STROKE CLINICAL UPDATES POST-STROKE LOWER EXTREMITY 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-tosevere spasticity is severe proximal and distal limb weakness on acute hospital or rehabilitation admission.6,10 Early development of spasticity in the shoulder joint has been associated with poor motor recovery.9 Spasticity is a direct cause of limitations in mobility and activities of daily living, and may increase the cost of care10 and reduce quality of life11 of the stroke survivor. This case provides a practical example of how clinicians manage stroke survivors with lower extremity spasticity throughout the continuum of care. Evidence- and consensus-based treatments are utilized to decrease spasticity and improve quality of life. CASE Ms. Jones (not her real name) is a 60-yearold right-handed white female, with a history of stroke in 2007 with residual left hemiparesis, hypertension, hyperlipidemia, and depression, who was admitted to an acute care hospital for pain after slipping on the floor. She was found to have an iliac wing fracture. CT and MRI Head were negative for new infarcts. MRI Cervical Spine demonstrated multi-level disk disease with no significant stenosis. She was noted to have near occlusion of her right internal carotid artery. Cerebral Angiogram demonstrated diffuse intracranial right internal carotid artery stenosis particularly in the supraclinoid area. She did not require surgery. For her previous stroke, she continued atorvastatin 80 mg by mouth at bedtime and aspirin 325 mg by mouth daily. She was transferred to a subacute rehabilitation unit, during which time she was noted to have spasticity of the left lower limb resulting in an equinovarus deformity. She remained in the rehabilitation unit for approximately 2 weeks, and was discharged home. She ultimately presented to the outpatient clinic for management of her spasticity. The patient denies the use of tobacco, alcohol, or illicit drug products. She is disabled from her stroke. She is single, and lives alone with her cat in a senior citizen’s apartment with no steps to enter the building. She ambulates independently with a left molded ankle-foot orthosis (MAFO) only. On physical examination, her extremities were symmetrical without cyanosis, clubbing, or edema. Range of motion is limited in the left ankle due to spasticity. Her left ankle is positioned in equinovarus deformity without toe clawing. Cognition and speech were grossly intact. Cranial nerves from II-XII were grossly intact except for her right eye being abducted and elevated due to the previous stroke. Sensation to light touch, pinprick, and proprioception was grossly intact in all extremities. Muscle strength was as follows: Right upper and lower extremities 5/5 throughout; left upper and lower extremities Brunnstrom grade III. The patient ambulated independently with only a left MAFO. Without the MAFO, the left foot was positioned in equinovarus position, and her gait was characterized by walking on the lateral aspect of her foot with foot drop during swing phase. She had difficulty donning the MAFO because of the severity of the equinovarus deformity, but ultimately could don it independently. Assessment and Treatment of Lower 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).12 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. 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 limited to the left lower limb. Assessment of lower limb spasticity in the stroke survivor involves evaluation of positioning in bed and wheelchair, as well as deviations during gait. Stroke survivors who are confined to wheelchairs may have deformities in hip and knee flexion. During gait, common deviations may include scissoring gait due to hip adductor tone, knee buckling due to quadriceps weakness, knee hyperextension due to hamstring weakness, foot drop due to gastrocnemius and soleus weakness, equinovarus deformity due to spasticity, and toe clawing due to toe flexor tone. Table 2 lists movements and corresponding muscles of the lower limb. Botulinum toxins currently used for the treatment of post-stroke spasticity include onabotulinumtoxinA (Botox®), abobotulinumtoxinA (Dysport®), incobotulinumtoxinA (Xeomin®), and rimabotulinumtoxinB (Myobloc®).i While no botulinum toxin currently is approved by the FDA for post-stroke lower limb spasticity, they, along with phenol, may play a significant role in correcting gait deviations and positioning issues. Scissoring gait may be treated by ablating the anterior and posterior branches of the obturator nerve using phenol, or with botulinum toxin injections into each of the hip adductor muscles. Equinovarus deformities may be treated with botulinum toxin injected into the ankle plantarflexor and inverter muscles,13,14,15 and may improve gait speed slightly.16 No studies have been conducted to determine whether botulinum toxin injections improve orthotic fit. The initial session of injections consisted of 500 units of onabotulinumtoxinA (Botox®) were injected into the left tibialis anterior (100 units), tibialis posterior (150 units), extensor hallucis longus (50 units), flexor digitorum longus (50 units), gastrocnemius (100 units), and soleus (50 units) muscles. The patient returned for recheck 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. At the current time, approximately 2 years after treatment was initiated, the patient now receives a total of 500 units of Botox injected into the left tibialis anterior (100 units), tibialis posterior (150 units), extensor hallucis longus (50 units), flexor digitorum longus (50 units), gastrocnemius (100 units), and soleus (50 units) muscles. Despite repeated injections, the equinovarus deformity has not significantly reduced. As a result, the patient was referred to an orthopedic surgeon for a splint anterior tibialis transfer (SPLATT).17 The SPLATT involves rerouting half of the tibialis anterior tendon posteriorly to the cuboid bone to address the varus deormity. It also involves lengthening of Achilles tendon, thus addressing the equinus deformity. Occasionally, the tibialis posterior tendon also must be lengthened. Prior to the surgery, gait analysis with surface electromyography should be performed to confirm the hyperactive muscles that need to be addressed. CONCLUSION This update has provided a definition of spasticity, a brief synopsis of the assessment and treatment of post-stroke spasticity, and presented a case of lower 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 21224-2735 F: 410-550-1345 V: 410-550-5299 Email: [email protected] 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. 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 TABLE 2. Movements of the Lower Limb and their Associated Muscles Movement Muscle(s) Hip Flexion Iliopsoas Sartorius Rectus femoris Hip Adduction Adductor magnus Adductor longus Adductor brevis Iliopsoas (weak) Pectineus (weak) Knee Extension Rectus femoris Vastus lateralis Vastus medialis Vastus intermedius Knee Flexion Lateral Hamstrings Medial Hamstrings Gastrocnemius Equinovarus with Flexed Toes Medial gastrocnemius Lateral hamstrings Soleus Tibialis posterior Tibialis anterior Flexor hallicis longus Long toe flexors Peroneus longus Striatal (Hitchhiker) Toe Extensor hallicis longus REFERENCES 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. Lance JW. Symposium synopsis. In: Feldman RG, Young RR, Koella WP, editors. Spasticity: Disordered control. Chicago: Yearbook Medical, 1980, pp. 485-494. Sheehan G. The pathophysiology of spasticity. Eur J Neurol 2002; 9 (Suppl 1): 3-9. Moura RCR, Fukujima MM, Aguiar AS, Fontes SV, Dauar RF, Prado Gf. 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