Spasticity A Clinical Review

Spasticity: A Clinical Review

http://www.medscape.com/viewprogram/14829_pnt

Spasticity: A Clinical Review CME Complete author affiliations and disclosures are at the end of this activity. Release Date: June 27, 2008; Valid for credit through June 27, 2009 Target Audience This activity is intended for any clinician who treats patients with spasticity. Goal The goal of this activity is to educate clinicians on diagnosing and treating spasticity. Learning Objectives for This Educational Activity Upon completion of this activity, participants will be able to: 1. 2. 3. 4.

Recognize common disorders commonly associated with spasticity Assess a patient with spasticity Describe objective testing for spasticity Recommend treatment options for patients with spasticity

Credits Available Physicians - maximum of 1.0 AMA PRA Category 1 Credit(s)™ for physicians All other healthcare professionals completing continuing education credit for this activity will be issued a certificate of participation. Physicians should only claim credit commensurate with the extent of their participation in the activity. Accreditation Statements For Physicians

Medscape, LLC is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide continuing medical education for physicians. Medscape, LLC designates this educational activity for a maximum of 1.0 AMA PRA Category 1 Credit(s)™. Physicians should only claim credit commensurate with the extent of their participation in the activity. For questions regarding the content of this activity, contact the accredited provider for this CME/CE activity: [email protected]. For technical assistance, contact [email protected]. Instructions for Participation and Credit There are no fees for participating in or receiving credit for this online educational activity. For information on applicability and acceptance of continuing education credit for this activity, please consult your professional licensing board. This activity is designed to be completed within the time designated on the title page; physicians should claim only those credits that reflect the time actually spent in the activity. To successfully earn credit, participants must complete the activity online during the valid credit period that is noted on the title page. Follow these steps to earn CME/CE credit*: 1. Read the target audience, learning objectives, and author disclosures. 2. Study the educational content online or printed out. 3. Online, choose the best answer to each test question. To receive a certificate, you must receive a passing score as designated at the top of the test. Medscape encourages you to complete the Activity Evaluation to provide feedback for future programming. You may now view or print the certificate from your CME/CE Tracker. You may print the certificate but you cannot alter it. Credits will be tallied in your CME/CE Tracker and archived for 6 years; at any point within this time period you can print out the tally as well as the certificates by accessing "Edit Your Profile" at the top of your Medscape homepage.

1 of 9

1/7/08 08:53

Spasticity: A Clinical Review

http://www.medscape.com/viewprogram/14829_pnt

*The credit that you receive is based on your user profile. This activity is developed and funded by Mescape.

Legal Disclaimer The material presented here does not necessarily reflect the views of Medscape or companies that support educational programming on www.medscape.com. These materials may discuss therapeutic products that have not been approved by the US Food and Drug Administration and off-label uses of approved products. A qualified healthcare professional should be consulted before using any therapeutic product discussed. Readers should verify all information and data before treating patients or employing any therapies described in this educational activity.

Copyright © 2008 Medscape.

Contents of This CME Activity To participate in this internet activity: (1) review the target audience, learning objectives, and author disclosures; (2) study the education content; (3) take the post-test and/or complete the evaluation; (4) view/print certificate View details. 1. Spasticity: A Clinical Review Richard D. Zorowitz, MD Joy B. Leffler, BS, MLA Catherine F. Murray, NASW, CSE Richard Robinson, BA

Spasticity: A Clinical Review

Description Spasticity: Spasticity is a motor disorder characterized by a velocity-dependent increase in tonic stretch reflexes with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex.[1]

Epidemiology To determine the epidemiology of spasticity, it is necessary to first identify the disorders in which spasticity is a common finding. Multiple sclerosis (MS): For MS, the incidence is 4.2 cases per 100,000 and the prevalence is 0.9 per 1000. In North America, the numbers are somewhat higher, with an incidence of 7.4 cases per 100,000, and a prevalence of 2.0 per 1000. Both the incidence and prevalence of MS are higher in women than in men.[2] Stroke: Among all ages, the estimated annual incidence of ischemic and hemorrhagic stroke is 183 per 100,000 in the US. Among people in the US aged 25 to 74 years, the prevalence of stroke is 2%, with higher rates in older populations.[2] Traumatic brain injury (TBI): The CDC estimates that at least 5.3 million Americans, approximately 2% of the U.S. population, currently have a long-term or lifelong need for help to perform activities of daily living as a result of a TBI.[3] Cerebral palsy (CP): A 2008 report from the CDC estimates the prevalence of CP as 3.6 per 1,000 children or about 1 in 278 children.[4] Spinal cord injury (SCI): The CDC estimates that the annual incidence of SCI in the US is approximately 11,000. Roughly 200,000 Americans currently live with a disability related to an SCI.[5] Within these populations, spasticity occurs at a variable rate. Studies have shown that spasticity affects between 37% and 78% of people with MS,[6,7] 40% of those with SCI,[8] approximately 35% of those with stroke,[9,10] more than 90% with CP,[11] and approximately 50% of patients with TBI, with higher rates in those patients with midbrain and pons lesions.[12]

Pathophysiology Although the pathophysiology of spasticity is not clearly understood, several theories have been proposed to explain this change in muscle tone, which comprises one component of the upper motor neuron syndrome. In general, spasticity develops when an imbalance occurs in the excitatory and inhibitory input to alpha motor neurons, leading to hyperexcitability.[13,14] The following are possible mechanisms of spasticity Increased neuronal excitability Enhanced excitatory synaptic input Segmental afferents Regional excitatory interneurons Descending pathways, i.e., lateral vestibulospinal tract Reduced inhibitory synaptic input

2 of 9

1/7/08 08:53

Spasticity: A Clinical Review

http://www.medscape.com/viewprogram/14829_pnt

Renshaw cell recurrent inhibition Ia inhibitory interneurons Ib afferent fibers Change in intrinsic electrical properties of the neuron Change in passive membrane electrical properties Change in voltage sensitive membrane conductance Enhanced stretch-evoked synaptic excitation of neurons gamma efferent hyperactivity Excitatory interneurons more sensitive to muscle afferent Lesion of the Upper Motor Neuron An upper motor neuron lesion, such as occurs with CP, stroke, TBI, or SCI, disrupts not only the pyramidal tract, but also the corticospinal tract that is involved in voluntary movement. The same damage to the higher centers provokes an imbalance in spinal reactivity through a modification of the descending input received by spinal neurons. After a variable period of time, spinal circuits undergo plastic rearrangements that lead to abnormal muscle contractions and abnormal reflex responses, some of which meet the classic definition of spasticity. A reciprocal potentiation is then likely to occur between spasticity and muscle shortening.[14] Pathophysiology of Impairment After a Central Nervous System Lesion Spinal versus Cerebral Models of Spasticity. The spinal model of spasticity posits that removal of inhibition on segmental polysynaptic pathways leads to a slow progressive rise of the excitatory state through cumulative excitation. What follows is afferent activity from one segment leading to muscle response many segments away and an overexcitation of flexors and extensors. In the cerebral model, enhanced excitability of monosynaptic pathways causes a rapid build-up of reflex activity, subsequently leading to a bias toward overactivity in the antigravity muscles and the development of hemiplegic posture.[15]

Spasticity may cause pain (which may also affect sleep and, subsequently, affect), joint deformity, macerated skin, difficulty performing activities of daily living or ambulating, muscle tightness or stiffness (particularly when the patient attempts to use fine-motor skills), muscle spasms, or fatigue. Spasticity also manifests in typical patterns, although they may not always be as readily apparent as those shown below.[15] (See Figures 1-11.) Figure 1. (click image to zoom) The Adducted/Internally Rotated Shoulder: This patient with head injury demonstrates an adducted/internally rotated shoulder, flexed elbow, pronated forearm, bent wrist, and clenched fist. The patient also has a thumb-in-palm deformity. Figure 2. (click image to zoom) The Flexed Wrist: Severe spastic wrist flexion may sometimes lead to wrist subluxation and carpal tunnel syndrome.

Figure 3. (click image to zoom) The Pronated Forearm: Pronator quadratus and/or pronator teres may contribute to the pronated forearm deformity.

Figure 4. (click image to zoom) The Clinched Fist: Two years after head injury, this patient illustrates a clenched fist with likely involvement of flexor digitorum sublimis. Flexor pollicis longus contributes to the thumb-in-palm deformity.

3 of 9

1/7/08 08:53

Spasticity: A Clinical Review

http://www.medscape.com/viewprogram/14829_pnt

Figure 5. (click image to zoom) The Flexed Elbow: This patient would often drive his fist into his throat because of severe elbow flexor spasticity.

Figure 6. (click image to zoom) The Thumb-in-Palm Deformity: Eleven months after head injury, this patient illustrates thumb-in-palm deformity when he tries to open his hand. Dynamic EMG studies reveal that flexor pollicis longus, adductor pollicis, and the thenar muscles all contributed. A parallelogram type of finger electrogoniometer records motion across the third finger PIP joint. Figure 7. (click image to zoom) Equinovarus: Varus posture may be seen in this patient from the anterior view. Excessive pressure typically occurs under the fifth metatarsal head.

Figure 8. (click image to zoom) Striatal Toe: Striatal toe (hitchhiker's great toe) caused by an overactive extensor hallucis longus.

Figure 9. (click image to zoom) Stiff Knee: Persistent knee extension of the "stiff knee," shown here with marked equinus. Note that the heel is not in contact with the foot pedal of the wheelchair.

Figure 10. (click image to zoom) Flexed Knee: Flexed knee deformity. Note taut hamstring tendons.

Figure 11. (click image to zoom) Adducted Thighs: The "scissoring thighs" caused by spastic adductors produce a narrow base of support at the feet.

Diagnosis and Assessment A key point in the assessment of spasticity is to standardize the environment, i.e., to perform the patient's assessment at the same time of day and in the same manner, at each visit. Exacerbating factors, such as urinary tract and other infections, pressure sores, ingrown toenails, and constipation, should be accounted for and removed to the extent possible before performing the assessment. Observing the person with spasticity perform activities such as walking, drinking from an open cup, and moving from one position to another often yields valuable information. In this manner, the assessment should examine the extent to which spasticity is limiting function: The amount of spasticity in each limb The impact of changing spasticity on function The degree of weakness The impact of weakness on function A standard evaluation of the nervous system forms the first step of the clinical examination, including an assessment of both strength and reflexes. Next, with the patient fully relaxed, each joint is moved through its full range of motion at various speeds. When stretching a limb affected with spasticity, the examiner will feel a "catch,"--a sudden increase in resistance to the stretch. Note should be made of the point at which the catch occurs and the speed with which the joint is moved when the catch occurs. Performing the range of motion may also elicit the "clasped-knife" phenomenon. Clasped knife occurs when the spastic muscle is stretched--the resistance to stretch is initially marked but then suddenly relents.[16] A variety of scales have been developed to standardize the recording of these findings from the clinical examination of spasticity. The most often used are the Modified Ashworth Scale and the Tardieu Scale.[17,18] Other scales are used less frequently, primarily for research purposes. The 6 points of the Modified Ashworth Scale (which includes a 1+ rating) correlate with clinician-determined increasing levels of spasticity during passive range of motion, from no change in or diminished muscle tone (0) to complete inability to move the joint (5). In

4 of 9

1/7/08 08:53

Spasticity: A Clinical Review

http://www.medscape.com/viewprogram/14829_pnt

addition to the degree of spasticity, the Tardieu Scale also includes the angle and velocity of the movement that elicits the response. Because one of the primary reasons to treat spasticity is its effect on function, the ability to measure change in function is important. Formal measures, such as the Fugl-Meyer Scale,[19] have been developed to measure functioning in patients with spasticity. However, these tools may not be sensitive to changes in spasticity per se and are infrequently used outside of the research setting. Therefore, the clinical assessment becomes more important and is likely to focus on patients' ability to complete a task, the quality of their completion of the task (e.g., ease of movement, normalization of gait), and the length of time that it takes them to complete the task. The clinical assessment should also include and evaluations of the change in level of pain, ease of caregiving or hygiene, or overall quality of life. Objective Measures of Spasticity Objective testing includes both electrophysiologic studies and biometric testing. An electromyogram (EMG), with simultaneous measure of agonist and antagonist muscles, can be used alone or in combination with gait analysis. The most widely employed electrophysiologic testing, multichannel EMG, provides quantification of the H-reflex to M-wave amplitude ratio (H/M ratio). F waves, the tonic vibration reflex, the flexor withdrawal response, and lumbosacral spinal evoked potentials.[20-26] Although biomechanical studies, because of the cost and size of the equipment, are typically reserved for use in research studies, they can provide objective measures of spasticity. Two types of studies are the Wartenburg pendulum test, in which an electrogoniometer is used to count the number and record the pattern of the swing when the knee is released from an extended position, and the torque motor test, which measures the amplitude and frequency oscillation during flexion and extension of the wrist.[18,27]

Treatment Left untreated, spasticity can lead to contracture. However, not all spasticity requires treatment Indeed, in some cases, the inappropriate treatment of spasticity may lead to loss of function, particularly when spasticity is counterbalancing the effects of paresis. Before beginning therapy, it is important for the clinician to differentiate rigidity and contracture from spasticity. Rigidity causes an overall involuntary increase in resistance of a muscle to passive stretch. In rigidity, this increased tone is uniform throughout the range of motion of the muscle being stretched and, unlike in spasticity, is not velocity dependent. In addition, spasticity causes an increase in deep tendon reflexes, whereas rigidity does not. Contracture is a fixed shortening of the muscle, tendons, or ligaments--or a combination thereof--that prevents normal movement of the associated joint or limb. Untreated contracture can result in permanent deformity. Another important consideration before commencing treatment is to determine which muscles are involved in spasticity. Standardized techniques to ascertain range of motion may yield valuable information regarding the effects of spasticity. However, motor point or nerve blocks may be necessary to clearly delineate the role of agonist and antagonist muscles. Spasticity may need to be treated when it causes Pain Difficulty performing activities of daily living Impaired mobility, whether related to ambulation or transfers Poor joint positioning An increased risk for the development of contracture Skin breakdown Outlining the Treatment Goals The primary aim of treatment is to improve quality of life for people with spasticity and for their caregivers. Therefore, the development of treatment goals should always include these key individuals, with realistic expectations clearly defined in collaboration with other members of the spasticity management team. The patient's ability to fully engage in and to have the resources necessary to participate in the rehabilitation program must be ensured prior to commencing therapy. Throughout the course of treatment, alterations in the treatment plan should be based on response to therapy, with expectations redefined at regular, agreed-upon intervals. Once the decision has been made that the spasticity should be treated and the patient, caregiver, and healthcare professionals are in agreement about the treatment goals, the question becomes which treatment to use. The patient's age, preferences, and ability to comply with treatment need to be taken into consideration. Other factors that determine the choice of treatment include the distribution (i.e., focal or diffuse), duration, and severity of the spasticity.[28] The treatment of spasticity is usually initiated with the most conservative treatments that have the fewest risks. Therapy directed at reducing or eliminating spasticity almost universally involves a multimodal approach.[28] A variety of factors may lead to or increase the severity of spasticity. These issues should be ruled out as underlying causes or exacerbating factors and should be effectively treated, if necessary, before attempting to treat the spasticity. Examples of commonly occurring causes of a new onset of spasticity or a worsening of existing spasticity include Urinary tract infections or retention Other sources of infection Pressure sores Extremes of heat or cold

5 of 9

1/7/08 08:53

Spasticity: A Clinical Review

http://www.medscape.com/viewprogram/14829_pnt

Fatigue Renal calculi Ill-fitting orthotics Constipation or bowel obstruction Physical and Occupational Therapy Physical therapy, occupational therapy, or both are included in most patients' treatment regimens, with the level of the patient's and caregivers' motivation strongly associated with outcome. These therapies are targeted at reducing muscle tone; improving range of motion, mobility, comfort, and strength; and enhancing independence and the performance of activities of daily living.[29,30] Orthoses include any device that is used to support, align, prevent, or correct deformities or to improve the function of movable parts of the body.[31,32] The primary goals in treating spasticity with orthoses include Preventing deformities and the breakdown of skin Inhibiting tone Maintaining the length of muscle fibers Elongating shortened tissues, thereby prolonging proper positioning Optimizing position Increasing or maintaining range of motion Decreasing pain Serial inhibitory casting involves the gradual stretching of a limb to provide "stress relaxation" to the muscle, thereby increasing the range of motion and preventing contracture or relieving a previously developed contracture. A temporary hard cast is placed on the affected limb at five degrees less than the maximum range that triggers spasticity. The cast is removed every three to five days, the limb is stretched slightly further, and another cast is applied, with the process continuing until maximum positioning of the joint is achieved. At that time, a bivalve cast is applied. Constant watchfulness is required to prevent skin breakdown and the formation of pressure sores.[32-34] (See Figures 12 and 13.) Figure 12. (click image to zoom) Clear plastic forearm orthosis.

Figure 13. (click image to zoom) Dynamic orthosis.

Chemodenervation and Neurolysis Chemodenervation, which interrupts neuronal signaling and is achieved with the use of botulinum toxin (BTX), or neurolysis, which destroys nerve tissue, is typically used to treat spasticity of focal origin and is often used before, after, or in combination with other therapeutic modalities, such as physical therapy or serial casting.[35] The agent is injected directly into the muscle (motor point block) or nerve (nerve block), preferably as close as possible to the motor end plates.[36,37,38] A key to the success of chemodenervation or neurolysis for the treatment of spasticity is patient selection.[39] In particular, if the injection of the targeted muscle or nerve would lead to a weakening that would decrease the current level of functioning, i.e., would reduce tone that is compensating for muscle weakness, the patient is not typically a candidate. Chemodenervation and neurolysis are also not effective in treating fixed contracture or other joint deformities.[40] Before the advent of the use of BTX in the treatment of spasticity, alcohol or phenol was often used.[41] Today, however, alcohol is rarely used for the treatment of spasticity, and phenol is typically reserved for use in those cases that require the injection of large muscles or a large number of muscles. Phenol and BTX may also be combined to achieve maximum effect in specifically targeted muscles.[40] Botulinum Toxin. BTX type A (BOTOX) affects the neuromuscular junction through binding, internalization, and inhibition of acetylcholine release. It must enter the nerve endings to exert its chemodenervating effect. Once inside the cholinergic nerve terminal cell, BTX-A inhibits the docking and fusion of acetylcholine vesicles at the presynaptic membrane.[42,43] BTX type-A does not have FDA approval for the treatment of spasticity. However, it has been well studied in the treatment of spasticity from all causes, particularly in cerebral palsy and post-stroke spasticity.[44-51] Clinical effects are usually seen within 24 to 72 hours. The maximum weakening effect is almost always seen at 2 weeks after injection. Duration of effect is usually 12 weeks but may be longer (sometimes up to 16 weeks or more) with adjunctive therapies such as stretching, casting, or other physical therapies. Gradually, muscle function returns by the regeneration or sprouting, which occurs when the blocked nerves form new neuromuscular junctions. BTX-A is dose dependent and reversible

6 of 9

1/7/08 08:53

Spasticity: A Clinical Review

http://www.medscape.com/viewprogram/14829_pnt

secondary to the regeneration process. Once begun, treatment with BTX-A is continually evaluated. Follow-up is crucial to gauge the response to BTX-A therapy and to fine tune muscle selection and the dosage.[49] The principal adverse effect is excess weakness in the injected muscle. Spread beyond the injected muscle does occur, although care in placing the injection in the muscle belly minimizes this possibility. BTX-A should be used with extreme caution in people with neuromuscular diseases such as myasthenia gravis or amyotrophic lateral sclerosis or in those taking aminoglycoside antibiotics. Although antibody formation appears to be rare with the use of BTX-A in the treatment of spasticity,[52] it is recommended, when possible, to wait at least 3 months between injections and to use the minimum effective dose. BTX-B or Myobloc has not been adequately evaluated in the treatment of spasticity to recommend its use in this patient population. The only randomized controlled trial that has assessed the use of BTX-B in spasticity found that 10,000 units of did not reduce muscle tone, and dry mouth was a common adverse event in the patients treated with BTX-B.[49] Phenol. Phenol causes nonselective tissue destruction in the injected area, including coagulation of nerves and muscle necrosis. As mentioned, phenol is typically used when treating large muscles, such as those of the anterior thigh.[53,54] The duration of effect of phenol can be quite variable, from less than 1 month to more than 2 years. There are several potential adverse events attributed to the use of phenol, such as dysesthesias. Nonselective tissue destruction to muscles or nerves may cause temporary or permanent pain in the muscle near the injection site. Oral Medications and Intrathecal Treatment A variety of medications are available for the treatment of spasticity. When spasticity is focal rather than diffuse in nature, the sedation and confusion associated with the use of oral medications may limit their effectiveness. Dantrolene. Dantrolene (Dantrium) has FDA approval for use in controlling the manifestations of chronic spasticity secondary to upper motor neuron disorders in children and adults.[55] The mechanism of action of dantrolene is to reduce the release of calcium into the sarcoplasmic reticulum of muscles. This drug, which has a half-life of 8.7 hours, affects fast muscle fibers more than it does slow muscle fibers.[56] The initial recommended dose of dantrolene for the treatment of spasticity in adults is 25 mg daily for 7 days. This may be increased to 25 milligrams 3 times daily for 7 days, then to 50 mg 3 times daily for 7 days and then to 100 mg 3 times daily. Before beginning therapy a therapeutic goal should be identified with doses increased accordingly. Therapy should be stopped if benefits are not seen within 45 days. The maximum dose in adults is 100 mg 4 times daily.[55] The initial recommended dose of dantrolene for the treatment of spasticity in children is 0.5 milligram/kilogram (mg/kg) once daily for 7 days. This may be increased to 0.5 mg/kg 3 times daily for 7 days, then 1 mg/kg 3 times daily for 7 days, and then 2 mg/kg 3 times daily. Doses higher than 100 mg 4 times daily should not be used. As in adults, a therapeutic goal should be identified before beginning therapy and doses should be increased accordingly. Therapy should be stopped if benefits are not seen within 45 days.[55] Although side effects include drowsiness, dizziness, weakness, malaise, fatigue, and diarrhea, dantrolene is less likely to cause problems with confusion or cognition than are the benzodiazepines and oral baclofen. Because of the potential for dantrolene to cause hepatotoxicity, regular monitoring of hepatic function is required with the use of this drug. The typical starting dose of dantrolene is 25 mg by mouth, daily, with titration to efficacy. There are no specific changes recommended for the dosing regimen for the geriatric patient.[47,57] Benzodiazepines. Benzodiazepines do not have FDA approval for the treatment of spasticity, although they are widely used for this condition. Diazepam acts by facilitating the postsynaptic action of gamma-aminobutyric acid (GABA), although it has no direct GABA mimetic effect. The half-life of diazepam is 27 to 37 hours. Common side effects include sedation, ataxia, and fatigue. The typical effective dose of diazepam for the treatment of spasticity is 2 to 10 mg, three or four times per day. In the geriatric population, a typical starting dose is 2.0 to 2.5 mg once per day.[58] Clonazepam is a sedative-anxiolytic, which decreases nocturnal spasms, hyperreflexia, and resistance to range of motion. Side effects include weakness, hypotension, ataxia, dyscoordination, sedation, depression, and memory impairment. Prolonged use may also increase the risk of addiction. Clonazepam is usually administered at bedtime, in a dose of 0.5 to 1.0 mg.[59] Imidazolines. Clonidine (Catapres tablet or transdermal patch) and tizanidine (Zanaflex) are imidazolines that reduce spasticity through their action on the central nervous system (CNS). These drugs typically cause less muscle weakness than do the benzodiazepines, which may be valuable when it is important for the patient to retain strength. The most common side effect of these drugs is sedation, and they may also cause hypotension, dry mouth, dizziness, renal impairment, and psychosis. Tizanidine is approved by the FDA for the treatment of spasticity. Tizanidine has a peak effect of 1 to 2 hours and a duration of action of 3 to 6 hours. The usual starting dose of tizanidine is 1 to 2 mg by mouth, which is then gradually increased in 1- to 2-mg increments. The drug may be repeated at 6- to 8-hour intervals as needed, up to 3 doses per 24 hours. However, the daily dose should not exceed 36 mg. The safety and efficacy of tizanidine have not been determined in children. Tizanidine may cause hepatotoxicity, and regular monitoring of hepatic function is required. Dantrolene and tizanidine are usually not prescribed together because they may each cause hepatotoxicity.[60] Concomitant use of tizanidine and either fluvoxamine or ciprofloxacin should be avoided.[55,61] Clonidine does not carry FDA labeling for the treatment of spasticity. Support for its use is derived from the results of open-label trials and clinical experience.[62] The half-life of oral clonidine is 12 to 16 hours. The usual starting dose of oral clonidine is 0.1 mg twice a day, with titration to 0.2 to 0.6 mg twice a day, to a maximum of 2.4 mg per day. The transdermal formulation of clonidine is typically initially administered as one TTS-1 patch (equivalent to 0.1 mg per 24 hours) per week, with titration to two TTS-3 patches (equivalent to 0.6 mg per 24 hours) per week. No dosing recommendations are available for geriatric patients. Clonidine is much more likely than tizanidine to cause hypotension. Baclofen. Orally administered baclofen (Lioresal) has FDA approval for the treatment in children and adults of spasticity resulting from multiple sclerosis and spinal cord injuries/diseases and intrathecally for spasticity related to cerebral palsy and spinal cord injury.[63] Baclofen is an analog of GABA and binds to the GABAB receptors found in the spinal cord, decreasing stretch reflexes, the rate of muscle

7 of 9

1/7/08 08:53

Spasticity: A Clinical Review

http://www.medscape.com/viewprogram/14829_pnt

spasms and clonus, pain, and tightness and improves range of motion. Oral Caclofen. The initial recommended dose of oral baclofen for the treatment of spasticity in adults is 5 mg 3 times a day. The dose may be increased by 15-mg/day increments every 3 days. Although 80 mg per day (divided into 3 or 4 doses) is a commonly accepted maximum, dosing up to 200 mg per day has been used safely and effectively. Keeping in mind that the safety and efficacy of oral baclofen have not been established in children younger than 12 years of age, the initial recommended starting dose of oral baclofen for the treatment of spasticity in children aged 2 to 7 years is 10 to 15 mg/day (in 2 to 3 divided doses). The dose may be increased by 5- to 15-mg/day increments every 3 days to a maximum dose of 40 mg/day (in 3 to 4 divided doses). For children older than 8 years, the initial recommended starting dose of baclofen is 10 to 15 mg/day orally (in 2 to 3 divided doses). The dose may be increased by 5- to 15-mg/day increments every 3 days to a maximum dose of 40 mg/day (in 3 to 4 divided doses). Side effects may include vertigo, urinary frequency, muscle weakness drowsiness, confusion, headache, nausea, seizures, constipation, dyspnea, impaired vision, severe fatigue, urticaria, and edema.[63] Intrathecal Caclofen Therapy. A programmable pump with a reservoir; a clear, flexible silicone catheter; and a programming device comprise the delivery system for intrathecal baclofen therapy (ITB). Typically, candidates for ITB therapy have severe spasticity that does not respond to conservative treatment with medications or have intolerable side effects at therapeutic doses. The system is surgically implanted after the patient has responded favorably to a test dose of the intrathecally delivered medication. The pump, which is implanted subdermally, is usually refilled in the physician's office on a four- to eight-week basis, depending on the capacity of the reservoir and the dosage of ITB that is administered, and typically lasts for five or more years. The usual starting dose is 25 mcg per day, with titration to efficacy, up to a maximum dose of 200+ mcg per day. Because ITB therapy delivers the drug directly to its site of action, much less baclofen is needed than when it is delivered orally. The drowsiness and sedation related to the use of ITB baclofen are much milder than when baclofen is delivered orally. However, approximately 5% of people develop infections that require temporary removal of the ITB therapy pump. Other equipment-related risks include pump failure, catheter kinking or breakage, or dislodgement of the catheter. Abrupt discontinuation of intrathecal baclofen is not advised--it may cause serious sequelae, including high fever, altered mental status, exaggerated rebound spasticity, and muscle rigidity. Rare cases have advanced to rhabdomyolysis, multiple organ-system failure, and death. To prevent withdrawal syndrome, families must be educated about the signs of baclofen withdrawal and have a plan to respond to possible emergencies. Surgery The goals of the surgical treatment of spasticity may include improving access for hygiene, improving the ability to tolerate braces, reducing pain, improving function such as walking, or reducing the risk of further deformity. Orthopedic Operations. With orthopedic surgery, muscles can be denervated, and tendons and muscles can be released, lengthened, or transferred. Spastic muscles in the shoulder, elbow, forearm, hands, and legs may all be treated with tendon or muscle lengthening. In tendon transfers, spastic muscles may be used to advantage by transferring them across the joint, relieving the deforming action of the muscle on the joint and simultaneously aiding the antagonist muscle. In some cases, a split transfer is desirable, for instance in the treatment of varus feet. In some situations, the transfer allows improved function. In others, the joint retains passive but not active function.[32] In contracture release, the surgeon partially or completely severs the contracted tendon and then repositions the joint at a more normal angle. The joint is encased in a cast over a period of several weeks while the tendon regrows, often requiring the use of serial casting to achieve maximum success. Once the cast is removed, physical therapy is necessary to strengthen the muscles and improve the patient's range of motion. Split tendons may also be employed in conjunction with osteotomy and arthrodesis to more fully correct the joint deformity. Osteotomies are most commonly used to correct hip displacements and foot deformities. Arthrodesis, a fusing together of bones that normally move independently, limits the ability of a spastic muscle to pull the joint into an abnormal position. Arthrodesis procedures are performed most often on the bones in the ankle and foot. Selective Dorsal Rhizotomy. Although performed most often for the treatment of spasticity in children with cerebral palsy, selective dorsal rhizotomy may be used in the treatment of post-stroke spasticity to treat spasticity of the legs that interferes with movement or positioning. In this procedure, electrophysiologic guidance is employed to identify abnormal sensory nerve rootlets, which are then sectioned, leaving the motor nerves intact. The best candidate for selective dorsal rhizotomy is a person with good strength and balance, spasticity in either or both legs with minimal or no fixed contractures, no spasticity in the arms, and strong motivation and support.[64] Assessing the Results of Treatment When developing the treatment plan, it is important to build in regularly scheduled formal assessments of treatment outcome.[65] According to Medicare guidelines, whenever the patient is undergoing physical or occupational therapy, the patient must return to the physician for a follow-up visit every 30 days. Because factors such as fatigue, time of day, and environmental conditions may affect the degree of spasticity, it is important to conduct the posttreatment examination in an environment similar to the pretreatment conditions. Replication of the conditions means that the evaluation should occur at the same time of day, with the patient in same position, and using a standard format for assessing the spasticity, whether that is with a standardized protocol such as the Modified Ashworth Scale or polygraphic recording techniques.

Authors and Disclosures As an organization accredited by the ACCME, Medscape, LLC requires everyone who is in a position to control the content of an education activity to disclose all relevant financial relationships with any commercial interest. The ACCME defines "relevant financial relationships" as financial relationships in any amount, occurring within the past 12 months, including financial relationships of a spouse or life partner, that could create a conflict of interest. Medscape, LLC encourages Authors to identify investigational products or off-label uses of products regulated by the US Food and Drug Administration, at first mention and where appropriate in the content.

8 of 9

1/7/08 08:53

Spasticity: A Clinical Review

http://www.medscape.com/viewprogram/14829_pnt

Author Richard D. Zorowitz, MD Visiting Associate Professor of Physical Medicine and Rehabilitation, The Johns Hopkins University School of Medicine; Chairman, Department of Physical Medicine and Rehabilitation, Johns Hopkins Bayview, Baltimore, Maryland Disclosure: Richard D. Robinson, MD, has disclosed that he has received grants for educational activities from Allergan, Inc. Joy B. Leffler, BS, MLA Senior Director of Education and Informatics, Movement Disorder Education Fund, dba WeMove, New York, NY Disclosure: Joy B. Leffler, BS, MLA, has disclosed no relevant financial relationships. Catherine F. Murray, NASW, CSE Science writer, WeMove, Ponte Vedra Beach, Florida Disclosure: Catherine F. Murray, NASW, CSE, has disclosed no relevant financial relationships. Richard Robinson, BA Freelance Medical Writer, New York, NY Disclosure: Richard Robinson, BA, has disclosed no relevant financial relationships.

Editor Carol Peckham Director, Editorial Development, Medscape, LLC Disclosure: Carol Peckham has disclosed no relevant financial relationships.

Registration for CME credit, the post test and the evaluation must be completed online. To access the activity Post Test and Evaluation link, please go to: http://www.medscape.com/viewprogram/14829_index

9 of 9

1/7/08 08:53