November 2009

Feedback-based rehab could lower risk of OA

11gait-figure-2

Figure 2

Injury and age make joints vulnerable to high rates of loading, which contribute to the onset of osteoarthritis. Early research suggests that feedback-based gait retraining can help reduce rates of loading by improving joint kinematics and proprioception.

by Jody L. Riskowski, PhD

Musculoskeletal symptoms and ailments are the number two reason, behind respiratory symptoms, for physician visits in the U.S. Annually they lead to more than two million first-time visits to physical therapy and movement rehabilitation centers,1 totaling an estimated $267.2 billion in direct and indirect costs.2 However, recent advances in engineering and technology have led to new devices that aid in physical rehabilitation and therapy, which are thought to bring a faster recovery while decreasing costs.3 Specifically, gait retraining is one area that has seen a rapid growth in product development.

To support the gait retraining efforts, there are a number of active assistive braces to aid in the restoration and/or enhancement of an individual’s ability to walk efficiently. Active assistive devices and braces as opposed to their passive counterparts use external monitoring and assistance to reestablish neuromuscular control. Though passive bracing may provide stability and maintain alignment of the joint, it lacks the ability to provide real-time feedback and to adapt to the individual.

The body has several intrinsic feedback systems to monitor movement and walking, such as vision, sound, and proprioception, defined as the body’s awareness of its actions. With vision, we watch our limbs move, with sound we listen to how our foot strikes the ground, and with proprioception we feel how our body moves. However, with disease and injury, one or more of these systems may become damaged and may not provide accurate information. In this case, external feedback, whether it is via sight, hearing, or touch, may augment our internal cueing and motion, aiding in motor learning and adaptation.

In our everyday world, many external feedback systems are employed: a coach films an athlete to show her how her hurdling technique changes from the start to the end of race, a musician replays a recording of his concert to listen to his timing, and a child learns to ride a bike through training wheels that guide his balance and movement. Over time, these external systems may develop our internal cueing and movement pattern.

Broadly speaking, internal and external feedback in gait monitors and measures the current movement status against a desired action. The feedback provides a goal for the user, allowing them to focus on their movements and actions. Feedback may also increase motivation by keeping individuals informed on their results and performance. This generally translates to greater effort during training sessions and more motivation for practice, yielding greater compliance and enthusiasm. All of this may lead to improved outcomes.

Feedback-based gait retraining

Figure 1

Figure 1

Feedback-based systems have been developed to assist gait retraining in patients with anterior cruciate ligament (ACL) injury4-6 and arthritis.7, 8 With these systems, feedback is relayed to the user visually,9-11 acoustically,4, 12-14 or vibrotactilely15 as well as in combination with one another.7,16-19 Regardless of the system, they all share a common function: to provide a quantitative measure of performance in real-time, which allows the individual to make adjustments on the subsequent step. These measures include muscular activity,16-18 kinematic,13, 20 or kinetic measures.12,14,16

Arthritis, or more specifically osteoarthritis (OA), is the most common arthropathy and a major contributor to disability in the elderly.21 OA is a degenerative joint disease that affects an estimated 27 million people in the U.S.22, generally targeting individuals over the age of 55, with 12% of the population 65 or older experiencing it in the knee joint.23 A secondary classification of OA, known as post-traumatic osteoarthritis, can develop in individuals much younger as a consequence of a previous injury, such as an ACL injury. Primary or secondary OA develops as the normally slippery articular surface becomes roughened and abrasive causing pain with movement. Further degeneration of the articular cartilage causes changes to the underlying bone,24 limits range of motion,25 and decreases joint strength.26 The associated pain as well as reduced strength and range of motion can lead to a decrease in mobility, independence and quality of life.27

Research has shown that a repetitive high force or rate of loading (ROL) during walking can be a predecessor to the onset of joint degenerative diseases, such as OA.28-34 In walking ROL refers to how quickly forces are imparted on a joint (Figure 1). Animal studies have demonstrated that repeated high impulse forces and a high ROL lead to osteoarthritic changes in the articular cartilage and surrounding bone.30,32,34 In gait, a high ROL tends to arise from improper gait kinematics at initial contact (IC), or heel strike.35, 36

To protect itself and prevent damage from the ROL, the body relies on several intrinsic, passive mechanisms, including the articular cartilage, menisci, and intervertebral discs.37 However, these structures by themselves cannot always withstand the repetitive forces of walking, and over a lifetime, they can experience fatigue failure.38 With the repeated exposure to a high ROL, these shock-absorbing and protective mechanisms become damaged, and the underlying bone at the joint experiences increased stress.29 Thus, simply relying passively on the body’s mechanical properties may not be effective to prevent the onset of OA, particularly if a person has experienced an injury, which tends to acerbate the ROL experienced.

In addition to the passive methods of affecting ROL, the body also utilizes active mechanisms to reduce the effects of IC39 by ensuring the body adequately prepares for IC.13,36,39 These methods include eccentric contraction of the quadriceps muscles and proper flexion of the knee to maximize the contact area of the articulating surfaces and disperse the load across the knee joint.37,40 Regardless of the active strategy the body utilizes to protect itself, an intact neuromuscular system is needed.

The neuromuscular system is the combination of the nervous system and muscles they innervate that work synergistically to permit movement. The nervous system activates the muscles to control the muscular stiffness and actions of the limbs. This system is also responsible for providing the proprioceptive feedback, which informs the body what limb actions occur. However, with aging or injury, some individuals’ proprioceptive feedback systems may be lacking, such as a patient post-ACL injury,41 or with pre-osteoarthritic35 and osteoarthritic42 conditions. These individuals tend to have poor intrinsic feedback systems, which suggest that they may benefit from an external feedback-based training system.

Tearing, rupturing or damaging the ACL can disrupt the joint mechanisms and may interrupt the proprioceptive signaling.43 Even after the ACL injury is rehabilitated and/or surgically repaired, the proprioceptive feedback may not be fully corrected.43 This means the body may be unable to provide appropriate feedback on the limb’s actions, which may result in further damage to the knee joint caused by incorrect movements. Studies analyzing gait post-ACL injury show that patients have disrupted joint mechanisms, altered force transmission, and unique muscle activation patterns compared to non-ACL injured subjects.44-52 This chronic knee instability can lead to further joint degeneration,53-56 changes in the meniscal properties,57,58 and alterations in the joint cartilage properties.59 The knee joint instability and subsequent altered joint mechanics that result from inaccurate proprioceptive feedback may be one reason that 14% to 60% of the ACL-injured population shows radiographic evidence of degenerative changes at the knee joint.53,60-67 As stated earlier, patients with poor intrinsic feedback may benefit from an external feedback-based gait training system.

There are a limited number of external monitoring systems that have been used for gait retraining in the post-ACL injured populations. One system is the force–driven harmonic oscillator (FDHO)4 that uses an individual’s body weight and thigh, shank, and foot lengths to determine the preferred walking cadence. This cadence is set with a metronome, and the patient is instructed to step to its frequency. Once the clinician calculates the preferred cadence, the metronome FDHO system can be used at home, with no need for the patient to be at the clinic for gait training therapy. Manipulating the step frequency is thought to alter the sensory and motor neuron signaling, as well as enhance the training stimulus, and the metronomic signaling increases directional attention and focus.4 The motor learning that results from this type of device is thought to promote greater quadricep activity and encourage focused attention on the actions of walking.4 Though this system has shown favorable results with regard to increasing knee flexion and improving gait speed post-ACL surgery, it does not account for the inherent variability of normal, healthy gait, nor does it account for differences in walking speed as the individual is recovering.4

Audio signaling for gait retraining has also been show to effectively increase muscle activation.17 In this work, Petrofsky developed a biofeedback training device to re-educate the neuromuscular activation in patients with Trendelenberg gait secondary to incomplete spinal cord injury. The device provided feedback, in the form of an audio signal, if improper muscular activation of the gluteus medius was noted. The system used electromyography (EMG) to monitor muscular activation, and after two months of home training, the subjects’ gait pattern was nearly fully restored with regard to hip drop.17 In a clinical setting, this muscular activation feedback also showed positive results with regard to developing quadriceps femoris strength in patients following ACL reconstruction.5 Although the quadriceps experience significant functional loss after ACL reconstruction, restoring strength to these muscles can be a challenge if patients have difficulty contracting the knee extensors and instead compensate by recruiting the hip musculature during rehabilitation exercises.

In recent work with gait retraining in ACL-injured and pre-osteoarthritic populations, a new feedback-based monitoring system (Figure 2) has been designed by our research group (described in detail elsewhere).13 This gait retraining system monitors an individual’s gait kinematics and provides an auditory signal if there is limited knee flexion ( < 5°) or high vertical acceleration (greater than 8.6 m/s2) at initial contact (IC), both of which are factors that may affect ROL.36 This gait retraining system is unique as it encourages the subject to develop awareness for the gait kinematics used in locomotion. In 30 minutes of training with this gait monitoring system, healthy subjects were able to effectively reduce their rate of loading (ROL) by 25%, without reducing their gait velocity. Previous research showed no significant kinematics changes by simply wearing this brace without the feedback component compared to normal walking without the brace, but with the added feedback significant changes in gait characteristics were detected, such as a reduced ROL and increased knee flexion. 13 Pilot data of the gait monitoring system suggest individuals are able to gain short-term neuromuscular changes through training. We found that training with the system was associated with an increase in proprioceptive acuity from baseline to post-training.68 In changing the knee joint kinematics, such as knee joint angle and vertical acceleration, and augmenting body awareness through the gait monitoring system, individuals effectively decreased the ROL experienced during walking.13,68

Conclusions

Currently, the potential long-term benefit of this system and the post-ACL injury gait retraining protocols is not just in developing a gait pattern that reduces rate of loading during walking, but also in preventing the early onset of osteoarthritis. Though the results from many of these gait retraining methods are positive, the efficacy of this training is still unknown. Although training with our group’s feedback-based monitoring system was associated with notable changes in the treatment subjects’ gait post-training, it is not feasible to state that this type of training is beneficial post-ACL rehabilitation. Moreover, there are still many questions that remain unanswered: When is the ideal time during rehabilitation to introduce gait retraining devices into the rehabilitation process? Are there specific patient or ACL injury characteristics that are more suited to using the gait monitoring system? Lastly, what are the effects of this type of gait training on an individual’s OA? Future large-scale and long-term studies are needed to address these questions.

Jody L. Riskowski, PhD, CSCS, is an assistant professor in the department of kinesiology at the University of Texas at El Paso, El Paso, TX.

Conflict of Interest Statement: None.

References

1. National Center of Health Statistics. National ambulatory medical care survey 2005. Hyattsville, MD: Public Health Service; 2007.

2. American Academy of Orthopaedic Surgeons. Burden of musculoskeletal diseases in the United States: Prevalence, societal and economic cost. Rosemont, IL: American Academy of Orthopaedic Surgeons; 2008.

3. Veltink PH, Koopman HF, Helm FCvd, Nene AV. Biomechatronics–assisting the impaired motor system. Arch Physiol Biochem 2001;109(1):1-9.

4. Decker MJ, Torry MR, Noonan TJ, et al. Gait retraining after anterior cruciate ligament reconstruction. Arch Phys Med Rehabil 2004;85(5):848-856.

5. Draper V. Electromyographic biofeedback and recovery of quadriceps femoris muscle function following anterior cruciate ligament reconstruction. Phys Ther 1990;70(1):11-17.

6. Feller J, Hoser C, Webster K. EMG biofeedback assisted KT-1000 evaluation of anterior tibial displacement. Knee Surg Sports Traumatol Arthrosc 2000;8(3):132-136.

7. Hirokawa S, Matsumura K. Biofeedback gait training system for temporal and distance factors. Med Biol Eng Comput 1989;27(1):8-13.

8. Weinberg B, Nikitczuk J, Patel S, et al. Design, control and human testing of an active knee rehabilitation orthotic device. IEEE International Conference on Robotics and Automation 2007:4126-4133.

9. Montoya R, Dupui P, Pages B, Bessou P. Step-length biofeedback device for walk rehabilitation. Med Biol Eng Comput 1994;32(4):416-420.

10. Bolek JE. A preliminary study of modification of gait in real-time using surface electromyography. Appl Psychophysiol Biofeedback 2003;28(2):129-138.

11. Aiello E, Gates DH, Patritti BL, et al. Visual EMG biofeedback to improve ankle function in hemiparetic gait. Conf Proc IEEE Eng Med Biol Soc 2005;7:7703-7706.

12. Aruin AS, Sharma A, Larkins R, Chaudhuri G. Knee position feedback: Its effect on management of pelvic instability in a stroke patient. Disabil Rehabil 2000;22(15):690-692.

13. Riskowski JL, Mikesky AE, Bahamonde RE, Burr DB. Design and validation of a knee brace with feedback to reduce the rate of loading. J Biomech Eng 2009;131(8):084503.

14. Batavia M, Gianutsos JG, Kambouris M. An augmented auditory feedback device. Arch Phys Med Rehabil 1997;78(12):1389-1392.

15. Femery VG, Moretto PG, Hespel JM, et al. A real-time plantar pressure feedback device for foot unloading. Arch Phys Med Rehabil 2004;85(10):1724-1728.

16. Mandel AR, Nymark JR, Balmer SJ, et al. Electromyographic versus rhythmic positional biofeedback in computerized gait retraining with stroke patients. Arch Phys Med Rehabil 1990;71(9):649-654.

17. Petrofsky JS. The use of electromyogram biofeedback to reduce Trendelenburg gait. Eur J Appl Physiol 2001;85(5):491-495.

18. Colborne GR, Olney SJ, Griffin MP. Feedback of ankle joint angle and soleus electromyography in the rehabilitation of hemiplegic gait. Arch Phys Med Rehabil 1993;74(10):1100-1106.

19. Krishnamoorthy V, Hsu WL, Kesar TM, et al. Gait training after stroke: A pilot study combining a gravity-balanced orthosis, functional electrical stimulation, and visual feedback. J Neurol Phys Ther 2008;32(4):192-202.

20. Batavia M, Gianutsos JG, Vaccaro A, Gold JT. A do-it-yourself membrane-activated auditory feedback device for weight bearing and gait training: A case report. Arch Phys Med Rehabil 2001;82(4):541-545.

21. World Health Organization (WHO). Annex 3: Burden of disease in disability-adjusted life-years (DALYs), by cause, sex, and mortality stratum, in WHO regions, estimates for 2001. Geneva: WHO; 2004.

22. Lawrence RC, Felson DT, Helmick CG, et al. Estimates of the prevalence of arthritis and other rheumatic conditions in the United States. Part II. Arthritis Rheum 2008;58(1):26-35.

23. Felson DT, Zhang Y. An update on the epidemiology of knee and hip osteoarthritis with a view to prevention. Arthritis Rheum 1998;41(8):1343-1355.

24. Jones G, Ding C, Scott F, et al. Early radiographic osteoarthritis is associated with substantial changes in cartilage volume and tibial bone surface area in both males and females. Osteoarthritis Cartilage 2004;12(2):169-174.

25. Oatis CA, Wolff EF, Lennon SK. Knee joint stiffness in individuals with and without knee osteoarthritis: A preliminary study. J Orthop Sports Phys Ther 2006;36(12):935-941.

26. Slemenda C, Brandt KD, Heilman DK, et al. Quadriceps weakness and osteoarthritis of the knee. Ann Intern Med 1997;127(2):97-104.

27. Tak SH, Laffrey SC. Life satisfaction and its correlates in older women with osteoarthritis. Orthop Nurs 2003;22(3):182-189.

28. Rogers LQ, Macera CA, Hootman JM, et al. The association between joint stress from physical activity and self-reported osteoarthritis: An analysis of the Cooper Clinic data. Osteoarthritis Cartilage 2002;10(8):617-622.

29. Voloshin AS, Wosk J. Shock absorption of meniscectomized and painful knees: A comparative in vivo study. J Biomed Eng 1983;5(2):157-161.

30. Simon SR, Radin EL, Paul IL, Rose RM. The response of joints to impact loading. II. In vivo behavior of subchondral bone. J Biomech 1972;5(3):267-272.

31. Radin EL, Ehrlich MG, Chernack R, et al. Effect of repetitive impulsive loading on the knee joints of rabbits. Clin Orthop Relat Res 1978;(131):288-293.

32. Radin EL, Martin RB, Burr DB, et al. Effects of mechanical loading on the tissues of the rabbit knee. J Orthop Res 1984;2(3):221-234.

33. Radin EL, Parker HG, Pugh JW, et al. Response of joints to impact loading. 3. Relationship between trabecular microfractures and cartilage degeneration. J Biomech 1973;6(1):51-57.

34. Radin EL, Paul IL. Response of joints to impact loading. I. In vitro wear. Arthritis Rheum 1971;14(3):356-362.

35. Radin EL, Yang KH, Riegger C, et al. Relationship between lower limb dynamics and knee joint pain. J Orthop Res 1991;9(3):398-405.

36. Riskowski JL, Mikesky AE, Bahamonde RE, et al. Proprioception, gait kinematics, and rate of loading during walking: Are they related? J Musculoskelet Neuronal Interact 2005;5(4):379-387.

37. Voloshin A, Wosk J. An in vivo study of low back pain and shock absorption in the human locomotor system. J Biomech 1982;15(1):21-27.

38. Whittle MW. Generation and attenuation of transient impulsive forces beneath the foot: A review. Gait Posture 1999;10(3):264-275.

39. Al-Zahrani KS, Bakheit AM. A study of the gait characteristics of patients with chronic osteoarthritis of the knee. Disabil Rehabil 2002;24(5):275-280.

40. Collins JJ, Whittle MW. Impulsive forces during walking and their clinical implications. Clin Biomech 1989;4(3):179-187.

41. Friden T, Roberts D, Zatterstrom R, et al. Proprioception in the nearly extended knee. Measurements of position and movement in healthy individuals and in symptomatic anterior cruciate ligament injured patients. Knee Surg Sports Traumatol Arthrosc 1996;4(4):217-224.

42. Lund H, Juul-Kristensen B, Hansen K, et al. Movement detection impaired in patients with knee osteoarthritis compared to healthy controls: A cross-sectional case-control study. J Musculoskelet Neuronal Interact 2008;8(4):391-400.

43. Muaidi QI, Nicholson LL, Refshauge KM, et al. Effect of anterior cruciate ligament injury and reconstruction on proprioceptive acuity of knee rotation in the transverse plane. Am J Sports Med 2009;37(8):1618-1626.

44. Beynnon BD, Fleming BC, Labovitch R, Parsons B. Chronic anterior cruciate ligament deficiency is associated with increased anterior translation of the tibia during the transition from non-weightbearing to weightbearing. J Orthop Res 2002;20(2):332-337.

45. Coury HJ, Brasileiro JS, Salvini TF, et al. Change in knee kinematics during gait after eccentric isokinetic training for quadriceps in subjects submitted to anterior cruciate ligament reconstruction. Gait Posture 2006;24(3):370-374.

46. DeVita P, Hortobagyi T, Barrier J. Gait biomechanics are not normal after anterior cruciate ligament reconstruction and accelerated rehabilitation. Med Sci Sports Exerc 1998;30(10):1481-1488.

47. Butler RJ, Minick KI, Ferber R, Underwood F. Gait mechanics after ACL reconstruction: Implications for the early onset of knee osteoarthritis. Br J Sports Med 2009;43(5):366-370.

48. Liden M, Sernert N, Rostgard-Christensen L, et al. Osteoarthritic changes after anterior cruciate ligament reconstruction using bone-patellar tendon-bone or hamstring tendon autografts: A retrospective, 7-year radiographic and clinical follow-up study. Arthroscopy 2008;24(8):899-908.

49. Kurz MJ, Stergiou N, Buzzi UH, Georgoulis AD. The effect of anterior cruciate ligament reconstruction on lower extremity relative phase dynamics during walking and running. Knee Surg Sports Traumatol Arthrosc 2005;13(2):107-115.

50. Hurd WJ, Snyder-Mackler L. Knee instability after acute ACL rupture affects movement patterns during the mid-stance phase of gait. J Orthop Res 2007;25(10):1369-1377.

51. Bonfim TR, Jansen Paccola CA, Barela JA. Proprioceptive and behavior impairments in individuals with anterior cruciate ligament reconstructed knees. Arch Phys Med Rehabil 2003;84(8):1217-1223.

52. Zantop T, Schumacher T, Diermann N, et al. Anterolateral rotational knee instability: Role of posterolateral structures. Arch Orthop Trauma Surg 2007;127(9):743-752.

53. Buckland-Wright JC, Lynch JA, Dave B. Early radiographic features in patients with anterior cruciate ligament rupture. Ann Rheum Dis 2000;59(8):641-646.

54. Daniel DM, Stone ML, Dobson BE, et al. Fate of the ACL-injured patient. A prospective outcome study. Am J Sports Med 1994;22(5):632-644.

55. Lohmander LS, Roos H. Knee ligament injury, surgery and osteoarthrosis. Truth or consequences? Acta Orthop Scand 1994;65(6):605-609.

56. Roos H, Adalberth T, Dahlberg L, Lohmander LS. Osteoarthritis of the knee after injury to the anterior cruciate ligament or meniscus: The influence of time and age. Osteoarthritis Cartilage 1995;3(4):261-267.

57. Killian ML, Isaac DI, Haut RC, et al. Traumatic anterior cruciate ligament tear and its implications on meniscal degradation: A preliminary novel lapine osteoarthritis model. J Surg Res 2009 Apr 5 [Epub ahead of print]

58. Vinson EN, Gage JA, Lacy JN. Association of peripheral vertical meniscal tears with anterior cruciate ligament tears. Skeletal Radiol 2008;37(7):645-651.

59. Yeow CH, Cheong CH, Ng KS, et al. Anterior cruciate ligament failure and cartilage damage during knee joint compression: A preliminary study based on the porcine model. Am J Sports Med 2008;36(5):934-942.

60. Lohmander LS, Englund PM, Dahl LL, Roos EM. The long-term consequence of anterior cruciate ligament and meniscus injuries: Osteoarthritis. Am J Sports Med 2007;35(10):1756-1769.

61. Louboutin H, Debarge R, Richou J, et al. Osteoarthritis in patients with anterior cruciate ligament rupture: A review of risk factors. Knee 2009;16(4):239-244.

62. Andriacchi TP, Mundermann A, Smith RL, et al. A framework for the in vivo pathomechanics of osteoarthritis at the knee. Ann Biomed Eng 2004;32(3):447-457.

63. Andriacchi TP, Briant PL, Bevill SL, Koo S. Rotational changes at the knee after ACL injury cause cartilage thinning. Clin Orthop Relat Res 2006;442:39-44.

64. Roe J, Pinczewski LA, Russell VJ, et al. A 7-year follow-up of patellar tendon and hamstring tendon grafts for arthroscopic anterior cruciate ligament reconstruction: Differences and similarities. Am J Sports Med 2005;33(9):1337-1345.

65. Segawa H, Omori G, Koga Y. Long-term results of non-operative treatment of anterior cruciate ligament injury. Knee 2001;8(1):5-11.

66. Lohmander LS, Ostenberg A, Englund M, Roos H. High prevalence of knee osteoarthritis, pain, and functional limitations in female soccer players twelve years after anterior cruciate ligament injury. Arthritis Rheum 2004;50(10):3145-3152.

67. von Porat A, Roos EM, Roos H. High prevalence of osteoarthritis 14 years after an anterior cruciate ligament tear in male soccer players: A study of radiographic and patient relevant outcomes. Ann Rheum Dis 2004;63(3):269-273.

68. Riskowski JL. Gait and neuromuscular adaptations after using a gait monitoring system. Gait Posture 2009 (In Review).

Figure Captions

Figure 1. Typical ground reaction curve demonstrating the heel strike transient. Point A represents the local maximum force generated within the 50 ms after contact. The dashed line represents the portion of the curve used to determine the rate of loading (ROL), and the graph is normalized by body weight (BW).

Figure 2. Subject wearing knee brace with feedback.

(Visited 19 times, 1 visits today)

Leave a Reply

Your email address will not be published. Required fields are marked *

Spam Blocker * Time limit is exhausted. Please reload CAPTCHA.