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Foot function and low back pain
The Foot (1999) 9, 175–180 © 1999 Harcourt Publishers Ltd
REVIEW ARTICLE
Foot function and low back pain A. R. Bird, C. B. Payne SUMMARY. The suggestion that foot posture may affect low back pain is one that has received some attention in the literature. This has principally involved theoretical mechanisms that may link the two. This paper reviews each of these mechanisms in turn, and comments upon directions for future research in the area. © 1999 Harcourt Publishers Ltd
how foot function may affect the lower back. The purpose of this paper is to review the diverse hypothetical mechanisms (Table 1) by which the foot may affect the low back.
Pain in the lower back is of major concern to health care systems, with an epidemic of low back pain (LBP) and disability occurring in the industrialized world since World War II. LBP has been defined as any pain between the 12th rib and the gluteal fold. After reviewing all published prevalence literature, Loney and Stratford1 estimated that the point prevalence rate of LBP in North America is 5.6%. Lifetime incidence has been estimated at 60%–85% of the Westernized population by a number of studies. Within the Victorian (Australia) compulsory worker’s compensation scheme during 1997–1998, back injury made up the largest component on non-fatal injuries, with the cost to the community in excess of A$410 million dollars (USS$270 million) for a population of approximately 4.5 million people.2 Most acute episodes of LBP tend to resolve or improve within 1–2 weeks, but chronic or recurrent back symptoms are variable. The traditional treatment of back pain has been bedrest; more recently the preferred approach to management involves light activity.3 Trends in management of LBP now also include ‘functional restoration’ programs that return people with back injury to the workplace to undertake light tasks. However, the positive outcomes of such programmes have been recently questioned due to poor research methodologies.4 The natural history of back pain is characterized by variability and change rather than predictability and stability.5 Due to this unpredictable nature, low back pain remains a difficult area to research. The cause of persistent back pain remains poorly understood. Approximately 70% of cases were described as ‘non-specific’ or ‘miscellaneous’ in a recent estimate of physician office visits in the USA.6 There are relatively few studies that look at
Table 1 Theoretical mechanisms that interrelate foot posture and LBP
Correspondence to: Adam Bird BPod (Hons), Department of Podiatry, School of Human Biosciences, La Trobe University Bundoora, Victoria, Australia 3083. Tel: +613 9479 5838; Fax: +613 9479 5787; E-mail: [email protected]
a. b. c. d. e.
HEEL HEIGHT AND FOOTWEAR Of all the features of shoes that might influence proximal mechanical function, increased footwear heel height (beyond approximately 2.5 cm) has long been implicated as being detrimental for wearers. High heels have been demonstrated to lead to an increase in such parameters as plantar pressures7,8 and increase knee joint compressive forces.9 Shoe heel height may have a large effect on the lower back due to changes in joint alignment and muscular activity. It is commonly believed that there is an increase in lumbar lordosis when wearing high heels.10 De Lateur et al.11 investigated static and dynamic lumbar lordosis with and without the participants wearing high-heeled shoes and found there was no significant difference in lumbar lordosis for female subjects. However, a small decrease in dynamic lumbar lordosis was measured in male subjects. Franklin et al.12 reported a trend of a reduction in lumbar lordosis when participants in their study stood on a 5.1 cm heel lift. The increase in lumbar lordosis previously considered to exist may have been overstated due to the greater gluteal prominence that is seen when wearing high-heeled shoes.13
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Heel height of footwear; inadequate shock absorption; factors related to excessive foot pronation; functional limb length discrepancy; sagittal plane blockade.
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Smith and Helms14 linked ‘improper’ shoes, in particular with ‘inappropriate’ heel height, with musculoskeletal pathology.14
INADEQUATE SHOCK ABSORPTION The foot interacts with the ground to introduce impulsive stress into the skeleton. This stress must be attenuated promptly and without damaging the more fragile structures of the body. ‘Shock’ is progressively attenuated as it travels proximally through the body and it is suggested that if this is impaired within the lower extremities, it may lead to pathology in the low back. Voloshin and Wosk15–18 have studied the shock attenuative ability of the body. Their first study measured propagation and attenuation of intermittent shock waves on 39 clinically healthy participants (average age 17.1 years) as they entered the body from the point of heel contact during gait. They strapped accelerometers to various points (the tibial tuberosities, medial femoral condyles, sacrum and forehead) and measured their output. The subject group was subsequently divided into two groups: balanced and unbalanced, referring to how symmetrical the impact forces were on each side of the body. They hypothesised that a deficiency or asymmetry in the attenuational capacity of different parts of the body may lead to joint degeneration. Testing similar to this may be useful in determining which people require preventative action to delay this process.15 A later study utilized the same protocol but divided the participants into four groups – ‘healthy’ persons, people with unilateral knee pain, people who had undergone a knee meniscectomy and people with LBP. The accelerometer signal intensity at the foreheads of all groups was approximately the same but the femoral signal in the LBP group was significantly less than the other groups. The authors postulated that this was to protect the lumbar spine from excessive shock (as it could not attenuate shock as effectively) and was a consequence of these subjects possibly using a different gait pattern. However, gait parameters were not measured in this study. An earlier study,16 looking at the effect of artificial shock absorbers (viscoelastic insoles), showed an average 42% reduction in the peak vertical impact force at heel strike. This was followed by a larger study involving participants with LBP, using viscoelastic inserts with ‘flexible and lightweight’ shoes.18 Use of this therapy lead to a ‘rapid and surprisingly significant improvement’ of pain and patient mobility in approximately 80% of the patients at the one-year follow-up. The viscoelastic insert group did not receive ongoing conservative treatment. A smaller control group of 54 patients was derived from participants who discontinued wearing the insoles of their own volition after 2–3 weeks – so were not a randomThe Foot (1999) 9, 175–180
ized control group. This group had a 45% improvement with normal conservative treatment which included bedrest, analgesia, sacroiliac joint manipulation, back-muscle strengthening and paraspinal infiltration of a methylprednisolone–lignocaine solution. This improvement in the control group with standard conservative treatments highlights the variable nature and natural history of lower back pain. Foot types such as club foot or cavus feet are often regarded as intrinsically lacking in the ability to properly shock absorb. Additionally, such foot types are suggested as being a predisposing factor to the development of LBP. Bjönness19 investigated 93 adults with club feet, 83% of whom had residual deformity after childhood surgery. He noted no significant difference between this group and the general population in terms of the prevalence of LBP. In contrast, a single subject case study by Builder and Marr20 investigated the positive effect that foot orthoses had on the LBP of a subject with cavus feet. The rationale for the prescription of orthoses focused on their proposed cushioning effect on the lower extremities. A recent study by Ogon et al.21 investigated the link between arch height and impact loading in the lower back during running. Twelve subjects ran with an accelerometer attached to their L3 spinous process, both barefoot and in a standard running shoe. The subjects had previously been split into two groups determined by arch height (high and low). This was based upon a static stance measurement of a single limb, and did not consider any other biomechanical measurements of the lower extremities. The researchers found that there was a significantly lower acceleration amplitude and rate in the ‘high-arch’ group compared to a ‘low-arch’ group. The authors concluded that a ‘high-arch’ foot type has an intrinsically better shock absorbing capacity than a foot with a ‘low arch’. The authors attempt to explain this by looking at other results derived from the study. These included a slight positive correlation between arch height and heel loading rate for the ‘medial force component’ measured by a force plate simultaneously with the accelerometry data. They suggested that a high-arched foot led to more internal rotation of the tibia at heel contact, and absorbed shock earlier (and therefore more distally) compared to a low-arched foot. This was also found by Nigg et al.22 Studies that reported higher incidence of lower extremity pathology with a high-arched foot (as compared to a lowerarched foot) were also used as supporting evidence.23,24 One variable that did substantially decrease acceleration rate and amplitude at the lower back in this study was the wearing of footwear compared to being measured barefoot. The type and softness of footwear worn (or the foot-surface interface) may be implicated in the development of LBP during prolonged upright activity such as standing or walking. Hansen et al.25 © 1999 Harcourt Publishers Ltd
Foot function and low back pain investigated this relationship using a simulated workplace. They used 8 subjects who undertook 2 hours of simulated standing and 2 hours of simulated work tasks using 4 combinations of soft running shoes, clogs, a soft mat and concrete underfoot. An EMG electrode placed over the erector spinae muscle during the testing indicated that there were signs of muscular fatigue as time progressed, particularly when the subjects were performing a simulated standing task. Subjects also reported a four- to sixfold increase in their perceived lumbar fatigue. The authors postulated that sustained trunk extensor muscle fatigue may lead to an overloading of the ligaments and other passive structures of the spine. Foot oedema halved when wearing running shoes rather than clogs whilst standing or working. The soft mat had no effect on foot oedema. No comparative analysis was made between footwear worn and muscular fatigue in the lower back (measured via EMG or subjective statement). The authors suggested that the ‘dampening’ effect of soft shoes during gait may influence the impact forces in the spine. The attenuation of ground reaction forces by the body in gait appears to be connected to problems in the lower back, but the literature is far from conclusive. Foot structure may also play a part with the transmission of such forces, but there is no obvious link from modified shock absorption to the development of LBP.
FACTORS RELATED TO EXCESSIVE FOOT PRONATION Within the literature, there are many theoretical explanations linking excessive foot pronation at heel contact or failed foot resupination during propulsion to abnormal motion within the pelvis and lower back. These theories interrelate the motion of body segments and surrounding neural, bony, ligamentous and muscular components during the gait cycle. A theoretical description of the chain of events involves the foot pronating excessively or for too long during the gait cycle. Theoretically, this results in increased internal rotation of the leg and an anterolateral pelvic tilt. This may place an increased strain on a number of pelvic muscles including the iliopsoas, piriformis and gluteus maximus, and subsequently lead to a rotation of the affected lumbar vertebral bodies resulting in a functional lumbar scoliosis. It is thought that the altered dynamic forces within the lower back may be a contributory factor to the development of LBP as they pull the inferior section of the sacroiliac joint forward. At the same time, to decrease the stretch on the iliopsoas, the subject may lean backward by active contraction of erector spinae, theoretically resulting in muscular fatigue.26–28 In Rothbart and Estabrook’s29 investigation of 97 participants with chronic LBP, 81 of whom were designated ‘excessive pronators’ by the difference © 1999 Harcourt Publishers Ltd
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between their neutral and resting calcaneal stance position measurements being greater than 6°, the participants subsequently were treated with foot orthoses and chiropractic manipulation. At a 6-month review, almost all related a ‘moderate-to-complete’ reduction in LBP symptoms. The authors deemed that therefore there was a ‘high correlation between excessive pronation and LBP’. The authors also considered forefoot to rearfoot position and one foot type that was suggested to require excessive foot pronation to achieve a plantigrade foot during gait was forefoot varus. Forefoot varus has been described as an osseous foot deformity whereby the plantar plane of the forefoot is inverted relative to the plantar plane of the calcaneous when the foot is in a neutral position.30 However, the existence of such a bony deformity has recently been questioned.31 A similarly aligned deformity, whose aetiology is related to soft-tissue adaptation, is known as a forefoot supinatus. The population prevalence of inverted forefoot reported is generally not separated into forefoot varus and forefoot supinatus categories. The majority of forefoot to rearfoot relationships are inverted,32,33 therefore an inverted forefoot deformity should not necessarily be viewed as an abnormality. The assertion by Root et al.30 that forefoot to rearfoot alignment should be parallel when the foot is in a neutral position is an ‘ideal’ and not a true representation of the asymptomatic population. Kidd31 argues that to have a bony forefoot varus is unlikely. It could be suggested that a forefoot supinatus deformity involving soft-tissue contracture is more likely to occur than an osseous forefoot varus. This distinction between the two deformities of the forefoot where the forefoot is inverted is important given the results of the largest clinical study that has investigated the connection between a ‘forefoot varus’ and LBP. Rothbart et al.34 investigated 208 subjects with chronic LBP – 202 of whom were classified as possessing a ‘forefoot’ varus deformity greater than 16 mm. This measurement was derived with a Biovector™, a triangular wedge with a vertical millimetre scale. The wedge was placed under the medial forefoot by varying amounts until the subtalar joint was determined to be maximally congruent by palpation, as the knee was flexed and extended. This device has not been tested for reliability.35 It could be suggested that the investigators were not testing for a ‘forefoot varus’ at all, but some measurement of forefoot supinatus related to motion around the putative longitudinal axis of the midtarsal joint. The subsequent foot orthoses that were prescribed were of a propriety design – having a medial extension running all the way along the first ray, with this extrinsic varus wedge equal in height at the most medial point to the Biovector™ measurement under the first MTPJ. Rothbart and Yerratt believed that this design was ‘… essential in controlling mid to late stance hyperpronation’ and was required as ‘forefoot varum only involves the medial column of the foot … The Foot (1999) 9, 175–180
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[any] … force under the second metatarsal diaphysis could cause jamming …’.34 The design of this device is inconsistent with the commonly held assumption that the first ray should be allowed to adequately plantarflex for efficient propulsion during gait. The suggestion that all the subjects possessed a forefoot varus raises issues about reliability and validity of measurement, given the assumed relative rarity of forefoot varus. However, overall results were very positive in this study, with over 80% of the participants reporting at least a 50% improvement in their LBP when responding to a mailed questionnaire one year after treatment. Travell36 considered the Morton foot type as a contributor to the development of LBP. The proposed sequencing of events was that, during gait, compensation for a Morton’s foot leads to strain of the peroneus longus muscle, internal rotation of the knee and hip, overloading the muscles gluteus medius and minimus, with referred pain to the sacrum, buttock and thigh. He advised treatment with foot orthoses and trigger point therapy. Given the relative rarity of a true Morton’s foot type in the population, it is unlikely that this theoretical mechanism will be fully investigated. Within the category of LBP related to excessive foot pronation, it could be suggested that the development of LBP is due to two factors, working independently or together. The first factor may be the excessive internal rotation of the lower extremity during gait and the second the poor shock-absorbing characteristics of a foot contacting the ground excessively pronated.
FUNCTIONAL LIMB LENGTH DISCREPANCY If there is asymmetrical leg length, it is widely thought that this may correlate to altered and uneven forces within the lower back, and contribute to the development of LBP. A subset of the aetiological factors related to a difference in leg length involve functional changes to joints within the lower extremities, including foot posture and motion. Botte26 suggested that unilateral excessive foot pronation may functionally shorten the affected limb. Sanner et al.37 investigated the effect of subtalar joint motion on ankle joint height of 33 participants using radiographic measures of the talar trochlear surface. Evaluation of the radiographs demonstrated that supination of the foot from relaxed to neutral calcaneal stance position resulted in a significant increase in ankle joint height an average of 0.3 cm. This would suggest that altering subtalar position can functionally lengthen or shorten a limb. The literature that interrelates foot posture, functional limb length discrepancies and LBP is principally based on clinical folklore and on a case report involving a runner with a 2 cm limb length discrepancy (LLD) (R>L), who was noted to exhibit excesThe Foot (1999) 9, 175–180
sive rearfoot pronation (L>R). Treatment consisted of orthoses and a heel lift in the left shoe of 1 cm height – this height was determined by an osteopathic formula. For this patient, this treatment led to complete symptomatic relief of his chronic LBP.38 Although anecdotally the correlation between a functional LLD and LBP would appear strong, this is not proven. However, a subtle change in foot posture related to asymmetrical foot pronation theoretically could alter spinal mechanics, and will remain a feature to note in the clinical biomechanical examination of a person with LBP.
SAGITTAL PLANE BLOCKADE The sagittal plane facilitation of motion theory of foot function focuses on the ability of the sagittal plane pivots of the foot to function efficiently during gait.39 The most important of these is considered to be the first metatarsophalangeal joint, as its function is believed to be commonly compromised during gait. If sagittal plane pivoting about these joints is impeded during gait, this is defined as a sagittal plane blockage, and compensations within other segments of the body are predicted to occur. In the case of first metatarsophalangeal joint dysfunction, this is commonly defined as a functional hallux limitus.40,41 One consequence of functional failure of first metatarsophalangeal joint dorsiflexion relates to insufficient hip joint extension (involving biceps femoris contraction) at the midstance phase of the gait cycle.41 Normally, the weightbearing limb is beginning to extend out from under the body at the midstance phase of the gait cycle. However, with a sagittal plane blockade at the first metatarsophalangeal joint, hip joint extension may be impeded, which may be clinically seen as a lack of normal knee joint full extension just prior to contralateral heel strike. One of the muscles responsible for hip joint extension, biceps femoris, attaches to the sacrotuberous ligament which in turn is attached to the sacrum. A lack of biceps femoris contraction may stop normal nutation of the sacroiliac joint whereby the sacral base should move anteriorly and the apex posteriorly. This is thought to be needed for self-bracing of the sacroiliac joint during the midstance and propulsion phases of the gait cycle.41 Repetitive loading and motion of this joint in this unstable position is suggested to be a contributory factor to the development of LBP. Other muscles, such as iliopsoas and quatratus lumborum are also believed to function abnormally when a sagittal plane block is present.41 Dananberg and Guiliano’s42 clinical study involved 32 participants with chronic LBP who were unresponsive to previous traditional conservative medical management. Foot orthoses were designed with the aid of two-dimensional video analysis and in-shoe plantar pressure measurement. The aim was to pre© 1999 Harcourt Publishers Ltd
Foot function and low back pain scribe devices that would optimize sagittal plane motion and normalize centre of plantar pressure patterns in gait. The Quebec Back Pain Disability Scale43 was utilized prior to treatment, as well as approximately 1 month and 6 months post initial treatment. The participants experienced twice the improvement in their pain, and for twice as long as compared to participants in a study using traditional back pain treatment. It should be noted that the control group they were compared to were part of the validation for the Quebec BPDS, so are not a true control group.
DISCUSSION This paper has reviewed a number of mechanisms by which foot structure and function may influence the lower back. It is unclear which of the mechanisms is more important or if they work in combination to affect LBP. Laboratory experiments will be needed to investigate well-defined postural changes of foot posture, structure and function and how they correlate with more proximal changes in structural, kinematic and neuromuscular variables. Prospective controlled clinical studies are needed to determine the role of foot structure and function on those with chronic problems of the lower back. Such studies are difficult as there are many different types of orthoses that could be used and each of these will have a number of prescription variables. Measures will also be needed to determine if the foot orthoses are inducing the assumed structural and functional changes of the foot. Blinding participants in a study to the type of foot orthoses is difficult. Problems with research on LBP include the classification and diagnosis, or the inclusion criteria for a study. Selective inclusion has potential to bias results. Many patients with LBP undergo spontaneous resolution and the natural history is one of variability and change, so it is difficult to attribute improvements to the intervention. Outcome measures to determine the effect of interventions are problematic. For clinical research, the outcomes need to be valid and sensitive to detect changes. Most available outcome measures involve some form of subject or investigator measures of pain. Pain interpretation is multidimensional and is very subjective and may not necessarily be subjective enough to detect small changes. Some measures have been shown to have some validity and reliability.43,44,45 CONCLUSION This paper has presented a number of theoretical explanations for the development of LBP via abnormal foot function. These include heel height of footwear, inadequate shock absorption, functional limb length discrepancy and sagittal plane blockade. © 1999 Harcourt Publishers Ltd
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Research on foot function and LBP is fraught with difficulties. However, given the high burden to individuals and society of this problem and the potential significance of foot orthoses, further research is essential. REFERENCES 1. Loney P L, Stratford P W. The prevalence of low back pain in adults: a methodological review of the literature. Phys Ther 1999; 79(4): 384–397. 2. Victorian WorkCover Authority Statistical Report 1997–1998. Melbourne: Victorian WorkCover Authority, 1998. 3. Waddell G. Low back pain: a twentieth century health care enigma. Spine 1996; 21(24): 2820–2825. 4. Teasell R W, Harth M. Returning patients with chronic low back pain to work – revolution or fad? Spine 1996; 21(7): 844–847. 5. Von Korff M, Saunders K. The course of back pain in primary care. Spine 1996; 21(24): 2833–2839. 6. Hart L G, Deyo R A, Cherkin D C. Physician office visits for low back pain: frequency, clinical evaluation and treatment patterns from a US national survey. Spine 1995; 20(1): 11–19. 7. Nyska M, McCabe C, Linge K, Klenerman L. Plantar foot pressures during treadmill walking with high-heel and lowheel shoes. Foot Ankle Int 1996; 17(11): 662–666. 8. Mandato M G, Nester E. The effects of increasing heel height on forefoot peak pressure. J Am Pod Med Assoc 1999; 89(2): 75–80. 9. Kerrigan D C, Todd M K, Riley P O. Knee osteoarthritis: wearing high heels may be a factor. Lancet 1998 (351): 1399–1401. 10. Rossi W A. The sex life of the foot and shoe. London: Routledge & Kegan Paul, 1976. 11. de Lateur B J, Giaconi R M, Questad K, Ko M, Lehmann JF. Footwear and posture: compensatory strategies for heel height. Am J Phys Med Rehab 1991; 70(5): 246–254. 12. Franklin M E, Chenier T C, Brauninger L, Cook H, Harris S. Effect of positive heel inclination on posture. J Orthop Sports Phys Ther 1995; 21(2): 94–99. 13. Bryan J M, Mosner E, Shippee R, Stull M A. Investigation of the validity of postural evaluation skills in assessing lumbar lordosis using photographs of clothed subjects. J Orthop Sports Phys Ther 1990; 12(1): 24–29. 14. Smith E O, Helms W S. Natural selection and high heels. Foot Ankle Int 1999; 20(1): 55–57. 15. Wosk J, Voloshin A. Wave attenuation in skeletons of young healthy persons. J Biomech 1981; 14(4): 261–267. 16. Voloshin A, Wosk J. Influence of artificial shock absorbers on human gait. Clin Orthop and related research 1981(160): 52–56. 17. 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. 18. Wosk J, Voloshin A S. Low back pain: conservative treatment with artificial shock absorbers. Arch Phys Med Rehab 1985;66(March):145–148. 19. Bjönness T. Low back pain in persons with congenital club foot. Scand J Rehabil Med 1975(7):163–165. 20. Builder M A, Marr S J. Case history of a patient with low back pain and cavus feet. J Am Pod Assoc 1980;70(6):299–301. 21. Ogon M, Aleksiev A R, Pope M H, Wimmer C, Saltzman C L. Does arch height affect impact loading at the lower back level in running? Foot Ankle Int 1999;20(4):263–266. 22. Nigg B M, Cole G K, Nachbauer W. Effects of arch height of the foot on angular motion of the lower extremities in running. J Biomech 1993;26:909–916. 23. Giladi M, Milgrom C, Stein M et al. The lower arch, a protective factor in stress fractures: a prospective study of 295 military recruits. Orthop Rev 1985(14). 24. Cowan D N, Jones B H, Robinson J R. Foot morphologic characteristics and risk of exercise-related injury. Arch Fam Med 1993 (2): 773–777. 25. Hansen L, Winkel J, Jørgensen K. Significance of mat and shoe softness during prolonged work in (sic) upright position:
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based on measurements of low back muscle EMG, foot volume changes, discomfort and ground force reactions. Appl Ergon 1998; 29(3): 217–224. Botte R R. An interpretation of the pronation syndrome and foot types of patients with low back pain. J Am Pod Assoc 1981; 71(5): 243–253. Minkowsky I, Minkowsky R. The spine, an integral part of the lower extremity. In: Valmassey R, ed. Clinical biomechanics of the lower extremities. St Louis:Mosby, 1996: 96–112. Michaud T C. Foot orthoses and other forms of conservative foot care, 2nd edn. Massachusetts: Thomas C. Michaud, 1997. Rothbart B A, Estabrook L. Excessive pronation: a major biomechanical determinant in the development of chondromalacia and pelvic lists. J Manipulative Physiol Ther 1988; 11(5): 373–379. Root M L, Orien W P, Weed J H. Normal and abnormal motion of the foot. Los Angeles: Clinical Biomechanics Corp, 1977, vol 2. Kidd R. Forefoot varus – real or false, fact or fantasy? Australasian J Pod Med 1997; 31(3): 81–86. Garbalosa J C, McClure M H, Catlin P A, Wooden M. The frontal plane relationship of the forefoot to the rearfoot in an asymptomatic population. J Orthop Sports Phys Ther 1994; 20(4): 200–206. Arstrom M, Arvidson T. Alignment and joint motion in the normal foot. Journal of Orthopedic and Sports Phys Ther 1995; 22(5): 216–222. Rothbart B A, Hansen K, Liley P, Yerratt M K. Resolving chronic low back pain: the foot connection. Am J Pain Management 1995; 5(3): 84–90. Rothbart B A, Yerratt M K. An innovative mechanical approach to treating chronic knee pain: a bio-implosion model. Am J Pain Management 1994; 4(3): 123–128.
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36. Travell J. Low back pain and the Dudley J. Morton foot (long second toe). Arch Phys Med Rehabil 1975; 56: 566. 37. Sanner W H, Page JC, Tolboe H R, Blake R, Bax C A. A study of ankle joint height changes with subtalar joint motion. J Am Podiatr Assoc 1981; 71(3): 158–161. 38. Blake R L, Fettig M H. Chronic low back pain in a longdistance runner: a case report. J Am Podiatr Assoc 1983; 73(11): 598–601. 39. Payne C B, Dananberg H J. Sagittal plane facilitation of the foot. Australasian J Podiatr Med 1997; 31(1): 7–11. 40. Dananberg H J. Functional hallux limitus and its relationship to gait efficiency. J Am Podiatr Medical Association 1986; 76(11): 648–653. 41. Dananberg H J. Lower back pain as a gait-related repetitive motion injury. In: Vleeming A, Mooney V, Snijders C J, Dorman T A, Stoeckart R, eds. Movement, stability and low back pain: the essential role of the pelvis. Edinburgh Churchill Livingstone, 1997: 253–267. 42. Dananberg H J, Guiliano M. Chronic Low-back pain and its response to custom-made foot orthoses. J Am Podiatr Med Assoc 1999; 89(3): 109–117. 43. Kopec J A, Esdaile J M, Abrahamowicz M et al. The Quebec back pain disability scale. Spine 1995; 20(3): 341–352. 44. Roland M, Morris R. A study of the natural history of back pain. Part 1: Development of a reliable and sensitive measure of disability in low back pain. Spine 1983 (8): 141–144. 45. Hudson-Cook N, Green P, Jones P. A revised Oswestry disability questionnaire. In: Roland MO, Jenner JR, eds. Back Pain: New Approaches to Rehabilitation and Education. New York: Manchester University Press, 1994: 187–204.
© 1999 Harcourt Publishers Ltd
REVIEW ARTICLE
Foot function and low back pain A. R. Bird, C. B. Payne SUMMARY. The suggestion that foot posture may affect low back pain is one that has received some attention in the literature. This has principally involved theoretical mechanisms that may link the two. This paper reviews each of these mechanisms in turn, and comments upon directions for future research in the area. © 1999 Harcourt Publishers Ltd
how foot function may affect the lower back. The purpose of this paper is to review the diverse hypothetical mechanisms (Table 1) by which the foot may affect the low back.
Pain in the lower back is of major concern to health care systems, with an epidemic of low back pain (LBP) and disability occurring in the industrialized world since World War II. LBP has been defined as any pain between the 12th rib and the gluteal fold. After reviewing all published prevalence literature, Loney and Stratford1 estimated that the point prevalence rate of LBP in North America is 5.6%. Lifetime incidence has been estimated at 60%–85% of the Westernized population by a number of studies. Within the Victorian (Australia) compulsory worker’s compensation scheme during 1997–1998, back injury made up the largest component on non-fatal injuries, with the cost to the community in excess of A$410 million dollars (USS$270 million) for a population of approximately 4.5 million people.2 Most acute episodes of LBP tend to resolve or improve within 1–2 weeks, but chronic or recurrent back symptoms are variable. The traditional treatment of back pain has been bedrest; more recently the preferred approach to management involves light activity.3 Trends in management of LBP now also include ‘functional restoration’ programs that return people with back injury to the workplace to undertake light tasks. However, the positive outcomes of such programmes have been recently questioned due to poor research methodologies.4 The natural history of back pain is characterized by variability and change rather than predictability and stability.5 Due to this unpredictable nature, low back pain remains a difficult area to research. The cause of persistent back pain remains poorly understood. Approximately 70% of cases were described as ‘non-specific’ or ‘miscellaneous’ in a recent estimate of physician office visits in the USA.6 There are relatively few studies that look at
Table 1 Theoretical mechanisms that interrelate foot posture and LBP
Correspondence to: Adam Bird BPod (Hons), Department of Podiatry, School of Human Biosciences, La Trobe University Bundoora, Victoria, Australia 3083. Tel: +613 9479 5838; Fax: +613 9479 5787; E-mail: [email protected]
a. b. c. d. e.
HEEL HEIGHT AND FOOTWEAR Of all the features of shoes that might influence proximal mechanical function, increased footwear heel height (beyond approximately 2.5 cm) has long been implicated as being detrimental for wearers. High heels have been demonstrated to lead to an increase in such parameters as plantar pressures7,8 and increase knee joint compressive forces.9 Shoe heel height may have a large effect on the lower back due to changes in joint alignment and muscular activity. It is commonly believed that there is an increase in lumbar lordosis when wearing high heels.10 De Lateur et al.11 investigated static and dynamic lumbar lordosis with and without the participants wearing high-heeled shoes and found there was no significant difference in lumbar lordosis for female subjects. However, a small decrease in dynamic lumbar lordosis was measured in male subjects. Franklin et al.12 reported a trend of a reduction in lumbar lordosis when participants in their study stood on a 5.1 cm heel lift. The increase in lumbar lordosis previously considered to exist may have been overstated due to the greater gluteal prominence that is seen when wearing high-heeled shoes.13
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Heel height of footwear; inadequate shock absorption; factors related to excessive foot pronation; functional limb length discrepancy; sagittal plane blockade.
176
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Smith and Helms14 linked ‘improper’ shoes, in particular with ‘inappropriate’ heel height, with musculoskeletal pathology.14
INADEQUATE SHOCK ABSORPTION The foot interacts with the ground to introduce impulsive stress into the skeleton. This stress must be attenuated promptly and without damaging the more fragile structures of the body. ‘Shock’ is progressively attenuated as it travels proximally through the body and it is suggested that if this is impaired within the lower extremities, it may lead to pathology in the low back. Voloshin and Wosk15–18 have studied the shock attenuative ability of the body. Their first study measured propagation and attenuation of intermittent shock waves on 39 clinically healthy participants (average age 17.1 years) as they entered the body from the point of heel contact during gait. They strapped accelerometers to various points (the tibial tuberosities, medial femoral condyles, sacrum and forehead) and measured their output. The subject group was subsequently divided into two groups: balanced and unbalanced, referring to how symmetrical the impact forces were on each side of the body. They hypothesised that a deficiency or asymmetry in the attenuational capacity of different parts of the body may lead to joint degeneration. Testing similar to this may be useful in determining which people require preventative action to delay this process.15 A later study utilized the same protocol but divided the participants into four groups – ‘healthy’ persons, people with unilateral knee pain, people who had undergone a knee meniscectomy and people with LBP. The accelerometer signal intensity at the foreheads of all groups was approximately the same but the femoral signal in the LBP group was significantly less than the other groups. The authors postulated that this was to protect the lumbar spine from excessive shock (as it could not attenuate shock as effectively) and was a consequence of these subjects possibly using a different gait pattern. However, gait parameters were not measured in this study. An earlier study,16 looking at the effect of artificial shock absorbers (viscoelastic insoles), showed an average 42% reduction in the peak vertical impact force at heel strike. This was followed by a larger study involving participants with LBP, using viscoelastic inserts with ‘flexible and lightweight’ shoes.18 Use of this therapy lead to a ‘rapid and surprisingly significant improvement’ of pain and patient mobility in approximately 80% of the patients at the one-year follow-up. The viscoelastic insert group did not receive ongoing conservative treatment. A smaller control group of 54 patients was derived from participants who discontinued wearing the insoles of their own volition after 2–3 weeks – so were not a randomThe Foot (1999) 9, 175–180
ized control group. This group had a 45% improvement with normal conservative treatment which included bedrest, analgesia, sacroiliac joint manipulation, back-muscle strengthening and paraspinal infiltration of a methylprednisolone–lignocaine solution. This improvement in the control group with standard conservative treatments highlights the variable nature and natural history of lower back pain. Foot types such as club foot or cavus feet are often regarded as intrinsically lacking in the ability to properly shock absorb. Additionally, such foot types are suggested as being a predisposing factor to the development of LBP. Bjönness19 investigated 93 adults with club feet, 83% of whom had residual deformity after childhood surgery. He noted no significant difference between this group and the general population in terms of the prevalence of LBP. In contrast, a single subject case study by Builder and Marr20 investigated the positive effect that foot orthoses had on the LBP of a subject with cavus feet. The rationale for the prescription of orthoses focused on their proposed cushioning effect on the lower extremities. A recent study by Ogon et al.21 investigated the link between arch height and impact loading in the lower back during running. Twelve subjects ran with an accelerometer attached to their L3 spinous process, both barefoot and in a standard running shoe. The subjects had previously been split into two groups determined by arch height (high and low). This was based upon a static stance measurement of a single limb, and did not consider any other biomechanical measurements of the lower extremities. The researchers found that there was a significantly lower acceleration amplitude and rate in the ‘high-arch’ group compared to a ‘low-arch’ group. The authors concluded that a ‘high-arch’ foot type has an intrinsically better shock absorbing capacity than a foot with a ‘low arch’. The authors attempt to explain this by looking at other results derived from the study. These included a slight positive correlation between arch height and heel loading rate for the ‘medial force component’ measured by a force plate simultaneously with the accelerometry data. They suggested that a high-arched foot led to more internal rotation of the tibia at heel contact, and absorbed shock earlier (and therefore more distally) compared to a low-arched foot. This was also found by Nigg et al.22 Studies that reported higher incidence of lower extremity pathology with a high-arched foot (as compared to a lowerarched foot) were also used as supporting evidence.23,24 One variable that did substantially decrease acceleration rate and amplitude at the lower back in this study was the wearing of footwear compared to being measured barefoot. The type and softness of footwear worn (or the foot-surface interface) may be implicated in the development of LBP during prolonged upright activity such as standing or walking. Hansen et al.25 © 1999 Harcourt Publishers Ltd
Foot function and low back pain investigated this relationship using a simulated workplace. They used 8 subjects who undertook 2 hours of simulated standing and 2 hours of simulated work tasks using 4 combinations of soft running shoes, clogs, a soft mat and concrete underfoot. An EMG electrode placed over the erector spinae muscle during the testing indicated that there were signs of muscular fatigue as time progressed, particularly when the subjects were performing a simulated standing task. Subjects also reported a four- to sixfold increase in their perceived lumbar fatigue. The authors postulated that sustained trunk extensor muscle fatigue may lead to an overloading of the ligaments and other passive structures of the spine. Foot oedema halved when wearing running shoes rather than clogs whilst standing or working. The soft mat had no effect on foot oedema. No comparative analysis was made between footwear worn and muscular fatigue in the lower back (measured via EMG or subjective statement). The authors suggested that the ‘dampening’ effect of soft shoes during gait may influence the impact forces in the spine. The attenuation of ground reaction forces by the body in gait appears to be connected to problems in the lower back, but the literature is far from conclusive. Foot structure may also play a part with the transmission of such forces, but there is no obvious link from modified shock absorption to the development of LBP.
FACTORS RELATED TO EXCESSIVE FOOT PRONATION Within the literature, there are many theoretical explanations linking excessive foot pronation at heel contact or failed foot resupination during propulsion to abnormal motion within the pelvis and lower back. These theories interrelate the motion of body segments and surrounding neural, bony, ligamentous and muscular components during the gait cycle. A theoretical description of the chain of events involves the foot pronating excessively or for too long during the gait cycle. Theoretically, this results in increased internal rotation of the leg and an anterolateral pelvic tilt. This may place an increased strain on a number of pelvic muscles including the iliopsoas, piriformis and gluteus maximus, and subsequently lead to a rotation of the affected lumbar vertebral bodies resulting in a functional lumbar scoliosis. It is thought that the altered dynamic forces within the lower back may be a contributory factor to the development of LBP as they pull the inferior section of the sacroiliac joint forward. At the same time, to decrease the stretch on the iliopsoas, the subject may lean backward by active contraction of erector spinae, theoretically resulting in muscular fatigue.26–28 In Rothbart and Estabrook’s29 investigation of 97 participants with chronic LBP, 81 of whom were designated ‘excessive pronators’ by the difference © 1999 Harcourt Publishers Ltd
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between their neutral and resting calcaneal stance position measurements being greater than 6°, the participants subsequently were treated with foot orthoses and chiropractic manipulation. At a 6-month review, almost all related a ‘moderate-to-complete’ reduction in LBP symptoms. The authors deemed that therefore there was a ‘high correlation between excessive pronation and LBP’. The authors also considered forefoot to rearfoot position and one foot type that was suggested to require excessive foot pronation to achieve a plantigrade foot during gait was forefoot varus. Forefoot varus has been described as an osseous foot deformity whereby the plantar plane of the forefoot is inverted relative to the plantar plane of the calcaneous when the foot is in a neutral position.30 However, the existence of such a bony deformity has recently been questioned.31 A similarly aligned deformity, whose aetiology is related to soft-tissue adaptation, is known as a forefoot supinatus. The population prevalence of inverted forefoot reported is generally not separated into forefoot varus and forefoot supinatus categories. The majority of forefoot to rearfoot relationships are inverted,32,33 therefore an inverted forefoot deformity should not necessarily be viewed as an abnormality. The assertion by Root et al.30 that forefoot to rearfoot alignment should be parallel when the foot is in a neutral position is an ‘ideal’ and not a true representation of the asymptomatic population. Kidd31 argues that to have a bony forefoot varus is unlikely. It could be suggested that a forefoot supinatus deformity involving soft-tissue contracture is more likely to occur than an osseous forefoot varus. This distinction between the two deformities of the forefoot where the forefoot is inverted is important given the results of the largest clinical study that has investigated the connection between a ‘forefoot varus’ and LBP. Rothbart et al.34 investigated 208 subjects with chronic LBP – 202 of whom were classified as possessing a ‘forefoot’ varus deformity greater than 16 mm. This measurement was derived with a Biovector™, a triangular wedge with a vertical millimetre scale. The wedge was placed under the medial forefoot by varying amounts until the subtalar joint was determined to be maximally congruent by palpation, as the knee was flexed and extended. This device has not been tested for reliability.35 It could be suggested that the investigators were not testing for a ‘forefoot varus’ at all, but some measurement of forefoot supinatus related to motion around the putative longitudinal axis of the midtarsal joint. The subsequent foot orthoses that were prescribed were of a propriety design – having a medial extension running all the way along the first ray, with this extrinsic varus wedge equal in height at the most medial point to the Biovector™ measurement under the first MTPJ. Rothbart and Yerratt believed that this design was ‘… essential in controlling mid to late stance hyperpronation’ and was required as ‘forefoot varum only involves the medial column of the foot … The Foot (1999) 9, 175–180
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[any] … force under the second metatarsal diaphysis could cause jamming …’.34 The design of this device is inconsistent with the commonly held assumption that the first ray should be allowed to adequately plantarflex for efficient propulsion during gait. The suggestion that all the subjects possessed a forefoot varus raises issues about reliability and validity of measurement, given the assumed relative rarity of forefoot varus. However, overall results were very positive in this study, with over 80% of the participants reporting at least a 50% improvement in their LBP when responding to a mailed questionnaire one year after treatment. Travell36 considered the Morton foot type as a contributor to the development of LBP. The proposed sequencing of events was that, during gait, compensation for a Morton’s foot leads to strain of the peroneus longus muscle, internal rotation of the knee and hip, overloading the muscles gluteus medius and minimus, with referred pain to the sacrum, buttock and thigh. He advised treatment with foot orthoses and trigger point therapy. Given the relative rarity of a true Morton’s foot type in the population, it is unlikely that this theoretical mechanism will be fully investigated. Within the category of LBP related to excessive foot pronation, it could be suggested that the development of LBP is due to two factors, working independently or together. The first factor may be the excessive internal rotation of the lower extremity during gait and the second the poor shock-absorbing characteristics of a foot contacting the ground excessively pronated.
FUNCTIONAL LIMB LENGTH DISCREPANCY If there is asymmetrical leg length, it is widely thought that this may correlate to altered and uneven forces within the lower back, and contribute to the development of LBP. A subset of the aetiological factors related to a difference in leg length involve functional changes to joints within the lower extremities, including foot posture and motion. Botte26 suggested that unilateral excessive foot pronation may functionally shorten the affected limb. Sanner et al.37 investigated the effect of subtalar joint motion on ankle joint height of 33 participants using radiographic measures of the talar trochlear surface. Evaluation of the radiographs demonstrated that supination of the foot from relaxed to neutral calcaneal stance position resulted in a significant increase in ankle joint height an average of 0.3 cm. This would suggest that altering subtalar position can functionally lengthen or shorten a limb. The literature that interrelates foot posture, functional limb length discrepancies and LBP is principally based on clinical folklore and on a case report involving a runner with a 2 cm limb length discrepancy (LLD) (R>L), who was noted to exhibit excesThe Foot (1999) 9, 175–180
sive rearfoot pronation (L>R). Treatment consisted of orthoses and a heel lift in the left shoe of 1 cm height – this height was determined by an osteopathic formula. For this patient, this treatment led to complete symptomatic relief of his chronic LBP.38 Although anecdotally the correlation between a functional LLD and LBP would appear strong, this is not proven. However, a subtle change in foot posture related to asymmetrical foot pronation theoretically could alter spinal mechanics, and will remain a feature to note in the clinical biomechanical examination of a person with LBP.
SAGITTAL PLANE BLOCKADE The sagittal plane facilitation of motion theory of foot function focuses on the ability of the sagittal plane pivots of the foot to function efficiently during gait.39 The most important of these is considered to be the first metatarsophalangeal joint, as its function is believed to be commonly compromised during gait. If sagittal plane pivoting about these joints is impeded during gait, this is defined as a sagittal plane blockage, and compensations within other segments of the body are predicted to occur. In the case of first metatarsophalangeal joint dysfunction, this is commonly defined as a functional hallux limitus.40,41 One consequence of functional failure of first metatarsophalangeal joint dorsiflexion relates to insufficient hip joint extension (involving biceps femoris contraction) at the midstance phase of the gait cycle.41 Normally, the weightbearing limb is beginning to extend out from under the body at the midstance phase of the gait cycle. However, with a sagittal plane blockade at the first metatarsophalangeal joint, hip joint extension may be impeded, which may be clinically seen as a lack of normal knee joint full extension just prior to contralateral heel strike. One of the muscles responsible for hip joint extension, biceps femoris, attaches to the sacrotuberous ligament which in turn is attached to the sacrum. A lack of biceps femoris contraction may stop normal nutation of the sacroiliac joint whereby the sacral base should move anteriorly and the apex posteriorly. This is thought to be needed for self-bracing of the sacroiliac joint during the midstance and propulsion phases of the gait cycle.41 Repetitive loading and motion of this joint in this unstable position is suggested to be a contributory factor to the development of LBP. Other muscles, such as iliopsoas and quatratus lumborum are also believed to function abnormally when a sagittal plane block is present.41 Dananberg and Guiliano’s42 clinical study involved 32 participants with chronic LBP who were unresponsive to previous traditional conservative medical management. Foot orthoses were designed with the aid of two-dimensional video analysis and in-shoe plantar pressure measurement. The aim was to pre© 1999 Harcourt Publishers Ltd
Foot function and low back pain scribe devices that would optimize sagittal plane motion and normalize centre of plantar pressure patterns in gait. The Quebec Back Pain Disability Scale43 was utilized prior to treatment, as well as approximately 1 month and 6 months post initial treatment. The participants experienced twice the improvement in their pain, and for twice as long as compared to participants in a study using traditional back pain treatment. It should be noted that the control group they were compared to were part of the validation for the Quebec BPDS, so are not a true control group.
DISCUSSION This paper has reviewed a number of mechanisms by which foot structure and function may influence the lower back. It is unclear which of the mechanisms is more important or if they work in combination to affect LBP. Laboratory experiments will be needed to investigate well-defined postural changes of foot posture, structure and function and how they correlate with more proximal changes in structural, kinematic and neuromuscular variables. Prospective controlled clinical studies are needed to determine the role of foot structure and function on those with chronic problems of the lower back. Such studies are difficult as there are many different types of orthoses that could be used and each of these will have a number of prescription variables. Measures will also be needed to determine if the foot orthoses are inducing the assumed structural and functional changes of the foot. Blinding participants in a study to the type of foot orthoses is difficult. Problems with research on LBP include the classification and diagnosis, or the inclusion criteria for a study. Selective inclusion has potential to bias results. Many patients with LBP undergo spontaneous resolution and the natural history is one of variability and change, so it is difficult to attribute improvements to the intervention. Outcome measures to determine the effect of interventions are problematic. For clinical research, the outcomes need to be valid and sensitive to detect changes. Most available outcome measures involve some form of subject or investigator measures of pain. Pain interpretation is multidimensional and is very subjective and may not necessarily be subjective enough to detect small changes. Some measures have been shown to have some validity and reliability.43,44,45 CONCLUSION This paper has presented a number of theoretical explanations for the development of LBP via abnormal foot function. These include heel height of footwear, inadequate shock absorption, functional limb length discrepancy and sagittal plane blockade. © 1999 Harcourt Publishers Ltd
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Research on foot function and LBP is fraught with difficulties. However, given the high burden to individuals and society of this problem and the potential significance of foot orthoses, further research is essential. REFERENCES 1. Loney P L, Stratford P W. The prevalence of low back pain in adults: a methodological review of the literature. Phys Ther 1999; 79(4): 384–397. 2. Victorian WorkCover Authority Statistical Report 1997–1998. Melbourne: Victorian WorkCover Authority, 1998. 3. Waddell G. Low back pain: a twentieth century health care enigma. Spine 1996; 21(24): 2820–2825. 4. Teasell R W, Harth M. Returning patients with chronic low back pain to work – revolution or fad? Spine 1996; 21(7): 844–847. 5. Von Korff M, Saunders K. The course of back pain in primary care. Spine 1996; 21(24): 2833–2839. 6. Hart L G, Deyo R A, Cherkin D C. Physician office visits for low back pain: frequency, clinical evaluation and treatment patterns from a US national survey. Spine 1995; 20(1): 11–19. 7. Nyska M, McCabe C, Linge K, Klenerman L. Plantar foot pressures during treadmill walking with high-heel and lowheel shoes. Foot Ankle Int 1996; 17(11): 662–666. 8. Mandato M G, Nester E. The effects of increasing heel height on forefoot peak pressure. J Am Pod Med Assoc 1999; 89(2): 75–80. 9. Kerrigan D C, Todd M K, Riley P O. Knee osteoarthritis: wearing high heels may be a factor. Lancet 1998 (351): 1399–1401. 10. Rossi W A. The sex life of the foot and shoe. London: Routledge & Kegan Paul, 1976. 11. de Lateur B J, Giaconi R M, Questad K, Ko M, Lehmann JF. Footwear and posture: compensatory strategies for heel height. Am J Phys Med Rehab 1991; 70(5): 246–254. 12. Franklin M E, Chenier T C, Brauninger L, Cook H, Harris S. Effect of positive heel inclination on posture. J Orthop Sports Phys Ther 1995; 21(2): 94–99. 13. Bryan J M, Mosner E, Shippee R, Stull M A. Investigation of the validity of postural evaluation skills in assessing lumbar lordosis using photographs of clothed subjects. J Orthop Sports Phys Ther 1990; 12(1): 24–29. 14. Smith E O, Helms W S. Natural selection and high heels. Foot Ankle Int 1999; 20(1): 55–57. 15. Wosk J, Voloshin A. Wave attenuation in skeletons of young healthy persons. J Biomech 1981; 14(4): 261–267. 16. Voloshin A, Wosk J. Influence of artificial shock absorbers on human gait. Clin Orthop and related research 1981(160): 52–56. 17. 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. 18. Wosk J, Voloshin A S. Low back pain: conservative treatment with artificial shock absorbers. Arch Phys Med Rehab 1985;66(March):145–148. 19. Bjönness T. Low back pain in persons with congenital club foot. Scand J Rehabil Med 1975(7):163–165. 20. Builder M A, Marr S J. Case history of a patient with low back pain and cavus feet. J Am Pod Assoc 1980;70(6):299–301. 21. Ogon M, Aleksiev A R, Pope M H, Wimmer C, Saltzman C L. Does arch height affect impact loading at the lower back level in running? Foot Ankle Int 1999;20(4):263–266. 22. Nigg B M, Cole G K, Nachbauer W. Effects of arch height of the foot on angular motion of the lower extremities in running. J Biomech 1993;26:909–916. 23. Giladi M, Milgrom C, Stein M et al. The lower arch, a protective factor in stress fractures: a prospective study of 295 military recruits. Orthop Rev 1985(14). 24. Cowan D N, Jones B H, Robinson J R. Foot morphologic characteristics and risk of exercise-related injury. Arch Fam Med 1993 (2): 773–777. 25. Hansen L, Winkel J, Jørgensen K. Significance of mat and shoe softness during prolonged work in (sic) upright position:
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