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

Botulinum toxins have an exciting and important role in treating the child with hypertonia. The guidelines presented in this article are those that have been published representing the safe use of botulinum toxins in children. Experience and a decade of research have provided the framework for using botulinum toxins in decreasing deformity and promoting function. In children, a window of opportunity exists with botulinum toxin that allows improved motor control and elongation of shortened muscles. Although 3 to 4 months in an adult life is short, for a child it is a relatively greater proportion of their life experience and may be long enough for skill development. The improvement noted in function after botulinum toxin use is facilitated by comprehensive rehabilitation. The pediatric physiatrist has a unique role in the management of children with cerebral palsy and other conditions with hypertonia. Their knowledge and training reflect an understanding of anatomy and development that allows accurate evaluation of specific functional problems in children related to hypertonia. The pediatric physiatrist has experience in localization of muscles by EMG, nerve stimulation, and surface anatomy. Although many other physicians inject botulinum toxins, goal-directed management is the cornerstone to the physiatrist's thinking and treatment plan. Orthopedic surgery ultimately may be the intervention of choice if persistent contracture or progression of contractures occurs. Working in collaboration with an orthopedist identifies the timing of optimal surgical intervention for alignment. For persistent and severe hypertonia, the treatment team includes a neurosurgeon. All options for spasticity, such as selective posterior rhizotomy and intrathecal baclofen, should be considered. Re-evaluation of the child after selective dorsal rhizotomy or intrathecal baclofen is appropriate and should be discussed with therapists for focal intervention. Communication between members of the team and the family is desirable and frequently is one of the major contributions of the pediatric physiatrist. For children with focal hypertonia, botulinum toxins offer a dramatic but temporary repeatable change that affects rehabilitation. Research rapidly has captured the positive effect of the toxins on impairment and functional limitations. Not to be overlooked are outcomes related to quality of life. The long-term use of botulinum toxins and the role the toxins play throughout the life span of the person with a childhood hypertonic disorder are yet to be determined.
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PMID:The use of botulinum toxin in pediatric disorders. 1458 33

Spasticity resulting from cerebral palsy can reduce the quality of life in affected children and can eventually cause more severe impairments, such as joint dislocation and scoliosis. Botulinum toxin type A (Botox) is widely used to temporarily alleviate the increased muscle tone associated with spasticity, and when combined with a comprehensive physical therapy regimen can result in permanent improvement. This report documents the successful use of Botox over a two-year period to treat spasticity secondary to cerebral palsy in a preschool-age child. Botox was used in conjunction with a specific physical therapy regimen in order to reach a functional goal of independent ambulation.
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PMID:Successful treatment of childhood spasticity secondary to cerebral palsy using Botox. 1463 60

The management of children and adults with upper motor neuron disorder is complex and multifaceted. This article reviews new information and potential treatment. As part of the upper motor neuron syndrome (UMNS), spasticity may occur in cerebral palsy, congenital brain malformation, head injury, or other etiologies. Within the UMNS the most recognizable clinical concern is the frequent abnormality of tone, which may have a significant functional impact. Tone reduction is not itself a goal, but is performed for the functional benefits it may allow. New approaches to treatment and management of hypertonia recently have become available. There are many other associated features of the UMNS that affect patient functioning. Ones that frequently occur are abnormalities of speech and other areas of oral motor control. A new area of intervention combines the use of botulinum toxin and ultrasonography to address the common problem of slalorrhea, which is a potential medical issue and a substantial social barrier in affected patients. This article also reviews new information and potential treatment for neuromuscular disorders.
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PMID:Approach to the rehabilitation of spasticity and neuromuscular disorders in children. 1474 53

Phenyl alcohol blocks are used to relieve spasticity. Such nerve conduction blocks result from phenol-induced axonotmesis and could potentially affect muscle properties related to the ability to generate, maximize, and reduce force. This study assessed the 12-week longitudinal effect of phenol on position (stiffness) and velocity (damping) components of hypertonia, in addition to strength (peak torque and times to generate and reduce torque) in an individual with chronic elbow flexor spasticity following stroke. Phenol motor point injections of flexor muscles paradoxically increased the magnitude of flexion torque and decreased the times required to generate and reduce flexion and extension joint torques, in addition to reducing elbow extension stiffness and damping. Large reductions in the velocity-related component of hypertonia (damping changes > 90%) occurred immediately following injection, which is a finding that supports the velocity-dependent definition of spasticity. Although the changes in damping were large and transient, changes in stiffness and strength variables were small, slower to occur, and maintained. This suggests secondary changes following nerve block, possibly facilitated by regular elbow use subsequent to spasticity reduction.
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PMID:Phenol reduces hypertonia and enhances strength: a longitudinal case study. 1522 7

To determine if oral/systemic delivery of baclofen can effectively decrease spastic hypertonia due to acquired brain injury (traumatic brain injury, stroke, anoxia, or encephalopathy). Tertiary care outpatient rehabilitation center directly attached to a university hospital. Patients were a convenience sample recruited consecutively who had been referred for treatment of their spastic hypertonia to our spasticity clinic over a 5-year period. The spastic hypertonia was due to an acquired brain injury by either traumatic brain injury (TBI), stroke, or anoxic brain injury. All patients were more than 6 months postinjury or illness. Retrospective review of patients before and after initiation of treatment with oral baclofen, per standardized clinical data sheets. Thirty-five patients (22 TBI patients) were started on oral baclofen and were reevaluated between 1 to 3 months after initiation of treatment. Data for motor tone (Ashworth scores), spasm scores (Penn spasm frequency score), and deep tendon reflex scores were collected on the affected upper extremity (UE) and lower extremity (LE) side(s). Normal extremities were not assessed. Differences over time were assessed via descriptive statistics and Wilcoxon signed-rank. After 1 to 3 months of treatment when subjects had reached their maximal tolerated dosage, the average LE Ashworth score in the affected lower extremities (LEs) decreased from 3.5 to 3.2 (P =.0003), the reflex score decreased from 2.5 to 2.2 (P =.0274), and there was no statistical difference in the spasm score (P >.05). When the 22 TBI patients are analyzed separately, the average LE Ashworth score decreased from 3.5 to 3.2 (P =.0044) and the reflex score decreased from 2.7 to 2.0 (P =.0003). There was no statistically significant change in UE tone, spasm frequency, or reflexes after 1 to 3 months of treatment (P >.05). The average dosage at follow-up was 57 mg/day of baclofen (range 15-120 mg/day). There was a 17% incidence of somnolence that limited the maximum daily dosage of the medication. The oral delivery of baclofen is capable of reducing LE spastic hypertonia resulting from acquired brain injury. The lack of effect upon the upper extremities may be due to receptor specificity issues. GABA-B receptors may be less involved in the modulation of UE spastic hypertonia.
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PMID:Orally delivered baclofen to control spastic hypertonia in acquired brain injury. 1524 21

A 28-year-old male sustained anoxic brain damage following aborted cardiac arrest, and subsequently developed severe muscular rigidity and spasticity involving all extremities. The spasticity was refractory to the standard regimens used for spastic hypertonia. Zolpidem dramatically inhibited muscular rigidity, spasticity, and dystonic posturing in a dose-dependent manner, resulting in a sustained improvement of his global performance over four years. The authors postulate a central mechanism of action by selective inhibition of GABAergic inhibitory neurons, and suggest a controlled clinical study to investigate the potential efficacy of zolpidem in relieving spasticity related to postanoxic brain injury.
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PMID:Zolpidem for postanoxic spasticity. 1535 81

Spasticity is a sensorimotor phenomenon related to the integration of the nervous system motor responses to sensory input. Although most commonly considered a velocity-dependent increase to tonic stretch, it is related to hypersensitivity of the reflex arc and changes that occur within the central nervous system, most notably, the spinal cord. Injury to the central nervous system results in loss of descending inhibition, allowing for the clinical manifestation of abnormal impulses. Muscle activity becomes overactive. This is mediated at several areas of the stretch-reflex pathway. Although spasticity is part of the upper motor neuron syndrome, it is frequently tied to the other presentations of the said syndrome. Contracture, hypertonia, weakness, and movement disorders can all coexist as a result of the upper motor neuron syndrome. Although basic science descriptions of spasticity are being elucidated, clinically, confusion exists.
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PMID:Spasticity: the misunderstood part of the upper motor neuron syndrome. 1544 72

A number of techniques attempt to objectively quantify various clinical characteristics associated with spastic hypertonia and related motor disorders. These range in cost, complexity, physiologic basis of measured response, and invasiveness. With a greater range of treatment options for spasticity and an increase in the number of centers participating in studies of interventions for spasticity, published reports reflect increasing use of objective quantification techniques. We review studies that highlight the potential utility of neurophysiologic techniques, including the H-reflex, F-wave, and flexion withdrawal reflex, in the objective evaluation of response to intrathecal baclofen administration. The accumulated knowledge suggests that neurophysiologic evaluation is useful for assessing spinal cord responsiveness, and we recommend it as an adjunct to clinical evaluation when judging the overall effectiveness of intrathecal baclofen administration.
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PMID:Neurophysiologic evaluation of spastic hypertonia: implications for management of the patient with the intrathecal baclofen pump. 1544 73

In the United States, the popularity of botulinum toxins as agents to treat muscle hypertonia has grown significantly over the last decade, despite lack of approval from the Food and Drug Administration for the indication of spasticity. Botox (botulinum toxin type A) and Myobloc (botulinum toxin type B) are Food and Drug Administration-approved for other indications, such as cervical dystonia. Another commercial preparation of type A, Dysport, has yet to reach the United States market as of this writing. Although botulinum toxin's efficacy in influencing spastic hypertonia is well accepted, the impact of certain clinical issues, such as dosing and dilution, on treatment outcome is not well established by published studies. This article will review important articles and selected abstracts on the use of botulinum toxin, specifically for spastic hypertonia in adults, with emphasis on current clinical practices as they relate to dosing and dilution.
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PMID:Botulinum toxin: dosing and dilution. 1544 75

Over the past decade a number of placebo-controlled studies have confirmed that intramuscular injections of botulinum toxin A (BTX A) has antispastic effects. Cerebral palsy is among the most frequent disorders of the growing locomotor apparatus during childhood. Weakness as well as spasticity due to lack of selective neuronal control causes functional impairment and additional mechanisms of compensation, retardation of motor development, secondary deformities of muscles and soft tissues due to a failure of muscle growth, subluxation/dislocation of joints, early osteoarthritis, and pain. Prevention of this vicious circle has to be the main goal of caring for children with spasticity. Quality of life in children with cerebral palsy can be improved by support of their daily living motor activities. Increased muscle tone can be reduced by physical exercises, by individually adapted orthoses, walkers, and wheelchairs, by manual therapy, serial casting and in certain cases by systemic drugs or by multiple-stage surgical procedures. BTX A can be used to enable these treatment possibilities or to increase their effect. In our clinical study (BTX A in 114 patients in 19952/2000) we found no major side effects. Weakness, pain or swelling occurred temporarily. Indications for the use of BTX A are pain, functional impairment, severe cosmetic problems, as well as prevention of secondary contractures, deformities, and dislocations caused by increased muscle tone. We consider the selection of patients for the use of BTX A and the development of a goal-orientated treatment plan by multidisciplinary team approach as the most important steps. Prerequisites are exact statomotoric and dynamic physical examinations, and standardised movement analysis. 3-D-gait analysis and dynamic electromyography is used in cases where functional improvement of gait is the goal of BTX A-treatment.
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PMID:[Botulinum toxin type A in the treatment plan for cerebral palsy]. 1550 50


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