A variety of electrical stimulation methods have been employed to reduce spasticity including direct muscle stimulation, sometimes also termed patterned electrical stimulation (PES) or patterned neuromuscular stimulation (PNS), functional electrical stimulation (FES) and transcutaneous electrical nerve stimulation (TENS). In the present section, we will examine the effect of interventions based on direct muscle stimulation (or stimulation of the motor nerve over the muscle belly). The objective of direct muscle stimulation is to produce a muscle contraction and related therapies are focused on the beneficial effects of series’ of muscle contractions. Often this stimulation is cyclical in nature (patterned) so as to simulate natural physiologic conditions such as might be seen in walking or cycling. With FES, the stimulation parameters are set to produce a coordinated contraction of several muscles with the intent of producing purposeful movement. This approach is often used to assist or simulate active exercise paradigms and therefore, the articles addressing FES have been summarized in the previous section on active movement-based approaches. TENS, on the other hand, is focused on stimulating large, low threshold afferent nerves so as to alter motor-neuron excitability and thereby reduce spasticity. Stimulation intensities are maintained sub threshold for eliciting muscle contraction when stimulating mixed motor and sensory nerves so that only lower threshold sensory nerves are selectively stimulated. For this reason articles concerning TENS will be included in the next section that is directed towards interventions based on afferent stimulation.
Murillo et al. (2011), Van der Salm et al. (2006), Seib et al. (1994) and Robinson et al. (1988a) tested the effects of a single session of muscle stimulation on spasticity. Each employed slightly different stimulation parameters and a variety of outcome measures. Of note, Van der Salm et al. (2006) and Seib et al. (1994) each employed prospective controlled trials of electrical stimulation and demonstrated immediate effects of reduced spasticity although these effects waned and were mostly absent by the next day. In particular, van der Salm et al. (2006) examined 3 different stimulation methodologies vs. a placebo condition and assessed ankle plantar flexor spasticity with the modified Ashworth scale, a clonus score and via EMG responses (i.e., H-reflex and H/M ratio). The various stimulation methods consisted of stimulation over the triceps surae (agonist), the tibialis anterior (antagonist) and the S1 dermatome vs. a control placebo condition of electrode application but no current generation. Presumably, subjects were not aware of this because subjects had no sensation in the stimulated areas. Significant spasticity reductions were only obtained with agonist muscle stimulation for the modified Ashworth scale (p<0.001) and not the clonus or EMG responses. This was not sustained for 2 hours post-stimulation although there was still a trend for reduced modified Ashworth scores at this time (p=0.113). Spasticity was also reduced (but not statistically significantly) with antagonist muscle stimulation but not for dermatomal or sham (placebo) stimulation. Murillo et al. (2011) applied vibration at 50Hz to the rectus femoris muscle for 10 min, of which a siginificant reduction in Modified Ashworth Scale scores was observed in all 28 patients.
Interestingly, van der Salm et al. (2006) noted that if they had examined their data by employing t-tests to test for pre-post effects (i.e., univariate analysis) within a specific stimulation method, they also would have demonstrated a reduction in spasticity for antagonist muscle stimulation, thereby illustrating the potential of obtaining false positives in uncontrolled or poorly controlled studies. Robinson et al. (1988a) conducted a pre-post study design without control conditions and Seib et al. (1994) conducted a prospective controlled trial but then inappropriately employed univariate analysis. Regardless, the results of these studies corroborate the finding of an immediate post-stimulation effect by van der Salm et al. (2006). Seib et al. (1994) and Robinson et al. (1988a) employed stimulation of different muscles (tibialis anterior, i.e., ankle dorsiflexion and quadriceps, i.e., knee extension respectively) and each demonstrated short lasting reductions in spasticity. Similar to the findings of van der Salm et al. (2006), Seib et al. (1994) reported that the effect of reduced spasticity waned quickly but was still evident up to 6 hours post-stimulation (mean 4.4 hours) as indicated by subject self-report.
In the only study of the long-term effects of stimulation, Robinson et al. (1988b) employed a similar stimulation protocol for the quadriceps as noted above over a period of 4–8 weeks with twice daily 20-minute sessions at least four hours apart, six days per week. Although 31 individuals initiated the study and 21 completed 4 weeks of the stimulation program, the study had severe subject retention issues with only 8 individuals continuing participation for the intended 8 weeks. Study results showed that most subjects actually had increased spasticity at four weeks but for the subjects who remained in the study for 8 weeks there was no significant difference. This null result begs further study of the long-term effects of muscle stimulation given the beneficial results obtained with short-term stimulation and in reports involving individuals with other etiologies (Chen et al. 2005; Ozer et al. 2006)
The other aspect of these studies worth noting is the variability across even just these 4 studies with respect to outcome measure selection. Within these papers there were measures that were clinical, neurophysiological, biomechanical and subject self-report in nature. The study with the strongest design (i.e., van der Salm et al. 2006) employed clinical and neurophysiological measures with the modified Ashworth scale, clonus score and H-reflex testing. Seib et al. (1994) employed a biomechanical approach by using a spasticity measurement system which monitored ankle viscoelastic stiffness through measurements of resistance torque to repetitive sinusoidal ankle movements. Robinson et al. (1988a; 1988b) used a clinical/biomechanical approach in measuring the normalized relaxation index (R2n) obtained from the pendulum drop test. Others have noted that spasticity is a multi-faceted construct with individual components of spasticity weakly related to each other suggesting that while different tools may measure unique aspects of spasticity the overall construct is best measured with an appropriate battery of tests (Priebe et al. 1996).
There is level 2 evidence from two prospective controlled trials supported by a single pre-post study that a single treatment of surface muscle stimulation reduces local muscle spasticity with agonist stimulation more effective than stimulation to the antagonist.
There is conflicting evidence for how long the effects of a single treatment of electrical stimulation on muscle spasticity persist, although they appear to be relatively short lasting (i.e., <6 hours).
Based on a single pre-post study, there is no evidence that a long-term program of muscle stimulation has an effect on reducing muscle spasticity and may even increase local muscle 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.