Passive Movement or Stretching

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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 Stretching

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). However, they are 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 three 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; Lechner et al. 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.

Prolonged Standing

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 2 (i.e., other than Odeen & Knutsson 1981) which outlines the specific investigations of effectiveness of these “passive” approaches. The individuals examined in all three 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).

Table 2 Studies of Passive Movement-based Approaches for Reducing Spasticity


The most prevalent therapeutic intervention involving passive movement to reduce spasticity is therapist or caregiver-mediated muscle stretching.

Fang et al. (2015) conducted a crossover RCT using a custom-made robot-assisted passive device for ankle hypertonia in individuals with chronic SCI. Study subjects (n=10) were randomly assigned in a crossover design to one of three interventions: high speed cyclic passive exercise (50 cycles/min), low speed cyclic passive exercise (20 cycles/min), or electrical stimulation-induced contractions (ES) for eight minutes, one time per week for three weeks, with a two week washout between conditions. H-reflexes, M-waves, total resistance during either slow or fast cyclic stretching, or isometric torque were assessed before each intervention and at 10 and 20 minutes after each intervention.

The amplitude of the H reflex was significantly reduced at 10 and 20 minutes post high-speed cyclic passive exercises (p<0.05), and 20 minutes post low-speed cyclic passive exercises (p<0.05) but not after repeated ES-elicited contractions. M-waves did not change with any condition (p>0.05). For study subjects who received ES, and then the high speed cyclic passive exercise, the total resistance during cyclic stretching increased significantly (p<0.05). Isometric torque did not decrease after either low or high speed cyclic passive exercise, although it did after eight minutes of ES along with reduction of reflex excitability which persisted up to 20 minutes (p<0.05). A key finding was that the change in the total resistance was specific to the testing speed in that resistance decreased with the low-speed cyclic stretch test after ES (p<0.05) and after low-speed but not high-speed cyclic passive exercise (p<0.05). For the high-speed cyclic stretch test, the total resistance decreased only after high-speed cyclic passive exercise (p<0.05). Clinical implications are that there may be some specificity related to the intended speed of movement and stretching or exercise (i.e, range of speed of exercises or stretching to reduce spasticity should consider intended range of speed of functional activities). In previous studies, it was observed that MAS scores decreased after one hour of repeated stretching of the ankle joint completed at a relatively high speed in individuals with chronic SCI which is comparable to the reduction of total resistance during the high-speed cyclic stretch test seen in this study.

Chang et al. (2013) conducted an RCT (n=14) to investigate whether five, one hour sessions per week over four weeks of continuous passive motion (CPM) of the ankle could increase post-activation depression (PAD), as measured by pairs of soleus H-reflexes elicited at 0.1 Hz, 1 Hz, Hz and 10 Hz in persons with chronic SCI. Before treatment, the H-reflex was not significantly depressed at 1 Hz or 5 Hz, but was significantly depressed in both groups at 10 Hz (p<0.05). PAD increased significantly (p=0.038) after CPM treatment compared with pretest conditions. MAS scores also decreased significantly (p=0.013) after CPM treatment compared with pretest conditions. The control group did not exhibit significant changes in either PAD or MAS after four weeks. One subject who completed 12 weeks of training displayed further increases in PAD at 1 Hz and 5 Hz stimulation frequencies, but not at the 10Hz stimulation frequency.

Harvey et al. (2009) conducted an RCT (n=20), with blinded assessment, in which persons with chronic SCI received six months of passive ankle movement (i.e., plantar and dorsi-flexion) on one 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 MAS 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 MAS score ranged from zero to two with a median score of one. Notably, there were no participants with a score of two 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 four-degree improvement was noted between the experimental and control conditions. This finding 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 versus no cycling one 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 two different speeds of knee flexion/extension. The majority of subjects tested (60%) reported subjectively that their spasticity was reduced following cycling; however, some subjects (30%) 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 by Rayegani et al. (2011) who had subjects using the cycle for 20 minute intervals, three times a day for a two-month period. This study also utilized a relevant outcome measure (Modified Ashworth) which identified that the passive cycling group showed a significant decrease (p=0.003) in spasticity. Hip, knee and ankle range of motion also significantly improved.

Rayegani et al. (2011) also employed a motorized cycle as part of an RCT (n=74; 10 subjects lost during follow up) to examine the effects on spasticity. Study subjects were randomly assigned to either a passive cycling group (n=37) or a physical therapy group (n=37), which received stretching, ROM and strengthening exercises. The treatment received 20 minutes of passive cycling for three sets per day over two months (# of times per week unspecified). Spasticity was assessed with MAS and electrodiagnostic parameters (H-reflex, H (max)/M (max), and F-wave). MAS scores significantly decreased post-intervention in the passive cycling group (p=0.003), but not with physical therapy. In the passive cycling group, the F/M ratio (p<0.027) and the H max/M max (p=0.001) decreased significantly. The H-reflex amplitude was not significantly different post intervention in either group.

Sköld (2000) employed a pre-post study design along with clinically relevant outcome measures (i.e., MAS, VAS) to assess the effect of standardized, repetitive passive movements of prone and supine hip flexion/extension and lumbar lateral flexion elicited by a motorized table in persons with AIS C and D paraplegia. These subjects were drawn from a larger study examining self- versus clinically-rated spasticity fluctuations. There was a significant reduction in the MAS and also a significant decrease in the self-report measure of spasticity immediately following passive movement. In addition, these reductions in spasticity were partially maintained as indicated by self-report assessments (but not clinical evaluations) conducted four 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 six-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 versus the neural facilitation techniques was also not assessed so it is uncertain as to the degree of effectiveness associated with these manual techniques.

Lechner et al. (2003 and 2007) have conducted two separate investigations demonstrating a short-term effect of hippotherapy on decreasing spasticity of the lower extremity. The more rigorous of these studies involved a small sample (n=12) crossover RCT during which each subject received twice weekly 25 minute sessions over four 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-versus post Ashworth Scale scores for all three intervention groups (i.e., 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-Skala scores) 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 four days (Lechner et al. 2003; Lechner et al. 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 nine 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 10-15 degrees 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 one RCT; Fang et al. 2015) that passive ankle movements may not reduce lower limb muscle spasticity in persons with initial mild spasticity.

There is level 2 evidence (from one RCT; Lechner et al. 2007) 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 study that 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.