Poststroke Considerations in AFO Usage

By Kyle Sherk, MS, CPO
Kyle Sherk, MS, CPO

Just as physicians and pharmacists must take into consideration the side effects of a single medication and its potential interactions with other medications when determining its appropriateness for a particular patient, so should the same consideration be given when providing an orthotic device to a person who has suffered a stroke.

The O&P profession and physiology researchers are becoming more aware of the impact that external O&P devices may have on body systems unrelated to those they are intended to treat. Variables such as the pressure, height, and weight of devices can be controlled to a certain extent through engineering principles. However, the disease or disability etiology may lead to unintended consequences of using an orthosis. For example, a poststroke patient will likely bear weight unevenly between his or her limbs. Then an improperly fitting AFO may lead the patient to hardly bear weight through the affected limb to avoid pain from edge pressure, further limiting the loading of the affected limb. Research on clinical populations is exposing practitioners of all disciplines to more of the consequences of current interventions, sometimes leaving professionals with more questions than answers about what effect prescribed devices may be having on patients.

Consider functional electrical stimulation (FES): Here is a treatment that has shown many positive effects on the body but is still categorized as experimental by many insurance companies. However, the continued development and expanding use of neuromuscular electrical stimulation in patients who have suffered stroke or have cerebral palsy has allowed patients' bodies to stabilize and returned function to otherwise paralyzed muscles.1 FES has also been shown to decrease edema, maintain or improve joint range of motion (ROM), and increase muscle size.2 While volitional muscle control may still be lacking, the increase in size equates to an increase in strength.3,4 This effect, in turn, may assist in the decrease of spastic responses by sending an inhibitory signal to retard the reflex arc effecting antagonist muscle(s) to the desired motion. This is a logical assumption from a neurological point of view, but it has only been suggested as an effect through scientific testing. This assumption is an important example of where anecdotal evidence meets scientific rigor and must be carefully evaluated. However, until coverage for FES use is more accepted, orthotists will rely upon AFOs to assist patients in returning to ambulatory status.

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The purpose of this article is to provide a rough outline of the physiological effects of general AFO design on the bones, muscles, and blood flow of stroke survivors. While treating poststroke patients with orthotic intervention is not new, the way O&P practitioners view treatment options for these patients is changing. No matter the method of assisting the patient, the importance of returning a patient to ambulatory status cannot be stressed enough. Minimizing the known effects of bed rest and disuse, by whatever method is acceptable to the patient, should be our first goal. As research continues to elucidate the effects of AFOs on the physiology of stroke survivors, the AFO's design should evolve to decrease any resulting negative effects.

Current Research

Bones

Our understanding of the poststroke patient population continues to grow as more researchers explore the physiological effects of stroke. Outside of the direct consequences of stroke on the nervous system, there are disuse effects from the recovery period and potential impacts on muscles and bones from orthotic use. Basic research on this patient population has shown that simply regaining the ability to ambulate does not lead to the normal increases in bone strength seen in the fracture immobilization population.3,5,6 Further, it is still not known if poststroke patients who use an AFO to ambulate are actually shielding the bones from the needed forces to return bones to healthy levels of mineralization and strength.7 It may seem difficult to differentiate between the effects of the bed-rest period and the effects of AFO usage, but remember that weight would be applied, at least partially, through the affected limb with any supporting device and definitely through the sound limb. Additionally, bones can take up to six months to show any significant change in size, density, or strength, so there is a lag in radiologically visible changes in the bones from any intervention. The few longitudinal studies that have been completed examined a heterogeneous poststroke population that included patients who would not return to independent ambulatory status.5,8-10 This gave the researchers a broader view of the possible effects of stroke and the subsequent recovery period but does not allow for the differentiation of the effects of the stroke from those of any assistive devices. Few studies have used orthotic use as an inclusion or exclusion criteria, which could be a confounding factor of the results.

Neuromuscular

Studies on the general effects of AFOs have shown that the muscular recruitment is altered simply by using an AFO.11 Limiting ankle ROM may also lead to decreased plantarflexor muscle activation, an unintended consequence of correcting swing-phase toe clearance with a posterior stop on an AFO. The data from fracture-healing studies show that limiting ROM leads to atrophy of the muscles that cross the limited joint.12 Additionally, placing a muscle in a shortened position accelerates the atrophy of the shortened muscle-accounting for the heel height of a shoe to set the shank vertically shortens the gastroc-soleus complex and could accelerate the atrophy of the calf musculature.8 So, while some neuromuscular effects of stroke are obvious and lead the patient to an O&P practitioner, some are not directly observable or are not evident until other factors change in the patient's situation. Consider this scenario: A patient presents with 3+ of 5 hamstring strength by manual muscle testing but still hyperextends his or her knee through stance phase while wearing an AFO. The hyperextension could be due to a recruitment timing issue, which was not seen at the initial evaluation due to limited walking ability and heavy reliance on parallel bars at that visit.

Blood Flow

Some poststroke patients suffer effects on the autonomic nervous system in addition to the volitional muscle or sensory systems, leading to uncontrollable changes in blood flow through the limbs.13-15 Differentiating effects on blood flow from stroke versus effects from AFO usage will be extremely difficult. Therefore, any potential orthosis-related physiological effect to blood flow may be best studied in another clinical patient population, such as individuals suffering from radiculopathy-induced foot drop, where autonomic effects are rarer. This difficulty in differentiating the source of a change in blood flow can stem from two causes: a direct autonomic effect from the stroke and the effect of the stroke on volitional control of the muscles on the affected side, since it is known that blood flow in the legs is partially controlled through muscular contractions.16,17 As mentioned previously, AFOs can further limit muscular contractions in the calf, which may exacerbate the decrease in blood flow in the affected calf and result in an increase in edema.

Monitoring AFO Effects

Simple video recording and analysis allow for thorough tuning of an AFO's alignment within the shoe to improve the patient's gait. These recordings allow for a digital record of gait changes as a result of orthotic use and can keep track of any changes and the amount of change in the patient's gait pattern that the tuning may have. Short videos, even ones that only record the patient's feet, can also track longitudinal changes in the patient's gait, revealing decrements or improvements in the patient's health. Continued physical therapy should lead to increased stride length, increased gait speed, and, potentially, increased cardiovascular potential.18 Conversely, inactivity could lead the patient to return to a stepto pattern after having achieved a more normal step-through pattern following his or her therapy regimen. As medical practitioners, we are all at least vaguely aware of the downward spiral that inactivity has on general health status.

The Future

As medicine turns to a more holistic view of the body and healing, we O&P practitioners should shift our focus toward more holistic fittings. For instance, checking for a functional leg-length discrepancy (fLLD) in association with knee hyperextension and ensuring the correcting orthosis does not lead to fLLD will keep patients more comfortable and satisfied that we care about them more than filling a prescription. Knowing what long-term effects our devices may have on the patients we serve, as discussed with poststroke patients and AFO usage, will help to elevate our profession from the art it began as to the science that it can be.

Kyle Sherk, MS, CPO, is a member of the Lower Limb Orthotics Society and the Lower Limb Prosthetics Society of the American Academy of Orthotists and Prosthetists (the Academy). He has been practicing orthotics and prosthetics for nine years. Sherk earned his master of science degree in exercise physiology from the University of Oklahoma, Norman, in 2011 while continuing to see patients. He is currently seeking new research avenues to assist in developing rehabilitation protocols to limit physiological deficits associated with amputation and the use of orthotic devices.

Society Spotlight is a presentation of clinical content by the societies of the Academy in partnership with The O&P EDGE.

References

  1. Damiano, D. L., L. A. Prosse, L. A. Curatalo, and K. E. Alter. 2013. Muscle plasticity and ankle control after repetitive use of a functional electrical stimulation device for foot drop in cerebral palsy. Neurorehabilitation & Neural Repair 27(3):200-7.
  2. Yan, T., C. W. Hui-Chan, and L. S. Li. 2005. Functional electrical stimulation improves motor recovery of the lower extremity and walking ability of subjects with first acute stroke: A randomized placebo-controlled trial. Stroke 36(1):80-5.
  3. Davies, C. T., and A. J. Sargeant. 1975. Effects of exercise therapy on total and component tissue leg volumes of patients undergoing rehabilitation from lower limb injury. Annals of Human Biology 2(4):327-37.
  4. Suetta, C., P. Aagaard, A. Rosted, A. K. Jakobsen, B. Duus, M. Kjaer, and S. P. Magnusson. 2004. Training-induced changes in muscle CSA, muscle strength, EMG, and rate of force development in elderly subjects after long-term unilateral disuse. Journal of Applied Physiology 97(5):1954-61.
  5. Jørgensen, L., B. K. Jacobsen, T. Wilsgaard, and J. H. Magnus. 2000. Walking after stroke: Does it matter? Changes in bone mineral density within the first 12 months after stroke. A longitudinal study. Osteoporosis International 11(5):381-7.
  6. Jørgensen, L., and B. K. Jacobsen. 2001. Changes in muscle mass, fat mass, and bone mineral content in the legs after stroke: A 1 year prospective study. Bone 28(6):655-9.
  7. Sherk, K. A., V. D. Sherk, M. A. Anderson, D. A. Bemben, and M. G. Bemben. 2013. Differences in tibia morphology between the sound and affected sides in ankle-foot orthosis-using survivors of stroke. Archives of Physical Medicine and Rehabilitation 94(3):510-5.
  8. Bainbridge, N. J., M. W. J. Davie, and M. J. Haddaway. 2006. Bone loss after stroke over 52 weeks at os calcis: Influence of sex, mobility and relation to bone density at other sites. Age and Ageing 35(2):127-32.
  9. Newham, D. J., and S. F. Hsiao. 2001. Knee muscle isometric strength, voluntary activation and antagonist co-contraction in the first six months after stroke. Disability and Rehabilitation 23(9):379-86.
  10. Hafer-Macko, C. E., A. S. Ryan, F. M. Ivey, and R. F. Macko. 2008. Skeletal muscle changes after hemiparetic stroke and potential beneficial effects of exercise intervention strategies. Journal of Rehabilitation Research & Development 45(2):261-72.
  11. Hesse, S., C. Werner, K. Matthias, K. Stephen, and M. Beteanu. 1999. Non-velocity-related effects of a rigid double-stopped ankle-foot orthosis on gait and lower limb muscle activity on hemiparetic subjects with an equinovarus deformity. Stroke 30(9):1855-61.
  12. Booth, F. W. 1977. Time course of muscular atrophy during immobilization of hindlimbs in rats. Journal of Applied Physiology 43(4):656-61.
  13. Kroese, A. J. 1977. The effect of inactivity on reactive hyperaemia in the human calf: A study with strain gauge plethysmography. Scandinavian Journal of Clinical & Laboratory Investigation 37(1):53-8.
  14. Ivey, F. M., A. W. Gardner, C. L. Dobrovolny, and R. F. Macko. 2004. Unilateral impairment of leg blood flow in chronic stroke patients. Cerebrovascular Diseases 18(4):283-9.
  15. Kroese, A. J. 1977. Reactive hyperemia in the calf of trained and untrained subjects: A study with strain gauge plethysmography. Scandinavian Journal of Clinical & Laboratory Investigation 37(2):111-5.
  16. Takeyasu, N., T. Sakai, S. Yabuki, and M. Machu. 1989. Hemodynamic alterations in hemiplegic patients as a cause of edema in the lower extremities. International Angiology 8(1):16-21.
  17. McDaniel, J., S. J. Ives, R. S. Richardson. 2012. Human muscle length-dependent changes in blood flow. Journal of Applied Physiology 112(4):560-5.
  18. Gardner, A. W., L. A. Killewich, L. I. Katzel, C. J. Womack, P. S. Montgomery, R. B. Otis, and T. Fonong. 1999. Relationship between free-living daily physical activity and peripheral circulation in patients with intermittent claudication. Angiology 50(4):289-97.