Mentally and physically handicapped individuals, such as those afflicted with Down syndrome and cerebral palsy , have gait problems that progress with age. These gait abnormalities frequently lead to the eventual development of foot pain if not corrected. No matter what the etiology, foot pain can lead to a decrease in activity and mobility and, for the mentally handicapped, the eventual removal of community participation [1]. Studies have found that early identification and correction with conservative care of lower extremity foot deformities commonly seen with the mentally and physically challenged can lead to improved development of the individual both physically and socially [2, 3]. This chapter covers orthoses, shoe gear, and shoe modifications to help with the most common pedal problems associated with active mentally and physically challenged individuals, with the hope of improving physical activity and wellness.

In 1948, Sir Ludwig Guttman held the first organized sporting event for the physically handicapped. The Paralympic Games , founded by Guttman, included athletes with visual and physical impairments, such as those with amputations and those requiring wheelchairs [4, 5]. Other programs have since been created that allow for the participation of a wide variety of athletes, including those with mental and physical disabilities, in national and international competition. One of the most noted organizations today is the Special Olympics. The Special Olympics is dedicated to providing training for 2.25 million mentally challenged athletes in 160 countries, promoting improvement in both physical and mental fitness [6]. In the United States , there are an estimated two to three million active athletes with mental and physical disabilities [5].

There is a vast volume of literature covering the physical improvements that exercise and physical activity can have on the human body. This literature mainly covers normal developing adults. Little research has been generated for the physically and mentally handicapped active population [4]. The small amount of research that has been conducted is dedicated to showing that with an increase in activity and interactive events such as sports, mentally and physically handicapped persons show improvements in daily activity, health, and social interactions [3–5, 7].

Before a handicapped individual participates in athletic events a thorough physical should be performed to assess physical limitations. Athletes with mental and physical challenges can have physical limitations and health risks that are non-conducive to certain athletic events. Physical limitations that should be considered before participation in individual sporting activity include endurance, strength, and mobility. Severe health risks, including those that can cause loss of body control or even death, need to be identified. For instance, in individuals with Down syndrome up to 25% have atlantoaxial instability from ligament laxity. Increased ligamentous laxity can allow subluxation of the C1 vertebrae on the C2 vertebrae. Vertebral subluxation will cause compression on the spinal cord by the dens. Spinal cord compression can present as abnormal neurological manifestations, quadriplegia, and death [1, 8]. In individuals with cerebral palsy , 40% of all children have an associated seizure disorder [3]. Seizure disorders need to be identified, addressed, and monitored by a medical professional before athletic clearance can be given.

A brief discussion on normal gait and development of the lower extremity is warranted. During a normal child’s growth the lower extremity rotates inwards and outwards around a central axis at three key osseous locations: the hip, knee, and ankle. The rotation is caused by a balance of soft-tissue development and growth of long bones. There are three key periods of growth that occur at approximately ages 1, 6, and 15. At each age the bones of the hip, knee, and ankle are rotating either inward or outward, ultimately causing the foot to retain an inward or outward position. Key rotating bones are the femur, fibula, and tibia at the tibial condyles and malleoli. Differences in femoral and tibial bone rotation result in bringing the knee into a progressively decreased varum position, rotating the knee inwards, and bringing the knees closer together throughout skeletal maturity. At the ankle, the external malleolar position increases with age.

The result of the combined bone rotation at all levels of the lower extremity causes out-toeing or an externally rotated flatfoot from 0 to 2 years old. Flat foot and out-toeing can be considered normal from birth to 2 years old as a child will be unable to form a foot arch due to lack of maturity of the neurological system until after age 2. Intoeing, or “pigeon toe,” will be present from 4 to 6 years old and again at 13–15 years old. At the age of skeletal maturity, 15–18 years old, the malleoli should be rotated 18–23° of external rotation forming the normal mildly everted foot position of about 18° from the body’s sagittal cardinal plane [9].

Common foot problems affecting normal gait can be classified into three general categories: pes planus , pes cavus , and equinus. These pathologies are the result of one or a mixture of three main biomechanical mechanisms: pronation, supination, and ankle equinus. Other problems commonly associated with mentally challenged athletes include hyperhidrosis syndromes.

Ankle equinus is the inability of the foot, at the ankle joint, to dorsiflex 10° past perpendicular to the leg. It is a common deforming force in the foot, typically causing the foot to pronate. Pronation is a frequent biomechanical compensation in normal gait. Primary manifestations of ankle equinus without biomechanical compensation, such as tiptoe walking, are not commonly seen except in certain neuromuscular diseases such as muscular dystrophy and cerebral palsy . Conservative treatment for ankle equinus consists of intrinsic and extrinsic heel lifts and will be discussed with the conservative treatments of pes cavus and pes planus .

Pes planus , or flat foot, is one of the most common foot conditions globally [10]. Flexible flat foot has been shown to occur in 44% of children aged 3–6 years [11]. Some experts consider flat foot a normal developmental stage in children up to 6 years old [12]. The most common cause of flat foot is excessive pronation at the subtalar joint.

Pronation of the foot inhibits mechanical dampening mechanisms by the bone and soft tissues, preventing internal rotation of the leg during heel contact and leading to foot and joint pain. Pronation is considered to be the foot at the subtalar joint functioning at maximum eversion. Quantitatively pronation can be described as a measurement equal to or greater than 10° eversion at the subtalar joint, leaving the calcaneus in a valgus position [8, 13].

Pronation can be visually identified in several ways: (1) an everted heel; (2) flat medial arch on or off weight bearing; (3) prominent talar head or midtarsal bones; (4) the inability of the heel to supinate with performance of the Jack’s test or Hubscher maneuver , activating the windlass mechanism to form the medial foot arch; (5) forefoot abduction causing “too many toes sign” on weight-bearing evaluation; and (6) the lateral border of the foot appearing shorter than the medial border [13, 14]. Appearance of a midtarsal bony collapse with a pronated foot is usually an indicator of more severe pes planus problems [13]. The degree of abnormal pronation leading to pes planus depends on a variety of factors.

Flat foot disorders can be classified as either pathologic or physiologic. Pathologic disorders are commonly seen at birth and cause rigid abnormalities. Examples of pathologic disorders include vertical talus syndrome, trauma, and spastic conditions. Physiologic disorders result from developmental abnormalities that cause a foot to gradually lose an arch throughout the first decade of life [11, 14].

Pes planus etiologies can be further classified as either genetic or acquired. Acquired pes planus is seen with (1) osseous fractures, (2) ligamentous tears, (3) muscular imbalances, (4) degenerative joint diseases, and (5) postural problems, resulting, for example, from obesity or pregnancy [10]. Genetic etiologies include (1) tarsal coalition; (2) obliquity of the ankle joint, where the medially located tibia grows faster than the fibula; (3) failure of tibial torsion; (4) Achilles tendon shortening; (5) ligamentous laxity (which is seen in Down syndrome , Ehlers-Danlos syndrome , and Marfan syndrome ) [10, 15]; and (6) increase or decrease in muscle tone, which can cause more complex forms of pes planus . Low muscle tone is seen in neurologically delayed subjects with or without anterior horn loss, in primary muscle damage and in collagen pathology. There is debate on whether latent cognitive and neurological system development of the cerebellum has an impact on abnormal physiological development causing ligamentous laxity, such as that found in Down syndrome . It is general consensus that a delay in cerebellar development does delay the age at which ambulation begins [1, 16].

High muscle tone pathology causing flat foot is seen with spastic peroneal muscles, the primary cause of a progressively rigid flat foot [8, 10, 13, 17]. Flat foot caused by peroneal spasticity can be corrected with a scaphoid pad, varus heel wedge, and orthosis [8].

Osseous developmental problems resulting in pes planus include acetabular dysplasia, hip dislocation syndromes, metabolic syndromes such as Blount’s disease, and physiological tibial varum [3, 7, 13]. These pathologies should be treated by surgical means. Foot pathologies include metatarsus adductus, hallux valgus, metatarsus primus varus, ligamentous laxity, joint hypermobility, foot and ankle equinus commonly caused by a tight Achilles tendon, pes cavus , forefoot supination, rigid forefoot varus, tarsal coalition, and foot rigidity [2, 16]. Most foot pathologies resulting in pes planus can be treated with appropriate shoe gear as long as the pes planus has not progressed to a symptomatic rigid state [7, 14].

Of the genetic disorders with associated flat foot , Down syndrome is the most common. It occurs in 1 in 660 live births [1, 2]. Down syndrome individuals are active and commonly participate in athletic events. Half of all people afflicted with Down syndrome have gait abnormalities appearing as gait imbalance and abnormal walking posture [1, 2]. Problems with ambulation are attributed to a delay in neurological development, ligamentous laxity, and muscular hypotonia, all of which are found in 88% of individuals with Down syndrome [1]. Ligamentous laxity and muscular hypotonia also allow for joint hypermobility causing increased foot width and potentially disabling osteoarthritis leading to rigid foot deformities if left untreated [1, 2, 16]. Flexibility, ligamentous laxity, and muscle hypotonia associated with Down syndrome decrease greatly with age but never fully resolve [1, 16].

Down syndrome individuals are also affected by osseous variations in bone torsion in the lower extremity. Developmental deformities include hip retroversion causing severe external rotation in hip flexion and extension and resulting in an out-toe gait. Hip dysplasia and dislocation can also be found; these are treated surgically. Knee problems are generally secondary to foot abnormalities. Knee pathology , which is relatively uncommon, includes patellofemoral instability, patellofemoral dislocation, knee flexion contracture, external tibial rotation, genu valgum, and rotary tibiofemoral subluxation. Knee pathologies are generally not inhibitory to activity or gait and tend to be well tolerated. Treatment consists of wearing a patellar sleeve during ambulation. At the ankle, the tibia is externally rotated causing an externally rotated foot [1, 7]. Although these examples of lower extremity problems are seen with Down syndrome, they are not limited to it and can found in other congenital pathologies [18].

Any deviation from normal development of the lower extremity will decrease the efficiency of gait in an active individual. Gait alteration with conservative measures that provide biomechanical and postural correction can dramatically improve activity and structural development in the lower extremity [2, 18].

Biomechanically, flat foot is a complex deformity. Pes planus can be caused from biomechanical imbalances in one body plane or a combination of all three: sagittal, transverse, and frontal. For pes planus treatment to be successful it must be addressed on the deformity’s main cardial plane [13, 17].

Structurally the foot is designed to bear weight on the rearfoot, lateral column, and first and fifth metatarsal heads [10]. In pes planus , as the medial foot arch collapses the foot shifts laterally along the lateral column shorting it and lengthening the medial column. The forefoot is hypermobile, allowing the first metatarsal to shift dorsally and medially, transferring weight further up the medial column which is not designed for weight bearing. The first metatarsal and sesamoid bones normally support 33% of the body’s weight during the normal stance phase. This percentage of weight bearing decreases with abnormal pronation, resulting in increased weight bearing in other areas of the foot [10].

In pes planus the rearfoot does not supinate on the forefoot, preventing locking of the midtarsal joints. If the forefoot joint complex is unlocked it is unstable. An unstable foot platform decreases the effectiveness of gait and allows joint subluxation to occur. Repetitive subluxation will result in eventual degenerative joint disease, foot pain, and possibly rigid foot deformities. Flat foot deformities that become painful and symptomatic are referred to as pes planovalgus deformities.