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

The relative importance of hyperreflexia and paresis in disturbances of voluntary arm movement was studied in a group of patients (n = 25) with spasticity arising from a unilateral ischemic cerebral lesion. Patient performance was evaluated against data obtained from normal subjects (n = 15). Spastic patients achieved lower maximum movement velocities during flexion or extension than did normal subjects. The more marked the paresis of the elbow flexor and extensor muscles of the patients, relative to the strength of the normal subjects, the greater was this reduction in maximum velocity. For a given velocity, however, the time taken to complete a movement and the time to reach the peak velocity were normal. No relationship was found between the degree of impairment of voluntary movement and the level of passive muscle hypertonia in the antagonist. Although overactivity of the antagonist muscle may play some role in disturbance of movements made at low velocities without an opposing load, antagonist activity during movements made against a load (i.e., under more natural conditions) was at or below normal levels, even in those patients with the most marked passive muscle hypertonia. It is concluded that agonist muscle paresis, rather than antagonist muscle hypertonia, plays the dominant role in the disturbance of voluntary elbow movement following stroke.
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PMID:Voluntary movement at the elbow in spastic hemiparesis. 808 Feb 47

Spasticity is a motor dysfunction affecting persons with an UMN injury in varying ways. Nurses can identify spasticity in their patients by the presence of hyperactive DTRs and hypertonicity (increased muscle tone). Other characteristics often present with spasticity are clonus and spasms. Spasticity interfering with recreation, work, or basic activities of daily living may be decreased through the use of a variety of nursing interventions. Some of these interventions are more advantageous for spasticity caused by brain injury, whereas others are more helpful for spasticity caused by the spinal cord injury. Interventions research has begun; however, more research needs to be done to identify the most effective nursing measures to decrease spasticity.
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PMID:Spasticity. Mechanisms and nursing care. 826 21

The effect of coated Mydocalm tablet, given in 3 x 150-mg daily doses for 3 weeks to 47 patients, simultaneously with physiotherapy, has been examined in comparison to the results of 47 patients treated with physiotherapy solely. In the group of patients receiving Mydocalm as an adjuvant to physiotherapy the alleviation of pain and moderation of muscular hypertonia and spasm were observed within a shorter period. On the basis of the results of these examinations the use of Mydocalm is recommended as an adjuvant to complex therapy, in 300-450-mg daily doses, for the treatment of locomotor diseases accompanied by muscular hypertonia, muscular spasticity, and contracture.
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PMID:Observations with high-dose Mydocalm therapy. 827 38

The motor disorders associated with human spasticity arise, partly from a pathological increase in the excitability of muscle stretch reflexes. In clinical practice, reflex excitability is commonly assessed by grading the reflex response to a blow delivered to the tendon of a muscle. This is a much simpler response than the complex patterns of activity which may be elicited following muscle stretch caused by active or passive movement. Changes in the biceps brachii tendon jerk response have been followed over the first year after stroke in a group of hemiparetic patients and compared with changes in short and medium latency reflex responses elicited by imposed elbow flexion of initially relaxed spastic muscle and with the development of the late reflex responses which contribute to spastic hypertonia. A progressive increase in tendon jerk responses occurred over the first year following stroke, whereas reflex responses to imposed displacement, in particular the late reflex responses contributing to muscle hypertonia, reached their peak excitability one to three months after stroke, with a subsequent reduction in activity. The tendon jerk reflex therefore provides an incomplete picture of the pathological changes in the reflex responses in spasticity.
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PMID:The limitations of the tendon jerk as a marker of pathological stretch reflex activity in human spasticity. 850 46

Clonidine, a centrally acting alpha 2 receptor adrenergic agonist, has been successfully used as adjunctive therapy in patients with spinal cord injury with problematic spasticity not adequately controlled by recognized spasmolytic agents. A transdermal system providing approximately constant and continuous systemic delivery of clonidine has been recently introduced to enhance patient compliance. However, experience with transdermal clonidine in the management of spasticity is limited. Three cases are presented of patients with spasticity as the result of cervical spinal cord injury, inadequately managed by oral baclofen, in whom transdermal clonidine was administered. Significant improvement in spastic hypertonia was observed in all three cases. Transdermally delivered clonidine was well tolerated, with reported side effects limited to dryness of the mouth.
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PMID:Effect of transdermal clonidine on spinal spasticity. A case series. 851 78

Flexor and extensor spasms associated with severe spasticity frequently cause pain and suffering in neurologically impaired patients, and greatly interfere with comfort and activities. When high doses of oral medications are necessary to keep the symptoms under control and are poorly tolerated, the long-term spinal-selective intrathecal infusion of baclofen by means of implanted drug pump and catheter is a safe, efficient and reversible alternative to destructive surgical procedures. Between September 1991 and March 1995, intrathecal baclofen was infused in 18 selected patients out of a series of 42 severely disabled spastic cases. We report here our preliminary experience with the criteria of selection, the initial intrathecal bolus test and the long-term benefit of the selected patients. Our results confirm the dramatic immediate and long-term benefit reported in other series. After a period of treatment of 1 to 42 months, 13 patients had a complete disappearance of their spastic symptoms without any oral treatment, one patient kept unchanged clonus despite the use of low-dose oral treatment and another one a severe, not improved dysuria although in both of them hypertonia and spasms were abolished. Finally, 2 patients had important joint stiffness slightly impairing the benefit from the treatment. None of the 18 patients had central side-effects related to baclofen. With time, a slight increase in daily dose (inferior to 10%) was necessary in most patients.
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PMID:Chronic intrathecal baclofen in severely disabling spasticity: selection, clinical assessment and long-term benefit. 900 75

Seventeen patients with severe disabling spinal spasticity were selected and treated by chronic intrathecal baclofen infusion using an implanted programmable pump. Nine patients were tetraparetic, seven were paraplegic and one paraparetic. Patients were regularly followed for 5 to 69 months (mean 37.5 months). The clinical efficacy of baclofen was estimated by means of evaluation of: hypertonia, spasms, pain and functional disability. All patients experienced significant amelioration of quality of life secondary to reduction of hypertonia, spasms and pain related to contractures. Neurogenic pain improved in 3 cases and remained unchanged in 3 others. In patients whose motor functions were partially preserved, various degrees of motor improvement were detected. Electrophysiological recordings of Polysynaptic flexion reflexes (FR) were obtained to control conditions, and under intrathecal baclofen, in order to quantify the spinal excitability responsible for spontaneous or induced spasms. Flexion reflex threshold was increased and amplitude proved to be very significantly reduced by chronic baclofen infusion in all our patients. Twelve patients with neurogenic bladder dysfunction were also evaluated by a clinically oriented questionnaire and by quantitative urodynamic recordings, before and after pump implantation. In patients with normal micturition, this was not changed by intrathecal baclofen. In patients with spastic bladder, intrathecal baclofen produced a decrease of detrusor hypertonia and hyperactivity in 50% of cases, with reduction of leakage and increase in functional bladder capacity.
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PMID:Long-term clinical, electrophysiological and urodynamic effects of chronic intrathecal baclofen infusion for treatment of spinal spasticity. 874 77

Spasticity following stroke reflects a spectrum of clinical problems including increased muscle tone, abnormal limb posture, excessive contraction of antagonist muscles and hyperactive cutaneous and tendon reflexes. The prevalence of stroke-related disability in stroke survivors is high, and spasticity may be a significant component of this. Management strategies include a multidisciplinary team approach utilising a variety of rehabilitation techniques. Although some interventions are well tolerated and fairly standardised, older adults may be particularly sensitive to drug treatment-related adverse effects. This article reviews some of the commonly employed interventions, such as oral medications, and some of the newer techniques, such as intrathecal baclofen infusion and botulinum toxin injections. The optimal management of spasticity following stroke in older adults requires careful goal setting and skilful combination of treatment modalities in order to produce the best outcome.
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PMID:Spasticity after stroke. Epidemiology and optimal treatment. 892 60

It has become increasingly recognized that the major functional deficits following brain damage are largely due to "negative' features such as weakness and loss of dexterity rather than spasticity. A variety of studies suggest that spasticity is a distinct problem and separate from the loss of dexterity, but that it may be implicated in the formation of muscle contracture and even in the recovery of strength. In order to address these issues, we examined the relationship between spasticity, contracture, strength and dexterity in the affected upper limb following stroke. Spasticity was measured both as increased tonic stretch reflexes and increased resistance to passive stretch (hypertonia). Twenty-four patients were recruited non-selectively from three rehabilitation units within 13 months of their stroke. Few patients exhibited increased tonic reflexes but half were found to have muscle contracture, the earliest at 2 months following stroke. Hypertonia was associated with contracture but not with reflex hyperexcitability. Increased tonic stretch reflexes were observed only in a subgroup of those with contracture and where present could usually be elicited only at the end of muscle range. This findings suggests that instead of spasticity causing contracture, contracture may actually potentiate spasticity in some patients. However, the majority of patients with contracture did not have increased tonic stretch reflexes. In addition, we found no relationship between spasticity and either weakness or loss of dexterity. Therefore, while hypertonia remains an important problem following cerebral lesions, it would appear that the amount of attention directed to reflex hyperexcitability associated with spasticity is out of proportion with its effects. Consequently, hypertonia needs to be clearly distinguished from reflex hyperexcitability in patients with spasticity.
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PMID:Spasticity and muscle contracture following stroke. 893 94

Mechanisms of spasticity and possible therapeutic interventions continue to dominate research into motor disorders following cerebral lesions. However, the accumulated evidence suggests that this focus on spasticity may be out of step with its effects. In contrast, hypertonia remains an important problem. Further investigation into its link with muscle contracture is required and it needs to be clearly distinguished from reflex hyperexcitability in patients with spasticity.
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PMID:Reflex hyperexcitability and muscle contracture in relation to spastic hypertonia. 900 4


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