The Effect of ASTYM on Recovery Time of Achilles Tendonitis as
Compared to Traditional Physical Therapy Methods
Jel Santos
Bio402
5/7/08
Final Draft
Table of Contents
AbstractIntroduction
Background
The Achilles tendon
Achilles tendonitis
Traditional physical therapy treatment
ASTYM treatment
Literature Review
Morphological changes associated with ASTYM in rat Achilles tendons
ASTYM pressure and fibroblast proliferation
Case studies
Specific Soft Tissue Mobilization (SSTM) and Achilles tendonitis
Graston technique and restrictive lumbar fascia
ASTYM and chronic ankle pain and fibrosis
ASTYM and chronic elbow pain
Comparing rehabilitation methods in patellar tendonitis
Research Implications and Hypothesis
Methods
Obtaining and screening data
Statistical analysis
Results
Discussion
Acknowledgments
Literature Cited / 1
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Abstract
Performance Dynamics®, Inc. claims that augmented soft tissue mobilization (ASTYM) is a “revolutionary” process that heals soft tissue dysfunctions. While this claim has been supported by past research, they provide little scientific evidence that ASTYM treatment is better than traditional physical therapy methods. This study was undertaken to determine whether a relationship exists between recovery time of Achilles tendonitis and ASTYM. Using past data, ASTYM treatment was compared to control (traditional physical therapy) treatment, with recovery time defined in both days and visit number. Resolved, uncomplicated Achilles tendonitis cases were collected from three locations of South Sound Physical and Hand Therapy: East Olympia, Lacey, and Downtown. Method of treatment, recovery time in visits, and recovery time in days were noted. Forty-seven cases in total were collected: 20 ASTYM and 27 control. A one way t-test at 95% confidence revealed a significant difference between ASTYM and control treatment for both recovery time in visit number and days (p < 0.001 and p < 0.050 respectively). ASTYM reduced treatment time in visits by 24.5% and in days by 21.0%. These results would suggest that ASTYM is a viable and more efficient method of therapy in the treatment of Achilles tendonitis compared to traditional physical therapy methods.
Introduction
Tendons are the tough, fibrous connective tissues that attach muscle to bone. When muscle generates tensile force, tendons serve as conduits that transfer this energy to bones, thus allowing movement to take place. In this way, tendons are responsible for the majority of movements for which the human body is capable (Kirkendall and Garrett, 1997). The Achilles tendon, for example, connects the gastrocnemius and soleus muscles (often referred to as the calf muscles) to the calcaneus, or ankle, and is responsible for an individual’s ability to walk. It is about 15 cm long, and as the strongest tendon in the body, has a high capacity to withstand tension (Cook et al., 2002). However, as with any other type of soft tissue, despite its strength and toughness, it is vulnerable to injury, such as tendonitis (Alfredson and Lorentzon, 2000).
Tendonitis refers to the inflammation of a tendon or the connective tissue that encases it (Martini and Welch, 2004). Achilles tendonitis typically encompasses a wide spectrum of chronic painful conditions in the tendon, including local degeneration of fibers, collagen disorganization, fibrosis (scar tissue build-up), scattered vascular ingrowth, calcification, and necrosis (Alfredson and Lorentzon, 2000, Grivas,2006). For the purposes of this study, the term “Achilles tendonitis” will refer to any chronic painful condition of the tendon, including, but not limited to, the aforementioned conditions.
Tendonitis is one of the most common injuries the Achilles tendon incurs (Martini and Welch, 2004), and it typically affects individuals who are athletically active, such as track and field athletes, soccer players, and individuals who run middle- to long-distances on a regular basis (Grivas, 2006). While the exact pathogenesis is unknown, it is generally associated with overuse, although the condition can occur in individuals who lead a sedentary lifestyle (Alfredson and Lorentzon, 2000). It is not an uncommon condition (for example, it affects 7-9% of top-level runners as reported by Lysholm and Wiklander, 1987), and can cause symptoms ranging from mild discomfort to immobility and restriction of lifestyle (Mehlham et al., 1998).
Because of its prevalence, especially among the athletic community, a variety of methods have been developed to treat Achilles tendonitis. Traditional physical therapy for Achilles tendonitis typically includes stretching, massage, therapeutic exercises, and cryotherapy (application of cold or ice to reduce pain and/or swelling). It can also include other methods of treatment (referred to as “modalities”) such as ultrasound and electrical stimulation (Grivas, 2006). Surgical intervention is also a possibility when traditional conservative treatment has failed; however, the success rate of surgery is variable (Alfredson and Lorentzon, 2000).
Augmented soft tissue mobilization (ASTYM) is an instrument-assisted, noninvasive treatment developed in 1998 by T.L. Sevier (Melham et al., 1998). Also referred to as instrument-assisted soft tissue mobilization (IASTM) or the Graston technique, it is designed to treat a range of soft tissue dysfunctions, including Achilles tendonitis (ASTYM Clinical Manual, 2003). During treatment, an ASTYM-certified therapist runs ergonomically-designed plastic instruments firmly along the patient’s skin following the direction of the injured soft tissue (ASTYM Clinical Manual, 2003). Once areas of dysfunction and fibrosis have been identified (typically by the presence of uneven tissues), the practitioner induces controlled microtrauma into the specific region by increasing the pressure with which the instruments are applied. This microtrauma promotes hyperemia (increase in blood flow in a region of the body), which in turn facilitates healing and reduces scar tissue (Gehlsen et al., 1999).
In 1997, Davidson et al. examined the morphological changes that were associated with ASTYM treatment. Twenty male rats were randomly assigned to one of four groups: A) control; B) tendonitis; C) tendonitis plus ASTYM; and D) ASTYM alone. An Achilles tendon injury was induced by a collagenase injection, and after the injection site had been allowed to heal for three weeks, treatment commenced. An ASTYM instrument was modified for use specifically on the rats, and groups C and D underwent treatment for three minutes every four days for a total of four treatments. Gait analysis of stride lengths and frequencies were performed prior to injection, after injection, and also every day prior to ASTYM treatments.
Ten days following the final treatment, the rats were killed via injection, and their tendons were harvested and examined through light and electron microscopy. Structural changes were noted, including collagen fiber alignment, presence of inflammatory cells, and number of fibroblasts. Activity of fibroblasts was also noted, as determined by the presence of numerous ribosomes, an abundance of rough ER, and exhibition of prominent nucleoli (Enwemeka, 1989).
Davidson et al. (1997)found that group A (control) had normal collagen fibers aligned in parallel and few fibroblasts. Group B (tendonitis) displayed disrupted and randomly aligned collagen fibers as well as an increased number of fibroblasts. Group C (tendonitis plus ASTYM) displayed randomly aligned collagen fibers, but also an abundance of highly active fibroblasts. Group D (ASTYM alone) displayed normal collagen fibers aligned in parallel with increased fibroblast numbers and high fibroblast activity. An ANOVA statistical analysis revealed a significant difference between group C fibroblast counts (p < 0.05) and all other groups. Significant differences (p < 0.05) were also noted between groups B and A, and B and D. Gait analysis indicated that group C was the only group that had returned to normal gait prior to death, while all other groups were still restricted in stride length and frequency.
From these results, Davidson et al. (1997) concluded that ASTYM improves limb function. Their results also suggest that ASTYM facilitates healing by not only increasing fibroblast proliferation, but facilitating fibroblast activation, which is one of the primary phases in tendon healing (Leadbetter, 1992). Additionally, because only group C fully returned to normal gait within the time frame of the study, Davidson et al. postulated that this might indicate an increase in healing rate, and that further research was warranted.
A similar study was performed by Gehlsen et al. (1999), who investigated fibroblast proliferation in response to varying ASTYM pressure. Thirty male rats were randomly assigned into five groups of six rats each: A) tendonitis only; B) tendonitis, light ASTYM (0.5 N/mm2); C) tendonitis, medium ASTYM (1.0 N/mm2); D) tendonitis, extreme ASTYM (1.5 N/mm2); and E) control. Gehlsen et al. induced Achilles tendonitis via collagenase injection, and the site was allowed to heal for three weeks. Once again, an ASTYM instrument was modified for use upon the rats; however a pressure indicator was also implanted to ensure accurate delivery of pressure. ASTYM treatment was administered to groups B, C, and D for three minutes every four days, for a total of six treatments. The rats were killed via injection, and their tendons harvested for examination via light and electron microscopy.
Group E (control) had few fairly inactive fibroblasts. Group A (tendonitis only) showed fiber misalignment (due to the tendonitis) and increased numbers of fibroblasts, which displayed increased activity. Groups B, C, and D all displayed fiber misalignment and had many more and more highly active fibroblasts than groups A or E. Groups A-D all displayed a statistically significant difference (p < 0.001) as compared to group E in the number of fibroblasts, but group D also showed a statistically significant increase (p < 0.05) compared to all other groups.
Gehlsen et al. therefore concluded that ASTYM treatment stimulates fibroblast production and that the magnitude of pressure was directly related to fibroblast proliferation, with extreme pressure resulting in the greatest amount of proliferation. The results of this study supported the findings and conclusions of Davidson et al. (1997): as fibroblasts stimulate healing (via other cell mechanisms) and create new collagen to replace old tissue (Prentice, 1994), ASTYM facilitates tendon healing by stimulating fibroblast production and activation.
Specific soft tissue mobilization, or SSTM, resembles ASTYM by using a graded and progressive application of force to induce controlled microtrauma. Like ASTYM, it also uses accessory devices; the difference between the two techniques is that SSTM relies on a combination of instrument-assisted massage as well as manual massage (Hunter, 1998).
Christenson (2007) examined the effectiveness of SSTM in treating Achilles tendonitis in a single case study. A previously athletically active female with a 5-year history of Achilles tendonitis underwent three phases of study: pre-treatment, treatment, and post-treatment. In the pre-treatment phase, pain, function, and muscle length were assessed once a week at the same time for six weeks. During the treatment phase, SSTM was applied to the injured Achilles tendon for 15 repetitions of 30 seconds of massage twice per week for the first three weeks of treatment, and then once per week during weeks four through six. During the post-treatment phase, pre-treatment assessments were repeated once a week for six weeks.
Throughout all three phases, the patient was instructed to continue her normal day-to-day activities and was given no other treatment. Following data analysis, Christenson (2007) reported an improvement in pain, function, and muscle length. Most notably, the patient experienced an increase from roughly 48% of normal functional ability to 100%, and a decrease in pain from about a 6.9/10 to 0/10, with zero being no pain and ten being the worst pain the patient can imagine (this scale is standard for usage in nearly all case-studies). Christenson (2007) concluded that as the patient’s condition had seen no change in the five years prior to treatment and as no other forms of treatment were administered, SSTM was directly correlated to the patient’s recovery.
The Graston technique is essentially the same treatment as ASTYM; the only difference between the two treatments is that the Graston technique uses stainless steel tools rather than plastic (Graston Technique, 2006). In 2005, Hammer and Pfefer examined the effects of the Graston technique upon restrictive tissue in the lumbar region. A 59-year-old male working in a retail setting had experienced low back pain intermittently for roughly one year. He reported that bed rest of two to three days and analgesic use relieved his symptoms and allowed him to return to work. At some point, however, his pain was not relieved, and Hammer and Pfefer (2005) determined that his pain was due to lumbar compartment syndrome brought about by restrictive fascia in the lumbar region extending down into the hamstring. Restrictive fascia is often caused by tissue adhesions and fibrosis (Martini, 2004).
The patient’s superficial and deep fascia were treated using the Graston technique two times a week for three weeks. After a total of six visits, the patient reported being completely asymptomatic. Tests for lumbar flexibility, which had previously been atypical due to the restriction of the fascia, now indicated normal range of motion, while tests for hamstring flexibility also indicated improvement.
Hammer and Pfefer (2005) had observed no neurological defects present in the patient during initial evaluation, nor did they observe any complicating factors or the presence of other dysfunctions. Thus they concluded that the patient’s pain and loss of motion and mobility was due to restrictive fascia alone. They noted that the Graston technique allowed them to introduce a greater pressure and thus a higher level of microtrauma to the area than conservative massage methods would have. As the patient had received no other form of treatment, this led them to believe that use of the Graston technique aided in the breakdown of adhesions and fibrosis in the fascia, which in turn led to pain reduction and restoration of motion.
Adhesions and fibrosis often form as a result of acute trauma, recurring microtrauma, immobilization, or surgical complications. These can lead to further complications, including but not limited to tendonitis, chronic pain, inflammation, dysfunction, and restrictive fascia, which can eventually contribute and lead to loss of function (Melham et al., 1998). These soft tissue traumas often respond poorly to conventional treatment, however Melham et al. documented an ASTYM success in a case study in 1998. A 20-year-old male college football player had been experiencing chronic ankle pain and functional limitation caused by post-traumatic scar tissue. He reported failure of conventional physical therapy treatment for his symptoms.
After an initial assessment documenting his pain and range of ankle motion, the patient underwent seven weeks of therapy with roughly ten minutes of ASTYM treatment two times per week. Assessment was performed a total of four times (pre-treatment, twice during the treatment phase, and post-treatment). Results indicated an increase in all planes of ankle motion (dorsi- and plantar-flexion, inversion, eversion, and soleus flexion). The patient had reported a pain rating of 6/10 prior to treatment; at the final assessment, he reported his pain at a 0/10 and a return to full function. The patient had undergone no other forms of therapy, and as he had not responded to traditional physical therapy and had shown no improvement since the occurrence of his injury, Mehlham et al. (1998)concluded that ASTYM aided his return to function, decrease of pain, breakdown of adherent scar tissue, and gains of flexibility.
In 1999, Haller et al. explored the affect of ASTYM in a case study on chronic elbow pain. The patient had a history of chronic elbow pain for 2.5 years and during that time had received extensive traditional physical therapy, as well as occupational therapy, nonsteroidal anti-inflammatory medications, and a steroid injection. Her symptoms remained unrelieved, and she had been offered surgery as the only remaining option.
Rather than undergoing surgery, which does not guarantee success, she opted to try ASTYM treatment first. After an initial assessment documenting her pain, grip strength, and functional ability, the patient underwent four weeks of therapy with roughly ten minutes of ASTYM treatment two times per week. Assessment was performed a total of three times (pre-treatment, once during the treatment phase, and post-treatment). The patient had reported a pain rating of 6/10 prior to treatment; at the final assessment, she reported her pain at a 0/10 and a return to full function. She was also able to forgo the use of an elbow support strap she had relied on for over two years. As she had been previously unresponsive to treatment and had received no other treatment than ASTYM, Haller et al. (1999) concluded that ASTYM aided in her recovery.
In 2000, Wilson et al. performed a study exploring the effectiveness of traditional physical therapy versus ASTYM treatment in patients with patellar tendonitis. Twenty subjects with physician-diagnosed patellar tendonitis were randomly placed in the ASTYM or traditional treatment groups. The traditional treatment group underwent conservative physical therapy protocol: stationary bicycling, stretching, five minutes of manual cross-friction massage manual on the patellar tendon, therapeutic exercises, and cryotherapy three times a week for four weeks (twelve total treatments). The ASTYM group was treated two times a week for four weeks (eight total treatments) and received ASTYM in place of the cross-friction massage in addition to the other forms of treatment.