Abnormal Biomechanics of the Foot and Ankle

Transcription

1 /67/ $02.00/0 THE JOURNAL OF ORTHOPAEDIC AND SPORTS PHYSICAL THERAPY Copyright (O 1987 by The Orthopaedic and Sports Physical Therapy Sections of the American Physical Therapy Association Abnormal Biomechanics of the Foot and Ankle ROBERT DONATELLI, MA, PT* The biomechanics of the foot and ankle is important to the normal function of the lower extremity. The foot is the terminal joint in the lower kinetic chain that opposes external resistance. Proper arthrokinematic movement within the foot and ankle influences the ability of the lower limb to attenuate the forces of weightbearing. It is important for the lower extremity to distribute and dissipate compressive, tensile, shearing, and rotatory forces during the stance phase of gait. Inadequate distribution of these forces could lead to abnormal stress and eventual breakdown of connective tissue and muscle. Pathologies such as heel spurs, hallux valgus, neuromas, hallux limitus, shin splints, and nonspecific knee pain result from abnormal mechanics of the foot and ankle. The use of orthotics to re-establish the normal biomechanics of the foot and ankle have profound clinical applications. The combined effect of muscle, bone, ligaments, and normal biomechanics will result in the most efficient force attenuation in the lower limb. Abnormal mechanics of the foot and ankle is the breakdown of the mechanisms designed to distribute and dissipate the normal forces of weightbearing. Pronation and supination are the arthrokinematic movements within the foot and ankle that are essential for proper attenuation of compressive, tensile, shearing, and rotatory forces during the stance phase of gait. For example, Mann8 describes a 150 Ib individual walking at a stride length of two 21/2 ft, for 1 mile, would apply 127 tons of force to his feet. If that same individual ran a mile with a stride length of q1/2 ft, he would increase the amount of force to 220 tons.8 A long distance runner's feet contact the ground approximately 5000 times in an hour's run, with 2-3 times the body weight at every heel strike.',' These excessive forces are normally attenuated by the dynamic action of muscle, periarticular tissue strength, flexibility, and proper arthrokinematics. Abnormal pronation and supination are nothing more than hyper or hypomobilities, respectively, within the joints of the foot and ankle. Excessive motion or restricted motion reduces the ability of the foot to act as a shock absorber, torque convertor, mobile adaptor to the terrain, and a rigid 'Assistant Professor. Master Degree Program Orthopaedic and Sports Physical Therapy, Georgia State University, Atlanta, GA lever to push off from. As a result of changes in the joint mobility, connective tissue changes occur, in addition to alterations in muscle function. This could result in pathological conditions such as neuromas, hallux valgus, tailors bunions, keratosis, shin splints, nonspecific knee pain, plantar fascitis, heel spurs, metatarsalgia, and achilles tendinitis.',l5 ABNORMAL PRONATION Abnormal pronation is a compensation for a soft tissue or osseous deformity.15 The deformity can be intrinsic or extrinsic to the foot. In the majority of cases, excessive pronation occurs at the subtalar joint to compensate for the abnormality.3z'5 The compensation is persistent and results in pathology.15 Maximum pronation is achieved at footflat and supination begins at midstance. Excessive pronation means that the foot is pronating beyond 25% of the stance phase.138s14915 Consequently, at midstance the foot does not begin to resupinate, it remains in maximum pronation. The foot may resupinate late in the stance phase or never resupinates, as seen in a rigid flatfoot. This results in the inability of the foot to effectively absorb the forces of weightbearing. The etiology of abnormal pronation can result from many different factors. Congenital, develop-

2 12 DONATELLI JOSPT Vol. 9, No. 1 mental, intrinsic, (within the foot) and/or extrinsic, (outside the foot), are the categories we will discuss. The most common intrinsic congenital deformities resulting in abnormal pronation in the adult foot include convex pes valgus (vertical talus), tarsal coalitions, and congenital metatarsus ~arus.~~','~ The developmental deformities intrinsic to the foot include talipes calcaneovalgus, talipes calcaneovarus, postural metatarsus adductus, and forefoot var~s.~~~.'~ The congenital deformities result from genetic factors, which are beyond the scope of this article. The developmental or postural deformities may result from a poor position in the uterus.17 Additional factors causing developmental flatfeet involve ligament laxity and/or a tight achilles tendon.17 CONGENITAL DEFORMITIES Convex pes valgus is a primary dorsal and lateral dislocation of the talocalcaneonavicular j~int.~.'~ The navicular articulates with the dorsal aspect of the talus, locking it in the vertical position. This deformity has been described as a "rocker bottom foot." Tarsal coalitions include complete or incomplete fusion of the major tarsal The coalitions producing a flstfoot are, calcaneonavicular or talocalcaneal at the middle, anterior, or posterior fa~et.~,'~ Clinical signs may exist, such as limitation and/or rigidity of the major tarsal articulations, valgus deformities of the rearfoot, and soft tissue contractures or spasm of the peroneus longus and brevis7, l7 Congenital metatarsus varus is medial subluxation of the tarsometatarsal joints with adduction and inversion deformity of the metatarsal^.^^'^ One important clinical finding is the inability of the forefoot to be passively abducted to the neutral position. This differs from the postural metatarsus adductus deformities, which can be reduced by passively moving the forefoot into abduction. In the newborn, the prognosis for 10O0/0 correction of the postural metatarsus adductus deformities is excellent within the first few month^.^.'^ POSTURAL DEFORMITIES Calcaneovalgus, the most common postural deformity, occurs in approximately 1 in 1000 births. There is a high correlation of calcaneovalgus in the newborn and the development of a flexible flatfoot in the older ~hild.~.'~ The appearance of the foot is one of dorsiflexion and eversion. The most important clinical observation is the limitation of plantarflexion at the ankle joint. The plantarflexion range is usually limited to 90' or less. Another clinical finding is dorsiflexion and eversion of the foot with stroking of the plantar surface of the foot. This sign is lost by the age of 4-6 months.17 Calcaneovarus can best be described as inversion of the entire foot, with no limitation in dorsiflexion at the ankle j~int.~,'~ Root et a1.15 and Tax1' report the most common intrinsic deformity resulting in abnormal pronation is forefoot varus. The definition of forefoot varus is an inversion of the forefoot on the rearfoot with the subtalar joint in neutral (Fig. l).15 Root et ai.l5 describe it as a frontal plane deformity, that is compensated at the subtalar joint by eversion or a valgus position of the calcaneus in weightbearing (Fig. 1). The compensation is nothing more than excessive talar adduction, plantarflexion, and calcaneal eversion (abnormal pr~nation).~.'~ This author has observed forefoot varus deformity as the single most common intrinsic cause of mechanical pain and dysfunction within the foot, lower one-third of the leg, and knee. McCreag defines forefoot varus as a sagittal plane deformity of the first ray. The first ray is dorsiflexed and hypermobile. This' hypermobility results from the inability of the peroneus longus to stabilize the first ray. The cuboid pulley allows the peroneus longus to plantarflex and abduct the first ray producing stability (Fig. 2).15 This pulley system is reinforced by a locking up of the midtarsal joint during supination of the subtalar j~int.'~~'~~'~ The cuboid becomes a rigid structure, producing a stable pulley for the peroneus longus. Abnormal or excessive pronation reduces the abil- Fig. 1. Uncompensated (A) and Compensated (B) forefoot varus. 1, First ray; 2, articular surface of talus and navicular; 3, Articular surface of calcaneus and cuboid; 4, calcaneus; 5, talus; 6, tibia; 7, fibula; 8, keratosis under second ray.

3 JOSPT July 1987 ABNORMAL BIOMECHANICS OF THE FOOT AND ANKLE 13 A common x-ray finding in a flatfoot is the change in the alignment of the midtarsal joint line. The lateral weightbearing x-rays demonstrate a line forming an S, called the Cyma line, which passes between the talus and navicular and cuboid and calcaneus (midtarsal joint) (Fig. 3).' With excessive pronation there is an anterior break in the Cyma line. The talus has moved anterior relative to the cuboid and calcaneus. The anterior movement of the talus compensates for the lack of anterior movement of the tibia. Fig. 2. Cuboidpulley. A, Normal pulley system for the peroneus longus, subtalar neutral; B, abnormal pronation and less efficient pulley system. A and F represent the vectors of the peroneus longus action; C, abduction vector; F, plantarflexion vector; P, peroneus longus. 1, Cuboid; 2, cuneiforms; 3, talus; 4, fibula; 5, tibia; 6, calcaneus. ity of the foot to return to supina:ion. Thus, the midtarsal joint, specifically the cuboid, is in a poor position. This creates an inefficient pulley for the peroneus longus, causing instability of the first ray.15 The dorsiflexed and hypermobile first ray can produce a hallux valgus, subluxation of the metatarsophalangeql joint of the big toe in the sagittal and transverse planes.15 The instability of the first ray during the stance phase of gait causes the weight to be shifted from the first to the second metatarsal. The first ray is twice as large and is four times as strong as any of the other rays6 It has stronger muscles attached to it than any other ray.6 It has progressed in evolution from an adducted position to a midline position to enhance it's weight-bearing ability." The second ray is not designed to deal with the excessive forces of weightbearing. As a result of first ray insufficiency, a callus or keratosis develops under the head of the second metatarsal and stress fractures are not uncommon in this area.6 This author and others have observed ankle jaint equinus to be a frequent factor in the development of abnormal pronati~n.~,'~ Root et ai,l5 define ankle joint equinus as the lack of dorsiflexion of the ankle joint with the subtalar joint in neutral. This inability of the tibia to move anterior to the talus from footflat to midstance can result from a tight achilles tendon or a flattened dome of the talus. The compensation for this deformity can occur at the subtalar joint by excessive pronation.14 If the tibia cannot move anterior to the talus, the talus will move anterior. EXTRINSIC CONGENITAL AND DEVELOPMENTAL DEFORMITIES The most common extrinsic congenital deformities causing abnormal pronation include hip dysplasia, femoral antitorsion, tibia1 torsions, and genu varum or valgus.' The most common developmental deformities this author has observed in the clinic include femoral antiversion secondary to tight internal rotators or anterior hip capsule, pelvic imbalances, and muscle imbalances within the pelvis and lower extremity. The above deformities produce a rotation of the lower limb that could be compensated by pronation of the subtalar joint. For example, excessive external rotation of the lower limb will shift the center of gravity in weightbearing to the medial aspect. This increase in medial stress to the foot causes the tibia and talus to rotate medially (plantarflexes and adducts), while the calcaneus rolls laterally (into v alg~s).~~~~'~ Internal rotation of the lower limb produces excessive forces to the lateral aspect of the foot. The center of gravity in weightbearing should pass through 'the center of the foot. In an attempt to shift the center of gravity more medially the fore- Fig. 3. Medial arch view on lateral weightbearing x-ray. A, Abnormal-anterior break in the Cyma line, with reduced height of the calcaneal inclination angle, cuboid, and navicular. Normal inclination angle of the calcaneus B, Normal alignment of the medial arch. "S" shaped Cyma line. 1, cuboid; 2, navicular; 3, calcaneus; 4, inclination angle of the calcaneus; 5, cyma line; 6, talus.

4 14 DONATELLI JOSPT Vol. 9, No. 1 foot abducts on the rearfoot or the foot abducts weightbearing x-rays, the inclination angle of the on the leg, producing excessive pronation of the calcaneus is reduced, reducing the height of the subtalar j~int.'~.'~ The toe-in gait abnormality in calcaneus to the ground. The normal angle of children is a good example of an internally rotated inclination is The height of the cuboid lower limb. Subtalar joint pronation is one possible and navicular is also reduced (Fig. 3).',l7 Patients compensation for this gait abnormality. with flatfeet (excessive pronators) demonstrate a As a result of the deformities listed, the align- wide foot, secondary to the spreading apart of ment of the calcaneus, talus, cuboid and navicular the tarsal bones. change. This in turn produces poor articular con- The change in the mechanics of the rearfoot gruity and changes in the arthrokinematics of the and midfoot produces certain anatomical changes ankle joint, subtalar joint, and midtarsal. The ex- typical to a flatfoot, that can be observed in the cessive arthrokinematic movements occur be- weightbearing position. These changes include a tween four bones, calcaneus, talus, navicular, and valgus (eversion) position of the calcaneus, bulgcuboid. The tibia, talus, and calcaneus move si- ing of the navicular tuberosity medially, abduction multaneously. As the talus and tibia rotated me- of the forefoot on the rearfoot, and a reduction in dially, the calcaneus rolls laterally (~algus).~~.~~.'~ the height of the medial In abnormal pronation the calcaneus is described as subluxing under the talus.' The talus during ABNORMAL SUPINATION weightbearing is fixed in the ankle joint.mortise, restricting movement in the frontal plane. The tibia There are three basic classifications for abnormoves anterior and medial producing internal ro- mal supination.'s16 First is a pes cavus foot. This tation of the talus and tibia. The talar movements foot demonstrates a fixed plantarflexed forefoot, are described as adduction and plantarflexion or an equinus forefoot. The rearfoot in the weight- (Fig. 4). The weightbearing stress is more medial bearing position is in neutral (no eversion or incausing a medial force to the heel, resulting in a version is visible). The second type is pes cavovalgus heel. varus. This foot demonstrates a fixed plantar- It is important to note that the above arthroki- flexed medial column or first ray. In the weightnematic movements are abnormal because they bearing position the calcaneus is in varus or inare excessive and persistent. Normal pronation verted. compensation is a temporary condition of the Root et ai.l5 defines forefoot valgus as eversion subtalar joint.14 The normal compensation might of the forefoot on the rearfoot with the subtalar occur in response to a change in the terrain. joint in neutral. The compensation for a forefoot The navicular and cuboid are influenced by the valgus is inversion of the calcaneus in the weightmovements of the talus and calcaneus. Excessive bearing position (Fig. 5).14,16 Forefoot valgus and/ pronation causes the navicular and cuboid to or a fixed plantarflexed first ray are the most move away from each other. As noted on lateral common intrinsic deformities resulting in abnormal supination of the subtalar joint. This author has observed a combined fixed plantarflexed first ray Fig. 4. Closed kinetic chain pronation. A, Anterior view of the subtalar joint and the talocrual joint; B, posterior view of the subtalar and talocrual joint. 1, ~alcaneal/cuboid articulation; Fig. 5. Uncompensated (A) and compensated (B) forefoot 2, talo/navicular articulation; 3, sustentaculum tali; 4, calca- valgus. 1, First ray; 2, talo/navicular articulation; 3, calcaneal/ neus anterior aspect; 5, talus; 6, tibia; 7, fibula. cuboid articulation; 4, calcaneus; 5, talus; 6, tibia; 7, fibula.

5 JOSPT July 1987 ABNORMAL BIOMECHANICS OF THE FOOT AND ANKLE 15 and a forefoot valgus present with rearfoot varus compensation at the subtalar joint. Pes equinovarus is the third clas~ification.~~'~ This foot demonstrates a fixed plantarflexed forefoot and rearfoot. No compensation is needed in the weightbearing position. The etiology of a pes cavus foot falls under two basic classifications, neuromuscular and idi- opathi~.~,'~ Several neuromuscular disorders can cause a pes cavus foot such as cerebral palsy, Charot-Marie-Tooth disease, Frederick's ataxia, and muscular dystr~phy.~.'~ The idiopathic type of cavus foot is thought to develop secondary to causative factors such as measles, scarlet fever, and diptheria causing a discrepancy in the growth of bone and m~scle.~*'~ Functionally, abnormal supination is the inability of the foot to pronate. At heel strike the foot should be in neutral and begin to pronate immediately. An excessive supinator remains supinated throughout the stance phase or pronates late in stance, (from heel-off to push-off). Root et ai.l5 state that more trauma occurs to the foot when pronation occurs during the push-off phase of gait. This can be observed during the gait cycle by a whipping or unstable heel in push-off. Patients that excessively supinate develop irritations within the foot such as plantar fascitis, heel spurs, achilles tendinitis, metatarsalgia, and calcaneal bursitis. FUNCTIONAL BIOMECHANICAL ORTHOTIC The functional biomechanical orthotic is designed to restore normal alignment of the subtalar and midtarsal joints, controlling excessive pronation and supination, reducing the abnormal forces through the kinetic chain. The general concept of a functional biomechanical orthotic is to support the forefoot varus or valgus deformity and reposition the rearfoot (subtalar joint) as close as possible to neutral. For example, to correct a forefoot varus a medial post or support is used to bring the ground up to the first ray (Fig. 6). In addition, a medial post is also used to prevent and/or control the calcaneus from rolling into valgus. A general rule to follow is "post what you see." If the forefoot varus deformity was measured at 5O, a 5O medial post should be prescribed in fabrication of the permanent orthotic. The post is designed to support the first ray and/or the forefoot foot deformity. SUMMARY Abnormal pronation and supination indicates excessive or restricted motion within the foot and ankle, secondary to soft tissue and/or bony abnormalities. A compensation for the deformity is necessary to allow the foot to function correctly during the gait cycle. A large majority of the time the compensation occurs at the subtalar joint. Consequently, the normal amount of pronation and supination required during the stance phase of gait occurs in addition to the amount needed to overcome the deformity. This is considered excessive pronation or supination. There are two basic types of abnormal pronators or supinators. The first type of foot remains pronated or supinated throughout the stance phase of gait. This type of foot never resupinates or repronates. The second type resupinates or pronates at the wrong time in the stance phase. For example, pronation might begin at heel lift or push-off. The foot needs to be supinating during the final phase of stance, to establish a rigid lever to push off from. If the foot is pronating, stability is lost producing trauma to the foot and a less efficient propulsive phase of gait. The use of orthotics to control the duration and the amount of pronation and supination during the stance phase of gait have profound effects on pain and dysfunction of the lower extremity. It is important to evaluate muscle imbalances extrinsic and intrinsic to the foot, in addition to evaluating forefoot and rearfoot deformities. The treatment must include correction of abnormalities within the foot and throughout the lower extremity. Fig. 6. Biomechanical orthotic posting. 1, First ray; 2, calcaneus in neutral; 3, medial forefoot post and rearfoot post. Acknodedgments: My wife Joni for her support and enwuragernent. My partners in practice and in Clinical Education Associates, Swt Irwin, Steve Kraus, Micheal Wooden, and Marty Kaput.

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