Cavus/Neuromuscular Foot

KEY FACTS

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The foot is a complex “machine” consisting of many bones and joints kept in a fine balance by many extrinsic (leg) and intrinsic (foot) muscles.
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Any disruption of the precise muscle balance leads to progressive deformity of the involved joints.
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If the imbalance arises prior to skeletal maturity, bone growth will be abnormal, and bones and joints will become dysplastic.
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  The shape of the bones begins with a fixed plan but is modified during childhood based on the forces (muscular and weight bearing) on them over time.
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If the imbalance arises after skeletal maturity, bones will have an essentially normal shape, and deformity will be through the joints.
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With time, the joints can erode in response to deformity, leading to secondary “dysplasia” of the bones.
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At the level of the ankle and hindfoot, there are several muscles pairs that balance each other.
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  The tibialis anterior dorsiflexes the 1st ray, while the peroneus longus plantar flexes it.
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  The posterior tibial muscle inverts the hindfoot, while the peroneus brevis everts.
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  The tibialis anterior and the extensor digitorum and hallucis longus all work in opposition to the triceps surae.
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    The triceps surae is by far the strongest of the leg and foot muscles.
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In the forefoot, balance between intrinsic and extrinsic flexors and extensors keeps the toes straight at the metatarsophalangeal and interphalangeal joints.
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Even when a muscle is weak, if there is no muscle to oppose it, then the weak muscle will eventually cause a deformity.
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Although muscle imbalance theoretically could lead to any imaginable foot deformity, neuromuscular deformities are generally some form of cavus.
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The neuromuscular cavus foot appears with a high arch, variable amounts of hindfoot varus, plantar flexion of the 1st ray or entire midfoot, and clawing of the toes.

Neuromuscular Deformity

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Upper motor neuron lesions, such as a stroke or cerebral palsy, lead to weakness with hyperreflexia and spasticity.
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Lower motor neuron lesions, such as poliomyelitis or traumatic nerve injury, lead to hyporeflexia.
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Muscle lesions (myopathy or untreated compartment syndrome) lead to weakness and hyporeflexia.

Symptoms From Neuromuscular Cavus Foot

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Neuromuscular imbalance leads to variably progressive deformity in the foot.
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The neuromuscular cavus foot appears with a high arch, variable amounts of hindfoot varus, plantar flexion of the 1st ray or entire midfoot, and clawing of the toes.
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Cavus or cavovarus deformity alters the distribution of pressure under the foot.
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  Focusing weight-bearing forces on smaller areas leads to higher pressures.
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  The cavus foot will have higher pressures under the heel and metatarsal heads.
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Patients may complain of pain &/or callusing in these high-pressure spots.
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If the hindfoot is in varus, then pressure may be focused on the 5th metatarsal.
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  This can cause pain and callusing and, in extreme cases, 5th metatarsal stress fractures.
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The high arch may make shoe fitting problematic.
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Shoe-fitting problems may also arise if clawing of the toes occurs with irritation over the dorsum of the interphalangeal joints.
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Clawing of the toes pulls the metatarsal fat pad distally.
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  It also uncovers the metatarsal heads and can lead to metatarsalgia.
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A varus hindfoot predisposes to ankle sprains, which is even more of a problem when the peroneus brevis is weak.
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Weakness may cause the patient to feel clumsy and fall.
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Severe deformity prevents the foot from being plantigrade.
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  In severe cases, the patient will become nonambulatory.
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If sensory neuropathy occurs, pressure sores may develop over high-pressure areas.
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Although many neuromuscular feet will have the same general cavus shape, the specific components of the cavus will vary with the cause of the imbalance.

Evaluation of Neuromuscular Patient

History and Physical Exam

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A full history and physical is appropriate, but there are several areas that should be explored more thoroughly.
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Family history should look for history of similar disease, because many neuromuscular diseases are inherited.
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Environmental exposures should be discussed; ask about residency in an area where polio might be present.
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On examination, the overall shape and symmetry of both feet are assessed.
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  Asymmetry is more common with acquired disorders (and some spinal cord abnormalities).
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  Systemic diseases tend to create symmetric deformity.
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The position of the hindfoot is assessed.
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  While the patient is standing, the observer notes the position of the heel from behind.
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  In the normal foot, the heel rests in slight valgus (just lateral to the long axis of the tibia).
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  Most neuromuscular deformities pull the heel into varus.
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If the heel is seen medial to the foot while looking at the patient from the front (the “peek-a-boo” heel), then it is in varus.
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The position of the forefoot can be assessed while the patient is seated with the legs hanging over the edge of the table.
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  With the heel straight, the metatarsal heads should be even.
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  A plantar flexed 1st ray is commonly seen with neuromuscular cavus.
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The Coleman block test is an important assessment of hindfoot flexibility when the hindfoot is in varus.
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  With the patient standing with the heel and lateral metatarsal heads on a block, the 1st metatarsal is allowed to drop medial to the block.
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  If the hindfoot is flexible, the 1st metatarsal will drop lower than the foot, and the heel will fall into slight valgus (forefoot-driven hindfoot varus).
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  If the hindfoot is rigid, the 1st metatarsal will not drop, and the heel will remain in varus.
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The alignment of the toes should be assessed, looking for the characteristic clawing [extension at metatarsophalangeal (MTP) and flexion at interphalangeal joints].
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The flexibility of the hindfoot, ankle, and toes must be assessed initially and with time.
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  Many diseases begin with a flexible deformity but become more rigid over time.
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The “quality” of the soft tissues should be assessed.
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  With longstanding deformity, the tissues may become contracted on the “concave” side of the deformity.
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    Example: Medial hindfoot in varus deformity
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  In such cases, realignment may put an unacceptable amount of stretch on these tissues.
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A full motor examination is performed, documenting the strength of each muscle group in both legs.
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A full sensory examination is listed either by dermatome or peripheral nerve, depending on the underlying pathology.
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The gait pattern must be observed.
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  A foot drop may be visible during the swing phase.
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Finally, the vascular supply to the foot should be assessed.

Imaging and Other Diagnostic Studies

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Weight-bearing radiographs are an important part of the deformity assessment.
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On the lateral view, calcaneal pitch > 30° is typical of cavus.
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The lateral talometatarsal angle will show the 1st metatarsal to be plantar flexed.
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  The 1st metatarsal may be plantar flexed much more than the other metatarsals in the cavus foot.
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Magnetic resonance (MR) imaging of the foot is rarely needed, but MR of the spine may be appropriate when the cause of deformity is not certain.
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  It might be especially useful in the asymmetric cavus foot when there is a suspicion for spinal cord lesions.
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  Unilateral progressive cavus deformity should prompt an MR to search for intraspinal pathology.
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  Cavus deformity, either unilateral or bilateral, in association with scoliosis should probably also be evaluated with an MR of the spine.
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Electromyographic tests with nerve conduction velocities (EMG/NCV) are helpful in the initial evaluation of the patient to better define the neuromuscular lesion.
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  EMG in cases of neuropathy show an increased amplitude and duration of response.
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  EMG in patients with myopathy show a decreased amplitude and duration of response with short polyphasic potentials.
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  Denervation or anterior horn cell loss demonstrates prolonged polyphasics, positive sharp waves, and fibrillations on EMG.
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  Abnormal NCV with prolonged latencies and minimal decrease in velocity suggest axonal degeneration.
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In rare cases, muscle or nerve biopsy may be needed to confirm a diagnosis.

Principles of Treatment of Neuromuscular Cavus Foot

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The underlying disease must be controlled as best as possible, usually in conjunction with a neurologist.
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In cases of spasticity, medication may be helpful.
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  Medications include baclofen, diazepam, and dantrolene.
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Specific muscle blocks with botulinum toxin may be helpful.
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  This is especially so if only 1or 2 muscles are involved.
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Once a muscle imbalance in the foot has been identified, the goal is to prevent further deformity.
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Frequent stretching by the patient must be done; otherwise, contracture will inevitably set in.
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Extra-depth shoes and orthotics will help accommodate a high-arched foot; a tall toe box will better fit claw toes.
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Custom accommodative orthotics can reduce peak pressures in the sole of the foot.
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Bracing of the weak or unstable ankle with a custom ankle-foot orthosis (AFO) can permit better ambulation and perhaps prevent further deformity.
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In patients with sensory deficits, Plastazote (or other cushioned) linings are required in the brace with frequent inspection of the skin for ulceration.

Surgery for Neuromuscular Cavus Foot

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Surgical intervention is indicated in certain situations.
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Surgery is appropriate when nonoperative treatment has failed, which most commonly means that the deformity is no longer braceable.
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Surgery is indicated in cases where an obvious muscle imbalance is expected to lead to progressive deformity.
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  If the muscle imbalance is corrected early, surgery may require only tendon transfers.
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  If surgery is delayed, a later deformity will require fusions &/or osteotomies, making the recovery longer and the final function poorer.
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The basic principle of surgical treatment is to restore muscle balance and osseous alignment.
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Muscle balance is corrected through muscle transfers, lengthenings, &/or releases.
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  Lengthenings weaken a muscle.
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  Releases (tenotomies) remove the muscle entirely.
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  Muscle transfers remove the deforming force of the muscle and redirect it to another location.
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Muscle transfers can be in phase or out of phase.
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  In-phase transfers take a muscle and transfer it into another muscle that normally fires during the same part of the gait cycle.
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    Example: Transfer of extensor digitorum longus to tibialis anterior
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  Out-of-phase transfers redirect a muscle to an insertion that is normally antagonistic.
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    Example: Posterior tibial tendon through interosseous membrane to tibialis anterior
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  Out-of-phase transfers are less likely to result in strong active motion in an adult.
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Osseous alignment can occasionally be corrected with capsulotomies in cases of mild deformity.
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Plantar fascia release (minimal incision or wide) can be used to “relax” the arch in some cavus feet.
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More severe deformity requires osteotomies or fusions.
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In adult patients with deformity secondary to brain injury, it may be appropriate to wait 18-24 months between injury and surgery to give enough time for any recovery.

Procedures for Clawed Hallux

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Many neuromuscular diseases result in severe clawing of the hallux, which interferes with shoewear.
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When nonoperative procedures have failed, surgical realignment can be helpful.
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A common procedure is to fuse the hallux interphalangeal joint and transfer the extensor hallucis longus to the 1st metatarsal or midfoot.