Spasticity Outcome Measures
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Key Points Spasticity Outcome Measures Although consensus has not yet been reached on clinically meaningful, feasible and effective outcome measures relevant to the treatment of spasticity and patient reported outcomes, development and inclusion of such a multidimensional test battery is required for understandable interpretations of and between future studies. Passive Movement-based Approaches for Reducing Spasticity Hippotherapy may result in short-term reductions in spasticity. A combination of neural facilitation techniques and Baclofen may reduce spasticity. Rhythmic passive movements may produce short-term reductions in spasticity. Prolonged standing or other methods of producing muscle stretch may result in reduced spasticity. Electrical passive pedaling systems may result in short-term reduction in spasticity. Active Movement-based Approaches for Reducing Spasticity Active exercise interventions such as hydrotherapy and FES-assisted cycling and walking may produce short-term reductions in spasticity. Direct Muscle Stimulation for Reducing Spasticity Electrical stimulation applied to individual muscles may produce a short term decrease in spasticity. There is also some concern that long-term use of electrical stimulation may increase spasticity. Various Forms of Afferent Stimulation for Reducing Spasticity Ongoing (TENS) transcutaneous electrical nerve stimulation programs result in short-term reductions in spasticity which may last for up to 24 hours. Penile vibration and rectal probe stimulation may be effective at reducing lower limb muscle spasticity for several hours. Other forms of afferent stimulation including massage, cryotherapy, helium-neon irradiation, and whole-body vibration may result in immediate spasticity reduction but require more research to examine long-term effects. Direct Spinal Cord and Transcranial Magnetic Stimulation Spinal cord stimulation may provide spasticity relief over a few months but long-term effectiveness and cost-effectiveness is less certain. Repetitive transcranial magnetic stimulation may provide spasticity relief over the short-term but long-term effectiveness is unknown. Neuro-Surgical Interventions for Spasticity Dorsal longitudinal T-myelotomy may result in reduced spasticity. Oral Baclofen Oral baclofen reduces muscle spasticity in people with SCI. Intrathecal Baclofen Bolus or long-term intrathecal baclofen decreases spasticity and may improve functional outcomes with low complication rates and is a cost effective intervention. Effect of Medications Other than Baclofen Tizanidine may be useful in treating SCI spasticity. Clonidine may be effective in treating SCI spasticity but more evidence is required to support its routine use. The usefulness of 4-Aminopyridine in the treatment of SCI spasticity requires confirmation through additional well-designed studies. Cyproheptadine may be useful in treating SCI spasticity but requires additional confirmatory research. Gabapentin may be useful in treating SCI spasticity but requires additional confirmatory research. Orphenadrine citrate may reduce spasticity in SCI but additional confirmatory research is needed. The use of L-threonine in the treatment of SCI spasticity requires confirmation through additional well-designed studies. Continued use of diazepam and dantrolene would benefit from controlled comparison studies. Cannabinoids Oral detra-9-tetrahydrocannabinol (dronabinol) may help to reduce spasticity but requires additional evidence from controlled studies. Nabilone has been shown to be effective in reducing spasticity but additional research is needed. Focal Neurolysis Botulinum neurotoxin appears to improve focal muscle spasticity in people with SCI. Phenol block may improve pain, range of motion and function related to shoulder spasticity in individuals with tetraplegia. Phenol block may reduce hip adductor spasticity in individuals with paraplegia and tetraplegia. Table of Contents 1.0 Introduction ........................................................................................................................ 1 2.0 Non-Pharmacological Interventions for Spasticity .......................................................... 5 2.1 Interventions Based on Passive Movement or Stretching ................................................. 5 2.2 Interventions Based on Active Movement (Including FES-assisted Movement) ...............12 2.3 Interventions Based on Direct Muscle Electrical Stimulation ............................................16 2.4 Interventions Based on Various Forms of Afferent Stimulation ........................................20 2.5 Interventions Based on Direct Spinal Cord or Transcranial Stimulation............................28 3.0 Neuro-Surgical Interventions for Spasticity ....................................................................32 4.0 Pharmacological Treatment for Spasticity ......................................................................34 4.1 Oral Baclofen ...................................................................................................................34 4.2 Intrathecal Baclofen for Reducing Spasticity ....................................................................38 4.3 Effect of Medications Other Than Baclofen on Spasticity After SCI ..................................50 Tizanidine ..........................................................................................................................50 Clonidine ............................................................................................................................52 4-Aminopyridine .................................................................................................................56 Cyproheptadine..................................................................................................................59 Gabapentin ........................................................................................................................61 Orphenadrine Citrate .........................................................................................................62 Other Potential Anti-Spasmodics .......................................................................................62 4.4 Cannabinoids for Reducing Spasticity after SCI ...............................................................64 4.5 Focal Neurolysis for Spasticity Management ...................................................................68 Botulinum Toxin .................................................................................................................68 Phenol ...............................................................................................................................71 5.0 Summary ...........................................................................................................................73 References ..............................................................................................................................77 This review has been prepared based on the scientific and professional information available in 2011. The SCIRE information (print, CD or web site www.scireproject.com) is provided for informational and educational purposes only. If you have or suspect you have a health problem, you should consult your health care provider. The SCIRE editors, contributors and supporting partners shall not be liable for any damages, claims, liabilities, costs or obligations arising from the use or misuse of this material. Hsieh JTC, Wolfe DL, McIntyre A, Janzen S, Townson AF, Short C, Connolly SJ, Mehta S, Curt A (2012). Spasticity Following Spinal Cord Injury. In Eng JJ, Teasell RW, Miller WC, Wolfe DL, Townson AF, Hsieh JTC, Connolly SJ, Mehta S, Boily K, editors. Spinal Cord Injury Rehabilitation Evidence. Version 4.0. www.scireproject.com We would like to acknowledge previous contributors: Keith Sequeira, Jeffrey Blackmer Spasticity Following Spinal Cord Injury 1.0 Introduction Definition Spasticity is quite commonly confused with tremor, rigidity, clonus, dystonia and various movement disorders (i.e. athetoid, ballisms, chorea). One of the earliest examples of this confusion is the term “spastic rigidity” used to refer to “excessive muscular contraction” first published in 1843 (Little WJ). Attempts to clarify this confusion have resulted in the most recent definition published by Pandyan et al. (2005) (adapted from Tardieau et al. 1954) as follows: “disordered sensori-motor control, resulting from an upper motor neuron lesion, presenting as intermittent or sustained involuntary activation of muscle”. This definition is intended to be more inclusive of clinical signs and symptoms of “spasticity” but has yet to be validated for clinical relevance. Perhaps the most common definition of spasticity was put forth by Lance (1980): “spasticity is 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 reflexes, as one component of the upper motoneuron syndrome.” Recent studies indicate that, besides changes in motoneuron activation (involuntary supraspinal descending inputs and inhibited spinal reflexes etc.), changes in muscle properties also contribute to the clinical appearance of limb spasticity and rigidity, which are frequently linked symptoms. In clinical practice, signs of exaggerated tendon tap reflexes associated with muscle hypertonia are generally thought to be responsible for spastic movement