Spasticity Following Spinal Cord Injury Jane TC Hsieh MSc Sandra J Connolly OT Amanda McIntyre RN MSc Andrea Townson MD Christine Short MD FRCPC FACP Viet Vu DO Brooke Benton BSc RDH Dalton Wolfe PhD www.scireproject.com Version 6.0 Key Points Spasticity Outcome Measures A multidimensional test battery of Spasticity Outcome Measures is needed for understandable interpretations of and between future studies. Passive Movement-based Approaches for Reducing Spasticity Short-term reductions in spasticity may be achieved by a variety of passive movement-based approaches (hippotherapy, neural facilitation combinations, rhythmic passive movements, prolonged standing of other methods of muscle stretching, and electrical passive pedaling systems. 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 Short-term reductions in spasticity may be achieved by various forms of afferent stimulation (ongoing (TENS) transcutaneous electrical nerve stimulation programs, penial vibration and rectal probe stimulation, massage, cryotherapy, helium-neon irradiation, and whole-body vibration). Direct Spinal Cord and Transcranial Magnetic Stimulation Short-or medium-term spasticity relief may be possible with repetitive transcarinal magnetic stimulation or spinal cord stimulation, respectively. 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 A variety of medications, other than baclofen, may be effective in treating SCI related spasticity (Tizanidine, Clonidine, cyproheptadine, gabapentin, orphenadrine citrate, and L-threonine). The usefulness of 4-Aminopyridine 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) and Nabilone may help to reduce spasticity. Focal Neurolysis Botulinum neurotoxin appears to improve focal muscle spasticity in people with SCI. Phenol blocks may assist in treating shoulder and hip adductor spasticity in individuals with SCI. Table of Contents 1.0 Introduction ........................................................................................................................ 1 1.1 Definition .......................................................................................................................... 1 1.2 Pathophysiology ............................................................................................................... 1 1.3 Impact............................................................................................................................... 2 1.4 Determining Impact of Treatment ...................................................................................... 2 1.5 Outcome Measurement and Spasticity ............................................................................. 3 1.6 Overview of Treatments .................................................................................................... 5 2.0 Non-Pharmacological Interventions for Spasticity .......................................................... 5 2.1 Passive Movement or Stretching ...................................................................................... 6 2.2 Interventions Based on Active Movement (Including FES-assisted Movement) ...............15 2.3 Interventions Based on Direct Muscle Electrical Stimulation ............................................34 2.4 Interventions Based on Various Forms of Afferent Stimulation ........................................38 2.5 Interventions Based on Direct Spinal Cord ......................................................................52 2.6 Repetitive Transcranial Magnetic Stimulation ..................................................................56 3.0 Neuro-Surgical Interventions for Spasticity ....................................................................59 4.0 Pharmacological Treatment for Spasticity ......................................................................62 4.1 Oral Baclofen ...................................................................................................................62 4.2 Intrathecal Baclofen for Reducing Spasticity ....................................................................67 4.3 Effect of Medications Other Than Baclofen on Spasticity after SCI ..................................81 4.3.1 Tizanidine..................................................................................................................82 4.3.2 Clonidine ...................................................................................................................84 4.3.3 Fampridine (4-Aminopyridine) ...................................................................................88 4.3.5 Gabapentin ...............................................................................................................94 4.3.6 Other Anti-Spasmodics .............................................................................................95 4.4 Cannabinoids for Reducing Spasticity after SCI ............................................................. 100 4.5 Focal Neurolysis for Spasticity Management ................................................................. 105 4.5.1 Botulinum Toxin ...................................................................................................... 105 4.5.2 Phenol ..................................................................................................................... 109 5.0 Summary ......................................................................................................................... 111 References ............................................................................................................................ 119 This review has been prepared based on the scientific and professional information available in 2015. 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, Connolly SJ, McIntyre A, Townson AF, Short C, Mills P, Vu V, Benton B, Wolfe DL. (2016). Spasticity Following Spinal Cord Injury. In Eng JJ, Teasell RW, Miller WC, Wolfe DL, Townson AF, Hsieh JTC, Connolly SJ, Curt A, Mehta S, Sakakibara BM, editors. Spinal Cord Injury Rehabilitation Evidence. Version 6.0. www.scireproject.com Spasticity Following Spinal Cord Injury 1.0 Introduction 1.1 Definition Spasticity is traditionally 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 reflexes, as one component of the upper motoneuron syndrome” (Lance 1980). Spasticity is quite commonly confused with tremor, rigidity, clonus, dystonia and various movement disorders (i.e., athetoid, ballisms, and 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. Regardless of the definitions presented, each eludes to various inter-related components of the upper motor neurone syndrome (i.e., tone, clonus, spasms, spastic dystonia and co- contractions). Therefore, a thorough clinical assessment of spasticity should always be undertaken as follows (Kheder & Nair 2012): 1) differentiate spasticity from other causes of increased tone, 2) identify potential triggers, 3) measure spasticity, 4) assess spasticity’s impact on function, and 5) gather input from patients, caregivers, therapists and other rehabilitation professionals. Spasticity is not static and therefore, assessments should be done regularly and combined with establishing goals of treatment to make decisions regarding treatment strategy (Rekand et al. 2012). 1.2 Pathophysiology Recent studies indicate that, besides changes in motoneuron activation (involuntary supraspinal descending inputs and inhibited spinal reflexes etc.), changes in muscle properties also