STROKE CLINICAL UPDATES. UPPER LIMB POST-STROKE SPASTICITY: Evidence and Opportunities

Transcription

1 STROKE CLINICAL UPDATES UPPER LIMB POST-STROKE SPASTICITY: Evidence and Opportunities Spasticity is defined as a motor disorder, characterized by a velocity-dependent increase in tonic stretch reflexes (muscle tone) with exaggerated tendon jerks, resulting from hyper-excitability of the stretch reflex as one component of the upper motor neurone syndrome." 1 The pathophysiology of spasticity is complex. It involves not only prolonged disinhibition of spinal reflexes under the control of inhibitory and excitatory descending pathways, but also may involve lesions of premotor and supplementary motor areas. Spasticity is part of a larger picture that includes spastic dystonia, co-contractions and associated reactions. Spastic dystonia is dependent on efferent drives, and cocontraction results from an inability to control reciprocal inhibition of agonist and antagonist muscle groups. 2 Post-stroke spasticity is a common complication. After 2 weeks, the prevalence of spasticity in any limb is 25%. After 6 months, it increases to 43%, and after one year it decreases back to 25%. 3,4,5 Within the first month post-stroke, the incidence of significant spasticity is 27%. 6 For stroke survivors admitted to an inpatient rehabilitation facility, the prevalence of spasticity in any limb is 42%, 7 and the incidence of upper limb spasticity over the first 3 months is 33%. 8 The strongest predictor of moderate-to-severe spasticity is severe proximal and distal limb weakness on acute hospital or rehabilitation admission. 6,9 Early development of spasticity in the shoulder joint has been associated with poor motor recovery. 10 Spasticity is a direct cause of limitations in mobility and activities of daily living, and may increase the cost of care 9 and reduce quality of life 10 of the stroke survivor. This case provides a practical example of how clinicians manage stroke survivors with post-stroke spasticity involving the upper limb. Evidence- and consensus-based treatments are utilized to decrease spasticity and improve quality of life. CASE: Upper Limb Post-Stroke Spasticity Mr. Smith (not his real name) is a 52-yearold right-handed white male who was referred for consultation by his stroke neurologist for right upper limb spasticity, status-post a left middle cerebral artery infarct he suffered in April, He is independent with his activities of daily living, but has difficulty with dressing as he cannot range his right shoulder adequately, and needs assistance to place his fisted hand through his sleeve. He is able to drive with adaptive equipment. He ambulates with a quad cane. For spasticity, he has tried tizanidine in the past, but it caused sedation. He also complains of a sharp shooting pain that emanates from his right shoulder and radiates to his forearm. The pain is associated with achiness and numbness in his right hand and leg. The pain occurs mainly at nighttime, when he is rolling over onto his right side, and he has difficulty with sleep.

2 The patient denies the use of tobacco, alcohol, or illicit drug products. He works full-time. He is married, and lives with his wife in a 2-level home with 5 steps to enter, and 15 steps to the second floor. There are no bedrooms and bathrooms on the first floor On physical examination, his extremities have no cyanosis, clubbing, or edema. Peripheral pulses are intact. Range of motion is full in the left arm and leg. Range of motion in the right upper limb is limited in active shoulder flexion to 30 degrees and in active abduction to 45 degrees. However, passive right shoulder flexion is 160 degrees, and passive right shoulder abduction to 110 degrees. Tone in the right biceps, triceps, wrist flexor, finger flexor, and thumb flexor muscles is rated as 3 on the modified Ashworth Scale. Active internal and external rotation of the right shoulder is within normal limits. His right arm is not functional for activities of daily living. Neurologically, the patient is alert and oriented. He is able to fully comprehend, but has mild deficits in verbal fluency. Cognition is intact. He demonstrates no sensory neglect. Deep tendon reflexes are 3+ in the right upper limb, 2+ in the left upper limb, 4+ with clonus in the right lower limb, and 2+ in the left lower extremity 2+. Babinski sign is positive on the right side. Muscle strength testing is Brunnstrom stage 3 in the right upper limb, with movement in flexor synergy in the shoulder and elbow only, but not in the wrist and fingers; Brunnstrom stage 3 in the right lower limb, with movement in extensor synergy in the hip and knee, but not in the ankle and toes; and 5/5 in the left upper and lower limbs. Sensation is impaired in the right upper and lower extremities. He ambulates with a large-base quad cane. Gait is characterized by the right upper limb in flexion synergy, and decreased toe clearance on the right. Assessment and Treatment of Upper Limb Post-Stroke Spasticity The assessment of spasticity includes the identification of impairments, activities limitations, and participation restrictions that spasticity affects. The clinician and stroke survivor should evaluate whether spasticity has resulted in or will lead to musculoskeletal deformity. If the clinician and stroke survivor come to a mutual decision to treat spasticity, goals of treatment should be identified and discussed. Goals may be as simple as reducing tone to increase range of motion, improve joint position, or reduce pain. Functional objectives may include improving transfers and ambulation, or easing the performance of activities of daily living. Patient preferences should be evaluated as some tone may be required to optimize mobility or activities of daily living. Any source of noxious stimulus that can increase the severity of spasticity should be identified and treated. The most common evaluation tool for spasticity is the modified Ashworth scale (Table 1). 11 While the Ashworth scale actually measures muscle tone and not spasticity, it is the most widely used scale in research and clinical applications. Muscle tone should be recorded in all appropriate pivots of each joint so that the effects of treatment can be assessed.

3 A comprehensive spasticity management program requires a multi-modal approach that may include any combination of physical therapy, occupational therapy, oral medications, intrathecal medications, intramuscular chemicals and biological agents, and surgery. One means to determine treatment is whether spasticity involves a discrete location or is diffuse throughout the body. If spasticity is discrete, appropriate treatments include intramuscular chemicals, such as phenol or denatured alcohol, or biological agents, such as the botulinum toxins. If spasticity is more diffuse, oral or intrathecal medications should be considered. For this case, spasticity is severe but is limited to the right upper limb. As a result, a decision to inject botulinum toxin into the affected muscles was made. Injection of botulinum toxin is indicated to treat upper limb post-stroke. 12,13,14,15,16 At present, only onabotulinumtoxina (Botox ) is approved by the United States Food and Drug Administration (FDA) for post-stroke spasticity of the upper limb. Other botulinum toxins currently used for poststroke spasticity but not approved by the FDA include abobotulinumtoxina (Dysport ), incobotulinumtoxina (Xeomin ), and rimabotulinumtoxinb (Myobloc ). i Injections of botulinum toxin A may have a small but statistically significant effect on activity, 17 but improvements were due to decreased muscle tone rather than increased functional use of the limb. The cost-effectiveness of botulinum toxin injections alone to manage spasticity is unclear, 18 but if caregiver burden is taken into account, the use of botulinum toxins with therapy may be costeffective. 19 This patient presented with spasticity involving the right elbow flexor, elbow extensor, wrist flexor, finger flexor, and thumb flexor muscles. In order to effectively treat spasticity, the clinician needs to have a good knowledge base of the muscles that are involved in these movements. Table 2 lists commonly observed pivots and the muscles that cause these movements. The initial session of injections consisted of 400 units of onabotulinumtoxina injected into the right biceps (100 units), triceps (100 units), pronator teres (50 units), flexor digitorum superficialis (50 units), flexor digitorum profundus (50 units), flexor pollicis longus (25 units), and thenar (25 units) muscles. The amount of onabotulinumtoxina injected is more than approved by the FDA indication, and the locations of some of the injections are in muscles not approved by the FDA. The patient returned for rechecks 2 weeks after the injections to assess the initial effects of the injections, and 6 weeks after injections to assess the maximal effects of the injections. It is very important to counsel the patient that several cycles of injections may be required to determine the dosage for optimal management of spasticity. Because spasticity in this patient was so severe, the dosage of onabotulinumtoxina was increased several times, and a number of muscles that initially were not treated were added. At the current time, approximately 3 years after treatment was initiated, the patient now receives a total of 700 units of onabotulinumtoxina

4 into the biceps (150 units), triceps (100 units), pronator teres (50 units), flexor carpi radialis (50 units), flexor carpi ulnaris (50 units), flexor digitorum profundus (100 units), flexor digitorum superficialis (100 units), flexor pollicis longus (25 units), abductor pollicis brevis (25 units), and lumbrical (50 units) muscles. He uses a resting hand splint to maintain range of motion, and he consistently performs a home exercise program consisting of stretching. CONCLUSION This clinical update has provided a definition of spasticity, a brief synopsis of the assessment and treatment of post-stroke spasticity, and presented a case of upper limb post-stroke spasticity. Post-stroke spasticity is a common complication with a complex pathophysiology. It affects activities and participation, can cause pain, and can lead to musculoskeletal deformity. The clinician and stroke survivor mutually should decide treatment modality and goals, and may include physical and occupational therapies, oral and intrathecal medications, intramuscular injections, and surgery. Appropriate treatment of spasticity can lead to improved function and quality of life. Faculty Richard D. Zorowitz, M.D. Associate Professor of Physical Medicine and Rehabilitation The Johns Hopkins University School of Medicine Chairman, Department of Physical Medicine and Rehabilitation Johns Hopkins Bayview Medical Center 4940 Eastern Avenue, AA Building, Room 1654 Baltimore, MD V: F: rzorowi1@jhmi.edu Disclosure Statement Dr. Zorowitz is a paid consultant for Allergan, Inc., Avanir Pharmaceuticals, and Medergy. i Doses among the different botulinum toxins are not interchangeable.

5 TABLE 1. Modified Ashworth Scale (Bohannon and Smith 1987) Score Description 0 No increase in tone 1 Slight increase in tone giving a catch, release and minimal resistance at the end of range of motion (ROM) when the limb is moved in flexion/extension 1+ Slight increase in tone giving a catch, release and minimal resistance throughout the remainder (less than half) of ROM 2 More marked increased in tone through most (more than half) of ROM, but limb is easily moved 3 Considerable increase in tone passive movement difficult 4 Limb rigid in flexion and extension

6 TABLE 2. Movements of the Upper Limb and their Associated Muscles Movement Shoulder Adduction/ Internal Rotation Elbow Flexion Elbow Extension Forearm Pronation Wrist Flexion Finger Flexion Thumb Flexion Muscle(s) Pectoralis major Latissimus dorsi Teres major Subscapularis Biceps Brachioradialis Brachialis Triceps Pronator Teres Pronator Quadratus Flexor Carpi Radialis Flexor Carpi Ulnaris Flexor Digitorum Profundus Flexor Digitorum Superficialis Flexor Pollicis Longus Adductor Pollicis Thenar Muscles

7 TABLE 3. Movements of the Lower Limb and their Associated Muscles Movement Hip Flexion Hip Adduction Knee Extension Knee Flexion Equinovarus with Flexed Toes Striatal (Hitchhiker) Toe Muscle(s) Iliopsoas Sartorius Rectus femoris Adductor magnus Adductor longus Adductor brevis Iliopsoas (weak) Pectineus (weak) Rectus femoris Vastus lateralis Vastus medialis Vastus intermedius Lateral Hamstrings Medial Hamstrings Gastrocnemius Medial gastrocnemius Lateral hamstrings Soleus Tibialis posterior Tibialis anterior Flexor hallicis longus Long toe flexors Peroneus longus Extensor hallicis longus

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9 REFERENCES (cont.) 17. Teasell R, Foley N, Pereira S, Sequeira K, Miller T. Evidence to practice: Botulinum toxin in the treatment of spasticity post stroke. Top Stroke Rehabil 2012; 19: Foley N, Pereira S, Salter K, et al. Treatment with botulinum toxin improves upperextremity function post stroke: a systematic review and meta-analysis. Arch Phys Med Rehabil 2013; 94: Shackley P, Shaw L, Price C, et al. Cost-effectiveness of treating upper limb spasticity due to stroke with boutlinum toxin type A: Results from the botulinum toxin for the upper limb after stroke (BoTULS) trial. Toxins 2012; 4: Doan QV, Gillard P, Brashear A, et al. Cost-effectiveness of onabotulinumtoxina for the treatment of wrist and hand disability due to upper-limb post-stroke spasticity in Scotland. Eur J Neurol 2013; 20(5):

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