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PubMed2002

Spasticity causes a fundamental rearrangement of muscle-joint interaction.

Sarcomere length was measured in flexor carpi ulnaris (FCU) muscles from patients with severely spastic wrist flexion contractures (n = 6), as well as from patients with radial nerve injury and a normally innervated FCU (n = 12). Spastic FCU muscles had extremely long sarcomere lengths with the wrist fully flexed (3.48 +/- 0.44 microm) compared to the FCU muscles of patients with radial nerve injury (2.41 +/- 0.31 microm). In three of the patients with spastic wrist flexion contractures, the slope of the FCU sarcomere length-joint angle relationship was measured and found to be, essentially, normal (0.017 +/- 0.005 microm/degree, n = 3) suggesting that serial sarcomere number (and therefore muscle fiber length) was unchanged in spite of the dramatic absolute sarcomere length change. These results indicate that spasticity results in a major alteration of normal muscle-joint anatomical relationships that has not previously been recognized to our knowledge. We hypothesize that the results are explained either by the inability of muscle fibers to add serial sarcomeres in response to growth, or the selective loss of FCU muscle length secondary to the central nervous system lesion.

Adaptation, Physiological↗

PubMed2003

Spastic muscle cells are shorter and stiffer than normal cells.

The mechanical properties of isolated single muscle fiber segments were measured in muscle cells obtained from patients undergoing surgery for correction of flexion contractures secondary to static perinatal encephalopathy (cerebral palsy). "Normal" muscle cells from patients with intact neuromuscular function were also mechanically tested. Fiber segments taken from subjects with spasticity developed passive tension at significantly shorter sarcomere lengths (1.84 +/- 0.05 microm, n = 15) than fibers taken from normal subjects (2.20 +/- 0.04 microm, n = 35). Elastic modulus of the stress-strain relationship in fibers from patients with spasticity (55.00 +/- 6.61 kPa) was almost double that measured in normal fibers (28.25 +/- 3.31 kPa). The fact that these muscle cells from patients with spasticity have a shorter resting sarcomere length and increased modulus compared with normal muscle cells suggests dramatic remodeling of intracellular or extracellular muscle structural components such as titin and collagen. Such changes in muscles of patients with spasticity may have implications for therapy.

Adult↗

PubMed2005

Pathophysiology of spastic paresis. II: Emergence of muscle overactivity.

In the subacute and chronic stages of spastic paresis, stretch-sensitive (spastic) muscle overactivity emerges as a third fundamental mechanism of motor impairment, along with paresis and soft tissue contracture. Part II of this review primarily addresses the pathophysiology of the various forms of spastic overactivity. It is argued that muscle contracture is one of the factors that cause excessive responsiveness to stretch, which in turn aggravates contracture. Excessive responsiveness to stretch also impedes voluntary motor neuron recruitment, a concept termed stretch-sensitive paresis. None of the three mechanisms of impairment (paresis, contracture, and spastic overactivity) is symmetrically distributed between agonists and antagonists, which generates torque imbalance around joints and limb deformities. Thus, each may be best treated focally on an individual muscle-by-muscle basis. Intensive motor training of the less overactive muscles should disrupt the cycle of paresis-disuse-paresis, and concomitant use of aggressive stretch and focal weakening agents in their more overactive and shortened antagonists should break the cycle of overactivity-contracture-overactivity.

Contracture↗

PubMed1996

Changes in voluntary motor control induced by intrathecal baclofen in patients with spasticity of different etiology.

We studied the effects of intrathecal baclofen upon voluntary movements. Eleven patients with spasticity of different etiology and one patient with idiopathic dystonia were studied. Six patients participated in a double-blind trial. Kinematic/dynamic and electromyographic (EMG) patterns were recorded during attempts at single-joint elbow or ankle voluntary movements and isometric contractions. Reflex responses were also recorded. Baclofen suppressed spastic signs in 10 patients: it eliminated clonus and decreased the co-contraction of antagonist and distant muscle groups. Baclofen could induce weakness, particularly in patients with cerebral palsy (CP). Patients with hemi-syndromes did not notice any effects of baclofen in their 'unaffected' limbs. Intrathecal baclofen could improve voluntary movements in some patients with spasticity resulting in better walking and usage of arms. We hypothesize that spasticity induces an adaptive reaction at a segmental level that includes an increase in the number and/or affinity of GABA-sensitive receptors.

Adaptation, Physiological↗

PubMed1993

H-reflexes are less depressed following muscle stretch in spastic spinal cord injured patients than in healthy subjects.

The size of the soleus H-reflex was measured after a slow (17 deg/s) passive stretch of ankle plantarflexors and compared to its control size without muscle stretch in ten neurologically healthy subjects and in six spastic spinal-cord-injured patients. Two seconds after the end of the stretch, the size of the H-reflex was reduced to about 30% of its pre-stretch size in the healthy subjects. The depression remained for 10-15 s. In the spastic, spinal-cord-injured patients, stretch caused significantly less reduction in the size of the H-reflex. The H-reflex also regained its pre-stretch size much faster than in healthy subjects. We suggest that the smaller depression of the H-reflex observed in spastic patients may be involved in the pathophysiology of spasticity.

Adult↗

PubMed1982

Tizanidine in the treatment of spasticity.

A double-blind crossover trial compared tizanidine with baclofen in 36 patients with spasticity. Tizanidine appeared to reduce lower limb spasticity more effectively and to have fewer side effects, but no statistically significant differences emerged when the two drugs were compared. An additional open study of tizanidine confirmed the beneficial action in a selected minority of patients with spasticity. This drug may have an important role in the management of spasticity, but further studies are required.

Adult↗

PubMed2006

Low dose treatment with the synthetic cannabinoid Nabilone significantly reduces spasticity-related pain : a double-blind placebo-controlled cross-over trial.

About 30% of patients with chronic upper motor neuron syndrome (UMNS) suffer from disabling spasticity-related pain not sufficiently correctable by conventional treatment. Delta9-tetrahydrocannabinol (Delta(9)-THC) was reported to add benefit in the treatment of pain in patients with multiple sclerosis (MS). The question arose whether synthetic cannabinoids with lower potential for psychotropic side effects could be effective as well. To evaluate the safety and efficacy of low dose treatment with the synthetic cannabinoid Nabilone (1 mg per day) on spasticity-related pain a placebo-controlled double-blind crossover trial was performed.11 out of 13 included patients completed the study. The 11-Point-Box-Test showed a significant decrease of pain under Nabilone (p < 0.05), while spasticity, motor function and activities of daily living did not change. 5 patients reported side effects: one moderate transient weakness of the lower limbs (Nabilone phase, drop out), three mild drowsiness (two Nabilone, one placebo) and one mild dysphagia (placebo). One patient was excluded from the study due to an acute relapse of multiple sclerosis (Nabilone phase, drop out). Nabilone 1 mg per day proved to be a safe and easily applicable option in the care of patients with chronic UMNS and spasticity-related pain otherwise not controllable.

Activities of Daily Living↗

PubMed2006

Four mutations of the spastin gene in Japanese families with spastic paraplegia.

Hereditary spastic paraplegia (HSP) is a group of genetically heterogeneous neurodegenerative disorders characterized by slowly progressive spasticity and weakness of the lower limbs. HSP is caused by failure of development or selective degeneration of the corticospinal tracts, which contain the longest axons in humans. The most common form of HSP is caused by mutations of the spastin gene (SPAST), located on chromosome 2p21-p22, which encodes spastin, one of the ATPases associated with diverse cellular activities (AAA). In this study, we detected four causative mutations of SPAST among 14 unrelated patients with spastic paraplegia. Two missense mutations (1447A-->G, 1207C-->G) and two deletion mutations (1465delT, 1475-1476delAA) were located in the AAA cassette region. Three of these four mutations were novel. Previous reports and our results suggest that the frequency of SPAST mutations is higher among Japanese patients with autosomal dominant HSP, although SPAST mutations are also observed in patients with sporadic spastic paraplegia.

Adenosine Triphosphatases↗

PubMed2004

Early onset autosomal dominant spastic paraplegia caused by novel mutations in SPG3A.

Hereditary spastic paraplegia (HSP) is a group of neurodegenerative disorders mainly characterized by progressive spasticity of the lower limbs. The major features of HSP are a marked phenotypic variability both among and within families and an extended genetic heterogeneity. More than 20 HSP loci and 10 spastic paraplegia genes (SPG) have been identified to date, including the genes responsible for the two most frequent forms of autosomal dominant spastic paraplegia (AD-HSP), encoding spastin (SPG4) and atlastin (SPG3A), respectively. To date, only eight mutations have been described in the atlastin gene, which was reported to account for about 10% of all AD-HSP families. We investigated 15 German and French AD-HSP families, including the 3 large pedigrees that allowed the mapping and subsequent refinement of the SPG3A locus. Three novel mutations were found in exons 4, 9, and 12 of the atlastin gene and the common R239C mutation located in exon 7 was confirmed in a 7th family of European origin. Overall, the comparison of the clinical data for all SPG3A-HSP families reported to date failed to reveal any genotype/phenotype correlation as demonstrated for other forms of AD-HSP. However, it confirmed the early onset of this form of HSP, which was observed in almost all affected individuals with a mutation in the atlastin gene.

Adolescent↗

PubMed2005

Botulinum toxin type A for upper limb spasticity following stroke: an open-label study with individualised, flexible injection regimens.

Current antispastic medications are unsatisfactory for spasticity treatment, but botulinum toxin type A (BTX-A) shows promise as a new therapeutic option. This open-label, prospective study aimed to assess the effectiveness of BTX-A in improving functional mobility in the early post-stroke population using an individualised, flexible range of doses and targeted muscle groups. Twenty-one stroke patients (13 male, 8 female) were enrolled and injected with BTX-A (Botox, Allergan, mean dose: 255 U; range: 185-300) according to individual spasticity patterns. Assessments were made at baseline and weeks 2, 4, 6, 10 and 16 post-treatment. Outcome measures comprised: Modified Ashworth Scale (MAS), finger flexion scale (Bhakta), MRC scale, Physician's Rating Scale (PRS), Nine Hole Peg Test (9HPT), Motor Assessment Scale, Clinical Global Impression (CGI), Global Assessment of Spasticity (GASS) and Visual Analogue Scale (VAS) for pain assessment. Statistically significant improvements in muscle tone as determined by the MAS were found in all areas (except arm) till week 16 (p<0.05). Finger positioning improved for the study duration, whilst muscle power increased only slightly in specific muscles. PRS revealed significant improvements to week 10 and slight improvement in 9HPT performance in selected patients was observed. Motor Assessment Scale results were statistically significant for arm, hand and advanced hand functions, although the overall functional benefit was mild. GASS and CGI results also showed improvement. Pain was present only in 11 patients and did not significantly improve following treatment. Individualised BTX-A injection regimens may be an effective, reversible and safe new treatment option for patients with spasticity. Nevertheless, functional improvement may be reached only in selected patients.

Adult↗

PubMed2002

Continuous intrathecal infusion of baclofen in patients with spasticity caused by spinal cord injuries.

The aim of this study was to determine the efficacy and safety of intrathecal baclofen therapy delivered by a programmable pump for the chronic treatment of spinal spasticity. Twelve patients with intractable spasticity caused by spinal cord injuries underwent implantation of a programmable continuous infusion pump after significant reduction in spasticity following an intrathecal test bolus of baclofen. No deaths or new permanent neurological deficits occurred following surgery or chronic intrathecal baclofen therapy. The follow-up (12 months) shows a reduction in rigidity in the lower limb of 2.0 points on the Ashworth scale and in the upper limb of 1.2 points. Muscle spasms were reduced from a mean preoperative score of 2.8 to a mean postoperative score of 1.0. In two cases, we observed postoperative catheter dislocation, a complication which could be corrected surgically. This study demonstrates that chronic intrathecal baclofen infusion is a safe and effective form of treatment of intractable spasticity in patients with spinal cord injury. There is considerable reduction in the risk of infection in view of the fact that interrogation and programming of the implanted programmed pumps is noninvasive.

Baclofen↗

PubMed2006

Hereditary spastic paraplegia.

The hereditary spastic paraplegias (HSPs) comprise a large group of inherited neurologic disorders. HSP is classified according to the mode of inheritance, the HSP locus when known, and whether the spastic paraplegia syndrome occurs alone or is accompanied by additional neurologic or systemic abnormalities. Analysis of 11 recently discovered HSP genes provides insight into HSP pathogenesis. Hereditary spastic paraplegia is a clinical diagnosis for which laboratory confirmation is sometimes possible, and careful exclusion of alternate and co-existing disorders is an important element in HSP diagnosis. Treatment for HSP is presently limited to symptomatic reduction of muscle spasticity, reduction in urinary urgency, and strength and gait improvement through physical therapy. Prenatal genetic testing in HSP is possible for some individuals with the increasing availability of HSP gene analysis.

Diagnosis, Differential↗

PubMed1989

Rehabilitation management of children with spastic diplegic cerebral palsy.

Spastic diplegia has been recognized as the type of cerebral palsy most frequently associated with prematurity. Due to constantly improving neonatal care in developed countries, more and smaller premature infants are surviving, and the number of spastic diplegic children can be expected to increase. This paper reviews the incidence, pathophysiology, and associated handicaps of patients with this type of cerebral palsy. The role of the physiatrist and aspects of traditional management are discussed. Recent advances in treatment of spasticity and lower extremity bracing are stressed as they seem to be particularly suitable to spastic diplegic patients.

Cerebral Palsy↗

PubMed1985

Effects of methyl beta-carboline-3-carboxylate, Ro 15-1788 and CGS 8216 on muscle tone in genetically spastic rats.

Genetically spastic rats were used for studying the effect on muscle tone of beta-carboline-3-carboxylic acid methylester (beta-CCM), an inverse benzodiazepine (BDZ) agonist, and that of Ro 15-1788 and CGS 8216, both putative antagonists of pharmacological actions of BDZs. These animals exhibit pathologically increased muscle tone, which can be recorded and quantified in the electromyogram (EMG) of the gastrocnemius (GS) muscle. beta-CCM, 2.5 and 3.0 mg/kg i.p., augmented the tonic activity in the EMG of GS muscle in spastic rats while it did not modify muscle tone at doses of 1.0 and 2.0 mg/kg. Diazepam, 0.4 mg/kg i.p., and Ro 15-1788, 5 mg/kg i.p., but not CGS 8216, 5 mg/kg i.p., antagonised the effect of the beta-carboline on muscle tone. Ro 15-1788, at doses of 0.1-5 mg/kg i.p., did not affect muscle tone in the genetically spastic rats, whilst at doses of 25-200 mg/kg the imidazodiazepine dose dependently increased the tonic activity in the EMG. The action of Ro 15-1788, 50 mg/kg i.p., was reversed by diazepam, 0.4 mg/kg i.p., and beta-CCM, 2 mg/kg i.p., while CGS 8216, 5 mg/kg i.p., facilitated the effect of Ro 15-1788 on muscle tone. CGS 8216 at doses of 5 and 25 mg/kg i.p. was devoid of any effect on muscle tone, whilst at doses of 50 and 200 mg/kg the pyrazoloquinoline increased the tonic activity recorded in the EMG from the GS muscle of the spastic rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1986

Bay K 8644 induces a reversible spasticity-like syndrome in rats.

The dihydropyridine Bay K 8644 exerts a positive modulation of Ca2+ channels. Administration of Bay K 8644 3-5 mg/kg i.p. to rats induces within 15 min a severe spasticity syndrome consisting of stiff tail, arched back, stretching and twisting of forelimbs and hindlegs and backwards motility and rolling over. The syndrome was effectively antagonized by nifedipine 3-30 mg/kg but not by the other Ca2+ channel blockers flunarizine, diltiazem and verapamil. Diltiazem even enhanced the spasticity. Diazepam 10-30 mg/kg i.p. completely blocked the spasticity whereas the other muscle relaxants (-)-baclofen and the beta-carboline ZK 93423 were completely inactive. These findings with Bay K 8644 suggest that spasticity may be caused by changed Ca2+ homeostasis.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗

PubMed1981

A histochemical and electron microscopic study of a fast- and a slow-twitch muscle in genetically spastic mice.

Fast and slow muscle fibers were studied in the flexor digitorum longus (FDL) and soleus (SOL) muscles, respectively, in control and spastic mice. HIstochemical and electron microscopic studies indicated an increased number of mitochondria, a decreased deposition of glycogen and a vesiculation and distension of the sarcoplasmic reticulum in many fast-twitch fibers of the spastic FDL. Similar findings were not evident in the slow-twitch fibers of the spastic SOL. Since the spastic condition causes increased muscular activity as a result of more rapid and prolonged nerve impulse firing, these findings reinforce the idea that a muscle fiber's oxidative capabilities are a function of its activity.

Adenosine Triphosphatases↗

PubMed1992

Isoform-selective deficit of glycine receptors in the mouse mutant spastic.

The mutant mouse spastic (spa) develops a characteristic motor disorder about 2 weeks after birth, with symptoms resembling sublethal poisoning by the glycinergic antagonist strychnine. Correspondingly, adult homozygotic mutants (spa/spa) exhibit a severe reduction of inhibitory glycine receptors in spinal cord and brain. Here we show that the spastic mutation selectively interferes with the postnatal accumulation of the adult isoform of the glycine receptor protein, whereas perinatal expression of the neonatal receptor isoform is not detectably affected. Heterologous expression in X. laevis oocytes of poly(A)+ RNA and Northern blot analysis indicate normal levels of glycine receptor alpha 1 subunit transcripts in spinal cord of adult spastic mutants. Thus, the age-dependent manifestation of spastic symptoms after birth reflects a selective effect of the mutation on the developmental expression of the adult glycine receptor isoform.

Age Factors↗

PubMed2005

[Spasticity. Physical therapy, preventive measures and treatment].

Spasticity is one of the most common motor and tonus disorders during the initial phase with traumatic brain injured patients. The evaluation of spasticity is mainly clinical but it is very important to prevent complications such as limitation of range of motion, pain, decubitus ulcers. The therapeutic options consist in classical indications such as baclofen, dantrolene, tizanidine, benzodiazepine, associated with physiotherapy. Other additive therapeutic options could be discussed: use of toxin botulinum in focal spasticity and intrathecal baclofen infusion in case of severe spasticity (often associated with dysautonomic disorders.).

Anti-Dyskinesia Agents↗