It has been reported that self-stretching, regular physiotherapy and physical activities affect spasticity and should be considered as a therapeutic approach prior to antispastic medication and surgical procedures (Merritt 1981). In particular, therapies based on physical interventions are advantageous as they generally have fewer related adverse events although they also typically have short-lasting effects. Movement therapies can be differentiated into passive or active maneuvers that are assumed to affect both spinal neuronal circuits and fibro-elastic properties of the muscles, thereby potentially reducing spasticity. An underlying physiologic paradigm that explains why passive movements have an influence on spasticity in patients with a lesion of the upper motor neuron is equivocal (Katz 1991).
Passive movement may be accomplished by therapist/care-giver or self-mediated limb movement focusing on muscle stretching or on preserving full range of motion over joints that may be immobilized (Harvey et al. 2009). Alternatively, a mechanical device may be employed such as a motorized therapy table (Skold 2000) or exercise cycle (Kakebeeke et al. 2005; Kiser et al. 2005; Rayegan et al. 2011). These mechanical devices have the advantages for research purposes of producing repeatable movements over a specific range and also in standardizing other parameters (e.g., frequency, speed). They are however, commonly not accessible for routine clinical use and may present an obstacle for multicentre trials.
Neurodevelopmental Therapy (NDT)
One class of therapies employed by physiotherapists and occupational therapists which utilize passive (and active) movement and stretching represent those developed mostly for stroke rehabilitation such as Bobath (neurodevelopmental) therapy and proprioceptive neuromuscular facilitation or other approaches such as those advocated by Rood or Brunnstrom. Although normalization of movement (sometimes associated with spasticity reduction) is at the basis of most of these approaches, it is noted that advocates for Bobath define this approach as more of a continually evolving, problem-solving concept that forms a framework for specific clinical practice (Raine, 2007). Anecdotally, these approaches appear to be in widespread practice although there are no reports that document the extent of their actual use in clinical practice within SCI rehabilitation. Li et al. (2007) recently conducted an RCT involving the use of 3 of these approaches (Bobath, Rood, Brunnstrom) in combination with Baclofen therapy to reduce spasticity.
Another approach to spasticity reduction is hippotherapy, which involves the rhythmic movements, associated with riding a horse, to regulate muscle tone (Lechner et al. 2003; 2007). Although the specific mechanisms by which an antispastic effect may be achieved with hippotherapy is unknown, it is postulated that it may be brought about by the combination of sensorimotor stimulation, psychosomatic effects and the specific postural requirements, and passive and active movements necessary for riding a horse (Lechner et al. 2003; 2007).
Although it has been suggested by some that repetitive movements are deemed necessary for obtaining a clinical effect (Rosche et al. 1997), there have been several reports of reduced spasticity associated with regular periods of passive standing (Odeen & Knutsson 1981; Bohannon 1993; Kunkel et al. 1993; Dunn et al. 1998; Eng et al. 2001; Shields & Dudley-Javoroski 2005). The majority of these are individual case reports (Bohannon 1993; Kunkel et al. 1993; Shields & Dudley-Javoroski 2005) or user satisfaction surveys (Dunn et al. 1998; Eng et al. 2001) and have not been included in Table 21.1 (i.e., other than Odeen & Knutsson, 1981) which outlines the specific investigations of effectiveness of these “passive” approaches. The individuals examined in all 3 case reports reported reductions in lower limb spasticity associated with passive standing despite the fact that different procedures and devices were used across the reports including a tilt table (Bohannon 1993), a standing frame (Kunkel et al. 1993) and a stand-up wheelchair (Shields & Dudley-Javoroski 2005). In addition, a significant number of people have indicated they receive benefit with respect to reduced spasticity in response to surveys about prolonged standing programs. Specifically, Eng et al. (2001) and Dunn et al. (1998) reported that 24% and 42%, respectively, of individuals engaged in this activity find it beneficial in reducing spasticity. However, it should be noted that in each of these studies some individuals also reported an increase in spasticity with this activity (13% and 3% respectively).
The most prevalent therapeutic intervention involving passive movement to reduce spasticity is therapist or caregiver-mediated muscle stretching. Harvey et al. (2009) conducted a RCT (n=20) with blinded assessment in which persons with chronic SCI received 6 months of passive ankle movement (i.e., plantar and dorsi-flexion) on 1 ankle (i.e., experimental condition) but not the other (i.e., control condition.) Although spasticity was only a secondary outcome measure in this trial, there was no apparent benefit of passive movement as indicated by no statistically significant changes in the modified Ashworth scale score (p not reported) for the hamstring and ankle plantar flexors. It should be noted that the participants in this study appeared to have predominately none or only mild spasticity as the initial modified Ashworth scale score ranged from 0 to 2 with a median score of 1. Notably, there were no participants with a score of 2 following treatment and there were subjective reports of reduced spasticity. Unfortunately, no further details were reported about spasticity given that the primary outcome measure for this study was range of motion, for which a 4o improvement was noted between the experimental and control conditions, which was statistically significant (p=0.002) but deemed to not be clinically significant.
Kakebeeke et al. (2005) employed externally applied repetitive cycling movements to the lower limbs with a specifically adapted motorized exercise bicycle. This study employed a prospective controlled design with each subject acting as his or her own control (i.e., cycling vs. no cycling 1 week apart). However, it involved only a single intervention session, not accounting for an order effect and no clinically relevant outcome measures were employed. In addition to a self-report measure of “more”, “less” or “equal” amounts of spasticity, a Cybex II isokinetic dynamometer was used to measure torque resistance to 2 different speeds of knee flexion/extension. The majority of subjects tested (i.e., 6 of 10) reported subjectively that their spasticity was reduced following cycling; however, some subjects (i.e., 3 of 10) also indicated it was reduced following the control (no cycling) condition. No changes were seen for either condition with the objective torque resistance response to movement. Given the mixed results of this study and uncertainty of the clinical relevance of the outcome measures, the findings of this study are deemed equivocal. Motorized cycle has been studied as a continuous intervention in a study by Rayegani et al. (2011) who had subjects using the cycle for 20 minute intervals, three times a day for a 2-month period. This study also utilized relevant outcome measures which identified that the passive cycling group showed a significant decrease (p=0.003) according to the spasticity scale and hip, knee and ankle range of motion also significantly improved.
Although a weaker study design (i.e., Pre-Post Trial), Sköld (2000) did employ clinically relevant outcome measures (i.e., modified Ashworth and a self-report visual analogue scale) and an intervention administered over 6 weeks. This intervention involved the evaluation of standardized, repetitive passive movements of prone and supine hip flexion/extension and lumbar lateral flexion elicited by a motorized table in a subset of subjects with AIS C and D paraplegia. These subjects were drawn from a larger study examining self- vs. clinically-rated spasticity fluctuations. Results of the study indicated that there was a significant reduction in the modified Ashworth Score and also a significant decrease in the self-report measure of spasticity immediately following passive movement. In addition, it was reported that these reductions in spasticity were partially maintained when self-report assessments (but not clinical evaluations) were conducted 4 days following the discontinuation of the intervention.
Passive stretching and active movements conducted with careful attention to postural positioning comprise important elements of the neural facilitation techniques (i.e., Bobath, Rood, Brunnstrom) examined by Li et al. (2007) in combination with Baclofen therapy to reduce spasticity. These investigators utilized an RCT (n=24) of individuals with thoracic SCI to examine the effect of a 6 week course of this combination of therapies to demonstrate significant spasticity reductions (p<0.05) and concomitant increases in ADL independence as compared to traditional rehabilitation approaches. Unfortunately, what constituted “traditional” rehabilitation was not described in this paper, which presumably would constitute stretching and movement, and the relative contribution of Baclofen vs. the neural facilitation techniques was also not assessed so it is uncertain as to the degree of effectiveness associated with these manual techniques.
Lechner and colleagues have conducted two separate investigations demonstrating a short term effect of hippotherapy on decreasing spasticity of the lower extremity (Lechner et al. 2003; 2007). The more rigorous of these studies involved a low n (n=12) crossover RCT during which each subject received twice weekly 25 minute sessions over 4 weeks of a) hippotherapy treatment, b) sitting on a rocker board driven by motor adjusted to mimic a horse’s rhythm and amplitude; c) sitting astride a bobath roll to mimic the postural demands associated with hippotherapy as compared to a similar period of pre-treatment (Control). The results of this study indicated that hippotherapy had a short term effect on decreasing spasticity of the lower extremity, as demonstrated by significant decreases in muscle tone (i.e., reduced Ashworth scores, p<0.05) and self-reported spasticity (p<0.05) in comparison to the other interventions. Significant differences were found when comparing pre- vs. post-session Ashworth Scale scores for all 3 intervention groups (hippotherapy, p=0.004; rocker board, p=0.003; bobath roll, p=0.005) but not for the control condition (p=0.083). In addition, improved mental well-being (i.e., reduced Befindlichkeits-Skalascores) was seen with hippotherapy (p=0.048) but not with sitting on the rocker board (p=0.933) or bobath roll (p=0.497). Neither study showed a carry-over effect from session to session or beyond 4 days (Lechner et al. 2003; 2007). As noted previously, it is difficult to know the primary mechanism for this antispastic effect, although the latter study suggests that it is the combination of sensorimotor stimulation, psychosomatic effects, specific postural requirements and passive and active movements that provide therapeutic benefits as individual aspects of this treatment (i.e., posture or rhythmic movements alone) demonstrated more modest beneficial effects than the full hippotherapeutic approach (Lechner et al. 2007).
Odeen and Knutsson (1981) employed a tilt table on 9 subjects with spastic paraparesis due to spinal cord lesions to examine whether benefits of reduced spasticity with passive activity were due to increased muscle load or muscle stretch. These investigators examined the effect of various conditions on resistance to passive sinusoidal ankle movement by loading the tibialis anterior or gastrocnemius by having the subject stand at an angle of 85º with the ankle dorsi- or plantar flexed by 10-15º or by applying stretch to the gastrocnemius muscles while supine. All procedures tested resulted in reduced resistance to passive movement (i.e., reduced tone or spasticity) with the most significant reductions noted for standing in forced dorsiflexion with load applied (i.e., stretch applied to calf muscles, p<0.001) (Odeen & Knutsson, 1981).
There is level 1b evidence from a single study that passive ankle movements may not reduce lower limb muscle spasticity in persons with initial mild spasticity.
There is level 2 evidence from a single study supported by level 4 evidence from another study that hippotherapy may reduce lower limb muscle spasticity immediately following an individual session.
There is level 2 evidence that electrical passive pedaling systems have an effect on spasticity and hip, knee and ankle range of motion.
There is limited level 1b evidence from a single studythat a combination of a 6 week course of neural facilitation techniques (Bobath, Rood and Brunnstrom approaches) and Baclofen may reduce lower limb muscle spasticity with a concomitant increase in ADL independence. More research is needed to determine the relative contributions of these therapies.
There is level 4 evidence from a single study that rhythmic, passive movements may result in a short-term reduction in spasticity.
There is level 4 evidence from a single study that externally applied forces or passive muscle stretch as are applied in assisted standing programs may result in short-term reduction in spasticity. This is supported by individual case studies and anecdotal reports from survey-based research.
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.