Systematic Review of the Management of Spasticity after Spinal Cord Injury, 2000 – 2010
Conducted by the Center for Psychiatric Rehabilitation with support from the National Institute on Disability and Rehabilitation Research.
Table of Contents
Plain language summary
Methods and procedures
Summary and conclusions
Acknowledgements and statement concerning conflict of interest
The Management of Spasticity after Spinal Cord Injury systematic review and narrative synthesis involved collecting and rating research information for rigor and meaning. The Shepherd Center Study Group used the Quality of Disability Research Instruments (Farkas, Rogers, & Anthony, 2008) to rate the rigor and meaning of disability research. The QDRI comprises two instruments: Standards for rating the rigor of program evaluation, policy or survey research, pre–post and correlational human subjects (Rogers, Anthony, Kash, & Farkas, 2008) and Standards for rating the meaning of disability research (Farkas & Anthony, 2008).
A complete list of contributors is contained in the Contributors section.
Spasticity is a fairly common problem in persons who sustain a spinal cord injury (SCI). The muscles in the arms, legs, and the trunk are often painful, resistant to movement, difficult to control, and prone to spasms or involuntary movements. Spasticity may be used to help with transfers and walking, or may help keep the muscles from decreasing in size. Muscles may appear to be healthier after SCI. However, there are problems that result from spasticity. Long-term spasticity can lead to decreased range of motion (ROM), prevent safe positioning, limit mobility, and impede hygiene. Spasticity can also lead to increased discomfort and pain.
Treatment for spasticity includes management with drugs as well as physical or occupational therapy (rehabilitation) approaches, surgery, and alternative medicine approaches (such as massage and acupuncture). Drugs that are commonly used include baclofen and dantrolene. Physical and occupational therapy generally focuses on ways to inhibit or decrease the spasticity, such as prolonged stretching and ROM exercises, casting or splinting, and the use of electrical stimulation and transcutaneous electrical nerve stimulation (TENS). Surgery may be needed if these treatments do not alleviate the spasticity or the problems associated with the spasticity. Surgery entails cutting pathways in the nervous system that are thought to be involved in spasticity. There are ongoing studies on other forms of electrical stimulation of the spinal cord (epidural spinal cord stimulation) and brain (transcutaneous magnetic stimulation).
Even though these treatments are routinely used to decrease spasticity, many persons with SCI continue to have problems related to spasticity. More than half of all persons surveyed with chronic SCI report symptoms of spasticity (Skold, 2000; Maynard, Karunas, & Waring, 1990). Persons with cervical and incomplete injuries (some motor function below the level of injury) seem to have spasticity more often and spasticity that is more severe.
Spasticity is actually a combination of problems. Specifically, spasticity is not just resistance to movement when an arm or leg is moved quickly. Some persons with spasticity also have spasms and clonus (repeated movement of a body part when positioned with the muscle stretched). It is not yet clear which treatment is best for these different aspects of spasticity. Furthermore, the literature related to spasticity has not been evaluated in terms of what is meaningful to persons with SCI.
The main purpose of this review was to evaluate all published research from the past 10 years related to the management of spasticity after spinal cord injury to determine which evidence may be meaningful to persons with SCI who have spasticity (e.g., level and completeness of injury) and that may be related to any type of spasticity a person may experience (increased reflexes, increased resistance to passive stretch, resistance to fast movements, clonus).
Seven clinicians assisted with this review. They identified and reviewed all articles published between 2000 and 2010 related to the treatment of spasticity in persons with SCI. They rated all articles on the quality of the science as well as the authors’ discussion of the meaningfulness of their research to persons with SCI, their caregivers and clinicians, or the payers. Any article that was rated as both of high quality and meaningful was considered for this summary. Forty-nine articles were considered for review, but only seven met the criteria for both meaning and quality; they are discussed in this report.
Two of the seven studies used randomized controlled trials—people were recruited for these studies and then randomly put into one of two groups: one that received the treatment or one that did not. Both studies used electrical stimulation for the treatment. One stimulated a nerve in the leg, and one stimulated the brain. The interesting finding from these two studies is that both uses of electrical stimulation led to a significant decrease in resistance to fast movements, clonus, and stretch reflex components of spasticity in persons with acute or chronic, motor complete or incomplete, paraplegia or tetraplegia. The study that used stimulation to the nerve in the leg also led to a decrease in muscle spasms. Further study is needed to see if these two types of treatment with electrical stimulation will work in the same ways for persons with different levels and completeness of injury.
Two of the studies used a different approach to assess the effects of electrical stimulation on spasticity in persons with SCI. They used a descriptive study design, collecting data at certain points from all persons in the study.
- One study evaluated the effects of epidural spinal cord electrical stimulation (SCS) for decreasing spasticity in persons with SCI.
- The other compared the effects of functional electrical stimulation (FES) cycling and passive cycling to evaluate which form of treatment would lead to the greatest decrease in spasticity. All study participants trained first on the FES cycle, and later on the passive cycle. Before and after each of these sessions, the researchers collected data related to their spasticity. There were no changes related to the passive cycling, but there were changes related to the treatments using electrical stimulation.
These studies revealed that both those who received spinal cord stimulation and those who trained on an FES cycle experienced decreased reflexes and decreased resistance to passive movement of their legs.
The findings from these four studies of different types of electrical stimulation suggest an interesting and powerful effect of electrical stimulation on disordered motor control in persons with SCI. Further study is required, however, to determine which technique confers greatest benefit—and which does not—in order to provide guidelines regarding the best intervention a for a person with SCI should to pursue.
Whole body vibration (WBV) is an intervention that has been explored more frequently in recent years in persons with SCI and spasticity. Whole body vibration involves a person standing or sitting on a plate that vibrates. The investigators who studied the effects of WBV on spasticity simply measured and described (using a descriptive study design) the effects of whole body vibration in 16 persons with chronic, motor incomplete American Spinal Injury Association Impairment Scale (AIS) C or D spinal cord injury. Some participants were using anti-spasticity medications before enrollment and continued with the medications during the study. All participants had to be able to stand with no more than moderate assistance for four 45-second bouts of vibration, with 1 minute of seated rest between each bout. The participants received WBV 3 days a week for 4 weeks. The only measure used related to quadriceps spasticity.
Most (11 of 16) of the participants in the study had some benefit from the whole body vibration, meaning that they experienced at least minimal reduction in quadriceps spasticity. Seven of the 16 participants had a significant decrease in spasticity, and 4 had a moderate decrease. This reduction in quadriceps spasticity was evident for up to 6 to 8 days after WBV. Participants on anti-spasticity medications and those who were not taking these medications experienced similar reductions in spasticity. Further study is needed to determine the full effect of WBV on spasticity in persons with different levels and completeness of SCI, as well as the functional effects of these changes in spasticity. In addition, because one third of the participants received little to no benefit from the WBV, further study is necessary to determine why certain persons with SCI benefited and others did not.
The final study in this review evaluated the effects of different doses (amounts) of oral and intrathecal baclofen therapy (ITB) in one person with spasticity, and also focused on determining if there is a relationship between decreasing spasticity and a person’s strength. The participant in this study was a 41-year-old man with chronic, motor incomplete (AIS D) T 11 paraplegia. Dosages included 80 mg of oral baclofen at baseline; 80 mg oral/50 µg ITB on Day 3; 80 mg oral/125 µg ITB on Day 5; 30 mg oral/125 ITB µg on Day 8; and 125 µg only ITB on Day 19. The investigators measured the resistance to passive movement and the hyper-reflexia components of spasticity after the person had taken each of these doses of baclofen. The participant demonstrated a dose-dependent change in spasticity, spasm strength, and flexion withdrawal reflex, suggesting that at different doses there were different responses on the tests. However, the study also found that even though spasticity was decreased, there was not a decrease in strength. These findings are similar to other reports showing that baclofen is effective for decreasing spasticity in persons with SCI. What is meaningful is that this reduction did not come at the expense of muscle strength in this one person with motor incomplete SCI.
Spasticity in SCI appears as several different aspects of motor function. The syndrome involves hyperactive reflexes, resistance to stretch, muscle spasms, and clonus. Some research shows that there are also changes in the muscle in persons with spasticity, suggesting that measuring the effects of treatments on the muscle itself is also important. The studies reviewed here include persons with both acute and chronic SCI. Those with chronic SCI may well have changes in their muscle due to chronic, long-term spasticity, yet the muscle was not studied in any of these studies. Therefore, it is not clear how these interventions affected the muscle. Further study is needed to see if these interventions have long-term effects and if they include both neural and muscle effects. Improving one and not the other may limit improvements.
Second, because none of the authors included functional outcome measures in their studies, the impact of these changes in spasticity on function remains unclear. At this point, whether reducing spasticity is necessary and sufficient for improving movement in persons with SCI, and thus improving function, remains unclear.
Finally, some reports indicate that the spasticity syndrome actually may be worse in people with cervical level injury than in those with thoracic and incomplete injury. All the studies reviewed here include both persons with paraplegia and those with tetraplegia. The results are reported for the groups as a whole. Therefore, it is not clear whether persons with different levels of injury have different responses. Further study is warranted to determine the responses of those with different levels and classifications of SCI.
Summary and Conclusions Related to the Management of Spasticity in Persons with Spinal Cord Injury
The evidence presented in this review suggests that electrical stimulation interventions applied either peripherally or centrally may lead to a reduction in certain aspects of spasticity in persons with different levels and completeness of SCI: acute or chronic, complete or incomplete, tetraplegic or paraplegic. In addition, there is minimal evidence to suggest that whole body vibration may reduce at least one component of spasticity, hyper-reflexia in the quadriceps, in these same individuals. Finally, there is promising evidence that baclofen, while reducing spasticity, may not decrease strength or function. Further study is warranted in all these areas, with a focus on determining the most beneficial timing and dosage of each intervention, the varying effects on the different aspects of the spasticity syndrome after SCI, and the varying effects in persons with different levels and completeness of SCI.
The limitations in these studies suggest that any stakeholder interested in the evidence related to the management of spasticity should first consider that none of these studies used the same measures, and that different aspects of spasticity may be affected by a given intervention. For example, if spasms are the worst aspect of spasticity in a person with SCI, they may be more inclined to pursue an intervention such as brain stimulation (transcranial magnetic stimulation [TMS]), spinal cord stimulation, or baclofen, all of which have been shown to reduce spasms in persons with SCI. On the other hand, those with velocity-dependent resistance to stretch may be able to use interventions such as transcutaneous electrical nerve stimulation (TENS) or TMS, but TMS may give the best results overall if there are multiple areas related to spasticity that continue to be a problem. However, how each intervention affects the spasticity in persons with different levels and completeness of injury is not clear from these studies, and any person pursuing these interventions should be aware of this.
Finally, it is not clear if the muscle consequences of spasticity will be affected by any of these interventions because this was not included in any of the outcome measures for these studies. Neural changes without accompanying muscle changes may preclude functional improvements. Persons with SCI who want to treat spasticity should consult with their physicians and therapists to diagnose which type of spasticity they have in order to determine the most effective treatment for their needs.
Deborah Backus, PhD, PT
Associate Director SCI Research
2020 Peachtree Rd, NW
Atlanta, GA. 30075
Shepherd Center Systematic Review Group
Deborah Backus, PhD, PT
David Apple, MD
Lesley Hudson, MA
Jennith Bernstein, PT
Amanda Gillot, OT
Ashley Kim, PT
Elizabeth Sasso, PT
Kristen Casperson, PT
Anna Berry, PT
Liz Randall, SPT
|AIS||American Spinal Injury Association Impairment Scale|
|ASIA||American Spinal Injury Association|
|CSS||composite spasticity score|
|IBT||intrathecal baclofen therapy|
|MAS||Modified Ashworth Scale|
|MPSFS||Modified Penn Spasm Frequency Scale|
|RCT||randomized control trial|
|ROM||range of motion|
|rTMS||repeated transcranial magnetic stimulation|
|SCAT||Spinal Cord assessment Tool|
|SCI-SET||Spinal Cord injury Spasticity Evaluation Tool|
|SCS||spinal cord electrical stimulation|
|SCI||spinal cord injury|
|TENS||transcutaneous electrical nerve stimulation|
|TMS||transcranial magnetic stimulation|
|VAS||visual analog scale|
|WBV||whole body vibration|
Rationale for the Review.
Spasticity after spinal cord injury (SCI) is a common, complicated, and often frustrating impairment that is generally considered both a “health” problem (Taricco, Pagliacci, Telaro, & Adone, 2006) and a deterrent to function and quality of life (Adams & Hicks, 2005). Various investigators strive to understand the underlying mechanisms of spasticity as well as the most efficacious way to treat spasticity in persons with sensory and motor dysfunction due to SCI. Much work has led to a definition of spasticity that can be used to guide studies of the pathophysiology and management of SCI. The classical definition of spasticity, as provided by Lance (1980), is a velocity-dependent resistance to stretch that includes both a tonic component, i.e., increased muscle tone, and a phasic component, i.e., increased tonic reflexes. This definition has been expanded to include hyperactive tendon reflexes, as well as clonus and spasms (Katz, Rovai, Brait, & Rymer, 1992; O’Dwyer, Ada, & Neilson, 1996).
While frustrating for some, the presence of spasticity can be viewed as beneficial for others. For instance, spasticity can aid in maintaining muscle bulk and blood circulation, both of which can prevent pressure sores. Spasticity can also be used to aid in mobility, such as for transfers and walking. However, the less desirable effects of spasticity, such as decreased range of motion (ROM), interference with positioning, mobility, and hygiene, and increased discomfort and pain often outweigh those that are beneficial, making intervention necessary. Clinical interventions include pharmacological approaches, as well as rehabilitation, surgical, and alternative medicine approaches. Pharmacological approaches include the use of oral medications that act within the central nervous system, such as baclofen, or that act directly on skeletal muscle, such as dantrolene (see Taricco et al., 2006 for review). Rehabilitation approaches mostly focus on inhibiting or modulating the spasticity and include prolonged stretching and ROM exercises, inhibitory strategies such as casting or splinting, and the use of electrical stimulation such as subthreshold sensory stimulation and transcutaneous nerve stimulation (TENS). Surgical approaches may be explored if the spasticity is resistant to any of these pharmacological or rehabilitation approaches and may include surgical rhizotomy or myelotomy. Alternative medicine approaches such as massage and acupuncture are often sought when these other interventions are not fruitful. Finally, experimental approaches are being investigated that include other forms of electrical stimulation to modulate neural activity, such as epidural electrical stimulation and cortical transcranial magnetic stimulation (TMS).
Despite these clinical and experimental approaches to the management of spasticity after SCI, persons with SCI continue to report difficulties with the appropriate management of the resulting impairments and continue to seek out ways to manage the spasticity. More than half of all persons surveyed with chronic SCI report symptoms of spasticity (Skold et al., 1999; Maynard et al., 1990). Furthermore, not all persons with SCI experience the same intensity and distribution of spasticity. Skold and colleagues (1999) reported that persons with cervical and incomplete injuries (International Standards of Spinal Cord Classification, American Spinal Injury Association Impairment Scale (AIS) ratings C or D experience spasticity most frequently and report greater fluctuations in their spasticity than those with thoracic injury. These findings suggest that the underlying pathophysiology may not be the same in persons with complete and incomplete injuries or with injuries at different levels of the spinal cord. For instance, those with incomplete injuries may be at a greater risk for spasticity due to the “noise” that may remain in the system with present but poorly functioning circuitry. Likewise, those with cervical level of injury may have exacerbated symptoms due to the autonomic dysfunction that accompanies higher levels of injury.
Although there have been recent reviews of the literature pertaining to the management of spasticity in persons with SCI (Adams & Hicks, 2005; Bovend’Eerdt et al., 2008; Taricco et al., 2006), two important questions remain. One pertains to the effects of any intervention on the various components of spasticity (e.g., hyper-reflexia, increased resistance to passive stretch, velocity-dependent resistance to stretch, clonus). For instance, does a specific treatment affect the tonic or phasic aspects of spasticity, or perhaps the hyper-reflexia and clonus? There also remains the question of which interventions are most useful or meaningful to any given person with SCI. Neither Adams and Hicks (2005) nor Taricco et al. (2006) were able to identify which interventions would be best for any given person. Furthermore, both acknowledged the poor quality and lack of standardization of outcome measures for studies exploring the various interventions for managing spasticity. Both report that, in general, the most conservative approach, regardless of level or completeness of injury, is to start with rehabilitation approaches, often combined with pharmacological approaches. Unfortunately, which are the best interventions for any given person is not yet clear.
Objectives of the Review
The main objective of this review was to evaluate all literature over the last 10 years (2000–2010) related to the management of spasticity after SCI to determine which evidence might be meaningful to any given person with SCI experiencing spasticity (e.g., level and completeness of injury) and might be related to any variety of spasticity a person may experience (hyper-reflexia, increased resistance to passive stretch, velocity-dependent resistance to stretch, clonus). Although there have been recent reviews related to the management of spasticity (Adams & Hicks, 2005; Bovend’Eerdt et al., 2008; Taricco et al., 2006), these have not taken into consideration one of the key elements of review endorsed by Rogers, Farkas, Anthony et al. (2008), namely, the meaning to the stakeholders.
The assumption for this systematic review was that important and significant literature has been published related to management of spasticity after SCI. This study group felt that the methods employed by the Supported Housing Study Group (E. Sally Rogers, Marianne Farkas, William Anthony, Megan Kash, Courtenay Harding, and Annette Olschewski at the Center for Psychiatric Rehabilitation at Boston University) would be useful for examining how spasticity is managed in persons with SCI in the existing literature and how this information might be meaningful to the stakeholders related to SCI (patients, caregivers, clinicians, educators, administrators of programs, and payers).
The secondary objective of this review was to develop and disseminate products that will inform consumers related to SCI about the efficacy of methods for managing spasticity in persons with SCI.
The methods employed for this systematic review were defined by the Supported Housing Study Group at the Center for Psychiatric Rehabilitation and modified only slightly to accommodate the needs of the SCI field and the literature available in the SCI field.
The following search terms were used:
- spasticity management
- pharmacological management
- physical therapy
All terms were paired with spinal cord injury or SCI, paraplegia, tetraplegia, and quadriplegia. The following websites/tools were explored with the search terms identified above:
- Search engines:
- Pubmed (Medline)
- Google Scholar
- Cochrane Reviews
- The citations contained in each article for additional potential articles and reports
The following types of studies/publications/documents were included in the primary review:
- policy statements
- needs assessments
- instruments related to outcome measures
- therapy satisfaction or quality of life studies
- program models
- conceptual models
- process evaluations
- reviews (included instead in the background)
Although such documents, as well as conference proceedings, dissertations, or government proceedings are important for the field, they were not included in the final review because they could not be subjected to ratings for their rigor and their meaning. Articles that discuss management of spasticity in patient populations other than SCI are not discussed here.
All studies published in the 10 years prior to the date of the systematic review (2000–2010) were included in this review. The lead reviewer queried the databases, located articles, and scanned the titles and abstracts of articles for relevance to management of spasticity in persons with SCI. If the title appeared relevant, the abstract was reviewed, and if it was deemed likely to meet inclusion criteria, the article was obtained.
The following study designs were accepted for this review:
- Experimental: Employed methods including a random assignment and a control group or a reasonably constructed comparison group.
- Quasi-experimental: No random assignment, but either with a control group or a reasonably constructed comparison group.
- Descriptive: Neither a control group nor randomization is used. These included case studies and reports, studies employing repeated measures, and pre-post designs.
Studies that were poorly described, or poorly defined, planned, and executed were deemed too difficult to determine the study design and were not accepted.
Training of Reviewers.
Seven clinicians assisted in this systematic review. All were affiliated with Shepherd Center, including the co-investigators of the SCI Model Systems grant and the associate director of SCI Research. Six of the clinicians participated in earlier systematic reviews, and one additional reviewer was added to this group and trained. Training of the reviewers focused on the goals of this review, how to perform a systematic review (using the guidelines set forth by Rogers and Farkas), the kind of evidence indicating rigor in research, and the criteria that would be used to determine if an acceptable rating for rigor and meaning had been achieved at each of the points on the respective rating scales. All persons were trained in the use of the rigor and meaning rating scales by reviewing each item in the scale and discussing the meaning of the item and the evidence that could be considered for each indicator.
Research articles were used as training devices by having each rater independently review articles and then discuss their ratings until agreement was achieved. Inter-rater reliability was established through two separate joint ratings of articles over the course of the review period. Each reviewer independently reviewed the same article for both meaning and rigor, and then the group met as a whole to review these ratings. When reviewers did not agree on a rating (the typical variation being only 1 point on a 4-point scale), these were discussed. Consensus was achieved by the group in 100% of the cases where there was originally a discrepancy, and the lead reviewer did not need to intervene or request further review by an additional outside reviewer.
The methodology employed by the Supported Housing Group considered both meaning and rigor of the studies reviewed. Meaning was determined based on the meaningfulness or perceived relevance of research information. The scale is divided into three major sections:
- meaningfulness derived from the conduct or design of the research,
- meaningfulness derived from the identification of the implications for use, and
- meaningfulness derived from the identification of support that is currently available to put the findings into use.
The scale accounts for the fact that meaningfulness is a subjective term and is difficult to rate in a standardized format. Therefore, the main determinant of meaning is based on the concept that research articles and reports should provide information to allow readers to make a determination about the usefulness and applicability of the findings for their own situation.
For “overall meaning,” individual items were scored on a yes or no basis—either the information was present or it was not. Then the number of Yes answers was tallied, and a level of meaning was assigned based on that number. The highest level that could be reached was Level 5. If all three sections had at least two indicators checked Yes, the overall rating was Level 5; if all three sections had at least one indicator checked Yes, the overall meaning was Level 4; if two out of three sections had at least one indicator checked Yes, the overall meaning was Level 3; if one out of three sections had at least one indicator checked Yes the overall meaning was Level 2. Finally, if no sections had a Yes checked, the overall meaning was Level 1. Only articles with a rating of Level 3, 4 or 5 were determined to have meaning.
The rigor scale ranged from a score of 1, which corresponded to no rigor or meaning, to a score of 4, which corresponded to excellent rigor or meaning. “Overall rigor” was determined first by the rating on the item that scored the overall methodology for the study: “Study/research uses rigorous or sound research methods that allow the questions of interest to be addressed.” This score had to be a 3 or 4 in order for the article to be considered “rigorous” for this synthesis. Then the overall average score was compared to the rating on this item. When there was a discrepancy (i.e., the average score indicated either greater or lesser rigor than the score on the overall methodology item), the lead reviewer examined the cause and sought out an additional reviewer for that article. The review from the original reviewer and the lead reviewer were then compared, and the lead reviewer determined the overall score. The articles that were deemed to be rigorous and meaningful were summarized for this review. In one case, the lead reviewer determined that an article did not meet the criteria for rigor, although the first reviewer had indicated a rigor rating of 3. Because the lead reviewer could not determine the methodology in enough detail for summarizing the study, this article was not included in the final summary.
Summary of Articles Reviewed
Forty-nine articles were considered for review. After various inclusion and exclusion criteria were considered, 30 articles were rated for rigor and for meaning; 20 of these met the criteria for rigor (as defined above), and 13 met the rating for meaning. When both rigor and meaning were considered, only seven met the criteria for both meaning and rigor and are discussed in this report.
Only two articles were classified as experimental, employing a randomized controlled trial. Five articles reviewed were classified as descriptive. Table 1 summarizes the studies, including authors, study design, type of intervention, and the number and characteristics of the study participants. None of the studies reported on the management of spasticity in children. All seven articles included persons with chronic SCI, and two of these also included those with acute injury (less than 1 year post-SCI). Five studies included those with motor incomplete injuries, AIS C and D (International Standards of Classification of Spinal Cord Injury [Taricco et al., 2006]), and four included those with motor complete (AIS A and B) classification. The interventions included pharmacological approaches as well as rehabilitation approaches (transcutaneous electrical nerve stimulation or TENS, epidural electrical stimulation, whole body vibration, and passive cycling). All studies evaluated the effects of the respective interventions on spasticity in the lower extremities, and none reported on effects in the upper extremities.
|n||Design||AIS||Acute (A), Chronic (C), Both (B)||Findings|
Chung & Cheng 2010
|18||RCT||A, B, C, D||B||Decreased spasticity (p = 0.017)
Decreased resistance to passive motion (p = 0.024)
Decreased clonus (p = 0.023)
Kumru et al. 2010
|15||RCT||C, D||B||Decreased MAS (p = 0.006)
Decreased MPSFS (p = 0.01)
Decreased SCAT (p = 0.04)
Maintained at 1 week post-intervention
Bowden & Stokic 2009
|1||D||D||C||Dose-dependent decease in spasticity (p = 0.01)
Decreased strength, less than decrease in spasticity (p = 0.001)
Decreased flexion withdrawal
|Passive LE ergometry
Kakebeeke, Lechner, & Knapp 2005
|10||D||A, B||C||6/10 reported subjective decrease in spasticity; no other significant changes|
|FES & Passive LE Ergometry
Krause, Szecsi, & Straube 2008
|5||D||A||C||FES > Passive ergometry
Decreased MAS (FES p = 0.001; Passive p = 0.05)
|Whole body vibration
Ness & Field-Fote 2009
|16||D||C, D||C||Decreased PSFS (p = 0.005)
Decreased MAS (p = 0.0117)
Maintained 6–8 weeks
Pinter et al. 2000
|8||D||A, B, C||C||Decreased amplitude on EMG left (p = 0.004), right (p = 0.0035)|
Only three of the studies defined “spasticity” in their articles (Bowden & Stokic, 2009; Kumru et al, 2010; Ness & Field-Fote, 2009). The other four did not provide any definition in either the introduction or the discussion. Table 2 provides the definitions as well as the aspects of spasticity that were assessed in each study. All but one study (Ness & Field-Fote, 2009) assessed the velocity-dependent resistance to stretch, part of the classical definition of spasticity (Lance 1980).
|Study||Definition of spasticity provided||Aspect of spasticity measured|
|Chung & Cheng 2010||None provided||Velocity-dependent resistance to stretch
|Kumru et al. 2010||“…a symptom of upper motor neuron syndrome, characterized by an exaggeration of the stretch reflex, spasms, and resistance to passive movement across a joint, secondary to hyperexcitability of spinal reflexes.”||Velocity-dependent resistance to stretch
Passive resistance to stretch
Spasms – frequency & severity
|Bowden & Stokic 2009||“…a motor disorder characterized by a velocity-dependent increase in tonic stretch reflex with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex, as one component of upper motor neuron syndrome”
“…include clonus, involuntary muscle contractions or spasms, and muscle co-contraction.”
|Passive resistance to stretch
Spasms: frequency & severity
|Kakebeeke, Lechner, & Knapp 2005||None provided||Velocity-dependent resistance to stretch|
|Krause, Szecsi, & Straube 2008||None provided||Passive resistance to stretch
Stretch reflex/quadriceps hyperreflexia
|Ness & Field-Fote 2009||“…spastic hypertonia with increased reflex excitability and disordered motor output (i.e., spasticity, clonus, spastic gait patterns)…”||Stretch reflex/quadriceps hyperreflexia|
|Pinter et al. 2000||None provided||Passive resistance to stretch
Stretch reflex/quadriceps hyperreflexia
Experimental Design Studies
Two of the seven studies reviewed used a randomized controlled trial (RCT). Chung and Cheng (2010) used an RCT design to determine how the application of transcutaneous electrical nerve stimulation (TENS) would affect lower extremity (LE) spasticity in persons with acute or chronic, complete or incomplete American Spinal Injury Association Impairment Scale (AIS) A, B, C, D, tetraplegia or paraplegia. Participants were randomized into one of two groups: an active TENS treatment group and a sham TENS group. The active TENS group received high-frequency, low-intensity (15mA, pulse width 0.25 ms, pulse frequency 100Hz) TENS for 60 minutes; no muscle contraction was elicited in the LE. The control group had the same application of TENS; however, the unit was never turned on. Thus, the authors could also determine if there was a placebo effect. The study recruited 18 participants with an SCI who also had noted LE spasticity, and the LE with the most severe spasticity was treated. Two electrodes were placed over the common peroneal nerve. Outcomes measures included the assessment of the amount of spasticity prior to and immediately post TENS application using the Composite Spasticity Score (CSS) (Levin & Hui-Chan, 1992) and the Ashworth Scale (Ashworth, 1964). The CSS includes measure of the phasic component of spasticity, assessing the Achilles tendon jerk, the resistance to ankle dorsiflexion, and ankle clonus. The Ashworth scale measures the resistance to passive stretch. Therefore, the authors studied the velocity-dependent resistance to stretch, clonus, and the stretch reflex.
The results of this study are summarized in Table 1. Most notably, the TENS group demonstrated significant reductions in CSS (29.5%, p = 0.017), and reductions in resistance to full passive range ankle dorsiflexion (31%, p = 0.024), and ankle clonus (29.6%, p = 0.023). These findings suggest that the application of 60 minutes of high-frequency, low-intensity TENS to the common peroneal nerve supplying the ankle dorsiflexors will lead to a reduction in the tonic and phasic components of spasticity of the ankle plantar flexors as well as clonus. Because there were no longer-term outcome measures, it is not known whether this reduction is maintained over time. All participants were grouped into one group, thus it remains unclear if persons with different levels or completeness of injury had differential responses to the TENS intervention.
Kumru et al. (2010) focused on determining if repetitive transcranial magnetic stimulation (rTMS) of the primary motor cortex would reduce LE spasticity in 15 persons with acute or early chronic (up to 17 months post-SCI), motor incomplete (AIS C or D) SCI. In this RCT, the researcher and participants were blind to the intervention. Participants were randomized to one of two groups: one group receiving real rTMS and one group receiving sham rTMS. Participants in the real rTMS group received rTMS for 20 minutes each morning for 5 consecutive days. The sham group received the sham rTMS for the same amount of time. The authors used the following outcome measures to measure spinal spasticity: the Modified Ashworth Scale (MAS), a Visual Analogue Scale (VAS), Modified Penn Spasm Frequency Scale (MPSFS), Spinal Cord Assessment Tool for Spasticity (SCAT), and the Spinal Cord Injury Spasticity Evaluation Tool (SCI-SET). These outcome measures are defined in Table 3. Neurophysiological measures were collected using electromyography (EMG) in the LE to assess the H-max to M-max ratio, as well as muscle activity during the T reflex and withdrawal reflex. Thus, the investigators measured the tonic and phasic aspects of spasticity as well as hyper-reflexia, spasms, and clonus.
|Ashworth Scale/Modified Ashworth Scale (MAS)||Measures the resistance of a muscle during passive movement with a 5-point scale ranging from 1 (no increase in tone) to 5 (limb rigid in flexion or extension).|
|Composite Spasticity Score (CSS)||Scores from a spasticity measure are summed to obtain one number, e.g., summing the MAS values for the elbow, wrist, and fingers.|
|Electromyography (EMG)||Surface electrodes are used to measure the activity of the muscles.|
|Pendulum Test||Measures quadriceps spasticity. The patient is seated or lying with the lower leg hanging over the edge of the surface; the leg is extended to horizontal, and the patient told to relax. The leg is released and allowed to swing. The swing of the leg about the knee joint is assessed.|
|Penn Spasm Frequency Scale (PSFS)||A two–part self-report measure of the frequency of muscle spasms that is commonly used to quantify spasticity. Part 1 is a 5-point scale assessing frequency. Part 2 is a 3-point scale assessing the severity of the spasms.|
|SCI Spasticity Evaluation Tool (SCI-SET)||A 7-day self-report questionnaire of the effects of spasticity on daily life in people with SCI|
|Spinal Cord Assessment Tool for Spasticity (SCAT)||A physiologically based measure to assess three types of spastic motor behaviors in SCI patients: clonus, flexor spasms, and extensor spasms.|
|Withdrawal reflex||A noxious stimulus is used to stimulate the dorsum of the foot to evaluate the spasm or spasticity that is elicited.|
There were no significant changes in any of the outcome measures after the sham rTMS. Furthermore, the neurophysiological measures did not change in either group. However, the MAS score, the MPSFS, SCAT, and VAS were all improved significantly (see Table 1 for p values) in the rTMS group. The improvements in the SCAT and MAS were maintained one week after the last session. All but one participant reported significant improvement in VAS one week after the intervention. None of the scores were significantly different between those with traumatic and those with non-traumatic SCI. Finally, two participants that received the rTMS reported decreased pain after the last session. Those participants who were in the sham group and later received the rTMS treatment demonstrated the same improvements as those who received the rTMS treatment initially. These findings suggest that persons with acute or early chronic SCI may benefit from rTMS by experiencing decreases in both the tonic and the phasic aspects of spasticity. The data from all participants was grouped, so how persons with different levels and completeness of injury respond to the rTMS intervention was not elucidated.
Conclusions from Experimental Design Studies
The interesting finding from these two studies is that in both cases electrical stimulation applied to peripheral structures (i.e., the common peroneal nerve or the nerve innervating the muscle antagonistic to the spastic muscle) (Chung & Cheng, 2010) and to central structures (i.e., over the primary motor cortex) (Kumru et al., 2010) led to a significant reduction in the velocity-dependent resistance to stretch, clonus, and stretch reflex components of spasticity in persons with acute or chronic, motor complete or incomplete, paraplegia or tetraplegia. Although the investigators exploring the effects of TENS (in & Cheng) did not evaluate the effects on spasms or stiffness, it is possible that the findings would be similar to those in the study that employed the rTMS (Kumru et al.), specifically that there would also be improvements in these parameters after common peroneal nerve stimulation. Further study is warranted to explore the effects of both peripheral and central electrical stimulation interventions in persons with SCI to determine the most efficacious approach to long-term reduction in spasticity, and specifically for persons with different levels and completeness of injury.
Two studies using a descriptive study design explored the effects of other forms of electrical stimulation on LE spasticity in persons with SCI (Pinter, Gerstenbrand, & Dimitrijevic, 2000; Krause, Szecsi, & Straube, 2008). Pinter and colleagues (2000) explored the efficacy of epidural spinal cord electrical stimulation (SCS) in reducing spasticity in the LE of persons with SCI. The study had eight participants with chronic, C5 to T6, AIS A, B, or C SCI. All participants underwent a surgical procedure to have an electrode placed in their lumbar spine. EMG was used during the Pendulum Test to measure the effects of spasticity on passive movements in the quadriceps. The authors also had an independent physiotherapist assess spasticity using the MAS. Thus, the investigators only evaluated the effects of SCS on hyper-reflexia of the quadriceps and passive resistance to stretch in the entire LE.
Six out of the eight participants showed a significant improvement in hyper-reflexia and the passive resistance to movement with long-term continuous SCS (see Table 1 for p values). The other two participants showed a moderate improvement in these parameters of spasticity with long-term continuous stimulation. The investigators recommend that the electrode should be placed on the upper dorsal roots during stimulation in persons with severe spasticity. On the other hand, those with mild spasticity may benefit more from an electrode placement that is below the level of the injury. Of note, only one participant continued to require anti-spasticity medication at the completion of the study, and all others discontinued anti-spasticity medication. Although this study employed outcome measures that were slightly different from those in the other studies exploring the effects of interventions using electrical stimulation (Chung & Cheng, 2010; Kumru et al., 2010), there were also improvements here as when the spinal cord was stimulated, thus supporting the use of electrical stimulation for the management of spasticity. Further research is necessary to compare the effectiveness of these peripheral and central approaches of application of electrical stimulation in persons with different levels and classifications of SCI.
Krause and colleagues (2008) evaluated the efficacy of functional electrical stimulation (FES) cycling and passive cycling using a descriptive cross-over design. Five participants with chronic, sensory, and motor complete (AIS A) paraplegia (T3 to T7) first participated in FES cycling. The parameters for cycling were determined during the FES cycling session (i.e., the duration and rpm for cycling) so that these same parameters could be used during the passive training sessions. Outcome measures were collected immediately before and within 30 minutes of completion of the cycling and included the MAS and the Pendulum Test.
There was a significant reduction in spasticity (i.e., the hyper-reflexia of the quadriceps) during the Pendulum Test after the FES cycling and not after the passive cycling. However, the MAS decreased significantly for both sessions, but more so for the FES cycling session than the passive session. These findings, along with those from Pinter et al. (2000), Chung and Cheng (2010), and Kumru et al. (2010), suggest an interesting and powerful effect of electrical stimulation on disordered motor control in persons with SCI.
These findings from Krause et al. (2008) support those of Kakebeeke, Lechner, and Knapp (2005), who evaluated the effects of passive cycling on spasticity. Kakebeeke and colleagues demonstrated that there was no change in velocity-dependent resistance to stretch in the LE of 10 participants with chronic, motor complete (AIS A or B) tetraplegia or paraplegia after they cycled on an ergometer that passively moved their LE.
There are other approaches that have been studied for the management of spasticity in persons with SCI. In their report, Ness and Field-Fote (2009) evaluated the effect of whole body vibration (WBV) on spastic hypertonia due to chronic, motor incomplete (AIS C or D) SCI. This pilot study enrolled 16 participants with SCI between C4 and T8. Some participants were using anti-spasticity medications before enrollment and continued use of the medication during the study. All participants had to be able to stand with no more than moderate assistance for four 45-second bouts of vibration with 1 minute of seated rest between each bout. The participants received WBV 3 days a week for 4 weeks. The only outcome measure was the Pendulum Test to measure quadriceps spasticity, and it was performed five times during each test session.
The study found that of the 16 participants, 7 had a significant decrease in quadriceps hyper-reflexia, 4 had moderate improvements, and 5 had little or no improvement in spasticity (Table 1 supplies specifics and p values). This reduction in quadriceps spasticity was evident for up to 6 to 8 days after WBV. Participants on anti-spasticity medications and those who were not taking these medications experienced similar reductions in spasticity. Whether WBV actually has more widespread effects is unclear because the authors explored only one aspect of the spasticity syndrome that often occurs after SCI and only one joint that might be affected. Further study is warranted to determine the full effects of WBV on spasticity in persons with different levels and completeness of SCI as well as the functional effects of these changes in spasticity. In addition, because one third of the participants received little to no benefit from the WBV, further study is necessary to determine why certain persons with SCI benefited and others did not.
The focus of the study by Bowden and Stokic (2009) was slightly different from the studies reported earlier. Namely, these investigators used a longitudinal, single-subject design to evaluate the effects of intrathecal baclofen using both clinical and neurophysiological assessments, and also focused on determining if changes in spasticity are correlated with measures of strength in persons with SCI. This case study evaluated the effects of varied doses of oral and intrathecal baclofen (ITB) on clinical and neurophysiological measures of spasticity and strength in a 41-year-old man with chronic, motor incomplete (AIS D) T 11 paraplegia. Dosages included 80 mg of oral baclofen at baseline; 80 mg oral/50 µg ITB on Day 3; 80 mg oral/125 µg ITB on Day 5; 30 mg oral/125 ITB µg on Day 8; and 125 µg only ITB on Day 19.
Outcomes measures included the Ashworth Scale for the LE, a spasm frequency scale and a spasm severity scale, motor function assessment using the International Standards for Neurological and Functional Classification of Spinal Cord Injury (Marino et al., 2003), and surface EMG during the H-reflex, the plantar withdrawal reflex, and maximal voluntary ankle dorsiflexion. Thus, these authors reported on the resistance to passive movement and the hyper-reflexia components of spasticity.
The participant demonstrated a dose-dependent change in spasticity, spasm strength, and flexion withdrawal reflex. Furthermore, the change in strength was not as great as the change in spasticity. Specifically, although the spasticity improved, this did not come at the expense of muscle strength. The neurophysiological measures also indicated improvements in spasticity with a reduction of the monosynaptic and poly-synaptic reflexes. The findings from these studies are in agreement with others showing the efficacy of baclofen for reducing spasticity in persons with SCI. However, this case report extends these findings to show that although there was a decrease in spasticity in this person with AIS D SCI, this was not to the detriment of muscle strength. These findings are meaningful and suggest that—at least in this person—decreasing spasticity should not lead to changes in strength or functional deficits.
Conclusions from Descriptive Studies
The findings from the descriptive studies reported here suggest that interventions that either stimulate the nervous system (e.g., electrical stimulation) or that alter the excitability in the nervous system (e.g., baclofen) lead to a reduction in spasticity in persons with SCI. The findings from these studies suggest that those with either complete or incomplete tetraplegia or paraplegia may benefit from these interventions.
Spasticity is traditionally defined as a motor disorder that is characterized by a velocity-dependent increase in tonic stretch reflex, exaggerated tendon jerks, and includes clonus, involuntary muscle contractions or spasms, and muscle co-contraction (Lance, 1980). Adams and Hicks (2005) discuss different definitions of spasticity and advocate including the intrinsic tonic spasticity (i.e., the exaggeration of the tonic component of the stretch reflex) or increased tone the intrinsic phasic spasticity (i.e., the exaggeration of the phasic component of the stretch reflex or hyper-reflexia and clonus), and extrinsic spasticity, (i.e., the exaggeration of extrinsic flexion or extension spinal reflexes). Gracies et al. (1997) suggests that to really study the effects of an intervention on spasticity, one should consider the musculoskeletal effects of spasticity, namely muscle shortening and contractures.
These studies reviewed here included persons with both acute and chronic SCI. Those with chronic SCI may well have musculoskeletal consequences to chronic spasticity, yet these parameters were not assessed in any of these studies, and it is therefore not clear how much of an effect these electrical stimulation interventions had on the musculoskeletal aspects of chronic spasticity. Further study is warranted to determine if there are long-term effects of these interventions and if these effects include both neural and musculoskeletal effects. Improving one and not the other may preclude maximal improvements.
Secondly, none of the authors included functional outcome measures in their studies, and the impact of these changes in spasticity on function remains unclear. At this point, whether reducing spasticity is necessary and sufficient for improving motor control in persons with SCI, and thereby improving function, remains unclear.
Finally, some reports indicate that the spasticity syndrome actually may be worse in people with cervical level injury than those with thoracic and incomplete injury (Kirshblum 1999; Maynard et al 1990; Skold et al 1999). All of the studies reviewed here included both persons with paraplegia and those with tetraplegia. The results are reported for the groups as a whole, and therefore whether there is a differential response to these interventions in persons with tetraplegia is not clear. Further study is warranted to determine the response in those with different levels and classifications of SCI.
Summary and Conclusions Related to the Management of Spasticity in Persons with Spinal Cord Injury
The evidence presented in this review suggests that electrical stimulation interventions applied either peripherally or centrally may lead to a reduction in certain aspects of spasticity in persons with either acute or chronic, complete or incomplete, tetraplegia or paraplegia. In addition, there is minimal evidence to suggest that whole body vibration may reduce at least one component of spasticity, namely hyper-reflexia in the quadriceps, in these same individuals. Finally, there is preliminary evidence that baclofen, while reducing spasticity, may not decrease strength or function. Further study is warranted in all of these areas, with a focus on determining the most beneficial timing and dosage of each intervention, and the varying effects on the different aspects of the spasticity syndrome after SCI as well as the varying effects in persons with different levels and completeness of SCI.
The limitations in these studies suggest that any stakeholder interested in the evidence related to the management of spasticity should first consider that none of these studies used the same measures, and that different aspects of spasticity may be affected by a given intervention. For instance, if spasms are the worse aspect of spasticity in a person with SCI, they may be more inclined to pursue an intervention such as rTMS, SCS, or baclofen—all shown to reduce spasms in persons with SCI. On the other hand, those with velocity-dependent resistance to stretch may be able to use interventions such as TENS or rTMS, but rTMS may give the best results overall if there are multiple areas related to spasticity that continue to be a problem. However, how each intervention affects the spasticity in persons with different levels and completeness of injury is not clear from these studies, and any person pursuing these interventions should be aware of this. Finally, it is not clear if the musculoskeletal consequences of spasticity will be affected by any of these interventions because this was not included in any of these studies’ outcome measures. Neural changes without accompanying musculoskeletal changes may preclude functional improvements.
The Systematic Review of the Management of Spasticity in SCI study group would like to thank the staff of the National Institute on Disability and Rehabilitation Research (NIDRR) for their support of this undertaking, including our project officer, Pimjai Sudsawad. In addition, we would like to thank the principal investigators, E. Sally Rogers and Marianne Farkas, for their guidance and support, as well as Megan Kash for development of and assistance with the database and analysis tools.
No study group member has a conflict of interest in this area of SCI research. Shepherd Center has one grant also funded by NIDRR related to evaluating the efficacy of a post-acute activity-based program for persons with incomplete tetraplegia. However, no member of the study group has a fiduciary interest in the delivery of activity-based interventions for persons with SCI or has any relation to any intervention used for the management of spasticity in persons with SCI.
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