Spasticity, defined as a velocity-dependent increase in muscle tone caused by the increased excitability of the muscle stretch reflex, is a challenging symptom that frequently accompanies severe neurological conditions including stroke, multiple sclerosis (MS), cerebral palsy (CP), and spinal cord injury.1 The mechanisms of spasticity are complex, involving an inhibitory/excitatory disruption to the spinal network that heightens muscle activity and spinal reflex responses as a result of compensatory structural neuronal reorganization to central nervous system damage or injury.1,2 The original site of the disrupted signal depends on the cause of central nervous system damage; stroke spasticity originates from the cerebral cortex, whereas spasticity associated with MS and spinal cord injury originates in the spinal cord.
The Role of Nonpharmacologic Therapies
Pharmacologic interventions including oral and injected drugs are a mainstay of spasticity management; however, drug therapies alone are not considered sufficient, and the general consensus supports a broader therapeutic strategy.2 “Spasticity management usually requires a multimodal approach, using nonpharmacological and pharmacological treatment strategies,” Patricia Branco Mills, MHSc, MD, FRCPC, physical medicine and rehabilitation specialist at GF Strong Rehabilitation Centre in Vancouver, British Columbia, Canada, told Neurology Advisor. “The goals are generally to improve function, quality of life, and medical/health status through a transdisciplinary, holistic approach,” Dr Mills said.
In a 2017 review of new technologic advances in neurorehabilitative treatments for spasticity, Naro and colleagues2 emphasized that physical therapy and occupational therapy should be included in any rehabilitation program for focal or generalized spasticity, with other therapies added to achieve optimal results. In a review of spasticity management in stroke, Francois Bethoux, MD,3 reported that because of complications associated with drug and surgical treatment that may exacerbate functional performance through weakness and compensatory hypertonia in weakened limbs, treatment should rely on nonpharmacologic approaches used either before or adjunctively to these strategies.3 In addition to PT, he pointed to multiple other modalities, including ultrasound, thermotherapy, neuromuscular electrical stimulation and muscle strengthening exercises applied to an agonist muscle, and robotic devices for stretching and movement training, as important to a treatment plan.3
Noninvasive Neuromodulation Therapies
Noninvasive neuromodulation therapies designed to modify neuroplastic mechanisms for better adaptive muscle responses via the application of electromagnetic stimuli in conjunction with weak currents and or biochemical agents show potential for reducing spasticity across a number of conditions.
Repetitive transcranial magnetic stimulation (rTMS) involving the indirect application of magnetic pulses in a repeating pattern to induce cortical excitability, has demonstrated more consistent magnitude and duration of benefits in studies of spasticity. In patients with MS, this modality, applied at high frequency (5 Hz, 900 pulses per 15-minute session) to the primary motor region of the brain for 10 sessions over the course of 2 weeks, improved lower limb spasticity for a week to a month after application in patients with relapsing remitting MS.4
Leo et al4 reported that several studies demonstrated that low-frequency rTMS applied to the healthy brain hemisphere reduced chronic stroke-associated upper limb spasticity for up to 1 month posttreatment, whereas high-frequency rTMS showed only limited benefits. It has also demonstrated lasting inhibitory aftereffects on corticospinal motor output that make it especially effective in conjunction with physical conditioning or other therapies for MS spasticity.4
Transcranial direct current stimulation (tDCS) is a method of direct application of low-amplitude current to the brain via rubber electrodes (with saline-dampened sponges) adhered to the scalp to induce excitability. The treatment exerts a neuromodulating effect on neuronal firing rates and plasticity with potential to restore normal balance of the polarity of the neurons. A few sham-controlled studies showed improved Modified Ashworth Scale scores and decreased lower limb spasticity after tDCS administered 5 times per week for 20 minutes, at a setting of 1 mA, for 1 to 4 weeks for patients with stroke as well as MS and CP.4 There were no complications, and adverse effects were minimal.4 A second review by the same group reported only short-term benefits of tDCS in MS and CP and concluded that the evidence in support of tDCS for spasticity was unconvincing, particularly when compared with more significant results from rTMS.
Other Noninvasive Therapies
Lacey Bromley, PT, DPT, NCS, MSCS, a physical therapist from Susan Bennett PT and Associates and a consultant in MS therapeutic strategies, explained that several inhibitory techniques can also be employed to reduce spasticity for a short period. “These include prolonged stretching of the spastic muscle (30-60 seconds), prolonged cold of the spastic muscle, biofeedback techniques, and cutaneous electric stimulation on the opposing muscle. However, these strategies will only reduce the tone temporarily.”
“We have had success utilizing [functional electrical stimulation] on the common peroneal nerve, which innervates the anterior tibialis muscle,” she told Neurology Advisor, referring to the task-directed stimulation therapy that, similar to neuromuscular electrical stimulation, delivers small impulses directly to the affected nerves to force muscle contraction that produces functional movement. Both therapies have demonstrated reductions in spasticity in CP, spinal cord injury, and stroke.2
A wide range of nonpharmacologic therapies and devices are under investigation for spasticity. Their benefits, however, rely largely on the hemisphere of application and the underlying mechanisms, which will require further study for better results.4 Dr Mills observed that many modalities that show promise include targeted exercises, casting/splints, and electromagnetic devices. “Given that pharmacological options can have side effects that patients want to avoid or minimize, there should be a high priority on investigating nonpharmacological treatment strategies that can be used on their own or to improve the effects of pharmacological strategies when given in combination,” Dr Mills said.
- Mukherjee A, Chakravarty A. Spasticity mechanisms – for the clinician. Front Neurol. 2010;1:149.
- Naro A, Leo A, Russo M, et al. Breakthroughs in the spasticity management: Are non-pharmacological treatments the future?J Clin Neurosci. 2017;39:16-27.
- Bethoux F. Spasticity management after stroke. Phys Med Rehab Clin N Am. 2015;26:625-639.
- Leo A, Naro A, Molonia F, et al. Spasticity management: the current state of transcranial neuromodulation. PM R. 2017;9(10):1020-1029.