The ‘measure’ I see most often used is static weight bearing. The patient stands and the clinician looks owlishly at the ankle (or if they are really keen, a bisection of the calc). ‘Aha’, they say ‘you're feet are pronated / overpronated / roll in. There’s your problem right there’.

Let us consider for a second how a normal healthy foot with a nice healthy function will appear in relaxed stance. The orientation of the subtalar axis means the centre of mass will tend to come down on the pronation side of the line, so the foot will pronate until something stops it. What structures limit pronation? The tibial muscles group certainly, but it would not be efficient for them to hold the patient in supination when in relaxed stance. The planter fascia / windlass? Sure but there is not a lot of tension there before heel raise (in most patients). Bony osseous limitation? Hope not, unless you are really arthritic! I contend that in most cases the limiting structure is the deltoid ligament complex, which limits the range generally. And what position will that keep the STJ in? Pretty near the maximally pronated position. It represents a position the foot CAN achieve and little more than that. It does not indicate the degree to which the calc everts during gait.^2,3 The position of a ‘normal’ healthy, effectively functioning foot during static weight bearing may be closer to maximally pronated than neutral, but it is certainly not neutral!⁴

Keep in mind also that correlation is not the same as causation. Just because a foot that hurts also pronates does not infer that it hurts BECAUSE it pronates.

‘Overpronation’ is at best a vague observation with little diagnostic value and different meanings to different people. It covers so much variation of pathological function that it informs the reader little of real value. All it tells me when I see it in a file is that A: the foot pronates (which it should) and B: the patient has a pathology of some description. One can be pretty sure that the foot pronates; after all it would be pathological if it didn’t. So by inference all diagnosis of ‘overpronation’ means that the assessor has blamed the pathology on a generally benign movement. It does not tell me why that benign movement has become pathological.

If we wish to make meaningful observations I believe we must rise above the ‘pronation causes all ills’ school of thought to which so many other AHPs subscribe when they ‘dabble’ in biomechanics. Pronation is a complex, benign system that can malfunction in a variety of ways, which can cause a variety of pathologies. How exactly it malfunctions may inform what problems it causes and what type / prescription of insole will work most effectively at treating it, and that is where we, as the professionals with the most knowledge of feet, should excel. Simply ascribing all pathology to ‘pathological pronation’ and treating with ‘anti-pronation devices’ or even (heaven forbid) ‘arch supports’ may have a success rate, but it does not elevate us far above the man I saw at a car boot sale selling ‘orthopaedic arch supports’ at £15 per pair (two for £20) last weekend for the treatment of every musculoskeletal pathology a suffering body can be plagued by.

References
1. Root ML, Orien WP, Weed JH, Normal and Abnormal Function of the Foot. Vol 2, Clinical Biomechanics Corporation, Los Angeles, 1977.
2. Hamill J, Bates BT, Knutzen KM, et al, Relationship between selected static and dynamic lower extremity measures. Clin Biomech 1989; 4: 217.
3. McPoil TG, Cornwall MW, The relationship between static lower extremity measurements and rearfoot motion during walking. J Orthop Sports Phys Ther 1996; 24: 309.
4. Kirby KA, Biomechanics of the normal and abnormal foot. JAPMA 2000; 90: 30.

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