Muscle & nerve. Supplement最新文献

Physical and occupational therapists play important roles in the evaluation and management of patients receiving botulinum toxin injections for spasticity. Baseline evaluation includes areas beyond the muscles being injected, since local spasticity reduction may lead to more widespread functional changes. Because the evaluation itself influences tone, a consistent order of muscle evaluation is recommended. The range of preinjection assessments includes evaluation of tone, mobility, strength, balance, endurance, assistive devices, and others. After injection, therapeutic interventions have multiple aims, including strengthening and facilitation, increasing range of motion, retraining of ambulation and gait, improving the fit and tolerance of orthoses, and improved functioning in ADLs.

An upper motor neuron syndrome often leads to the development of stereotypical patterns of deformity secondary to agonist muscle weakness, antagonist muscle spasticity and changes in the rheologic (stiffness) properties of spastic muscles. Identification of the spastic muscles that contribute to deformity across a joint allows therapeutic denervation to be implemented with the maximum likelihood of success. Identifying responsible muscles can be complex, since many muscles may cross the joint involved, and not all muscles with the potential to cause deformity will be spastic. Strategies including polyelectromyography and diagnostic blocks with local anesthetics can be used to test hypotheses regarding the deformity, providing information for more long-term denervation. In this review, we discuss frequently observed patterns of deformity associated with problematic spasticity, paresis, contracture, and impaired voluntary motor control.

Development of validated and reliable outcome measures for spasticity rehabilitation has been hampered by the difficulty of quantifying functionally important parameters such as pain, ease of care, and mobility. Nonetheless, a combination of measures designed to assess technical and functional outcomes, patient satisfaction, and the cost effectiveness of treatment can be used together to evaluate status and track change in spasticity management, including treatment programs involving botulinum toxin. While double-blind, placebo-controlled studies remain the gold standard for clinical testing, the single-subject design is a useful alternative in many treatment protocols. Because no single tool can measure the many types of changes possible with treatment, the choice of assessment tools must be based on the functional changes expected from the treatment. A wide range of assessment tools are critically reviewed for their sensitivity, reliability, validity, and ease of administration.

The surgical treatment of spasticity has been aimed at four different levels: the brain, the spinal cord, peripheral nerves, and the muscle. Stereotactic neurosurgery, whether involving the globus pallidum, ventrothalamic nuclei, or the cerebellum, has had little success. Cerebellar pacemakers have been tried: results have been mixed but not ultimately encouraging. Selective posterior rhizotomy is currently the most widely used and effective central nervous system procedure. Posterior rootlets in L2-S2 are exposed and tested with electrical stimulation. Those showing abnormal response are transected. Contraindications include weakness and marked fixed contracture. Neurectomy has been tried for spasticity, but the results have not been encouraging and the adverse effects may be severe. Musculoskeletal surgery remains an important procedure for treatment of contractures secondary to spasticity.

Botulinum toxin has been tested as a treatment for spasticity resulting from cerebral palsy, multiple sclerosis, traumatic brain injury, spinal cord injury, and stroke. The results of 18 studies are reviewed in this article. In both open label and double-blind, placebo-controlled trials, botulinum toxin has proven to be an effective measure for reduction of focal spasticity. Improvements have been documented in tone reduction, range of motion, hygiene, autonomic dysreflexia, gait pattern, positioning, and other criteria, though not all criteria tested showed improvement in all studies. In none of the studies were there significant adverse effects. Future trials may be improved by refinement of several design parameters, including patient selection, treatment timing, and selection of dose and injection site.

Spasticity is a disorder of the sensorimotor system characterized by a velocity-dependent increase in muscle tone with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex. It is one component of the upper motoneuron syndrome, along with released flexor reflexes, weakness, and loss of dexterity. Spasticity is an important "positive" diagnostic sign of the upper motoneuron syndrome, and when it restricts motion, disability may result. The "negative" signs--weakness and loss of dexterity--invariably alter patient function when they occur. In an upper motoneuron syndrome, the alpha motoneuron pool becomes hyperexcitable at the segmental level. This hyperexcitability is hypothesized to occur through a variety of mechanisms, not all of which have yet been demonstrated in humans. Spasticity caused by spinal cord lesions is often marked by a slow increase in excitation and over-activity of both flexors and extensors with reactions possibly occurring many segments away from the stimulus. Cerebral lesions often cause rapid build-up of excitation with a bias toward involvement of antigravity muscles. Chronic spasticity can lead to changes in the rheologic properties of the involved and neighboring muscles. Stiffness, contracture, atrophy, and fibrosis may interact with pathologic regulatory mechanisms to prevent normal control of limb position and movement. In the clinical exam, it is important to distinguish between the resistance due to spasticity and that due to rheologic changes, because the distinction has therapeutic implications. Diagnostic nerve or motor point blocks and dynamic or multichannel EMG are useful to distinguish the contributions of spasticity and stiffness to the clinical problem.

Spasticity is a velocity-dependent increase in stretch reflex activity. It is one of the forms of muscle overactivity that may affect patients with damage to the central nervous system. Spasticity monitoring is relevant to function because the degree of spasticity may reflect the intensity of other disabling types of muscle overactivity, such as unwanted antagonistic co-contractions, permanent muscle activity in the absence of any stretch or volitional command (spastic dystonia), or inappropriate responses to cutaneous or vegetative inputs. In addition, spasticity, like other muscle overactivity, can cause muscle shortening, which is another significant source of disability. Finally, spasticity is the only form of muscle overactivity easily quantifiable at the bedside. Under the name pharmacological treatments of spasticity, we understand the use of agents designed to reduce all types of muscle overactivity, by reducing excitability of motor pathways, at the level of the central nervous system, the neuromuscular junctions, or the muscle. Pharmacologic treatment should be an adjunct to muscle lengthening and training of antagonists. Localized muscle overactivity of specific muscle groups is often seen in a number of common pathologies, including stroke and traumatic brain injury. In these cases, we favor the use of local treatments in those muscles where overactivity is most disabling, by injection into muscle (neuromuscular block) or close to the nerve supplying the muscle (perineural block). Two types of local agents have been used in addition to the newly emerged botulinum toxin: local anesthetics (lidocaine and congeners), with a fully reversible action of short duration, and alcohols (ethanol and phenol), with a longer duration of action. Local anesthetics block both afferent and efferent messages. The onset of action is within minutes and duration of action varies between one and several hours according to the agent used. Their use requires resuscitation equipment available close by. When a long-lasting blocking agent is being considered, we favor the use of transient blocks with local anesthetics for therapeutic tests or diagnostic procedures to answer the following questions: Can function be improved by the block? What are the roles played by overactivity and contracture in the impairment of function? Which muscle is contributing to pathologic posturing? What is the true level of performance of antagonistic muscles? A short-acting anesthetic can also serve as preparation to casting or as an analgesic for intramuscular injections of other antispastic treatment. Alcohol and phenol provide long-term chemical neurolysis through destruction of peripheral nerve. Experience with ethanol is more developed in children using intramuscular injection, while experience with phenol is greater in adults with perineural injection. In both cases, there are anecdotal reports of efficacy but studies have rarely been controlled. Side effects are numerou