The Big Toe and Windlass Mechanism

by Carson Boddicker

While it is not a big joint, the first metatarsophalangeal joint may be one of the most important joints in running gait. There is no question that dysfunctional patterns can result from too much or not enough movement at any joint, however, when the metatarsophalangeal joint does not play, a great deal of compensations can result.

As I noted in a previous post, proper gait requires the ability to flex the knee to 40 degrees, the dorsiflex the ankle at minimum of 20 degrees, and to be able to extend the first MTP joint to a minimum of 65 degrees (Oatis, 2004). When any of these ranges of motion are unable to be reached, compensation will and must occur to maintain a pattern that is similar to a “functional” pattern. In the event of hallux restriction, a number of compensations can occur to enable a person to still get from point “A” to point “B” but we know that less than optimal patterns, practiced regularly can snowball into bigger problems down the road.

The inability to extend the first MTP joint due to joint degeneration, structural change, or general restriction is commonly known as hallux limitus and is often seen in running athletes.

This range of motion is very important in the grand scheme of the Windlass Mechanism, which is a passive loading mechanism that occurs as the calcaneus clears the ground in late stance and the weight transfers over the heads of the metatarsals. Combined, these motions load the plantar fascia and intrinsics of the foot that help to transform the foot into a stable lever off of which to push (Fuller, 2000). As demonstrated by Carlson, there seems to be an incremental, linear relationship between hallux dorsiflexion and increased tensile strength of the plantar fascia (Carlson, 2000). As you know, the plantar fascia and Medial Longitudinal Arch are capable of producing a great deal of elastic return in running, so imagine the detrimental effects when this mechanism cannot function well. Those with reduced hallux extension and pronated feet often have diminished effects of this mechanism and ultimately less efficient (Dananberg, 1986).

When the big toe does not extend well during late stance, plantar flexion torque decreases and occurs in a delayed fashion (Hall, 2004), knee flexion increases (potentially as a result of tension from the distal end as the calcaneus raises early), and hip extension decreases. To compenstate, there must be an increased drive of the hip flexors to advance the leg. When the foot is fixed upon the ground, this contraction creates potential for lumbar rotation and lateral flexion can occur stressing the intervetebral disks and potentially leading to low back pain and dysfunction (Kapandji, 1974). Add to that the possibility of the body compensating with an anterior tilt to facilitate hip flexion and you have a gamut of issues that sounds a lot like the makings of Janda’s lower crossed syndrome with excessively toned hip flexors, inadequate gluteal strength, and possibly an increased full body anterior tilt placing the plantar flexors under excessive load. It is very common in the running world. Additionally, the early knee joint flexion and limited extension of the hips can beget a loss of transverse plane stability possibly as a result of ineffective use of the “screw home mechanism” at the tibiofemoral joint and ineffective activation of the hip extensors.

Put all of the above together and you have a recipe for increased forces at the PFJ, shearing across the iliotibial band, potentially increased contact pressures at the anterior hip capsule, excessive activation of the deep hip rotators forcing the hip into a hyperextended position causing decreased sacral rotation during gait, low back pain, and SIJ instability.

Clearly, limited hallux extension is not something to be ignored. Tomorrow we’ll discuss how it should be assessed and addressed.


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