Luis Rodil Peralta
MULTIMEDICA VISTA HERMOSA
During hyperpronation the astralagus is forced to adduce and plantarflex in excess, while the calcaneus simultaneously is everted (A). These actions markedly affect the calcaneo-navicular ligament and the plantar capsule of the scaphoid-astralagus articulation. With time, these exaggerated movements tend to provoke pathological hypermobility in such structures.
Additionally the excess of pronation affects the aponeurosis (plantar fascia) and/or the soft parts of the forefoot, because the astralagus is moved to the front approximately 1.5mm for every 10° of calcaneus eversion. (B). To a greater eversion of the calcaneus, more movement of the astralagus. While this anterior movement may be insignificant in a biomechanically balanced foot, it can play a critical role in the pathomechanics associated to an excessive subtalar pronation because the anterior movement of the astralagus causes the scaphoid and the first three radii to move to the front and in abduction in relation to the fourth and fifth radius. The anterior movement of the medial column irritates the plantar fascia producing tension in a relatively inelastic tissue, which generates an increase in the traction forces at the periostic insertion and fascia at the calcaneus level, producing plantar fasciitis, heel spur.
The abduction movement of the medial column may also be co-responsible for lesions being that it generates compression forces in the union of the lateral and medial column. The anterior leads to intermetatarsophalangeal bursitis and interdigital neuritis.
Additionally to producing lesions at foot level, excessive subtalar pronation may be responsible for a wide range of lesions along all the kinetic chain. For example, it has been widely documented that excessive pronation is the cause of tibial periostitis (shinsplints), pain along the distal two thirds of the tibia.
It has been documented (Matheson et al.) that tibial rotation caused by excessive pronation predisposes to fractures, possibly because the distal side of the tibia due to its relatively low polar momentum of inertia, is unable to tolerate such torsional increases.
The excessive internal rotation of the tibia can also be responsible for pain at medial level in the knee because the tibial medial plate is forced to slide behind the internal femoral condyle. This movement presses the medial meniscus and the medial capsule producing pes anserines bursitis. Lutter documented that in a study of 213 injured knees, 77% had disequilibrium in the foot.
Even though many authors sustain that excessive pronation affects the medial face of the knee, Noble, in a study of 100 individuals diagnosed withiliotibial band syndrome concluded that excessive subtalar pronation was a significant ethiological factor. Apparently the excessive internal rotation of the tibia “drags” the distal portion of the iliotibial band over the lateral femoral epicondyle, predisposing to this friction syndrome.
Retropatellar pain is also related to excessive subtalar pronation. Even though it is notorious that excessive subtalar pronation produces an increase of Q angle, and therefore predisposes to retropatellar artralgia, this only happens while still, when the crossed ligaments maintain the blocked knee extended. When the knee is bent (like it is during the phase of contact of the heel) the tibia rotates internally more than the femur and therefore decreases Q angle. This may be a causing factor of lesions at the medial retropatellar level. Huerti and Hayes demonstrated that the reduction in the Q angle will result, in 50% of the cases, in reduction of the pressure behind the patellar lateral facet with a redistribution of the pressure to another side and therefore increasing proclivity to a chondromalacia. Maybe this is why Kegerreis et al. sustain that excessive subtalar pronation is causally related with the synovial plica syndrome and that the increased Q angle is related to dysfunction in the extensor mechanism.
Posture Effects associated with excessive subtalar pronation:
- Increases traction in the gluteus maximus insertion and hence
- may be responsible for tendonitis at that level. Also the bursa of the trocanter major is more inclined to be injured because the proximal femur rotates at a greater range of movement, which produces greater friction in such bursa which is located between the trocanter major and the proximal section of the iliotibial band.
- Of greater clinical significance is the effect of internal femur rotation in the pelvis. The internal rotation of the femur moves the femur head to the back,
- which causes the pelvis to tilt to the front. The aforementioned may be a cause of a wide range of lesions because the angle of the base of the sacrum is increased, the invertebrate discs and the vertebrate spinal process move closer together.
- Lumbar lordosis is increased.
- Anterior tilting of the pelvis tractions at the level of the ischiotibial insertion.