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At least 235 records · Page 13Linked to original sources
PubMed2000

Intrasubject repeatability of gait analysis data in normal and spastic children.

OBJECTIVE: To evaluate intrasubject repeatability of data obtained from computer-aided motion analysis in normal and spastic children. DESIGN: Prospective controlled study. BACKGROUND: Information from gait analysis is used in selecting therapeutic interventions for gait improvement in cerebral palsy. While there are several studies regarding repeatability of normal gait, there are no studies evaluating the repeatability of spastic gait. METHODS: Forty children (20 normal, 20 with diplegic type of cerebral palsy) were subjected to gait analysis. Kinematic, kinetic and time distance parameters obtained from gait analysis were studied for intrasubject variability within-day and between-day using statistical measures. RESULTS: Normal children had lower variability in time distance parameters than spastic children both within and between days. The repeatability of kinetics was better than those of kinematics, and values for normal children were better than those for spastic children. Within-day repeatability of kinematics and kinetics was better in normal children. Between-day repeatability of kinematics was better in normal children, while spastic children showed better repeatability for kinetics. CONCLUSIONS: We found lower repeatability of gait analysis data in spastic children compared to normal children. Restricted joint range of motion due to spasticity in the group of cerebral palsy patients may be responsible for the lower repeatability of data. Some errors due to marker placement are inadvertent and contribute to the lower between-day repeatability. RELEVANCE: The results of this study should be of interest to clinicians who make therapeutic decisions in patients with cerebral palsy using gait analysis data, and for scientists studying normal and pathological gait.

Adolescent↗
PubMed2002

The effect of gamma-aminobutyric acid (GABA) receptor drugs on morphine-induced spastic paraparesis after a noninjurious interval of spinal cord ischemia in rats.

UNLABELLED: We have previously demonstrated that intrathecal morphine given after a noninjurious interval of spinal cord ischemia induced transient spastic paraparesis in a rodent model. However, the mechanism of this paraparesis is unknown. We hypothesized that morphine inhibits gamma-aminobutyric acid (GABA)ergic interneurons that control the tonus of spinal cord alpha-motoneurons and that inhibition of spinal cord interneurons may cause spastic paraparesis. In this study, we investigate interactions between morphine and GABAergic agonists or antagonists on motor function after spinal cord ischemia and then clarified the mechanism of the spastic paraparesis induced by intrathecal morphine. Spinal cord ischemia was induced by aortic occlusion lasting 6 min. We first determined whether intrathecally administered GABA agonists (muscimol or baclofen) improve the spastic paraparesis in this model. GABA agonists did not improve the paraparesis. Next, we examined the effect of GABA antagonists (bicuculline or 5-aminovaleric acid) and determined the interaction between morphine and GABA antagonists. In an isobolographic analysis, the 50% effective dose decreased below the theoretical additive line, indicating a synergistic interaction between morphine and GABA antagonists. These results indicate that the spastic paraparesis induced by intrathecal morphine may be mediated in part by GABA receptors. IMPLICATIONS: The purpose of this study was to investigate interactions between morphine and GABAergic agonists or antagonists on motor function after spinal cord ischemia and then clarify the mechanism of the spastic paraparesis induced by intrathecal morphine. The spastic paraparesis induced by intrathecal morphine may be mediated in part by GABA receptors.

Analgesics, Opioid↗
PubMedDate not supplied

Computer modeling of the pathomechanics of spastic hip dislocation in children.

Spastic muscles about the hip cause subluxation, dislocation, and lead to acetabular dysplasia. Spastic hip disease occurs when the muscles about the hip exert forces that are too high or in the wrong direction or both. To determine the role of the hip forces in the progression of spastic hip disease and the effect of both muscle-lengthening and bony reconstructive surgeries, a computerized mathematical model of a spastic hip joint was created. The magnitude and direction of the forces of spastic hips undergoing surgery were analyzed preoperatively and postoperatively to determine which procedure is best suited for the treatment of spastic hip disease. The muscle-lengthening procedures included (a) the adductor longus, (b) the psoas, iliacus, gracilis, adductor brevis, and adductor longus, and (3) the psoas, iliacus, gracilis, adductor brevis, adductor longus, semimembranosus, and semitendinosus. The bony reconstructive and muscle-lengthening procedures included (a) lengthening the psoas, iliacus, gracilis, adductor brevis, adductor longus, semimembranosus, and semitendinosus combined with changing femoral neck anteversion from 45 to 10 degrees , (b) lengthening of the psoas, iliacus, gracilis, adductor brevis, adductor longus, semimembranosus, and semitendinosus combined with changing neck-shaft angle from 165 to 135 degrees , and (c) lengthening of the psoas, iliacus, gracilis, adductor brevis, adductor longus, semimembranosus, and semitendinosus combined with changing femoral neck anteversion from 45 to 10 degrees and neck-shaft angle from 165 to 135 degrees . Results show that a child with spastic hip disease has a hip-force magnitude 3 times that of the a child with a normal hip in the normal physiologic position. Based on this mathematical model the best to normalize the magnitude of the hip-joint reaction force, the muscles to be lengthened should include the psoas, iliacus, gracilis, adductor brevis, and the adductor longus. To normalize the direction of the hip force, the extremity should be positioned in the normal physiologic position. The impact of decreasing the femoral anteversion or femoral neck-shaft angle or both had little additional effect on the direction or magnitude of hip forces.

Biomechanical Phenomena↗
PubMed1998

Electrophysiological monitoring during selective dorsal rhizotomy, and spasticity and GMFM performance.

The relation between abnormal electrophysiological responses to intraoperative stimulation during selective dorsal rhizotomy (SDR) and the degree of spasticity and motor dysfunction was explored in 92 children with spastic cerebral palsy (CP) who underwent SDR at a single center. The proportion of abnormally responding rootlets was compared with the degree of spasticity measured with the modified Ashworth Scale (MAS) and with the spasticity measurement system (SMS) at discrete segmental levels. Motor impairment measured with the Gross Motor Function Measure (GMFM) was also compared with the proportion of abnormally responding dorsal rootlets. A consistent relation between the proportion of abnormally responding rootlets and the degree of spasticity and gross motor abnormality at the corresponding muscles could not be demonstrated. There was also no consistent association between the proportion of rootlets ablated during SDR and the change in spasticity measured with the MAS and SMS, or to the change in motor function as measured with the GMFM. These data suggest that the intraoperative monitoring technique most commonly used for SDR is unlikely to identify accurately those neural elements which contribute to spasticity in children with CP.

Adolescent↗
PubMed2005

Pressure sores with associated spasticity: a clinical challenge.

Paraplegic and quadriplegic patients particularly those suffering from spinal cord injuries are at a high risk of developing pressure ulcerations. Unlike pressure ulcers in geriatric patients, which usually can be controlled with pressure relieving devices and local wound care, pressure ulceration complicating spinal cord injuries should be viewed from another perspective. Clinical management is also more complex because of the associated spasticity. Although it is now recognised that spasticity control is critical for management of patients with cerebral or spinal cord diseases or injuries, published risk assessment studies and risk assessment pressure sore scales fail to recognise spasticity as a major risk factor. Identification of spasticity should heighten the awareness of medical and paramedical personnel and have a positive impact on prevention as well as on treatment of pressure sores in this particularly difficult group of patients. We present our experience with a young quadriplegic patient with severe spasticity presenting with a large infected ischial pressure sore. All surgical as well as conservative attempts to achieve healing failed because of our failure to recognise the importance of spasticity control in the overall treatment scheme. Spasticity control should be included as a prerequisite for any treatment protocol of such patients.

Adult↗
PubMedDate not supplied

Evaluation and treatment of recurrent spasticity after recurrent laryngeal nerve section. A preliminary report.

Of 365 spastic dysphonia patients treated by recurrent laryngeal nerve (RLN) section to date, 44 (12%) have experienced recurrence of the spastic dysphonia. Most of these 44 patients had moderately severe to very severe spastic dysphonia before the RLN section was performed. We believe, therefore, that preoperative severity is an important predictor of the likelihood of recurrence. Twenty-eight patients with recurrent spastic dysphonia following RLN section were further treated by one or more carbon dioxide laser thinnings of the paralyzed vocal fold. Following this procedure, 23 patients (50%) achieved eradication of spasticity, while a mild degree of spasticity remained in 17 (39%). These findings lead us to conclude that even though spastic dysphonia may recur following RLN section, a viable secondary surgical procedure is available.

Humans↗
PubMed2001

Intrathecal baclofen therapy for stroke-related spasticity.

Intrathecal baclofen (ITB) therapy is a widely recognized management technique for severe, disabling spasticity in individuals with cerebral palsy and spinal and brain injuries. Its utility in the stroke population has only been recognized recently. Unlike the aforementioned patient populations, many stroke survivors are ambulatory and are able to maintain a certain degree of functional independence through compensatory use of the uninvolved limbs. Clinicians often fail to recognize the potential enhancement in the function of these individuals if they gain better control of their spastic limbs. Other spasticity treatments, such as oral medications and neurolytic procedures, offer the advantage of being nonsurgical; however, not every stroke patient will respond well to them. Some patients may not tolerate the systemic side effects of oral medications, such as drowsiness and sedation. In patients with severe multilimb spasticity, phenol and even high doses of botulinum toxin may not adequately control spasticity. ITB therapy offers the advantage of effectively decreasing severe, diffuse spasticity without causing untoward effects on arousal and cognition. This article will review the efficacy of ITB therapy in treating spasticity and enhancing function in stroke survivors.

Journal Article↗
PubMed1998

Spasticity and strength changes as a function of selective dorsal rhizotomy.

This investigation quantified pre- and postsurgery (8 months) hamstring muscle spasticity and strength in children with cerebral palsy (CP) undergoing a selective dorsal rhizotomy. Nineteen children with CP (CP group) and six children with able bodies (AB group) underwent testing with a dynamometer. For the spasticity measure, the dynamometer measured the resistive torque of the hamstring muscles during passive knee extension at four different speeds. Torque angle data were processed to calculate the work done by the machine to extend the knee for each speed. Linear regression was used to calculate the slope of the line of best fit for the work velocity data. The slope simultaneously encompassed three key elements associated with spasticity (velocity, resistance, and stretch) and was considered the measure of spasticity. For the strength test, the dynamometer moved the leg from full knee extension to flexion while a maximum concentric contraction of the hamstring muscles was performed. Torque angle data were processed to calculate the work done on the machine by the child. Hamstring spasticity values for the CP group were significantly greater than similar values for AB group prior to surgery; however they were not significantly different after surgery. Hamstring strength values for the CP group remained significantly less than those for the AB group after surgery, but were significantly increased relative to their presurgery values. The results of spasticity testing in the present investigation agreed with previous studies indicating a reduction in spasticity for the CP group. The results of strength testing did not agree with those in the previous literature; a significant increase in strength was observed for the CP group.

Journal Article↗
PubMed1990

Epidemiology of spasticity following traumatic spinal cord injury.

Two epidemiologic studies of spasticity at discharge and first annual follow-up in patients with traumatic spinal cord injury (SCI) are reported. Study 1 analyzed occurrence of spasticity and its severity for 96 subjects at one SCI center, with 67% of subjects developing spasticity by discharge and 37% receiving antispasticity medication. By follow-up, these figures were 78% and 49%, respectively. Incidence of spasticity was higher among cervical and upper thoracic than lower thoracic and lumbosacral levels of injury groups (p less than 0.001). Study 2 analyzed presence of spasticity severe enough to have warranted treatment on 466 subjects at 13 collaborating SCI centers, where 26% of subjects received treatment by discharge and 46% by follow-up. Probability of spasticity treatment was significantly related (p less than 0.05) to days from injury to discharge and level of injury group, whereas age, gender, and Frankel grade were not related. Among only cervical and upper thoracic subjects, Frankel grade was significantly related (p less than 0.01), with grades A (27%) and D (29%) being less frequently treated than grades B (50%) and C (52%). Importance of controlling the above significantly related factors is emphasized for future studies of methods to reduce incidence or severity of spasticity.

Adult↗
PubMed1993

Preserved endothelial function in the spastic segment of the human epicardial coronary artery in patients with variant angina--role of substance P in evaluating endothelial function.

This study aimed to determine whether or not endothelium-dependent vasodilation is preserved in spastic segments of human epicardial coronary arteries. Segmental responses of coronary arteries to substance P were examined in 30 patients with variant angina and in 10 patients with atypical chest pain using a quantitative angiographic technique. Coronary diameter at the basal state was matched between spastic and non-spastic segments in patients with variant angina, normal coronary arteries and with atypical chest pain (2.3 +/- 0.2 mm, 2.3 +/- 0.4 mm, 2.4 +/- 0.3 mm, respectively). In segments where vasospasm was induced by ergonovine and/or acetylcholine, changes in diameter in response to substance P did not differ from those in non-spastic segments; maximal dilation averaged 27.1 +/- 9.5% in the spastic segments and 24.4 +/- 9.6% in the non-spastic segments (expressed as a percent increase over the value before drug administration). It would appear that the potential of the endothelium to release endothelium-dependent relaxant factor (EDRF) and the vasodilator response to EDRF are preserved, even in spastic segments.

Acetylcholine↗
PubMed1992

Long-term intrathecal baclofen treatment in supraspinal spasticity.

Baclofen, a derivate of gamma-amino butyric acid (GABA), is known to be a useful drug in spasticity treatment. To achieve a good therapeutic response higher oral dosages have to be administered related with central side effects. Intrathecal application of Baclofen in microgram range dosages is proved to be effective in spinal spasticity. The efficiency of intrathecal Baclofen in patients suffering from supraspinal spasticity is discussed controversially. We report on 9 patients with long-term intrathecal Baclofen treatment, all of them responding well presenting a marked reduced muscle tone. In most cases an improvement of motor performance and in two cases improved bladder function was observed. The therapeutical dosages administered to patients with supraspinal spasticity exceed those administered to patients with spinal spasticity by approximately 100% without provoking central side effects. Despite the risks connected with this method it has to be considered as treatment of choice in cases of severe supraspinal spasticity.

Adult↗
PubMed2004

Novel mutation in the SPG3A gene in an African American family with an early onset of hereditary spastic paraplegia.

BACKGROUND: Mutations in a novel GTPase gene SPG3A cause an autosomal dominant hereditary spastic paraplegia linked to chromosome 14q (SPG3), which accounts for approximately 10% to 15% of all autosomal dominant hereditary spastic paraplegia cases. The mutational spectrum of the SPG3A gene and the phenotype/genotype correlations have not yet been established. OBJECTIVE: To describe a kindred with an infantile onset of hereditary spastic paraplegia caused by a novel mutation in the SPG3A gene. PATIENTS: Complete neurological examination and genetic analysis were performed on 6 affected members of a small African American kindred. Linkage analysis to genetic markers near autosomal dominant hereditary spastic paraplegia loci on chromosomes 2p and 14q was performed. The coding sequence of the SPG3A gene was analyzed, and the identified change in the sequence was tested for being a benign polymorphism by sequencing 200 chromosomes from normal controls. RESULTS: Every affected individual had signs of uncomplicated spastic paraparesis without additional neurological abnormalities. None of the affected family members had ever walked normally. The history was consistent with an infantile onset, despite the normal acquisition of motor milestones. Genetic analysis suggested linkage to the SPG3A locus on chromosome 14q. Analysis of the SPG3A gene revealed a missense mutation C635T, predicted to result in a threonine to isoleucine substitution at codon 156. Analysis of 200 normal chromosomes did not identify the same change in healthy subjects. CONCLUSION: We report a novel mutation in the SPG3A gene in an African American family with an infantile onset of autosomal dominant hereditary spastic paraplegia.

Adolescent↗
PubMed2004

Atlastin1 mutations are frequent in young-onset autosomal dominant spastic paraplegia.

BACKGROUND: Hereditary spastic paraplegias are disorders that are very heterogeneous, both clinically and genetically. The atlastin1 gene has recently been implicated in SPG3A, a form of autosomal dominant pure spastic paraplegia. Atlastin1 mutations have been identified in 8 families so far. OBJECTIVES: To determine the relative frequency, phenotype, and mutation spectrum of SPG3A in patients with pure autosomal dominant spastic paraplegia and onset before age 20 years. PATIENTS AND METHODS: We sequenced the atlastin1 gene in a large series of patients (31 families) in which mutations in the spastin gene, corresponding to the frequent SPG4 locus, had previously been excluded. The phenotype was compared with 126 SPG4 patients. RESULTS: We identified 12 families (39%) including 34 patients with 9 different missense atlastin1 mutations, 7 of which are newly described. The main clinical characteristic of these SPG3A patients was pure spasticity with very young onset of symptoms (mean age, 4.6 +/- 3.9 years) and slow progression. However, additional signs such as decreased vibration sense and wasting in lower limbs, sphincter disturbances, and scoliosis were found in a minority of patients. In addition, several gene carriers were clinically affected but still asymptomatic (n = 5) or had no clinical signs (n = 2), indicating incomplete penetrance. Compared with patients from other families meeting the same diagnostic criteria (43 patients) and families with SPG4 (126 patients), the major form of autosomal dominant spastic paraplegia, SPG3A patients had earlier symptom onset, less frequently increased reflexes in the upper limbs, decreased vibration sense in the lower limbs, and fewer sphincter disturbances, but more frequently observed wasting in the lower limbs and scoliosis. These particularities, as well as frequent abnormal motor evoked potentials, could help identify patients to be screened for atlastin1 gene mutations. CONCLUSIONS: This study enables us to estimate the frequency of the SPG3A mutations in France at 39% in families with young-onset autosomal dominant spastic paraplegia after exclusion of SPG4 cases. So far, most mutations have been private, although they were all found in exons 7, 8, 12, and 13. These exons should be given priority when performing molecular diagnoses for SPG3A.

Adolescent↗
PubMed2004

Treatment for spasticity in amyotrophic lateral sclerosis/motor neuron disease.

BACKGROUND: Spasticity commonly affects patients with motor neuron disease and it is likely to contribute to worsening muscle dysfunction, increased difficulty with activities of daily living and deteriorating quality of life. OBJECTIVES: The objective of this review is to systematically review all types of treatments for spasticity in amyotrophic lateral sclerosis, also known as motor neuron disease. SEARCH STRATEGY: We searched the Cochrane Neuromuscular Disease Group specialised trials register (searched January 2003), MEDLINE (January 1966 to January 2003), EMBASE (January 1980 to January 2003), CINAHL (January 1982 to January 2003), AMED (January 1985 to January 2003) and LILACS (January 1982 to January 2003) for randomized controlled trials. We reviewed the bibliographies of the randomized trials identified, and contacted trial authors and known experts in the field. SELECTION CRITERIA: We included quasi-randomized or randomized controlled trials of participants with probable or definite amyotrophic lateral sclerosis according to the El Escorial diagnostic criteria (or a revised version) or the Airlie House revision. We would have included trials of physical therapy, modalities, prescription medications, non-prescription medications, chemical neurolysis, surgical interventions, alternative therapies. Our primary outcome measure was reduction in spasticity at three months or greater as measured by Ashworth (or modified Ashworth) spasticity scale. Our secondary outcome measures were: validated measures based on history, physical examination, physiological measures, measures of function, measures of quality of life, serious adverse events, and measures of cost. DATA COLLECTION AND ANALYSIS: We identified only one randomized controlled trial that met the inclusion criteria for this review. Two authors extracted the data. We also contacted the author of the paper and obtained further information not available in the published article. MAIN RESULTS: The included study was a trial of moderate intensity, endurance type exercise versus 'usual activities' in 25 patients with amyotrophic lateral sclerosis. At three months patients performing the 15 minute twice daily exercises had significantly less spasticity (mean reduction of 0.43 Ashworth grades versus an increase of 0.25 in controls), as measured by the Ashworth scale. REVIEWER'S CONCLUSIONS: Individualized, moderate intensity, endurance type exercises for the trunk and limbs may help to reduce spasticity in motor neuron disease. No other medical, surgical or alternative treatment and therapy has been evaluated in a randomized fashion in this patient population.

Amyotrophic Lateral Sclerosis↗
PubMed2005

Mapping of a new form of pure autosomal recessive spastic paraplegia (SPG28).

Pure hereditary spastic paraplegias are characterized by isolated and progressive spasticity in the lower limbs. We mapped the spastic paraplegia 28 (SPG28) locus to chromosome 14q21.3-q22.3 in a Moroccan family with autosomal recessive hereditary spastic paraplegia. Affected patients experienced development of progressive spastic gait during childhood and required help walking in their early 40s. Nine additional hereditary spastic paraplegia families were not linked to this locus, demonstrating further genetic heterogeneity. No mutations were found in exons of GCH1 and SPG3A, two genes from the candidate region involved in movement disorders.

Adult↗
PubMed2001

A comprehensive model of spastic hypertonia derived from the pendulum test of the leg.

We propose a comprehensive model of spastic hypertonia based on clinical neurophysiology and validated using experimental data obtained from the pendulum test of the leg in 8 healthy volunteers and 15 spastic patients. This nonlinear computational model includes mechanical parameters and a stretch reflex representation involving three neural parameters: a threshold coefficient, the gain of the stretch reflex, and a time lag accounting for the reflex loop latency and the electromechanical coupling delay. Variation of the threshold coefficient alone allowed an overall reproduction of experimental data obtained from spastic and healthy subjects. We propose that this parameter could represent the supraspinal drive, supposed to be preserved in control subjects and decreased in spastic patients. No subsequent variation of the reflex gain was required to simulate spastic traces. Adjustment of the time lag influenced the duration of the swinging phase and oscillatory phenomena possibly occurring during the pendulum test. It could be related to the involvement of either short- or long-latency stretch reflex loops. With respect to current neurophysiological concepts of motor control, this modeling approach may help in understanding mechanisms underlying spastic hypertonia, and in predicting the clinical effect of antispasticity agents.

Adult↗
PubMed1996

Selective neurotomies for relief of spasticity focalized to the foot and to the knee flexors. Results in a series of 58 patients.

Fifty-eight patients with a mean age of 24 years (range 5 to 65 years) who underwent selective neurotomies (SN) for harmful spasticity focalized to the lower limb are presented. In 43 of the patients who suffered spastic foot, SN was directed to the tibial nerve. In 10 others who had spastic knee flexors, the target was the hamstring branches of the sciatic trunk. In the remaining 5 patients, SN concerned both nerves. The aim of the section was to reduce partially the number of the fascicles conveying the excessive spasticity. A stimulation of the nerve above and below the section is performed to check the effectiveness of surgery on the corresponding muscle(s). At long-term follow-up evaluation (mean duration: 4.2 years), this study shows that 40 patients (i.e., 68.9% of the cases) experienced a better quality of life, related to the disappearance or a notable regression of the spasticity in 72.4% of the cases and to improved motor capacities in 65.5% of the cases. Post-operative complications were few, consisting of talus foot in 2 cases and dysaesthesias of the foot on the plantar aspect in 3 cases. This study shows that SN is able to take its place in the surgical armamentarium for treating disabling localized spasticity when it cannot be successfully controlled by rehabilitation and medical therapy. An appropriate candidate selection and intensive postoperative rehabilitation are mandatory to obtain good and long lasting results.

Adolescent↗
PubMed2005

Pharmacologic interventions for reducing spasticity in cerebral palsy.

Motor function abnormalities are a key feature of cerebral palsy. Spasticity is one of the main motor abnormalities seen in children with cerebral palsy. Spasticity is a velocity dependent increased resistance to movement. While in some children, spasticity may adversely impact the motor abilities, in others, it may help maintain posture and ability to ambulate. Thus, treatment to reduce spasticity requires careful consideration of various factors. Non-pharmacologic interventions used to reduce spasticity include physiotherapy, occupational therapy, use of adaptive equipment, various orthopedic surgical procedures and neurosurgical procedures. Pharmacologic interventions used for reducing spasticity in children with cerebral palsy reviewed in this article include oral administration of baclofen, diazepam, dantrolene and tizanidine, intrathecal baclofen, and local injections of botulinum toxin, phenol, and alcohol.

Administration, Oral↗