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Poststroke Spasticity Management

2012; Lippincott Williams & Wilkins; Volume: 43; Issue: 11 Linguagem: Inglês

10.1161/strokeaha.111.639831

1524-4628

Gerard E. Francisco, John R. McGuire,

Parkinson's Disease Mechanisms and Treatments

HomeStrokeVol. 43, No. 11Poststroke Spasticity Management Free AccessResearch ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessResearch ArticlePDF/EPUBPoststroke Spasticity Management Gerard E. Francisco, MD and John R. McGuire, MD Gerard E. FranciscoGerard E. Francisco From the Department of Physical Medicine and Rehabilitation, University of Texas Health Science Center–Houston, TX (G.E.F.); S.T.A.R.(Spasticity Treatment and Research) Clinic and the UTHealth Motor Recovery Laboratory at TIRR Memorial Hermann, Houston, TX (G.E.F.); Department of Physical Medicine and Rehabilitation, Stroke Rehabilitation and Comprehensive Spasticity Management, Medical College of Wisconsin, Milwaukee, WI (J.R.M.). and John R. McGuireJohn R. McGuire From the Department of Physical Medicine and Rehabilitation, University of Texas Health Science Center–Houston, TX (G.E.F.); S.T.A.R.(Spasticity Treatment and Research) Clinic and the UTHealth Motor Recovery Laboratory at TIRR Memorial Hermann, Houston, TX (G.E.F.); Department of Physical Medicine and Rehabilitation, Stroke Rehabilitation and Comprehensive Spasticity Management, Medical College of Wisconsin, Milwaukee, WI (J.R.M.). Originally published13 Sep 2012https://doi.org/10.1161/STROKEAHA.111.639831Stroke. 2012;43:3132–3136Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: January 1, 2012: Previous Version 1 Poststroke spasticity (PSS) is a common complication associated with other signs and symptoms of the upper motor neuron syndrome, including agonist/antagonist co-contraction, weakness, and lack of coordination. Together, they result in impairments and functional problems that can predispose to costly complications. The goal of PSS management should take into consideration not only reduction of muscle hypertonia but also the impact of PSS on function and well-being. Therapeutic interventions focus on peripheral and central strategies, such as physical techniques to increase muscle length through stretching and pharmacological modulation. Although there are few comparative studies on the superiority of one method over another, it appears that optimal management of PSS involves a combined and coordinated compendium of therapies that encompass cost-effective pharmacological and surgical interventions, along with rehabilitative efforts.What is PSS and How Common Is It?Spasticity, commonly defined as "a motor disorder characterized by a velocity-dependent increase in tonic stretch reflexes with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex, as one component of the upper motor neuron syndrome,"1 is a common complication of stroke. It contributes to the impairments and disabilities that negatively impact functional recovery. Consequently, PSS, along with weakness and lack of coordination, result in gait abnormalities and problems with arm use. In addition to functional limitations, spasticity, when inappropriately treated, may lead to reduced quality of life, increased pain, and joint contractures.Three community-based studies that followed-up stroke survivors for 3 to 12 months reported an incidence of PSS between 17% and 43%.2–4 Certain factors are recognized as predictors of PSS: stroke lesions in the brain stem; hemorrhagic stroke and younger age;5 and severe paresis and hemihypesthesia at stroke onset.3How Is PSS Measured?To quantify the full impact of PSS, assessment should include a measure of passive stretch, volitional movement, and active/passive function.6,7 The benefit of using multiple measures in the evaluation of PSS is to differentiate the various components of the upper motor neuron syndrome, such as spasticity, spastic co-contraction, spastic dystonia, synergistic limb patterns, weakness, soft tissue contractures, and the functional implications of these impairments.The most commonly used clinical measure of spasticity is the Ashworth Scale or its modified version. This ordinal scale is a simple clinical test of resistance to passive stretch and is limited8–10 by poor inter-rater reliability. The Tardieu Scale7,11 has advantages over the Ashworth Scale because it is an interval scale and takes into consideration the velocity-dependent nature of spasticity. Tardieu Scale measures the spasticity angle, which is the difference between the angle at the end of passive range of motion at slow stretch and the angle of catch at fast stretch. This estimates the relative contribution of neural mechanisms (ie, spasticity) and mechanical restraint attributable to rheological changes in soft tissues.Electrophysiological tests, such as the H-reflex and H/M ratio, have been used to quantify PSS but tend to correlate poorly with the degree of spasticity.12 Biomechanical measurements of spasticity using a servo-controlled motor-driven device can provide a more objective measure of resistance to passive stretch.13Measures of passive function, such as the Carer Burden Scale, assess the impact of upper limb spasticity on the physical ability of caregivers to provide assistance.14 Measures of active function of the upper limb, such as the Composite Functional Index15 and Disability Assessment Scale,16 show a positive correlation with reduction of arm spasticity. Timed ambulation tests are clinically useful measures of the ability to walk.6 The Goal Attainment Scale, although not a measure of spasticity, can identify symptoms that a specific therapeutic intervention is meant to change.17When and Why Should PSS Be Treated?Some argue that the importance of spasticity may be overstated,2,18 but it is widely acknowledged that treatment of disabling PSS is beneficial. In many instances PSS is a significant contributor to the multitude of impairments and disabilities and decreased quality of life that challenge stroke survivors. For example, PSS resulting in an adducted internally rotated shoulder can limit overhead reaching activities and make underarm cleaning more difficult. When it involves wrist and finger flexors, PSS interferes with object grasp and release. The "clenched fist" deformity can lead to skin breakdown and nail bed infections. Lower extremity spasticity can limit ambulation, such as when an equinovarus foot prevents the foot flat position during the stance phase of gait, resulting in instability, and resulting in knee pain attributable to excessive recurvatum when ankle plantar flexor spasticity overwhelms. Severe spasticity of hip adductor muscles can make perineal care and toileting difficult. There are instances when even "mild" PSS causes significant limitations and warrants attention to enhance function or comfort. An example is mild spasticity of finger flexors that limits typing on a keyboard or object manipulation, or mild spasticity of the great toe extensor that causes pain attributable to friction against footwear when walking.The presence of PSS is not an indication for treatment because it may not have a negative impact on the stroke survivor's well-being. PSS can aid in some functional tasks, such as using increased knee extensor tone for standing and transfers, and possibly can preserve muscle bulk and retard osteoporosis. The most reasonable approach is to treat PSS whenever it becomes disabling or problematic. The treatment goals can be active, ie, tasks performed by the patient, and for the lower-level patient they tend to be passive, ie, performed for the patient. Frequently, however, treatment goals are a combination of passive and active. For example, treatment of elbow flexor spasticity is expected to facilitate hygiene and prevent contractures (passive goal) and at the same time is anticipated to improve limb movement (active goal). Table 1 lists common passive and active goals.Table 1. Treatment Goals for Problematic Poststroke SpasticityLow-Level Patient: Passive FunctionImproved positioning, orthotic fit, and complianceDecreased associated spasms, pain, caregiver burden, and nursing carePrevention of complications (ie, contractures and learned nonuse of paretic limb)High-Level Patient: Active FunctionUpper extremityImproved prehension and grasp and releaseImproved reaching and overhead activitiesReduced shoulder pain during movementADLIncreased independence in performanceDecreased time to accomplish ADLMobilityImproved speed, balance, quality, and safety of gaitPrevent long-term injury attributable to alteration in joint biomechanicsOthersDiscontinuation of oral spasmolytic drugs to decrease risk for adverse eventsDecreased time spent on exercise programADL indicates activities of daily living.Rehabilitation TechniquesReducing spasticity alone without addressing the negative components of the upper motor neuron syndrome will limit meaningful recovery. A combination of rehabilitation techniques is needed to facilitate functional improvements. Most rehabilitation studies for spasticity management are limited to small, randomized, controlled trials. There is emerging evidence of effectiveness of electric stimulation delivered to muscles after botulinum toxin injections, serial casting of ankle and elbow joints, partial body weight support gait training, and EMG-triggered electronic stimulation of wrist and finger extensors (Table 2). Studies on the use of an upper limb neuroprosthesis are limited, but there is more evidence that lower limb neuroprosthesis can improve gait speed.19Table 2. Rehabilitation Techniques for Poststroke SpasticityPotentiate medicationNeuromuscular electrical stimulation after BoNT injectionsRestore biomechanicsOrthoticsStretching, including serial castingImprove motor controlBody weight–supported treadmill trainingRobot-assistedNeurofacilitatory techniquesFunctional electrical stimulationStrengthen weak musclesResistance training programsAquatic therapyIntegrate into functional tasksConstraint-induced movement therapyNeural prosthesisImprove enduranceAquatic therapyTreadmill exercisesCircuit trainingOthersElectroacupunctureBiofeedbackPhysical modalities (ultrasound, vibration, thermotherapy)BoNT indicates botulinum neurotoxins.Pharmacological ManagementThe choice of drugs to treat PSS depends on severity, anatomic distribution (see Figure), presence of comorbidities, and drug cost, among others. Many stroke survivors have cognitive deficits that may be worsened by the central effects exerted by oral medications, or they are receiving other drugs that are relatively contraindicated for use with certain antispasticity drugs (eg, clonidine and tizandine act in synergy, resulting in hypotension; dantrolene sodium used concurrently with statins may induce hepatotoxicity.)Download figureDownload PowerPointFigure. Treatment algorithm for poststroke spasticity (PSS).Oral MedicationsAntispastic oral medications (baclofen, tizanidine, dantrolene, and benzodiazepines) can effectively reduce PSS, but their use islimited by many adverse effects. Because of this, and because of the limited evidence of efficacy attributable to inadequate sample size and lack of quality-of-life measures, it is best to limit the use of these drugs in PSS.20 However, oral drugs may be cost-effective choices for individuals who achieve adequate spasticity reduction without experiencing adverse events. The somnolent effect of oral medications may benefit a stroke survivor who has difficulty sleeping because of muscle spasms. Antispasticity drugs are discussed in greater detail in other reviews.21,22NeurolysisNerve blocks are effective in managing focal PSS.23,24 Depending on the dose and concentration used, these agents (phenol and alcohol) denature proteins in axons and membranes in afferent and efferent nerve fibers, leading to denervation and degeneration of muscle spindles.25 Adverse effects include postinjection dysesthesia, localized swelling, and excessive weakness.26 Although nerve blocks are widely used to manage PSS, there is paucity of evidence of efficacy and safety based on randomized controlled studies.Botulinum NeurotoxinsRecent consensus articles support the use of botulinum neurotoxins (BoNT) for focal spastic conditions in adults with PSS,27–31 as do individual trials involving the upper16,32–37 and lower limbs.28,38–41 It has been suggested that proper choice of muscles and individualized doses of BoNT type A can improve function in selected poststroke patients.42 Advantages of BoNT over oral medications is target specificity (ie, exerting significant changes only in injected muscles) and better adverse event profile. Drowsiness and sedation, which are commonly associated with oral spasmolytics, are practically nonexistent with BoNT. BoNT is superior over tizanidine in terms of efficacy and safety in treating PSS.37 Many clinicians also appear to favor BoNT over phenol and alcohol neurolysis, which are more technically challenging and have a higher incidence of complications, among them dysesthesia.Clinical Issues in the Use of BoNTUnlike in other countries where payors dictate the total dose of BoNT that can be used, dosing in the United States is not standardized and is empirical or largely based on expert recommendation and consensus. A few injection cycles using different doses may be needed before determining the optimal dose, defined by these authors as the BoNT units required to achieve a predetermined outcome without causing adverse event unique to an individual with PSS. It is unclear where the common practice of administering BoNT not more frequently than every 3 months was based, because the early studies of immunoresistance were in the cervical dystonia, not stroke, population.43 Although no prospective investigation of antibody formation to repeated BoNT injection has been reported, it is estimated that the incidence of antibody to BoNT in the spastic hypertonia population is <1%, which is lower than in cervical dystonia.44 Repeated BONT injections appear to result in sustained reduction of spastic hypertonia.45,46 Most studies on BoNT efficacy and safety reported improvement in muscle tone and reduction of impairment, but only a few use functional improvement as the primary outcome measure. A randomized, controlled, multicenter trial36 found that BoNT type A treatment was safe and efficacious in reducing upper limb spasticity but did not result in a change in quality of life using standardized measures. However, the treatment appeared to result in achievement of patient-centered goals.Intrathecal Baclofen TherapyIn the past decade, intrathecal baclofen (ITB) has been increasingly used to treat generalized or regional PSS recalcitrant to oral medications or injection therapy. Previous concerns that an intrathecally administered medication is not selective and, thus, will result in weakness of the noninvolved side were unfounded.47–49 ITB therapy has been shown to be effective in managing PSS,49 potentially enhancing functional recovery of gait47 and upper limb use,50 and improving quality of life.48 A consensus statement by a panel of experts recommended that ITB therapy be considered as early as 3 to 6 months poststroke, whenever it causes significant functional impact or hinders progress in rehabilitation.51 Common side effects of ITB are similar to the oral form but occur less frequently, largely because much lower intrathecal (and, hence, not required to cross the blood–brain barrier) doses are needed to exert therapeutic effects. Additional potential adverse effects are procedure-related or device-related, such as surgical infection, pump malfunction, or catheter interruption.Despite the potential benefits of ITB, 1 mechanism that underlies PSS. A better understanding of these mechanisms would help clinicians determine the type, timing, degree, and duration of the most effective combination of treatments. Although some predictors of disabling spasticity have been suggested, they are limited in their ability to forecast the onset of disabling spasticity during the poststroke recovery period, severity and regional distribution of spasticity, and response to therapies. If the characteristics of PSS evolve during the course of recovery, then it might be possible that a particular treatment will be effective only during a certain phase of spasticity evolution. An important question that needs to be answered is whether spasticity is a constraint on recovery, and would early intervention improve long-term outcomes?There is a dearth of research on the comparative efficacy, safety, and cost-effectiveness of various therapies, both pharmacological and nonpharmacologic. With the introduction of newer BoNT, there are now three different type A and one type B toxins available in the United States, but how these toxins measure up against each other is unknown. The same is true of the effects of combination therapies, eg, different drugs or drug plus exercise. Outcomes of long-term use of antispasticity drug therapy rarely have been reported.ConclusionsSelecting the appropriate treatment strategy and goals for the management of PSS should result in favorable functional outcomes. Inappropriate PSS management can interfere with functional recovery and increase complications. Function is a complex phenomenon that relies not only on muscle tone but also on strength, coordination, endurance, and sensation. In many instances, spasticity is incorrectly blamed as the main cause of dysfunction, when in fact the negative components of the upper motor neuron syndrome are most problematic. Thus, PSS management should be guided by its potential impact on function and well-being, rather than merely on the difficulty with passive muscle stretch or loss of range of motion. Other factors to consider before management include duration of condition, previous response to therapies, topographical involvement, response to medication, potential side effects, and cost. Therapeutic efforts have focused on peripheral (ie, altering muscle properties through physical techniques) and central (ie, influencing neurotransmission through GABA-mediated medications and modifying reciprocal inhibition) strategies. The optimal combination of rehabilitation techniques along with cost-effective medical and neurological management may provide the most favorable outcomes for PSS treatment.55DisclosuresDr Franciscois consultant to Allergan, Merz, and Ipsen, and has received speaking honoraria from Allergan. Dr McGuire is consultant and member of the speakers' bureau for Allergan, Ipsen, and Medtronic, and has received research grants from these companies.FootnotesCorrespondence to Gerard E. Francisco, MD, Chairman and Professor, Department of Physical Medicine and Rehabilitation, University of Texas Health Science Center–Houston, Chief Medical Officer and Director, S.T.A.R. (Spasticity Treatment and Research) Clinic and the UTHealth Motor Recovery Laboratory at TIRR Memorial Hermann, 1333 Moursund, Houston, TX 77030. E-mail [email protected]References1. Lance JW. Symposium synopsis. In: , Feldman RG, Young R, Koella WP, eds. Spasticity:disordered Motor Control. Chicago, IL: Year Book Medical Publishers; 1980:485–494.Google Scholar2. Sommerfeld DK, Eek EU, Svensson AK, Holmqvist LW, von Arbin MH. Spasticity after stroke: Its occurrence and association with motor impairments and activity limitations.Stroke. 2004; 35:134–139.LinkGoogle Scholar3. 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