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Query: UMLS:C0026838 (spasticity)
 6,471 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of dantrolene sodium and diazepam were compared in a double crossover study of 42 patients with spasticity due to stable multiple sclerosis. Both drugs reduced the findings of spasticity, clonus, and hyperreflexia, and the complaints of muscle stiffness and cramping. Each drug had different side effects which suggest indications and contraindications for its use in spastic patients.
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PMID:Comparison of dantrolene sodium and diazepam in the treatment of spasticity. 77 44

The changes in passive mechanical muscle properties due to cooling of the calf in healthy human volunteers were investigated. The technique, using sinusoidal driving of the foot, permitted the separation of muscle stiffness response into its elastic and viscous components. Cooling the calf with ice for 30 minutes increases the rate of change of elastic stiffness with frequency, and it increases the frictional stiffness over a frequency range of 3 to 12Hz. Such cooling would produce an estimated 3% to 10% increase in total stiffness, on average, in a spastic person. This increase in stiffness would counteract reductions in total stiffness achieved during the application of cryotherapy to relieve spasticity. However, one could expect that for a clinically significant reduction of spasticity, the increase in passive stiffness of the muscle generated by cooling would be largely overshadowed by the decrease in reflex reactivity.
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PMID:Influence of muscle cooling on the viscoelastic response of the human ankle to sinusoidal displacements. 240 81

Is characterized by several various signs. One of these, spasticity, involves a velocity dependent increase in muscle stiffness during stretch and by hyperactive tendon jerks. When intense, spasticity impedes residual strength in antagonistic muscles and interferes with attempts to move, especially if complicated by clonus and/or spasms. Assessment of spasticity is multifactorial and implies clinical as well as instrumental methods. The pathophysiological mechanisms responsive for the hyperexcitability of the myotatic reflex can be studied by methods of clinical neurophysiology. It appears that there are various factors involved at the spinal level, involving reduction in both pre- and post-synaptic inhibitions. Although spasticity is not responsible for the major part of the disability imposed by upper motor neurone syndrome, it should be reduced. The therapeutic methods are medical, surgical or from physical medicine. In many cases, the results have been validated by blind studies. As paresis is the most disabling effect, it would be worthwhile to develop drugs able to reduce spasticity and increase muscle strength at the same time. Recent trials suggest than TRH-T may be effective in this regard.
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PMID:[Pyramidal syndrome: its physiopathology and treatment]. 269 2

The term spasticity is used to describe many relatively unrelated syndromes and, because they share few common pathophysiologic mechanisms, it is not possible to define the physiology or pharmacology of spasticity. In patients with spastic paresis, it is the latter negative symptom (rather than the spasticity) that accounts for almost all the functional disability. Clinical neurophysiologic techniques are useful for categorization of patients with clinically identical syndromes into subgroups which respond to different therapies. Fusimotor or spindle primary afferent hyperactivity have not been demonstrated in spastic patients; reduction in central inhibitory mechanisms probably accounts for spastic hyper-reflexia. Increased passive muscle stiffness may also be clinically significant. Therapies for spasticity include elimination of causative or enhancing factors, frequent muscle stretching, surgical approaches and chemotherapy. The latter includes dantrolene (which weakens muscles), baclofen (particularly useful for reduction of flexor spasms and flexor dystonia in patients with spinal lesions) and diazepam.
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PMID:Physiologic and pharmacologic approaches to spasticity. 332 74

The aims of this study were to determine whether changes in the non-reflex component of spastic plantarflexors had developed 2 and 4 months after stroke and to study their relationship with the level of impairment. One group of adults with hemiparesis (HPs) was tested 2 and 4 months after the onset of stroke, and data were compared with a control group (CTLs) tested once. Twenty-two patients (14 males) admitted over a 4-month period in a rehabilitation centre (mean = 62 yrs +/- 14), and 11 (6 males) non-disabled (CTLs) subjects (mean = 57yrs +/- 12.8) agreed to participate in the study. The resistive torque (RT) recorded with a myometer during slow (8-10 degrees/s) passive dorsiflexions imposed manually served as the primary outcome, whereas, the Ashworth score (spasticity), ankle ROM and Fugl-Meyer motor subscore were used as secondary measures to determine the level of impairment. The mean RT values measured at 0 degrees dorsiflexion on the affected and unaffected sides were compared with those in CTLs. As expected, the RT values 2 and 4 months post-stroke on the unaffected side did not differ from corresponding values in CTLs. Significantly higher RT values on the affected side when compared to the unaffected side were found both at 2 months (39%; p < 0.05) and at 4 months (43%; p < 0.01). No significant difference existed on the affected side between the 2nd and 4th months. A high (r = 0.80) and significant (p < 0.0001) correlation coefficient was calculated between the changes in RT values recorded at 2 and 4 months. Low and not significant correlations were computed between these RT changes and factors such as the ROM (r = -0.24), the Ashworth score (r = 0.23) and the Fugl-Meyer lower extremity motor subscore (r = -0.26). Present results indicate that: (1) changes in the non-reflex component are already present 2 months after stroke but do not increase significantly between the 2nd and 4th months; (2) these changes are not related to the level of impairment; and (3) myometry testing at 2 months could be used as a preventive measure to detect patients more at risk of developing severe passive muscle stiffness.
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PMID:Non-reflex mediated changes in plantarflexor muscles early after stroke. 927 Nov 48

Based on the results of several electrodiagnostic and biomechanical studies, the following classification of muscle dysfunction in spastic hemiplegia is proposed: changes in muscle activation (excess symptoms, e.g., spasticity, and deficit symptoms, e.g., paresis); changes in muscle stiffness; and changes in muscle length. The clinical significance of this classification is that different types of muscle dysfunction might require specific treatment. The authors have developed techniques to measure quantitatively each type of muscle dysfunction: free frequency repetitive movement (FFRM) and torque angle diagram (TAD). Surface EMGs of tibialis anterior, gastrocnemius, and soleus muscle are recorded during active (FFRM) and passive (TAD) ankle movements. EMG data are converted to parameters for abnormal muscle activation (excess and deficit symptoms). Parameters for muscle stiffness and muscle length are derived from the hysteresis curve of the TAD. This article describes the measurements and the results of a validation study. For the validation study, four hypotheses were formulated: 1) in nonimpaired control subjects, parameters expressing abnormal muscle activation are low; 2) in hemiplegic subjects, differences between the affected and the unaffected sides will be found for all types of parameters; 3) after local anaesthesia of the tibial nerve on the hemiplegic side, excess symptoms will decrease, while muscle stiffness remains unchanged; and 4) despite a uniform gait pattern, between-subject differences can be detected with regard to muscle activation, stiffness, and length. The first hypothesis was tested and confirmed in two controls; the remaining three were tested and confirmed in ten hemiplegic subjects (mean age 47.7 yrs, mean time since onset 10.7 yrs). However, the level of co-contraction of the gastrocnemius muscle was low, probably indicating that the clinical significance of this phenomenon might be limited. The results support the validity of the proposed classification and measurements.
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PMID:Measurement of impaired muscle function of the gastrocnemius, soleus, and tibialis anterior muscles in spastic hemiplegia: a preliminary study. 970 15

This paper presents the objective and quantitative measurement of muscle stiffness described by Rack and Lehmann. This method allows analysis of the pathophysiological mechanism of spasticity and assessment of anti-spastic treatment. This is illustrated by a case report, showing the objective effect of intrathecally administered baclofen in a spastic patient.
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PMID:[Objective measures of muscle stiffness in the ankle. Evaluation of the effect of intrathecal injection of baclofen in spastic patients]. 982 36

Muscle function often becomes progressively more compromised in children with spastic cerebral palsy, leading to reduced mobility. This study aimed to examine the role that muscle connective tissue plays in this process. Severity of spasticity as determined by a range of clinical measures was assessed in 26 children (14 males 12 females; age range 4 to 17 years) with either diplegic or quadriplegic cerebral palsy (CP). Muscle biopsies from the vastus laeralis muscle were obtained for biomedical and histological analysis during orthopaedic surgery as part of the child's ongoing care. Total collagen was quantified by hydroxyproline determination. Two clinical measures of severity, Modified Ashworth Scale and Balance, were shown to have a highly significant correlation with collagen content, and Ambulatory Status, Clonus, and Selective Muscle Control all showed positive trends. Collagen I accumulated in spastic muscle's endomysium which appeared to be thickened, and fibrotic regions with sparse muscle fibres were evident in more severe cases. This suggests that collagen may be involved in increases in muscle stiffness observed in spasticity. Once developed, these changes are essentially irreversible and we suggest that future treatments should consider including prevention of muscle fibrosis.
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PMID:Collagen accumulation in muscles of children with cerebral palsy and correlation with severity of spasticity. 1136 84

Despite the lack of consensus of the role of spasticity in the observed motor disability in cerebral palsy (CP), alleviation of spasticity remains a primary focus in the clinical management of these patients. The purposes of this study were to: (1) quantify voluntary torque and passive resistance across speeds in the hamstrings and quadriceps muscle groups with respect to the presence of stretch responses and/or passive muscle stiffness in patients with CP compared to age-related children without disability, and (2) relate these parameters to each other and to functional performance, as measured by the Gross Motor Function Measure (GMFM), in CP. Included were 23 subjects with CP, sub-grouped by the presence or absence of stretch responses as determined by electromyography, and 9 subjects without CP. Results indicated that peak torque was considerably greater in the comparison group than for each of the CP groups and resistance was greater in the CP group with spasticity compared to the nonspastic CP group in both muscles at all speeds. Stiffness differed between the spastic CP group and the comparison group only for the quadriceps at the fastest speed. Higher passive resistance torque and stiffness were correlated with decreased voluntary torque, particularly for the antagonists, and with lower GMFM scores. In conclusion, strength and motor function are related to the magnitude of resistance torque and stiffness in CP, although the small amount of variance explained reinforces the multidimensional nature of this disorder, and the challenges inherent in managing it.
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PMID:Spasticity versus strength in cerebral palsy: relationships among involuntary resistance, voluntary torque, and motor function. 1185 33

Spasticity is an abnormal increase in muscle contraction often caused by damage to central motor pathways that control voluntary movement. During clinical examination, spasticity manifests as an increase in stretch reflexes, producing tendon jerks and resistance appearing as muscle tone. There are many causes of spasticity, including demyelination from multiple sclerosis, congenital damage from diseases such as cerebral palsy, trauma to the brain or spinal cord, hemorrhage or infarction, and other pathologic conditions that interrupt neural pathways. Effects of spasticity range from mild muscle stiffness to severe, painful muscle contractures and repetitive spasms that reduce mobility and substantially impede normal activities of daily living. Botulinum toxin therapy reduces spasticity and pain associated with several disorders. Local treatment with botulinum toxins can be used as adjunctive therapy, along with oral antispasticity medications, or alone to provide localized decrease in symptoms of spasticity and pain. Botulinum toxin therapy may be particularly useful for patients with spasticity due to stroke, whose treatment can be tailored based on recovery of function over time. In addition, botulinum toxin therapy is safe for pediatric patients, including children with cerebral palsy, who may not be able to tolerate the cognitive side effects of oral medications. Results of studies evaluating botulinum toxin for the treatment of spasticity due to various causes are presented here.
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PMID:Treatment of spasticity with botulinum toxin. 1256 67


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