Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Spasticity”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 937 records · Page 52Linked to original sources
PubMed2002

The vegetative and minimally conscious states in children: spasticity, muscle contracture and issues for physiotherapy treatment.

The neuropathology of the vegetative (VS) and minimally conscious (MCS) states and the pathophysiology of spasticity are reviewed. Current treatment options available in the physical management of children in a low-level state and factors influencing the physiotherapy treatment of children in a low-level state will be discussed. The complex neuropathology of VS and MCS helps to explain the varied clinical presentations of children in VS and MCS. Spasticity and muscle contracture are common motor sequelae of VS and MCS. Loss of inhibition by descending motor pathways is thought to result in increased muscle tone or spasticity. However, secondary changes in muscle fibre structure and periarticular connective tissue may be an additional component to increased muscle tone. A multimodal approach combining physical, pharmacological and surgical interventions is likely to be the most effective. Knowledge of the likelihood of recovery from VS and MCS can be helpful in determining the frequency and intensity of physiotherapy. Ethical issues in the management of children in a low-level state include a consideration of the benefits to the child and the child's family and the costs to the health care team and the medical institution.

Adolescent↗
PubMed2006

Ashworth Scales are unreliable for the assessment of muscle spasticity.

Ashworth Scales are the most widely used tests to assess the severity of muscle spasticity. These scales offer qualitative and subjective information; consequently, there are issues concerning validity and reliability. This article presents the results of a study comparing interrater reliability of the original and of the modified Ashworth Scales for measuring muscle spasticity in elbow flexors. Fifteen patients with hemiplegia (nine men and six women) with a median age of 52 years (interquartile range, 28-64) participated in this study. Two physiotherapists rated the muscle tone of elbow flexors according to ratings criteria of the Ashworth and the modified Ashworth Scales. Kappa values for the original Ashworth and the modified Ashworth Scales were 0.17 (SE 0.21; p = 0.41) and 0.21 (SE = 0.12; p = 0.08), respectively. The scales showed similar levels of reliability (chi2= 0.0285, df=1, p = 0.7). The Ashworth Scales are not reliable for the assessment of muscle spasticity. In the absence of interrater reliability, the validity of the measurements may also be questioned.

Adult↗
PubMed2005

The lowest effective dose of botulinum A toxin in adult patients with upper limb spasticity.

OBJECTIVE: To define the lowest effective dose of botulinum toxin type A (Dysport) and safety in the treatment of adult patients with upper limb spasticity. DESIGN: This was a prospective, randomized, double-blind, dose-ranging study. Patients received either a placebo or one of three does of Dysport (350, 500 100) U) into five muscles of affected arm by anatomical and electromyography guidance. Efficacy was assessed periodically throughout the 6-month study period by the Modified Ashworth Scale (MAS), the Action Research Arm Test (ARA), the Barthel Index (BI) and the Visual Analogue Pain Scale (VAS). RESULTS: fifty patients were recruited. The four study groups were comparable at baseline with respect to their demographical characteristics and severity of spasticity. All doses of Dysport studied showed a significant reduction from baseline of muscle tone and pain compared to placebo. However, the effect of functional disability was best at a dose of 500 U and the peak improvement was at week 8 after injection. A dose of 1000 U Dysport produced such an excess degree of muscle weakening that the number of randomized patients was reduced to five. BI and ARA of all patients were decrease after injection. No other adverse event was considered related to the study medication. CONCLUSION: This study suggest that treatment with Dysport reduces muscle tone in adult patients with upper limb spasticity. The optimal dose for treatment of patients with residual voluntary movement in the upper limb appears to be 500 U.

Adult↗
PubMed2005

Conventional magnetic resonance imaging features in patients with tropical spastic paraparesis.

Conventional brain and spinal cord magnetic resonance images were performed in 21 patients with human T-cell lymphotropic virus (HTLV)-1 associated myelopathy/tropical spastic paraparesis, to assess the role of conventional magnetic resonance imaging (MRI) in the disease diagnosis. These patients had no other central nervous system conditions or related risk factors at the time of tropical spastic paraparesis diagnosis. Eleven (52.4%) patients showed nonspecific brain abnormalities on T2-weighted images. The majority (77.2%) of brain abnormalities were located in the deep white matter. A transient contrast-enhancing lesion was identified in the brain of only one patient. In the brain of another patient, 9.0% of the T2-hyperintense lesion load was hypointense on the correspondent T1-weighted images. No differences in terms of demographic, biological, or clinical variables were present between patients with abnormal brain images and those with normal brain magnetic resonance images. Spinal cord T2-weighted images were abnormal in three (14.3%) patients. In one of these three patients, a diffuse but transient edema was found along the entire tract of the spinal cord. White matter lesions were present in the central nervous system of 60% of the cases in this study. However, no correlations between magnetic resonance imaging and clinical findings, and no specificity of lesions were observed. Hence, conventional magnetic resonance imaging is a sensitive but not highly specific tool for diagnosis of tropical spastic paraparesis.

Adult↗
PubMed2006

Human T-lymphotropic virus type 1-associated myelopathy/tropical spastic paraparesis: viral load and muscle tone are correlated.

Human T-lymphotropic virus type 1 (HTLV-1) infections are associated with varying degrees of HTLV-1 viral load and spasticity. Increased viral load is associated with higher risk of developing HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). The authors performed a cross-sectional study of 24 people with HAM/TSP in Lima, Perú, to determine if higher HTLV-1 viral load was correlated with increased muscle tone, measured with a device providing quantitative spasticity assessment (QSA). Median HTLV-1 viral load was 17.0 copies/100 peripheral blood mononuclear cells and QSA value was 39.9 Newton-meters/radian. HTLV-1 viral load was significantly correlated with QSA value (Spearman rho = .48, P = .02), suggesting viral load may play a role in expression of symptomatic neurologic disease. Longitudinal studies are needed to determine if treatments that reduce viral load will reduce muscle tone.

Cross-Sectional Studies↗
PubMed2003

Hereditary spastic paraplegia: clues from a rare disorder for a common problem?

Hereditary spastic paraplegia is a rare disorder with gait disturbance due to a degeneration of the corticospinal tract, sometimes accompanied by involvement of other systems. Out of the 20 loci known so far, eight genes have now been identified, allowing the first molecular and cell studies in the pathophysiology of the disorder. These should also help to understand the function of the corticospinal tract at the molecular level and design strategies to prevent and treat spasticity due to more common causes. The proteins encoded by these genes play a role in development, in signal transduction between axons and myelinating cells, in cellular, particularly axonal trafficking or in energy metabolism. Some of them have actions in several areas of cellular function. Here we review the present knowledge about the genes involved in hereditary spastic paraplegia, a field presently undergoing rapid change.

Adenosine Triphosphatases↗
PubMed2002

Effects of functional electrical stimulation training for six months on body composition and spasticity in motor complete tetraplegic spinal cord-injured individuals.

The effect of functional electrical stimulation (FES) training on body composition, assessed by computed tomography, and the effect of spasticity, assessed by both objective and subjective measures, are evaluated. Fifteen motor-complete spinal-cord-injured men participated in the study. Eight of the 15 subjects undertook FES cycling 3 times weekly for 6 months. Whole body computed tomography scans evaluated changes in body composition. Simultaneous Modified Ashworth Scale and electromyography (EMG) measurements, resistive torque (Kin-Com) and EMG measurements, and self-ratings with Visual Analogue Scale during four consecutive days were used to evaluate changes in spasticity. Lower extremity muscle volume increased by an average of 1300 cm3 (p < 0.001) in the training group compared to the control group, who experienced no change. Otherwise no changes in body composition were seen. Significant correlations (Spearman) were found between individual EMG activity recordings and movement-provoked Modified Ashworth Scale ratings in 26% of the test situations, irrespective of group and time. The objective and subjective evaluation of movement-provoked passive (viscoelastic) and active (spasticity-related) resistance remained unchanged.

Adult↗
PubMed2002

Treatment of upper extremity spasticity in stroke patients by focal neuronal or neuromuscular blockade: a systematic review of the literature.

Studies published from January 1966 until October 2000 on the clinical effects of focal neuronal and neuromuscular blockade in post stroke upper limb spasticity were identified. Twelve studies were included and evaluated on 13 methodological criteria. Ten studies on Botulinum toxin type A (BTX-A) treatment were found (of which 4 were randomised controlled trials (RCTs) and 6 were uncontrolled observational studies) as well as one uncontrolled observational study on phenol blockade of the subscapular muscle and one on alcohol blockade of the musculocutaneus nerve. The homogeneity of the patient groups with regard to diagnosis and their comparability with regard to functional prognosis and other sources of bias were generally unsatisfactory. Only two RCTs met predetermined criteria of minimal validity. There is evidence of effectiveness of BTX-A treatment on reducing muscle tone (varying between 0.8 and 2.0 points on the modified Ashworth scale) and improving passive range of motion at all arm-hand levels in chronic stroke patients for approximately 3-4 months. There is also preliminary evidence of a synergistic effect of concomitant electrostimulation. Taking into account a critical maximum dose of 100 MU Botox" (300-500 MU Dysport) for preserving active finger flexion, BTX-A treatment seems to be a safe focal spasmolytic treatment. Effectiveness of BTX-A treatment on improving functional abilities could not be convincingly demonstrated, although two subgroups may be identified that might specifically benefit at a functional level: (1) patients with mild spasticity and a potential for voluntary extensor activity and (2) patients with severe spasticity suffering from problems with positioning and taking care of the affected arm and hand. Larger controlled studies are needed to compare the effectiveness of BTX-A with other focal spasmolytic techniques paying special attention to individual goal assessment, the (duration of) functional benefits, co-treatment and aftercare, side-effects and cost-effectiveness.

Botulinum Toxins↗
PubMed2006

Focal spasticity therapy with botulinum toxin: effects on function, activities of daily living and pain in 100 adult patients.

OBJECTIVE: Analysis of the effects of a comprehensive focal spasticity program in adult patients. DESIGN: Retrospective study of an out-patient cohort. PATIENTS: One hundred patients were enrolled in the study (54 men and 46 women, mean age 41 years (SD 14). Cerebral palsy and stroke were equally common (80% in total). The remaining patients had miscellaneous diagnoses, including traumatic brain injury. METHODS: On average 230 units (SD 101) of botulinum toxin A Botox was given for 227 principal therapy targets chosen by the patient or the caregiver. One patient could have several targets for therapy. Administration of botulinum toxin was combined with 260 additional therapeutic interventions, most of which were forms of physical therapy. The effects were assessed after 6 weeks and compared with baseline functional abilities 1-2 weeks prior to therapy. RESULTS: Improvement was observed for 211 (93%) therapy targets, no change in 15 (7%), and impairment in 1, corresponding to an overall improvement in 90 patients (90%), 9 unchanged (9%) and worsening in 1. Spasticity assessment (Ashworth scale 0-4; 30 patients) showed a statistically significant improvement (median at baseline was 3 vs 2 after therapy, mean difference 1.2, p<0.001). CONCLUSION: Improvement was observed in >or=90% of patients and in their principal therapeutic targets in a cohort receiving their first focal spasticity treatment with botulinum toxin A and additional therapy. A strict strategy for patient selection and comprehensive management was followed.

Activities of Daily Living↗
PubMed1999

Genetic mapping to 10q23.3-q24.2, in a large Italian pedigree, of a new syndrome showing bilateral cataracts, gastroesophageal reflux, and spastic paraparesis with amyotrophy.

We have recently observed a large pedigree with a new rare autosomal dominant spastic paraparesis. In three subsequent generations, 13 affected individuals presented with bilateral cataracts, gastroesophageal reflux with persistent vomiting, and spastic paraparesis with amyotrophy. Bilateral cataracts occurred in all affected individuals, with the exception of one patient who presented with a chorioretinal dystrophy, whereas clinical signs of spastic paraparesis showed a variable expressivity. Using a genomewide mapping approach, we mapped the disorder to the long arm of chromosome 10 on band q23.3-q24.2, in a 12-cM chromosomal region where additional neurologic disorders have been localized. The spectrum of phenotypic manifestations in this family is reminiscent of a smaller pedigree, reported recently, confirming the possibility of a new syndrome. Finally, the anticipation of symptoms suggests that an unstable trinucleotide repeat may be responsible for the condition.

Abnormalities, Multiple↗
PubMed2000

A new locus for autosomal recessive spastic paraplegia associated with mental retardation and distal motor neuropathy, SPG14, maps to chromosome 3q27-q28.

Hereditary spastic paraplegias (HSPs), a group of neurodegenerative disorders that cause progressive spasticity of the lower limbs, are characterized by clinical and genetic heterogeneity. To date, three loci for autosomal recessive HSP have been mapped on chromosomes 8p, 16q, and 15q. After exclusion of linkage at these loci, we performed a genomewide search in a consanguineous Italian family with autosomal recessive HSP complicated by mild mental retardation and distal motor neuropathy. Using homozygosity mapping, we obtained positive LOD scores for markers on chromosome region 3q27-q28, with a maximum multipoint LOD score of 3.9 for marker D3S1601. Haplotype analysis allowed us to identify a homozygous region (4.5 cM), flanked by markers D3S1580 and D3S3669, that cosegregates with the disease. These data strongly support the presence, on chromosome 3q27-28, of a new locus for complicated recessive spastic paraplegia, which we have named "SPG14."

Adult↗
PubMed2002

A kinesin heavy chain (KIF5A) mutation in hereditary spastic paraplegia (SPG10).

We have identified a missense mutation in the motor domain of the neuronal kinesin heavy chain gene KIF5A, in a family with hereditary spastic paraplegia. The mutation occurs in the family in which the SPG10 locus was originally identified, at an invariant asparagine residue that, when mutated in orthologous kinesin heavy chain motor proteins, prevents stimulation of the motor ATPase by microtubule-binding. Mutation of kinesin orthologues in various species leads to phenotypes resembling hereditary spastic paraplegia. The conventional kinesin motor powers intracellular movement of membranous organelles and other macromolecular cargo from the neuronal cell body to the distal tip of the axon. This finding suggests that the underlying pathology of SPG10 and possibly of other forms of hereditary spastic paraplegia may involve perturbation of neuronal anterograde (or retrograde) axoplasmic flow, leading to axonal degeneration, especially in the longest axons of the central nervous system.

Amino Acid Sequence↗
PubMed1991

Tropical spastic paraparesis/HTLV-1-associated myelopathy (TSP/HAM): treatment with an anabolic steroid danazol.

Tropical spastic paraparesis or HTLV-I-associated myelopathy is a progressive spastic disorder associated with the human T-lymphotropic virus type I. Some cases have responded to prednisone. Danazol is an attenuated androgen with minimal virilizing effects. It is used in the treatment of endometriosis and various autoimmune hematologic diseases shown to be responsive to prednisone. Because danazol is anabolic, useful in prednisone-responsive diseases, and less toxic than prednisone, we gave danazol to 6 patients with TSP and 1 with HIV, HTLV-I-associated myelopathy. Five patients had a favorable response. Two became ambulatory after having been confined to a wheelchair. Three were able to ambulate greater distances (in walkers) than prior to danazol. Three had noticeable decreases in spasticity. Urinary incontinence resolved in two. Physical therapy was variably employed in all except one patient. Two patients who had not responded to physical therapy responded to physical therapy and danazol. One patient did not tolerate danazol and one patient did not improve. Toxicities noted were mild elevations in liver enzymes in 4 patients; these responded to a decrease in dose of danazol; amenorrhea in one and mild fluid retention in one. We conclude that danazol is a useful agent in the management of TSP.

Adult↗
PubMed1986

Spinal cord stimulation for the control of spasticity in patients with chronic spinal cord injury: II. Neurophysiologic observations.

We sought neurophysiologic evidence that spinal cord stimulation could modify the behavior of spinal reflexes in 15 chronic SCI patients who showed the beneficial effect of SCS on spasticity. We studied the behavior of passive stretch, clonus, cutaneous touch, plantar reflex irradiation, and the response to the neck flexion reinforcement maneuver during spinal cord stimulation by use of surface PEMG recordings. Fifty-five percent of the responses were changed during spinal cord stimulation, but with widely varying patterns of response in individual patients. Exceptional patients showed changes in most or all responses; most showed changes in two or three. Thirty of seventy-five responses showed a reduction in motor unit activity in the recordings. Eleven of seventy-five responses were increased. Excessive stimulation strength enhanced spasticity in patients in whom another stimulus setting suppressed spasticity. We conclude that spinal cord stimulation could modify segmental reflexes but that the effects were selective, probably dependent on the preserved segmental structures and ascending and descending pathways.

Adolescent↗
PubMed2005

Mu and delta, but not kappa, opioid agonists induce spastic paraparesis after a short period of spinal cord ischaemia in rats.

BACKGROUND: Intrathecal (IT) morphine given after a short interval of aortic occlusion in a rodent model induced transient spastic paraparesis via opioid receptor-predicted actions in spinal cord. To determine the role(s) of spinal opioid receptor subtypes we investigated whether IT administration of various selective opioid receptor agonists can induce paraparesis following a short period of spinal cord ischaemia in rats. METHODS: In Sprague-Dawley rats implanted with an IT catheter, spinal cord ischaemia was induced for 6 min using an intraaortic balloon. Mu ([D-Ala2, N-Me Phe4, Gly-ol5] enkephalin), kappa (U50488H) or delta ([D-Pen(2,5)] enkephalin) selective agonists were injected intrathecally 30 min after reperfusion. A separate group of animals was used to investigate the dose-response effect on this motor dysfunction. For this purpose, three doses of mu, kappa, or delta agonists were injected intrathecally after ischaemia. After IT injection, recovery of motor function was assessed periodically using the motor deficit index (0=complete recovery; 6=complete paraplegia). RESULTS: IT administration of mu and delta but not kappa agonists produced dose-dependent effects in the induction of spastic paraparesis. In addition, this spasticity induced by IT mu and delta agonists was reversed completely by IT naloxone and naltrindole, respectively. CONCLUSION: These results suggest that the effect of various opioids on motor function after a short period of spinal cord ischaemia depends upon individual opioid receptor subtypes.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1981

Electrophysiological studies of gait in spasticity and rigidity. Evidence that altered mechanical properties of muscle contribute to hypertonia.

The surface electromyogram (EMG) of mm. tibialis anterior and triceps surae was recorded in 10 patients with spasticity, 10 patients with rigidity and 20 normal subjects and correlated with the changes in ankle joint angle during the different phases of the gait cycle. While the strength and timing of EMG activity recorded from triceps surae during the stance phase of gait did not differ from that of normal subjects, the EMG of tibialis anterior was significantly stronger during the swing phase in both groups of patients. Although the reciprocally organized innervation pattern of the leg muscles was preserved, spastic patients could hardly lift up the affected foot during the swing phase despite the enhanced activity of tibialis anterior. There was no coactivation of the calf muscles during the hyperactivity of tibialis anterior. Therefore, no electrophysiological explanation could be found for the increased muscle tone in either group of patients. The possibilities of reduced force development by the muscle fibres of tibialis anterior or of some mechanical obstruction in the ankle joint were largely excluded as alternative explanations underlying the impeded elevation of the foot. We suppose that in both diseases the muscle fibres undergo changes which are responsible for increased muscle tone in spasticity and rigidity. The pathophysiological mechanism of these changes remains unknown.

Adolescent↗
PubMed1982

The effects of cerebellar stimulation on the stretch reflex in the spastic monkey.

The effects of stimulating the cerebellar surface on abnormal segmental reflexes were examined in monkeys rendered spastic by either bilateral or unilateral decortication of areas 1, 2, 3, 4 and 6. Rectified, integrated electromyographic (EMG) activity from the biceps and triceps as well as the torque were recorded and averaged during successive flexion-extension movements of the arm produced by a displacement controlled torque motor. Two movement paradigms were employed. The first consisted of a ramp and hold paradigm with an initial rapid flexion of the forearm, a subsequent two second period during which the arm position was held constant, and a rapid extension returning the limb to the initial position. In the second paradigm, the forearm was modulated sinusoidally at several different frequencies. Cerebellar stimulating electrodes were placed over the paravermal region bilaterally. Different frequencies (10 to 300 HZ) and different charge densities (1.5 to 10 microC/cm2) were used in each animal. In each experimental trial short periods of cerebellar stimulation (10 to 30 minutes) were interspersed between control periods. As observed in some types of clinical spasticity, flexion or extension of the extremity was capable of evoking coactivation of the biceps and triceps. Cerebellar surface stimulation reduced the amplitude of the phasic and tonic stretch reflexes recorded from the triceps during flexion and decreased the abnormal triceps response during passive shortening. The biceps response to stretch was increased by cerebellar stimulation and its abnormal response to flexion was decreased. These combined effects modified the organization of the segmental reflexes, producing a more normal reciprocal relationships of the EMG activity in the biceps and triceps. Evaluation of many different combinations of stimulus parameters revealed that not only the magnitude of the passive reflex but also the nature of the effect was dependent on stimulus parameters. Although these studies demonstrate an improvement in the abnormal reflexes present in spastic primates, they emphasize the complexities of the response evoked by cerebellar stimulation and the importance of stimulus parameters in the modifications produced by this technique.

Animals↗
PubMed1990

A quantitative study of sensory function in hereditary spastic paraplegia.

Somatic sensation was studied in 23 patients from 14 families with hereditary spastic paraplegia. Quantitative sensory testing revealed significantly raised thermal, heat pain, vibratory and tactile thresholds in patients as compared with normal controls. Cutaneous sensitivity was more severely impaired in the feet than in the hand. All patients had at least one elevated sensory threshold. Sensory nerve conduction studies were abnormal in 6 patients, 5 of whom were members of the same family. Somatosensory evoked potentials were reduced on average to half the size of those of controls. Although the clinical picture is dominated by a spastic paraparesis, subclinical sensory impairment is common in hereditary spastic paraplegia and may reflect involvement of peripheral nerves, afferent pathways in the spinal cord or both.

Adult↗