August 2010

Spinal cord injury: Role of ankle foot orthoses

Figure 2: Individual walking with a unilateral, posterior leaf spring ankle foot orthosis.

The current approach to gait retraining after incomplete spinal cord injury emphasizes restoration of normal walking patterns rather than compensation, which is changing the way practitioners think about the use of AFOs in this patient population.

By Preeti M Nair, PT, PhD, and Andrea L Behrman, PT, PhD

Spinal cord injury (SCI), an injury to the neural elements within the spinal cord, results in a multitude of dysfunction, loss of sensation and motor function being the most profound.1,2 Although there is a significant rate of mortality associated with injury, survival after SCI has improved considerably because of efficient critical care, improved urinary rehabilitation and respiratory management.3,4 About 253,000 people currently in the United States live with SCI and there are an additional 11,000 new cases every year.5 The American Spinal Injury Association (ASIA) impairment scale (AIS) is used to classify the level and severity of injury in relation to the loss of sensation and motor function.6,7 According to the scale, a person with some amount of motor sparing and retention of sensation below the level of injury is classified as having an incomplete SCI (ISCI). Although upright mobility may be spared or achieved with assistance, walking is typically impaired in persons with ISCI as a result of varying levels of muscular paralysis, sensory deficits, spasticity and poor trunk control.8-10

Gait in an individual with ISCI is often characterized by one or combination of the following deviations (i) inadequate active hip extension during terminal stance; (ii) limited hip flexion; (iii) limited knee flexion; (iv) excess ankle plantar flexion during swing; and (v) impaired initial foot contact, with excess plantar flexion of the ankle  and/or the characteristic foot slap associated with weakness of the ankle dorsiflexors.11 Consequently, these individuals are often seen taking slow, asymmetrical and uncoordinated steps over a wide base of support and having limited adaptability to the environment, which tends to increase the risk of falls and decrease patient mobility.11,12

Orthoses and the compensation based approach

Figure 1: Individual with incomplete spinal cord injury undergoing locomotor training on treadmill, with body weight support and manual assistance to facilitate a normal walking pattern involving upright trunk posture, rhythmical lower limb stepping pattern with symmetrical limb loading and arm swing.

Conventional physical therapy interventions for improving walking function in persons with ISCI emphasize the use of assistive and orthotic devices to improve ambulation potential13,14 and teach new strategies for upright mobility.13,15,16 The goals of prescribing orthotic devices for walking are to support the paralyzed or weakened musculoskeletal structure, add stability to joints, improve mobility, correct alignment and improve overall functional independence.14

Ankle foot orthoses (AFOs) are usually prescribed for individuals with ISCI to provide support for weakened musculature around the ankle joint, specifically to address the excess plantar flexion observed during initial contact, stabilize the joint for effective push-off during late stance, and prevent toe-drag during swing.14,17 Since an AFO supports one single joint, it is considered by clinicians and patients to be less cumbersome and less energy demanding compared to multi-joint supporting orthotic devices, such as knee-ankle foot orthoses (KAFOs) and hip-knee-ankle foot orthoses (HKAFOs). The guiding principles for recommendation are to control the ankle joint by limiting excursion range, provide safe joint mechanics, prevent toe drag during the stance-to-swing transition, minimize the risk of falls and enhance the ability to walk faster and efficiently.14,18

The current rationale for use of AFOs for persons with ISCI is based on adaptation to loss of sensorimotor deficits associated with the injury.19,20 Conventional rehabilitation therefore typically consists of a compensatory approach to deal with walking impairments in persons after ISCI.21,22 The approach utilizes the use of compensatory orthotic devices that utilize other spared abilities to accomplish the task or modify the task and/or the environment to make it easier for a person to accomplish the goal.  For example, in individuals who are unable to stand upright and have limited lower limb mobility, the task of walking is modified to include assistive devices such as the walker and utilize the spared upper extremities to provide stability and mobility. Similarly, by utilizing orthotic devices such as the solid AFO around the weakened ankle joint, the task of walking is modified to utilize more proximal hip and knee joint control. The prevailing assumption that neural recovery is not possible following SCI has led to the extensive use and development of orthotic and assistive devices that compensate for walking impairments.23-25

Activity-dependent plasticity of the nervous system and locomotor training

Compelling evidence from neuroscience examining the neural control of walking, however, challenges this assumption.26-31 Neuroscientists have investigated the ability of the nervous system, particularly the spinal cord, to adapt and reorganize after complete transections at the level of the cord.32-34 The ability of the spinal cord to respond to peripheral sensory input, generate and modulate rhythmic activity in the lower limbs and reorganize after injury make it a viable substrate for intervention.29,35-37

Animal and human research on the neurobiological control of stepping and the skill-dependent plasticity of the nervous system have challenged the compensation based approach of rehabilitation after SCI. Research has revealed that task-specific, repetitive training following SCI in animals and humans promotes skill-dependent plasticity in the spinal cord and plays a critical role in the recovery of locomotor abilities including stepping.28,37-39 The emerging training strategy is to provide the central nervous system with peripheral sensory input related to locomotion in order to stimulate a stepping response.40-48 Processing of task-specific, kinematic and kinetic sensory input facilitates performance of the task and learning.49 This strategy is based upon evidence that the lumbosacral spinal cord is capable of recognizing and processing functional sensory input to produce a functional motor response.50 Simply put, generation of the stepping pattern would involve the provision of motion-related sensory input associated with stepping and postural control. Two of these inputs related to stepping are limb loading and unloading and hip position.51-54A therapeutic intervention termed as “locomotor training” has been developed based on such research.

In the locomotor training environment, this motion-related sensory input is made available by having a person with ISCI walk over a treadmill in a harness connected to a body weight supporting system with manual assistance.45 This assembly in addition to the manual assistance provides an environment where normal walking speeds, bilateral limb loading and proper limb and trunk kinematics can be safely and effectively trained to enhance the neural output generating walking.45 Evidence supporting the benefits of locomotor training in facilitating the recovery of walking in humans has been recorded in the literature as early as the 1990s.55-59 Persons who participated  in this intervention demonstrated significant improvements in pattern of stepping, walking speed, endurance,  inter-limb coordination and  increased electromyograhic activity in the muscles of the lower limbs.60-62

Differing perspectives about the use of an ankle foot orthosis

As this novel intervention is evolving, effort is being made to identify and introduce strategies that facilitate the task of stepping by contributing to the provision of appropriate kinematic and kinetic input to promote recovery.41,63 Since lower limb orthoses have been used for such a long time in conventional rehabilitation, the assumption that they facilitate stepping has been undisputed.  Although functional ambulation, characterized by modifying the task or the environment and quantified by functional outcome measures such as speed to reach  destination, improves with orthotic devices in individuals with ISCI, the impact of the devices on normalizing the walking pattern and providing appropriate motion-related sensory input however is unknown.63

In a recent study, Nair et al examined the kinematic and kinetic contributions of a posterior leaf spring ankle foot orthosis (PAFO), a device of minimal assistance, during stepping.63 The results of their study revealed that use of the orthosis failed to produce desired proximal joint kinematics such as hip extension during the transition from stance-to-swing phase of walking and meet the functional task requirements such as rate of loading during the transition from swing-to-stance phase of walking in able-bodied individuals. Since the orthosis limited hip extension and prolonged limb loading; both motion-related sensory inputs that are crucial to normal walking, its effect on the pre-existing walking impairments in individuals with ISCI could be more pronounced as a result of the increased reliance of the spared spinal cord on peripheral, motion-related sensory input to sculpt the pattern of walking. Continued examination of AFOs in individuals with ISCI might be important to assess their ability to generate appropriate kinematics and kinetics consistent with normal stepping.63

Although the goal is to improve ambulation potential, the theoretical approach utilized by conventional interventions and neurobiologically driven rehabilitation interventions such as locomotor training are quite distinct and different in their principles. In conventional interventions, prescription of assistive and/or orthotic devices often does not take into account the influence of the device on the user’s resultant stepping pattern.64,65 For example, rigid support provided at the ankle by the PAFO might limit the excursion of the contingent joints, affecting the control of the transition from stance-to-swing.

Under the supposition that neurological function ceases to exist below the level of injury, clinical assessments for the prescription of ambulatory devices utilize a frame work for substitution of impaired function rather than the restitution of function.22 Therefore, the ambulatory ability of a person in moving from one place to another rather than the walking pattern utilized in achieving this mobility is emphasized. While wearing orthotic devices like the PAFO, Ounpuu et al reported an inability to generate sufficient power in the transition from stance-to-swing phase of stepping in children with cerebral palsy with gait impairments similar  to those observed in individuals with ISCI.66 Likewise, Romkes et al reported a decrease in terminal stance phase hip extension with an AFO in children with cerebral palsy.67 However, conclusions drawn from these studies contend that ambulatory devices are still capable of fulfilling various assistive functions during walking, although they affect posture and walking pattern in different neurological populations.67 The inability to generate normal walking mechanics was concluded to be the result of the irreversible nature of the injury rather than the inability of the device to provide or assist normal stepping.

In neurobiologically driven (activity-based) rehabilitation interventions such as locomotor training, the individual’s stepping pattern is of utmost importance.41It is important to provide the spinal cord appropriate motion-related sensory input that it can utilize to relearn a normal stepping pattern. Normal walking is not only energy efficient but also useful for the modulation of spinal reflexes that are processed at the level of the spinal cord and are often times exaggerated post injury. Therefore, the primary goal is to progressively retrain the ability to step rather than to immediately substitute for impaired stepping. The emphasis is on training without an orthotic device while step training on the treadmill. The commercially available, off-the-shelf AFO is designed to stabilize the joint and therefore is rigid, range limiting, and more likely to change the individual’s stepping pattern than hinge or dynamic AFOs that are more permissible for movement. Thus, a compromise for home and community ambulation is to use a hinged AFO if deemed necessary for safety and endurance purposes; however, this again is temporary or used intermittently only. Additionally, since the emphasis of locomotor training is on retraining the ability to walk independently, we favor a dynamic approach of use across training, such as progression from an orthotic device that permits a normal walking pattern and can be adjusted to provide varying degrees of support before the patient is finally weaned off. Other design recommendations for the AFO are development and manufacture of softer foot plates which feel like regular footwear insoles rather than rigid plastic plates. Plastic foot plates are likely to create pressure on the plantar surface of the foot throughout the swing phase of walking, while motion-related sensory input from the plantar surface is minimal during swing.  


With the advent of new interventions and new evidence about the control of stepping during locomotor training, a casual, omnipresent approach for the use of AFOs may be inappropriate. Orthotics could therefore have different roles, functions and durations of use based on the goals and perspectives of the intervention. An AFO could be used extensively and permanently to compensate for impaired ankle function and to enable adaptive mobility, or it could be used judiciously and intermittently as a safety measure alone while retraining stepping.  The ultimate decision about the use of orthotics lies in the hands of the clinician in partnership with the patient and his/her goals. However, in each scenario, careful evidence-based decision making is essential.

Preeti M. Nair, PT, PhD, is an associate professor in the department of physical therapy at Seton Hall University in South Orange, NJ. Andrea L. Behrman, PhD, PT is an associate professor in the department of physical therapy at the University of Florida and a research scientist at the Malcom Randall VA Medical Center’s Brain Rehabilitation Research Center, both in Gainesville, FL.


1. Stover SL, DeLisa JA, Whiteneck GG. Spinal cord injury: clinical outcomes from the model systems. Gaithesburg, MD: Aspen Publishers; 1995).

2. Staas WE, Freedman MK, Fried GF. Spinal cord injury and spinal cord injury medicine. In: DeLisa JA, Gans BM, eds. Rehabilitation Medicine: Principles and Practice. 3rd ed. Philadelphia: Lippincott-Raven Publishers; 1998.

3. McDonald JW, Sadowsky C. Spinal-cord injury. Lancet 2002;359(9304):417-425.

4. DeVivo MJ, Stover SL. Long term survival and causes of death. In: Stover SL, DeLisa JA, Whiteneck GG, eds. Spinal cord injury: clinical outcomes from the model systems. Gaithersburg, MD: Aspen Publishers;1995:289-316.

5. National Spinal Cord Injury Statistical Center University of Alabama at Birmingham. Annual statistical report. Birmingham, AL: University of Alabama, National Spinal Cord Injury Statistical Center; 2004.

6. Maynard FM Jr, Bracken MD, Creasey G, et al. International standards for neurological and functional classification of spinal cord injury. American Spinal Injury Association. Spinal Cord 1997;35(5):266-274.

7. American Spinal Injury Association. Standards for neurological classification of spinal injury patients. Chicago: American Spinal Injury Association; 1984.

8. Conrad B, Benecke R, Meinck HM. Gait disturbances in paraspastic patients. In: Delwaide PJ, Young RR, eds. Clinical neurophysiology in spasticity. Amsterdam: Elsevier;1985:155-174.

9. Fung J, Barbeau H. A dynamic EMG profile index to quantify muscular activation disorder in spastic paretic gait. Electroencephalogr Clin Neurophysiol 1989;73(3):233-244.

10. Krawetz P, Nance P. Gait analysis of spinal cord injured subjects: effects of injury level and spasticity. Arch Phys Med Rehabil 1996;77(7):635-638.

11. van der Salm A, Nene AV, Maxwell DJ,. et al. Gait impairments in a group of patients with incomplete spinal cord injury and their relevance regarding therapeutic approaches using functional electrical stimulation. Artif Organs 2005;29(1):8-14.

12. Nene AV, Hermens HJ, Zilvold G. Paraplegic locomotion: a review. Spinal Cord 1996;34(9):507-524.

13. Somers M. Spinal cord injury: functional rehabilitation. London: Prentice-Hall; 2001.

14. Atrice MB. Lower extremity orthotic management for the spinal-cord-injured client. Spinal Cord Inj Rehabil 2000;5(4):1-10.

15. O’ Sullivan SB, Schmitz TJ, eds. Physical rehabilitation – assessment and treatment. Philadelphia: F.A. Davis Company; 2000.

16. Umphred DA. Neurological rehabilitation. St. Louis: Mosby; 2001.

17. Maxwell DJ, Granat MH, Baardman G, Hermens HJ. Demand for and use of functional electrical stimulation systems and conventional orthoses in the spinal lesioned community of the UK. Artif Organs 1999;23(5):410-412.

18. Lehmann JF. Biomechanics of ankle-foot orthoses: prescription and design. Arch Phys Med Rehabil 1979;60(5):200-207.

19. Craik RL. Recovery processes: maximizing function. In: Liser MJ, ed. Contemporary management of motor problems. Fredericksburg, VA: Bookcrafters; 1991: 165-174.

20. Gordon J. Assumptions underlying physical therapy intervention: Theoretical and historical perspectives. In: Carr JH, Shepherd RB, eds. Movement science: Foundations for physical therapy in rehabilitation. 1st ed. Rockville: Aspen Publishers; 1987: 1-30.

21. Ramon y Cajal S. Degeneration and regeneration of the nervous system. London: Oxford University Press; 1928.

22. American Physical Therapy Association. Guide to physical therapy practice. 2nd ed. Alexandria, VA: 2001.

23. Kasaoka K, Sankai Y. Predicting control estimating operator’s intention for stepping-up motion by exo-skeleton type power assist system. Proceedings: IEEE/RSJ International Conference on Intelligent Robots and Systems 2001;3:1578-1583.

24. Kawamoto H, Sankai Y. Power assist method based on phase sequence driven by interaction between human and robot suit. Proceedings: IEEE International Workshop on Robot and Human Interactive Communication 2004;1:491-496.

25. Ferris DP, Sawicki GS, Domingo A. Powered lower limb orthoses for gait rehabilitation. Top Spinal Cord Inj Rehabil 2005;11(2):34-49.

26. Van de Crommert HW, Mulder T, Duysens J. Neural control of locomotion: sensory control of the central pattern generator and its relation to treadmill training. Gait Posture 1998;7(3):251-263.

27. Edgerton VR, Tillakaratne NJ, Bigbee AJ, et al. Plasticity of the spinal neural circuitry after injury. Annu Rev Neurosci 2004;27:145-167.

28. Grillner S. Interaction between central and peripheral mechanisms in the control of locomotion. Prog Brain Res 1979;50:227-235.

29. Grillner S. Neurobiological bases of rhythmic motor acts in vertebrates. Science 1985;228(4696):143-149.

30. Wolpaw JR. Acquisition and maintenance of the simplest motor skill: investigation of CNS mechanisms. Med Sci Sports Exerc 1994;26(12):1475-1479.

31. Rossignol S, Chau C, Brustein E, et al. Locomotor capacities after complete and partial lesions of the spinal cord. Acta Neurobiol Exp 1996;56(1):449-463.

32. Barbeau H, Danakas M, Arsenault B. The effects of locomotor training in spinal cord injured subjects: a preliminary study. Restor Neurol Neurosci 1993;5:81-84.

33. Lovely RG, Gregor RJ, Roy RR, Edgerton VR. Effects of training on the recovery of full-weight-bearing stepping in the adult spinal cat. Exp Neurol 1986;92(2):421-435.

34. Barbeau H, Julien C, Rossignol S. The effects of clonidine and yohimbine on locomotion and cutaneous reflexes in the adult chronic spinal cat. Brain Res 1987;437(1):83-96.

35. Duysens J, Pearson KG. Inhibition of flexor burst generation by loading ankle extensor muscles in walking cats. Brain Res 1980;187(2):321-332.

36. de Leon RD, Hodgson JA, Roy RR, Edgerton VR. Locomotor capacity attributable to step training versus spontaneous recovery after spinalization in adult cats. J Neurophysiol 1998;79(3):1329-1340.

37. Dobkin BH. Neuroplasticity. Key to recovery after central nervous system injury. West J Med 1993;159(1):56-60.

38. Edgerton VR, de Leon RD, Tillakaratne N, et al. Use-dependent plasticity in spinal stepping and standing. Adv Neurol 1997;72:233-247.

39. Barbeau H, McCrea DA, O’Donovan MR, et al. Tapping into spinal circuits to restore motor function. Brain Res Brain Res Rev 1999;30(1):27-51.

40 Barbeau H, Blunt R. A novel interactive locomotor aproach using body weight support to retrain gait in spastic paretic subject. In: Wernig A, ed. Plasticity of motoneuronal connections. Amsterdam: Elsevier Science; 1991: 461-474.

41. Behrman AL, Bowden MG, Nair PM. Neuroplasticity after spinal cord injury and training: an emerging paradigm shift in rehabilitation and walking recovery. Phys Ther 2006; 86(10):1406-1425.

42. Behrman AL, Harkema SJ. Locomotor training after human spinal cord injury: a series of case studies. Phys Ther 2000;80(7):688-700.

43. Behrman AL, Lawless-Dixon AR, Davis SB, et al. Locomotor training progression and outcomes after incomplete spinal cord injury. Phys Ther 2005;85(12):1356-1371.

44. Wernig A, Muller S., Nanassy A, Cagol E. Laufband therapy based on ‘rules of spinal locomotion’ is effective in spinal cord injured persons. Eur J Neurosci 1995;7(4):823-829.

45. Barbeau H, Wainberg M, Finch L. Description and application of a system for locomotor rehabilitation. Med Biol Eng Comput 1987;25(3):341-344.

46. Harkema SJ. Neural plasticity after human spinal cord injury: application of locomotor training to the rehabilitation of walking. Neuroscientist 2001;7(5):455-468.

47.  Harkema SJ, Hurley SL, Patel UK, et al. Human lumbosacral spinal cord interprets loading during stepping. J Neurophysiol 1997;77(2):797-811.

48. Dobkin BH, Harkema S, Requejo P, Edgerton VR. Modulation of locomotor-like EMG activity in subjects with complete and incomplete spinal cord injury. J Neurol Rehabil 1995; 9(4):183-190.

49. Schmidt RA, Young DE. Methodology for motor learning: A paradigm for kinematic feedback. J Mot Behav 1991;23(1):13-24.

50. Edgerton VR, Roy RR, Hodgson JA, et al. A physiological basis for the development of rehabilitative strategies for spinally injured patients. J Am Paraplegia Soc 1991;14(4): 150-157.

51. Pang MY, Yang JF. The initiation of the swing phase in human infant stepping: importance of hip position and leg loading. J Physiol 2000;528 Pt 2:389-404.

52. Dietz V, Muller R, Colombo G. Locomotor activity in spinal man: significance of afferent input from joint and load receptors. Brain 2002;125(Pt 12):2626-2634.

53. Dietz V, Duysens J. Significance of load receptor input during locomotion: a review. Gait Posture 2000;11(2):102-110.

54. Dietz V. Evidence for a load receptor contribution to the control of posture and locomotion. Neurosci Biobehav Rev 1998;22(4):495-499.

55. Dietz V. Locomotor training in paraplegic patients. Ann Neurol 1995;38(6):965.

56. Wernig A, Muller S. Laufband locomotion with body weight support improved walking in persons with severe spinal cord injuries. Paraplegia 1992;30(4):229-238.

57. Wernig A, Nanassy A, Muller S. Laufband (treadmill) therapy in incomplete paraplegia and tetraplegia. J Neurotrauma 1999;16(8):719-726.

58. Gardner MB, Holden MK, Leikauskas JM, Richard RL. Partial body weight support with treadmill locomotion to improve gait after incomplete spinal cord injury: a single-subject experimental design. Phys Ther 1998;78(4):361-374.

59. Wirz M, Colombo G, Dietz V. Long term effects of locomotor training in spinal humans. J Neurol Neurosurg Psychiatry 2001;71(1):93-96.

60. Barbeau H, Pepin A, Norman KE, et al. Walking after spinal cord injury: control and recovery. Neuroscientist 1998;4(1):14-24.

61. Behrman AL, Harkema SJ. Recovery of walking: locomotor training after human spinal cord injury. (submitted).

62. Dietz V, Colombo G, Jensen L, Baumgartner L. Locomotor capacity of spinal cord in paraplegic patients. Ann Neurol 1995;37(5):574-582.

63. Nair PM, Rooney KL, Kautz AL, Behrman AB. Stepping with an ankle foot orthosis re-examined: A mechanical perspective for clinical decision making. Clin Biomech 2010;25(6):618-622.

64. Mandzak-McCarron K, Drayton-Hargrove S. Ambulation aids. Rehabil Nurs 1987;12(3): 139-141.

65. Mulley G. Walking frames. BMJ 1990;300(6729):925-927.

66. Ounpuu S, Bell KJ, Davis RB 3rd, DeLuca PA. An evaluation of the posterior leaf spring orthosis using joint kinematics and kinetics. J Pediatr Orthop 1996;16(3):378-384.

67. Romkes J, Brunner R. Comparison of a dynamic and a hinged ankle–foot orthosis by gait analysis in patients with hemiplegic cerebral palsy. Gait Posture 2002;15(1):18-24.

(Visited 1,015 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.

This site uses Akismet to reduce spam. Learn how your comment data is processed.