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The reverse windlass mechanism

Discussion in 'Biomechanics, Sports and Foot orthoses' started by admin, Dec 17, 2007.

  1. admin

    admin Administrator Staff Member

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    The Role of the Reverse Windlass Mechanism in Foot Pathology
    Anna Aquino & Craig Payne

    Reprinted with permission from the Australasian Journal of Podiatric Medicine 34(1)32-33 2000

    The plantar fascia is the subcutaneous fibrous covering of plantar surface of the foot composed mostly of collagen fibres and divided into medial, central and lateral components. The central component is considered aponeurotic in nature as the medial and lateral components are thinner and appear to have minor functional significance (Pontious et al., 1996). The plantar aponeurosis originates from the medial calcaneal tubercle, becoming broader distally before dividing into five slips just below the metatarsal shafts. Each slip has a deep and superficial component, inserting into a complex network in the plantar forefoot area, ending at the bases of the proximal phalanges.

    The foot can be viewed as an arch-like structure known as a ‘truss’, in which the calcaneus and talus serve as the posterior strut, the midfoot tarsal bones and metatarsals serve as the anterior strut and the plantar aponeurosis serves as the ‘tie rod’ (Snijders, 1999). In a static weightbearing situation, the osseous ‘struts’ of the truss are compressed and the tie-rod is tensed. The plantar aponeurosis can therefore be considered to function as a strong ligament that sustains tension between the calcaneus and the proximal phalanges (Aquino & Payne, 1999). During gait however, the timing and amount of this aponeurotic tension is perceived to change significantly, particularly upon dorsiflexion of the digits at the metatarsophalangeal joints (Perry, 1983).

    The windlass mechanism was first described by Hicks in 1954 as a phenomenon whereby passive dorsiflexion of the hallux caused the medial longitudinal arch to rise, the rearfoot to supinate, the leg to externally rotate and the plantar aponeurosis to become more tense. This phenomenon was likened to the winding of a cable (the plantar aponeurosis) around the drum of a windlass (first metatarsophalangeal joint) by pulling a handle (proximal phalanx of the hallux). The effect of this windlass can be demonstrated by a test first described by Jack in 1953 and also sometimes referred to as the Hubscher manoeuvre (Kirby, 1997).

    The role of the windlass mechanism is assumed to assist with making the foot a more rigid structure during the propulsive phase of gait as well as assumed to help facilitate the establishment of the foot’s autosupport mechanisms (Payne & Dananberg, 1997). This is considered necessary to enable the efficient transfer of body weight from the rearfoot to the metatarsophalangeal joints during propulsion. The windlass mechanism and the foot supination that occurs with it also co-ordinates with the external rotation of the limb and pelvis during gait due to the contralateral leg swing. Bojsen-Moller (1979) described two kinds of propulsion, which he termed high gear or low gear, identified by the respective presence or absence of a visible protrusion of the medial slip of the plantar aponeurosis. The greatest amount of plantar fascial tension was observed to occur during the high gear push off, when toe-off occurred over the transverse axis across the first and second metatarsal heads. This was believed to indicate an effective establishment of the windlass mechanism. An ineffective establishment of the windlass mechanism is hypothesised to be related to pathology. This may be due to the foot’s inability to direct weight flow from the oblique axis (located across metatarsal heads two to five) to the transverse axis and subsequently hindering windlass establishment (Payne & Dananberg, 1997).

    The effect of winding the windlass via dorsiflexion at the first metatarsophalangeal joint is well described, but Hicks (1954) also referred to the mechanism as occurring at the lesser metatarsophalangeal joints. Minimal consideration has been given in the literature as to the role of this mechanism and the consequences of a perceived defect in the mechanism. While the plantar aponeurosis’ windlass function has been well documented, very little attention has been given to the unwinding or ‘reverse’ of the windlass mechanism. On weightbearing, the windlass unwinds as the arch flattens and the foot elongates. This is seen to place a compressive force upon the posterior and anterior struts of the ‘truss’ structure of the foot, which produces tension in the plantar aponeurosis ‘tie-rod’. This causes a powerful plantarflexory force to the proximal phalanges, as the insertions of the aponeurosis’ digital slips is wound around the plantar surface of each metatarsophalangeal joint to attach to the base of the proximal phalanges. Thus the plantar plate helps to stabilise the proximal phalanx against the ground and the mechanism as a whole provides a static resistance to dorsiflexion of the digits (Yao et al, 1996). Because the interphalangeal joints remain mobile while the reverse windlass mechanism is active, Stainsby (1997) considers that the long flexor and extensor tendons of the foot are not responsible for this plantarflexory influence. Rather it is the tethering effect of the tightened digital slips on the plantar plates that brings about the plantarflexion observed in the reverse windlass mechanism.

    A number of descriptions have been given in the literature for the cause of hammer toes (Jimenez et al., 1987). Scheck (1977) suggested that hyperextension of the proximal phalanx was due to “age-related inefficiency of plantar structures” causing elongation of the plantar joint capsule and the plantar aponeurosis’ digital slips beyond normal physiological limits. Stainsby (1997) suggests that a stretched plantar plate and displaced fascial slips renders the reverse windlass mechanism ineffective. The stretching could be hypothetically due to a high-heeled shoe causing hyperextension of the proximal phalanx, thus being made to pull the plantar plate in an anterior direction. If the proximal phalanx cannot plantarflex, the structures remain stretched. Support for this hypothesis was illustrated by Pontious et al. (1996), where the development of post-operative hammertoes was described after partial plantar fasciectomy. This alteration of fascial structure can be considered to lessen the tension on the tie-rod function of the plantar aponeurosis. Thus the stabilising plantarflexory influence exerted on the proximal phalanges by the aponeurosis is lost, due to an ineffective reverse windlass mechanism.

    Similarly, Stainsby (1997) considers claw toes as being due to chronic metatarsophalangeal joint extension serving to stretch the plantar plate distally following the proximal phalanx. The hyperextension can be so severe that this displaces the plate onto the lateral or dorsal aspect of the metatarsal head. This leaves the metatarsal head exposed in a prominent position on the plantar surface with little fibrofatty padding. The metatarsal head becomes depressed as the deep transverse metatarsal ligament (attached to the plantar plate) holds down the dorsally displaced plantar plate. Stainsby (1997) refers to this as the ‘plunger effect’. The aponeurosis’ digital slips become stretched around the medial and lateral sides of the metatarsal head, and are unable to adequately plantarflex the proximal phalanx. The tethering effect of the plantar aponeurosis, combined with the action of the long and short flexor tendons, thus serve to enhance the ‘plunger effect’ of the deep transverse metatarsal ligament and force the digit into a clawed position. Therefore, the displaced plantar plate and elongated digital slips lead to a defective reverse windlass mechanism, which in turn leads to a clawed toe.
    Taylor et al. (1998) noted plantar fascial rupture in 12 consecutive patients with diabetic sensory neuropathy and dorsiflexed toes on magnetic resonance imaging scans. No ruptures were observed in a control group. The fascial rupture could be hypothesised to lead to a decrease in tension of the plantar aponeurosis, thus the tethering effect on the proximal phalanges is lost. The ineffective reverse windlass mechanism may then lead to clawing of the toes, increasing pressure on metatarsal heads and increasing the risk of ulceration. A rupture or dysfunction of the plantar fascia has been reported in all cases of Charcot’s neuroarthropathy compared to the contralateral foot and control subjects (Chuter & Payne, 2001) indicating that a loss of reverse windlass may be a significant factor in changes in the structure and function of the diabetic foot.

    Several anatomical and biomechanical hypotheses are suggested in the literature with regard to the aetiology and development of hallux abductovalgus. A recent theoretical model by Fuller (2000) postulates that an increased plantarflexion moment on the first metatarsophalangeal joint due to increased tension on its aponeurotic slip could create a medial deviation of the first metatarsal head, which can lead to or enhance the hallux abductovalgus (HAV) deformity. Stainsby (1997) considers that if the hallux is forced laterally into a valgus position, eg. by tight footwear, the medial slip of the plantar aponeurosis leading to the first MPJ will bowstring or pull across to the lateral side of the joint. Tension in the medial slip forces a lateral displacement of the plantar plate complex of the first MPJ, which pushes the medial sesamoid against the crista of the metatarsal head. In severe HAV, the crista may become eroded, thus the stability afforded by the sesamoids in resisting lateral displacement is eradicated, and serves only to enhance the valgus orientation of the hallux. The ability of the aponeurosis to plantarflex the proximal phalanx and resist MPJ dorsiflexion is progressively lost as the lateral displacement of the plantar plate increases, rendering the reverse windlass mechanism ineffective.

    Stainsby (1997) first described the “footstool-edge weightbearing test” (FEWBT) to clinically assess the reverse windlass mechanism. The subject stands on the edge of a surface with the toes dangling over the edge. The reverse windlass mechanism is observed to be functioning when plantarflexion is noted in all of the proximal phalanges, and whether they are all plantarflexed at the same level. Kirby (1997) has utilised this test to evaluate the amount and integrity of plantar fascial tension in normal and pathological feet. Stainsby (1997) has observed that those with severe HAV demonstrated no plantarflexion at the level of the hallux’s proximal phalanges, and that the toes maintained their dorsiflexed and everted position.

    The concepts and implications of the ‘reverse windlass mechanism’ are still being developed and explored. Based on what is understood about the mechanism currently, it can be assumed that the reverse windlass mechanism is an important contributor in keeping the digits straight during the toe off phase of gait and in resisting digital deformity. Current research is investigating the windlass & reverse windlass mechanisms and their roles in foot function and foot pathology (Hamel & Sharkey, 1999; Aquino & Payne, 2001). More work is needed to fully understand its role in pathology and the clinical implication of the mechanism.

    Aquino A & Payne CB (1999): Function of the Plantar Fascia. The Foot, 9, 73-78.
    Aquino A & Payne CB (2001): The Role of the Windlass Mechanism in Pronated Feet. Journal of the American Podiatric Medical Association 91(5)245-250
    Bojsen-Moller, F. (1979): Calcaneocuboid joint and stability of the longitudinal arch of the foot at high and low gear push off. Journal of Anatomy, 129 (1), 165-176.
    Chuter V & Payne CB (2001): Limited Joint Mobility and Plantar Fascia Function in Charcot’s Neuroarthropathy. Diabetic Medicine 18(7)558-561
    Fuller, E.A. (2000): The windlass mechanism of the foot: a mechanical model that can theoretically explain selected pathology in the foot. Journal of the American Podiatric Medical Association, Vol 90, Issue 1 35-46
    Hamel AJ & Sharkey NA (1999): Proper Force Transmission Through the Toes and Forefoot is Dependent on the Plantar Fascia. Presented at the 23rdAnnual Meeting of the American Society of Biomechanics. University of Pittsburgh. October 1999
    Hicks, J.H. (1954): The mechanics of the foot II. The plantar aponeurosis and the arch. Journal of Anatomy, 88, 25-31.
    Jack, E. (1953): Naviculo-cuneiform fusion in the treatment of flatfoot. Journal of Bone and Joint Surgery, 35B, 75-82.
    Jimenez, A.L., McGlamry, E.D. & Green, D.R. (1987): Lesser Ray Deformities. In E.D. McGlamry (ed), Comprehensive Textbook of Foot Surgery, Vol. I., Baltimore, Williams & Wilkins, pp. 57-113.
    Kirby, K.A. (1997): Foot and Lower Extremity Biomechanics: a Ten Year Collection of Precision Intricast Newsletters. Payson, Arizona: Precision Intricast, Inc.
    Payne C.B. & Dananberg H. (1997): Sagittal plane facilitation of the foot. Australasian Journal of Podiatric Medicine, 31 (1), 7-11.
    Perry J (1983): Anatomy and biomechanics of the hindfoot. Clinical Orthopaedics and Related research 177:9-15
    Pontious, J., Flanigan, K.P. and Hillstrom, H.J. (1996): Role of the plantar fascia in digital stabilization: a case report. Journal of the American Podiatric Medical Association, 86 (11), 538-546.
    Scheck, M. (1977): Etiology of acquired hammertoe deformity. Clinical Orthopaedics and Related Research, 123, 63-69.
    Snijders CJ (1999): Plantar Fascia: Mechanical and Clinical Perspectives. In Ranawat CS & Positanbo RG: Disorders of the heel, rearfoot, and Ankle. Churchill Livingstone. New York.
    Stainsby, G.D. (1997): Pathological anatomy and dynamic effect of the displaced plantar plate and the importance of the integrity of the plantar plate-deep transverse metatarsal ligament tie-bar. Annals of the Royal College of Surgery in England 79, 58-68.
    Taylor, R., Stainsby, G.D. & Richardson, D.L. (1998): Rupture of the plantar fascia in the diabetic foot: a common complication. Diabetic Medicine, 15 (Supplement), A29.
    Yao, L., Cracchiolo, A., Farahani, K et al. (1996): Magnetic Resonance Imaging of Plantar Plate Rupture. Foot and Ankle International, 17, 33-3
    Last edited: Dec 19, 2007
  2. Admin2

    Admin2 Administrator Staff Member

  3. Here's the best paper I have seen on the subject of the "reverse windlass":

    Sharkey NA, Donahue SW, Ferris L: Biomechanical consequences of plantar fascial release or rupture during gait. Part II: Alterations in forefoot loading. Foot Ankle Intl, 20:86-96, 1999.
  4. Dananberg

    Dananberg Active Member

    In observing this phenomena for many years, I would agree w/ Stainsby that the digital contraction and stretching of the plantar plate are inter-related.

    As I have previously written, F-scan pressure analysis does show a decrease in CoP advancement during the single support phase of the step in patients with what we have long considered "pronation" related issues. As the CoP slows, the foot is essentially "behind" the movement of the CoM, and an abnormal sequences of events (ie hinderance of heel lift via the normal metatarsal sagittal plane rotation of the bases about the heads) demonstrates this delay. When single support phase terminates and pre-swing phase begins, the trailing foot has not yet moved to an efficient position to coordinate an efficient, propulsive pre-swing sequence. Since this entire pre-swing phase is normally 20% of the entire gait cycle, the duration of this phase is a brief 150-200ms. The result is a vertical lift off of the foot from the ground vs. the normal propulsive toeoff. (I believe that Eric Fuller refers to this as a hip pull off). The digits contract with this vertical lift off maneuver, causing the plantar plate to move distally towards the sulcus and away from under the metatarsal heads. On examination of these patients, the plantar fat pad appears to have moved distally to the sulcus and is easily palpated in this position. Since this event will occur millions of times/year, form would appear to follow function with regards to these sequence of repetitive events. The net result is a deterioration of the reverse windlass and its effect of foot stabilization.

  5. What is sometimes called the "reverse windlass mechanism" was first reported over a half century ago by John Hicks in his classic paper on the function of the plantar fascia (Hicks JH: The mechanics of the foot. II. The plantar aponeurosis and the arch. J Anatomy. 88:24-31, 1954). Even though I am not too fond of this terminology "reverse windlass mechanism", it is certainly descriptive.

    I consider this "reverse windlass mechanism" to simply be a passive increase in plantar fascial tension that occurs with weightbearing loads being placed on the plantar foot. Loading of the plantar forefoot by ground reaction force (GRF) dorsiflexes the forefoot on the rearfoot which, by also increasing the length of the medial and lateral longitudinal arches, will cause increased tension within the plantar fascia (i.e. central component of plantar aponeurosis). The plantar fascia will not only act to help prevent longitudinal arch flattening (i.e. help prevent forefoot dorsiflexion) but will also cause a digital plantarflexion moment, and digital plantarflexion, due to its distal insertion onto the bases of the proximal phalanx of all the digits.

    If the digits are suspended off the edge of a flat surface (i.e. "footstool edge weightbearing test"), the digits will normally plantarflex and the longitudinal arches will be also seen to flatten slightly at the same time that the digits plantarflex. This test of hanging the digits of the subject's feet off the edge of an orthoposer was first shown to me in the hallway of Module C at CCPM by Jack Morris, DPM, during my Biomechanics Fellowship in 1984. Therefore, to give credit to Stainsby as the creator of this test may not be appropriate. However, I know of no other earlier reference within the medical literature to such a test. This "footstool edge weightbearing test" is an excellent test to see the effects of the plantar fascia on arch height in many individuals since the plantarflexion action of the plantar fascia on the digits in combination with the arch lowering effects that occur with decreasing the tension within the plantar fasca can be easily observed using this test on many feet.

    Tearing of the plantar plate is not just likely due to increases in tensile forces on the plantar plate but also due to the considerable compression forces that this structure also is subjected to during weigthbearing activities. I often see plantar plate tears in patients that do not have distal migration of the plantar fat pad into the sulcus, so I am not sure that there is a good correlation between plantar plate pathology and fat pad displacement. One thing is certain that as we learn more about this often injured structure, the plantar plate, I believe we will be amazed, in retrospect, that we didn't pay more attention to it in years past.

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