Prolonged lateral overload and recurrent sprain can lead to peroneal tendon problems. Rigid joints can progress to joint destruction and develop arthritis over time.Ĭhronic lateral ankle instability and recurrent sprain is inevitable in a patient with cavus foot. Haglund deformity can become symptomatic more easily if the heel is in varus because the posterior superior calcaneal tuberosity will become more prominent. Reduced shock absorption due to rigid hindfoot and tight heel cord can lead to plantar fasciitis or Achilles tendinitis. Recurrent dislocation of the peroneal tendons
Peroneal tendon problems (tear or split, rupture, tendinopathy)Įnlarged or posteriorly placed distal fibular Sesamoid problems (sesamoiditis, chondromalacia, avascular necrosis) Clinical manifestations associated with cavus foot. Chronic ankle instability with a varus-tilted mortise can also result in a cavovarus foot. Although the exact etiology for this entity has been subject to debate, both intrinsic and extrinsic muscle imbalances may play a role. This foot shape has been referred to as the subtle, nonneurologic, or idiopathic cavus. Ī mild variation of the cavovarus deformity without an identifiable underlying neurological deficit has been increasingly reported in recent literature. With the rigid hindfoot varus, the Achilles tendon becomes a secondary invertor and becomes contracted. Hindfoot varus is initially flexible, but can gradually become rigid over time. The plantar flexed forefoot forces the hindfoot into varus. The resultant claw toe deformity and plantarflexed metatarsal heads amplify forefoot equinus. With weak intrinsic muscles, the unopposed extensor digitorum longus hyperextends the unstable lessor toes at the metatarsophalangeal joint while the flexor digitorum longus and brevis flex the phalanges. Recruitment of extensor hallucis longus produces cock up deformity of the great toe, which further depresses the metatarsal head. The flexion power of the peroneus longus becomes much stronger as the foot is positioned in equinus. Weak anterior tibial relative to the peroneus longus results in plantar flexion of the first metatarsal. Muscle imbalance can occur between the extrinsic and intrinsic muscles, between the posterior tibial and the peroneus brevis muscles, and between the anterior tibial and the peroneus longus muscles. Structural deformation is more substantial when the motor imbalance begins before maturation of the skeleton. Relative weakness in one of the two opposing muscles causes muscle imbalance and structural deformity.
Extensor hallucis longus is relatively spared. The progressive muscle involvement from distal to proximal, most frequently affects the intrinsic muscles, the tibialis anterior, and the peroneus brevis. The probability of a patient who has bilateral cavovarus feet being diagnosed with CMT is 78%. Among them, Charcot-Marie-Tooth (CMT) disease, a hereditary sensory motor neuropathy, is most frequently reported. Two thirds of adults with symptomatic cavus foot have an underlying neurological condition. The etiology is most frequently attributed to the neuromuscular disorders involving brain, spinal cord, or the peripheral nerves. High arch of the foot is frequently associated with hindfoot varus, forefoot adduction and plantar flexion, and ankle equinus. The term “pes cavus” or “cavus foot” is used to describe a wide spectrum of foot shapes that have an abnormal elevation of the medial longitudinal arch.
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