskeletal problems, 9 (52.9%) had epilepsy, 16 (94.1%) had visual impairment, 13 patients (76.5%) were unable to walk independently, while all 17 patients (100%) had speech impairment and mental retardation. The aetiology of CP was prenatal in 2 of these 17 patients (11.8%) and perinatal in 15 patients (88.2%). Thirteen patients (76.5%) had cortical atrophy determined by either computed tomography or magnetic resonance imaging, two patients (11.8%) had an infarct picture and two patients (11.8%) had maldevelopment of the central nervous system. There was a definite statistically significant association between abnormal BAEP recordings and full-term delivery, perinatal aetiology of CP, spastic tetraplegia, speech, visual and myoskeletal impairments, epilepsy, mental retardation, inability to walk independently and cortical atrophy on neuroimaging (p < 0.001). We conclude that abnormal BAEP recordings in children with spastic CP are indicative of poor prognosis and associated with a "multihandicap state". BAEP testing should be incorporated into the diagnostic plan of all children with spastic CP newly referred to neurodevelopmental centres.

Cerebral Palsy↗
PubMed1999

[Spasticity and physical methods for controlling it].

Spasticity is one of the greatest difficulties in patients with central nervous system injuries and diseases. Severe spasticity makes treatment, rehabilitation and care of patient very difficult and sometimes even impossible. It has been sought for many years for an objective method to evaluate the degree of spasticity, necessary to establish the results of treatment and rehabilitation. In this study we present subjective and objective methods of evaluating the spasticity in order to classify every patient to adequate therapeutic group. The authors present physical methods that not only contribute to control of spasticity together with pharmacotherapy and surgical treatment, but can be used alone. The big advantage of this therapy is a low invasiveness and the very few side effects.

Humans↗
PubMedDate not supplied

The influence of eccentric contractions and stretch on alpha motoneuron excitability in normal subjects and subjects with spasticity.

Application of eccentric contractions and muscle stretch are clinically effective in reducing spasticity and increasing ROM (7). This may be explained by a change in the excitability of motoneurons supplying the spastic muscle. Excitability of motoneurons can be indirectly assessed using the H-reflex. Experiments were performed on 20 normal subjects and 17 subjects with spasticity resulting from neurological disorder. Subjects were seated in a secure position and the ankle joint was moved from 30 degrees plantarflexion to 20 degrees dorsiflexion at a velocity of 30 degrees/sec. Sixty eccentric contractions of the triceps surae muscle were performed using a Kin-Com dynamometer (Chattanooga Corp, Tennessee). Two protocols were used: (1) eccentric contractions only, and (2) eccentric contractions with a 5s stretch of the relaxed triceps surae after each contraction. Two sets of 10 H-reflexes were collected from the soleus muscle before (trial 1 & 2) and after (trial 3 & 4) eccentric and eccentric + stretch protocols. The mean peak to peak H-reflex amplitude was calculated for each trial and compared using ANOVA. Eccentric contractions resulted in a significant and maintained increase in the H-reflex in neurological compared to normal subjects (P < 0.05). Eccentric contractions in subjects with spasticity resulted in an increase in motoneuron excitability which may assist in corticospinal activation of motoneurons during voluntary movement. The eccentric + stretch protocol, resulted in a decrease in the mean amplitude of H-reflexes in neurological subjects, however, this was not significant. The application of a stretch following eccentric contractions decreased motoneuron excitability and may thus be beneficial to decrease spasticity whilst strengthening muscle.

Adult↗
PubMed2001

[Spasticity and multiple sclerosis].

Spasticity is a common symptom in MS patients. It is easy to recognize and evaluate spasticity at rest. The efficacy of numerous treatments has been well documented. Nevertheless, it is difficult, particularly in MS patients, to assess the functional disability due to spasticity and the functional benefit due to treatment. This is why it is appears more appropriate to use therapeutic tests with transitory effects such as anesthetic blocks in case of focal spasticity or intrathetical baclofen in case of diffuse spasticity. It is also possible to use reversible treatments such as botulinum toxin injections before proposing section of a peripheral nerve.

Disability Evaluation↗
PubMedDate not supplied

[Treatment of spasticity in cerebral palsy with botulinum toxin].

OBJECTIVE: A review of the pathophysiological and developmental basis, measurement scales and the usefulness of botulinum toxin A injections in selected muscles for the treatment of spasticity in children with cerebral palsy. DEVELOPMENT: Cerebral palsy is the most common cause of spasticity in children. The increase in muscle length is achieved through the addition of sarcomeres in series at the level of the muscle tendinous junction. The regulation of the number of sarcomeres seems to be determined by the lengthening of the muscle. The muscle contracture is a shortening of the length of a muscle as a result of a decrease in the number of sarcomeres. Spasticity and motor function assessment scales used in children with cerebral palsy: a) Modified Ashworth scale for the assessment of spasticity; b) modified Tardieu scale for the assessment of dynamic muscle length; c) muscle spasms frequency scale; d) modified Medical Research Council scale for muscle strength; e) hip adductor muscle tone scale; f) global pain scale with affective facial expression represented in a drawing; g) goniometric measurement of the joint range of movement; h) Palisano gross motor function measure; i) observational video gait analysis scale. Recommended guidelines for dosing the botulinum toxin A: 1. Total maximum dose administered per visit up to 15 U/kg or a total of 400 U; 2. Dose range of large muscles 3 to 6 U/kg per visit; 3. Dose range of small muscles 1 to 3 U/kg per visit; 4. Maximum dose per injection site: 50 U dividing the total planned unit dose/muscle into equal amounts/injection site; 5. Frequency: no more than one injection every 3 months, frequently once every 6 or more months. CONCLUSION: Botulinum toxin A injection is a well tolerated, safe and effective procedure in the treatment of children with spastic cerebral palsy.

Botulinum Toxins, Type A↗
PubMed2001

[A family of hereditary spastic paraplegia with dementia, ataxia, and dystonia].

We reported three siblings with complicated hereditary spastic paraplegia. The striking features in these patients were characterized by early onset of gait disturbance, mental deficiency, and dystonia. The most likely diagnosis was Mast syndrome. Patient 1: A 44 years-old woman. She first developed gait disturbances at age of 8. She was admitted in our hospital because of progressive spastic paraplegia. Neurological examination revealed mental deficiency, saccadic pursuit eye movement, speech disturbance of cerebellar type, ataxia, and spastic paraplegia. She showed also dystonia in the face, tongue, and trunk. MRI showed cerebellar atrophy. Patient 2: A 51 years-old brother of the patient 1. He had mentally retarded. Late teens he developed gait disturbance. Gradually he manifested spastic paraplegia, dysarthria, dysphasia, mental deficiency, and ataxia. He also showed incontinence of urine and feces. Then he became bedridden, apathetic, and showed forced crying. MRI showed diffuse brain atrophy. Patient 3: A 48 year-old woman. This woman, a sister of the patient 1, showed progressive gait disturbance and dysarthria. She also developed incontinence, apathy, and dystonia. She became bedridden, responding to simple questions with only occasional single-word answers. Her speech was slurred, and spastic paraplegia was noted. MRI showed diffuse brain atrophy including marked atrophy of the cerebellum.

Brain↗