Category: Pediatrics

Growing pains are one of the most common causes of recurrent limb pain in childhood, yet they remain poorly understood and sometimes misunderstood by both parents and clinicians. Despite the name, growing pains are not directly associated with growth spurts, nor do they signal any underlying musculoskeletal pathology. Rather, they represent a benign, self-limiting syndrome characterized by intermittent pain, typically occurring in the lower limbs of children aged between three and twelve years. Understanding growing pains requires examining their clinical features, possible pathophysiological mechanisms, differential diagnoses, and management strategies.

Epidemiology

Growing pains affect approximately 10–30% of children, with the reported prevalence varying widely across studies due to differing diagnostic criteria. The condition appears to occur equally among boys and girls, though some studies suggest a slight female predominance. The peak incidence typically occurs between ages 4 and 9, and there is no known correlation with height, weight, or accelerated growth rate—contrary to popular belief. A family history of childhood limb pain is frequently reported, suggesting a possible genetic or familial predisposition. Growing pains are most often seen in otherwise healthy children with normal growth and physical development.

Clinical Presentation

The typical presentation of growing pains involves intermittent, bilateral pain in the lower extremities—especially the thighs, calves, or behind the knees. The pain usually arises in the late afternoon or evening, sometimes waking the child at night, but is absent by morning. Episodes may occur sporadically, several times per week, or intermittently across months or years. Importantly, the pain is not localized to joints, and there is no associated swelling, redness, or warmth. The child’s gait remains normal, with no limitation of activity during the day, and physical examination between episodes is unremarkable.

Pain severity can vary from mild to moderate, occasionally prompting crying or restlessness at night. Parents often note that the pain can follow days of increased physical activity, suggesting a possible relationship between muscle fatigue and symptom onset. The episodic nature of symptoms, coupled with normal examinations, distinguishes growing pains from more serious musculoskeletal or systemic conditions.

Pathophysiology

The cause of growing pains remains unclear, but several hypotheses have been proposed:

1. Muscular fatigue hypothesis: One of the most widely accepted theories suggests that growing pains result from muscle overuse or fatigue following daily physical activity. The discomfort may stem from microtrauma or metabolic accumulation in muscles unaccustomed to sustained exertion.
2. Joint hypermobility and mechanical stress: Some children with joint hypermobility syndromes are more prone to musculoskeletal pain, potentially due to the increased mechanical stress on muscles and connective tissue.
3. Bone strength and microvascular factors: A subset of research indicates that children with growing pains may have lower bone density or altered vascular perfusion in the limbs, making periosteal structures more sensitive to strain or transient ischemia.
4. Central pain sensitization: Another perspective implicates altered pain perception or lowered pain thresholds. Evidence suggests that children experiencing growing pains may also have an increased prevalence of headaches or abdominal pain, hinting at a generalized pain amplification mechanism rather than a purely localized musculoskeletal process.
5. Psychological and hereditary influences: Some studies link growing pains with stress, temperamental traits, or family patterns of episodic pain. Parental anxiety and attention to pain can also shape the child’s pain perception and coping behavior.

No single mechanism adequately explains all clinical features, and it is likely that growing pains represent a multifactorial condition involving mechanical, vascular, psychological, and neurophysiological components.

Differential Diagnosis

Though growing pains are benign, clinicians must exclude other potential causes of limb pain in children. The key differential diagnoses include:

• Juvenile idiopathic arthritis (JIA): Presents with persistent joint pain, swelling, and morning stiffness—unlike the transient and non-articular nature of growing pains.
• Infectious or inflammatory conditions: Osteomyelitis or septic arthritis causes localized tenderness, systemic symptoms, and often fever.
• Orthopedic disorders: Conditions such as Legg–Calvé–Perthes disease, slipped capital femoral epiphysis (SCFE), or Osgood–Schlatter disease produce localized pain associated with joint dysfunction or activity.
• Malignancies: Bone tumors or leukemia can present with bone pain, nocturnal discomfort, and systemic signs like weight loss, fatigue, or pallor.
• Vitamin D deficiency: Low vitamin D levels can contribute to limb and muscle pain, though typically accompanied by other skeletal symptoms.

A careful history and physical examination are usually sufficient for diagnosis. Red flags warranting further investigation include localized pain, unilateral symptoms, functional impairment, constitutional symptoms (fever, malaise, weight loss), or any abnormal findings on musculoskeletal examination.

Diagnosis

There is no specific laboratory or imaging test for growing pains. The diagnosis is primarily clinical and based on exclusion. Routine investigations are not necessary unless atypical features are present. Parents can be reassured when the child exhibits the classic triad: (1) bilateral limb pain, (2) normal daytime activity, and (3) normal clinical examination. However, if red flags are noted, further assessment—such as radiographs, blood tests (ESR, CRP), or bone scans—may be warranted to exclude other pathology.

Management

The management of growing pains is mainly supportive, focusing on symptom relief and parental reassurance. Since the condition is benign and self-limiting, the primary goal is to ensure comfort and reduce anxiety.

1. Parental reassurance:
Education is central. Parents should be informed that growing pains do not signify underlying disease and usually resolve spontaneously by adolescence. Clear communication about the benign course of the condition alleviates unnecessary anxiety and prevents overmedicalization.

2. Physical comfort measures:

• Gentle massage of affected areas often provides immediate relief.
• Application of warmth, such as a heating pad or warm bath, can soothe muscles.
• Stretching exercises targeting the quadriceps, hamstrings, and calf muscles may reduce recurrence in some cases.
• Adequate rest and moderation of excessive physical activity, especially high-impact sports, may also help.

3. Pharmacological measures:
Simple analgesics like paracetamol or ibuprofen can be used for pain episodes, though regular use is rarely necessary. There is no evidence supporting the use of stronger analgesics or specific pharmacotherapy for growing pains.

4. Addressing contributing factors:
Children showing signs of biomechanical abnormalities—such as flat feet, hypermobility, or gait asymmetry—may benefit from assessment by a podiatrist or physiotherapist. Orthotic supports, while not universally indicated, can be helpful in select cases.

5. Psychosocial support:
For children who experience anxiety or sleep disruption due to pain, nighttime reassurance and relaxation techniques can be valuable. Encouraging normal activity and reinforcing positive associations around physical play fosters resilience.

Prognosis

The prognosis for growing pains is excellent. Most children outgrow them by adolescence without any long-term consequences. The episodes tend to diminish in frequency and severity over time. Although some studies suggest a modest association between childhood growing pains and later musculoskeletal sensitivity or chronic pain syndromes, the majority of cases resolve completely.

Current Research and Emerging Insights

Emerging studies are exploring links between vitamin D deficiency and growing pains, with some reporting symptom improvement following supplementation. Other research is examining genetic predispositions and correlations between growing pains and sensory processing differences, providing a more holistic understanding of pediatric pain syndromes. Future insights into pain modulation pathways could refine management strategies, potentially linking growing pains to broader pediatric pain research.

Growing pains represent a benign, recurrent pain syndrome of childhood that, despite its commonality, continues to raise diagnostic uncertainties. Characterized by intermittent bilateral lower limb discomfort, typically occurring at night, the condition has no identifiable structural or inflammatory cause. Its multifactorial etiology likely encompasses mechanical, vascular, and neurophysiological components. The cornerstone of management lies in reassurance, symptomatic relief, and careful exclusion of more serious conditions. With appropriate understanding and parental guidance, children with growing pains can maintain normal physical activity and quality of life, free from undue concern about their natural growing process.

Gait plates are a specialised orthotic modification used to influence the angle of gait and can be a useful tool in managing in‑toe gait in children when applied to the right patient and integrated into a broader treatment plan. This essay will outline the biomechanics and causes of in‑toe gait, the design and mechanism of gait plates, the evidence for their effectiveness, clinical indications and limitations, and practical considerations for their use in paediatric practice.

In‑toe gait in children

In‑toe gait (or pigeon‑toeing) describes a walking pattern in which the feet point medially relative to the line of progression. It is common in early childhood and is most frequently associated with three main anatomical contributors: metatarsus adductus, internal tibial torsion, and increased femoral anteversion.

In many toddlers, mild in‑toeing is considered a normal variant of development and often improves spontaneously as rotational alignment normalises with growth. However, persistent or severe in‑toe gait can be associated with frequent tripping, reduced participation in play or sport, pain, and cosmetic or psychosocial concerns for the child and family. For these children, intervention may be warranted, beginning with careful assessment to determine the primary level of rotational deformity (foot, tibia, or femur) and to exclude neuromuscular or structural pathology.

Gait plate design and mechanism

A gait plate is an orthotic design feature that modifies the distal contour and line of flexion of the device to alter the child’s angle of gait. Unlike traditional functional orthoses that typically terminate just proximal to the metatarsal heads, gait plates extend distally beyond the metatarsophalangeal joints asymmetrically to influence how the shoe flexes and how the foot operates within the shoe.

For in‑toe gait, the gait plate is commonly extended laterally so that the distal edge finishes under or past the lateral toes, shifting the effective flexion line and making it easier and more comfortable for the foot to externally rotate during propulsion. The device is thought to act via a combination of mechanical constraint and proprioceptive feedback: as the child attempts to toe‑in, contact with the orthosis and shoe encourages a subtle out‑toe position that gradually becomes the preferred pattern while the device is worn.

Gait plates can be fabricated as modifications to custom orthoses or as stand‑alone flat plates sourced from rigid materials such as polypropylene or carbon fibre, then posted or contoured as required. They are typically used inside everyday footwear, including school shoes and runners, provided there is sufficient depth and width to accommodate the extended forefoot section.

Evidence for effectiveness

The literature on gait plates is relatively limited but suggests that they can produce a measurable improvement in the angle of gait and reduce functional problems such as tripping in children with in‑toe gait. Early work by Schuster in the 1960s reported improvements of around 15° in angle of gait with gait plate use in children with rotational gait abnormalities. Subsequent studies have shown more modest but statistically significant reductions in in‑toeing, along with decreased tripping and high levels of parental satisfaction.

A more recent study of children with in‑toe gait due to increased femoral anteversion found that a gait plate insole worn in ordinary shoes increased the angle of gait by approximately 11.1° compared with barefoot walking and by around 7° compared with shoes alone. The same study reported changes in centre of pressure displacement in the anterior–posterior direction, indicating a subtle alteration in gait mechanics rather than a purely cosmetic change. Importantly, these improvements occurred immediately when the device was worn, which supports the view that gait plates primarily modify gait while in situ rather than permanently correcting underlying torsional deformities.

Clinical reports from podiatry practices indicate that gait plates can noticeably reduce tripping and improve the appearance of gait in children with more severe in‑toeing, with many parents reporting that children adapt quickly and find the devices comfortable. However, there is limited high‑quality long‑term data on whether these devices influence structural rotational alignment over time, so they should be viewed as functional aids rather than definitive corrective tools.

Indications, limitations, and clinical decision‑making

Gait plates are most appropriately indicated in children who have persistent in‑toe gait beyond the expected age of spontaneous resolution, particularly when it is associated with frequent tripping, pain, or psychosocial distress. They can be especially useful when the in‑toe gait is functionally significant but surgery would be disproportionate or inappropriate given the child’s age and overall function.

Before prescribing a gait plate, practitioners should identify the primary source of in‑toeing, as some causes are less responsive to conservative approaches. For example, tibial torsion is often reported not to respond meaningfully to splints, footwear modifications, or physical therapy alone; surgical derotation may be considered only in older children with severe functional limitations. In contrast, in‑toe gait related to increased femoral anteversion has shown measurable improvement in angle of gait when a gait plate insole is used, suggesting that in these cases the device can be an effective adjunct to monitoring and exercise.

A key limitation is that gait plates are generally effective only while worn; they do not necessarily resolve the underlying torsional deformity. Clinicians should therefore avoid over‑promising structural correction and instead frame the goal as improving function, reducing tripping, and enhancing the cosmetic appearance of gait during use. Additionally, the extended distal profile may limit footwear options, and careful shoe selection is essential to avoid pressure on the toes or poor fit.

Practical application in a paediatric treatment plan

In practice, gait plates should be prescribed as part of a comprehensive management plan for the child with in‑toe gait rather than as a stand‑alone cure. This plan typically begins with a detailed history and physical examination, including assessment of rotational profiles (foot progression angle, thigh–foot angle, hip rotation range), neuromuscular status, and any associated pain or functional limitations.

When gait plates are selected, custom devices are often designed from a cast or scan to incorporate both standard orthotic features (such as rearfoot posting or arch support) and the specific gait plate extension tailored to the child’s pattern of in‑toeing. The child and family are counselled on a gradual wear‑in schedule to allow adaptation and to monitor for pressure areas or discomfort, with follow‑up reviews to assess changes in gait and function over time.

Adjunctive therapies frequently include stretching and strengthening programs targeted at identified deficits, such as hip external rotator strengthening or calf and hamstring stretching, as well as postural and balance work. Many clinicians also incorporate gait retraining strategies, using verbal cues, visual feedback, and sometimes video to help the child internalise a straighter foot progression pattern. In this context, the gait plate can be seen as a facilitative device that reinforces the desired movement pattern with each step, complementing active rehabilitation efforts.

Ultimately, gait plates represent a useful tool in the paediatric podiatrist’s repertoire for managing symptomatic or functionally significant in‑toe gait, offering a non‑invasive means to improve gait appearance and reduce tripping while a child continues to grow and develop. Used judiciously and with clear expectations, they can play an important role in supporting both physical function and the child’s confidence during everyday activities.

Freiberg disease, also called Freiberg infraction, is an osteonecrosis of a lesser metatarsal head that most commonly affects the second metatarsal in adolescent or young adult females, causing forefoot pain and stiffness at the metatarsophalangeal (MTP) joint. It represents a spectrum from subtle subchondral collapse to advanced arthrosis and deformity, with early stages often responding well to conservative off‑loading and later stages sometimes requiring joint‑preserving or joint‑sacrificing surgery.pmc.ncbi.nlm.nih+3​

Definition and epidemiology

Freiberg disease is defined as a localized osteonecrosis/osteochondrosis of a lesser metatarsal head, characterized by collapse, fragmentation, and subsequent deformity of the articular surface. Pathologically it is a form of osteonecrosis rather than classic inflammatory arthritis, and it most frequently involves the second metatarsal head, with the third less often affected and the fourth or fifth rarely involved.

Epidemiologically, Freiberg disease predominates in females and typically presents in adolescence or early adulthood, although later presentations occur in both sexes. The female preponderance is often attributed to both biomechanical factors (a relatively long second metatarsal and forefoot loading patterns) and footwear factors such as high‑heeled or narrow toe box shoes that increase pressure under the lesser metatarsal heads.

Etiology and pathophysiology

The precise cause is multifactorial, with several overlapping theories. A traumatic theory proposes that repetitive microtrauma to the metatarsal head—seen in running, dancing, jumping sports, or high‑heel use—produces cumulative injury to the subchondral bone plate and vascular supply, leading to collapse. A vascular theory emphasises disruption or insufficiency of intraosseous blood flow to the metatarsal head, predisposing to osteonecrosis in structurally vulnerable metatarsals such as a long second ray.wikipedia+4​

Biomechanical and systemic contributors also appear relevant. Altered forefoot loading from cavus or planus foot types, hallux valgus with transfer loading, or iatrogenic overload after first ray surgery can increase stress on the second metatarsal head. Systemic factors such as collagen disorders, endocrine abnormalities, or vascular compromise are occasionally reported, although strong causal links remain less clear.

Clinical presentation and staging

Clinically, patients usually report insidious forefoot pain localised to the affected lesser MTP joint, worsened by weight‑bearing, particularly push‑off and activities that load the forefoot. Swelling, joint tenderness dorsally over the metatarsal head, and difficulty with high‑heeled or fashion shoes are typical, and patients may develop a limp or lateralised gait to avoid painful loading. Stiffness and reduced range of motion at the affected MTP joint, plantar callus under the involved metatarsal, and sometimes mechanical catching or locking can also occur as the articular surface fragments.

Radiographically, Freiberg disease classically demonstrates flattening and sclerosis of the metatarsal head with varying degrees of fragmentation and joint space irregularity. MRI is useful in early disease, showing bone marrow oedema and subchondral changes in the metatarsal head before plain radiographs become diagnostic, which helps prompt off‑loading at a reversible stage. The Smillie classification describes five stages, from subchondral fissuring (stage 1) through dorsal collapse, fragmentation, and deformity (stages 2–4) to end‑stage arthrosis with a flattened, deformed head and secondary degenerative change (stage 5).

Management strategies

Treatment aims to relieve pain, preserve or restore joint congruity, and maintain functional gait, with strategies tailored to stage, symptoms, and patient demands. In early Smillie stages (1–3), nonoperative management is the mainstay, focusing on reducing load through the diseased metatarsal head so that bone remodelling and revascularisation can occur. Common measures include activity modification, temporary immobilisation or casting in more acute cases, metatarsal pads or bars, stiff‑soled or rocker‑soled footwear, and custom orthoses designed to off‑load the affected ray while redistributing pressure to adjacent metatarsals and the midfoot.

When conservative measures fail or in more advanced stages (typically Smillie 3–5), surgery is considered, balancing joint preservation against pain relief and long‑term function. Joint‑preserving options include dorsal closing‑wedge osteotomy of the metatarsal head to rotate a relatively preserved plantar cartilage segment dorsally into the weight‑bearing zone, osteochondral autologous transplantation (OAT) of cylindrical plugs from the knee to reconstruct the joint surface, and microfracture or drilling procedures for smaller focal lesions. For end‑stage deformity, interposition arthroplasty using soft‑tissue spacers, implant arthroplasty, or resection/shortening arthroplasty of the metatarsal head can relieve pain and restore shoe wear, though at the expense of some power at push‑off and with careful consideration of transfer metatarsalgia risk.

Prognosis and clinical implications

Prognosis is generally favourable when Freiberg disease is recognised early and appropriately off‑loaded, with many patients in early stages achieving pain relief and radiographic remodelling without surgery. Later‑stage disease can still be managed effectively, but may leave residual stiffness or mild deformity even with well‑executed reconstructive procedures, and return to high‑impact sport may be limited depending on the extent of osteonecrosis and the technique used.

From a clinical standpoint, Freiberg disease is an important differential diagnosis for chronic lesser MTP joint pain in adolescents and young adults, particularly active females or those with a long second metatarsal and a history of high‑heel or forefoot‑loading activities. Early detection using targeted imaging, meticulous assessment of forefoot biomechanics, and timely implementation of footwear and orthotic strategies can reduce progression to advanced collapse, while contemporary surgical algorithms—including dorsal osteotomy, OAT, and interposition arthroplasty—offer structured options for those who remain symptomatic despite conservative care.

Congenital vertical talus (CVT) is a rare, complex congenital foot deformity in which the normal alignment and structure of the foot are profoundly disrupted, resulting in a rigid “rocker-bottom” flatfoot. This condition poses both diagnostic and therapeutic challenges, drawing the attention of orthopedic surgeons, pediatricians, and geneticists.

Defining Congenital Vertical Talus

Congenital vertical talus is defined by a fixed dorsal dislocation of the navicular bone on the talus, causing the talus to assume a vertical orientation within the foot. The calcaneus is typically in equinus, and the forefoot is abducted and dorsiflexed. This combination of deformities creates a visible convexity of the sole (hence “rocker-bottom foot”) and obliterates the normal arch. CVT is distinguished from the more common flexible flatfoot and from positional foot deformities by its rigidity and the vertical appearance of the talus on radiographs.

Epidemiology and Incidence

CVT occurs in approximately one out of every 100,000 to 150,000 live births, making it a rare condition. About half of the cases are bilateral. The incidence does not show clear sex predilection, and while it can appear in isolation, it is frequently associated with neuromuscular disorders or genetic syndromes, such as arthrogryposis, spina bifida, or trisomy syndromes

Etiology and Pathogenesis

The precise cause of congenital vertical talus remains poorly understood. About half of cases are associated with underlying neuromuscular or genetic syndromes, while the remainder were termed idiopathic, although increasing evidence shows a genetic basis even in these. Mutations in the HOXD10 gene and other genetic loci have been implicated, demonstrating an autosomal dominant inheritance with variable expressivity in some families.

Proposed pathophysiological mechanisms include:

• Abnormal muscular or neuromuscular influences during fetal development, such as muscle imbalance or abnormal intrauterine positioning.
• Abnormal development or displacement of the talonavicular joint in utero, sometimes related to connective tissue disorders or chromosomal aberrations.
• Congenital contractures of foot musculature (e.g., tightness of the tibialis anterior, peroneals, or Achilles tendon).

Clinical Features

The most distinctive physical finding in congenital vertical talus is a rigid, convex plantar surface of the foot with the hindfoot in fixed equinus and valgus, the midfoot and forefoot dorsiflexed and abducted relative to the hindfoot. Other features include:

• Prominent talar head on the plantar aspect, sometimes forming a callus.
• Crease on the dorsum of the foot and convexity of the sole.
• Stiffness, inability to plantigrade the foot even with manipulation.
• In older children, difficulty fitting into shoes and an abnormal “peg-leg” gait.
• Associated anomalies such as limb contractures or spinal dysraphism (when syndromic).

Diagnosis

Early and accurate diagnosis is essential to prevent disability. Diagnosis relies on clinical examination and radiography:

• Clinical: The foot is in equinus and valgus, with the forefoot abducted and dorsiflexed, sole convex, and normal plantar arch reversed.

Differential Diagnosis

Congenital vertical talus must be differentiated from:

• Flexible flatfoot (physiologic, resolves with growth).
• Oblique talus (features overlap but with residual movement and partial reducibility).
• Clubfoot (talipes equinovarus: foot is inverted and adducted rather than abducted and everted).
• Metatarsus adductus and cavus foot (distinct orientation and mobility).

Pathoanatomy

Surgically and in postmortem studies, the talonavicular joint is found irreducibly dislocated dorsally, with the talus in a vertical sagittal plane. The calcaneus is in equinus, and the navicular becomes hypoplastic from abnormal articulation. There are varying degrees of contractures in the anterior tibial, peroneal, and extensor tendons. The rigidity of the deformity relates to contractures and abnormal development of both bone and soft tissues.

Associated Conditions

Fifty percent of cases are associated with other disorders:

• Arthrogryposis multiplex congenita.
• Spina bifida and other neural tube defects.
• Cerebral palsy.
• Trisomy 13, 15, 18.
• Other genetic syndromes and familial cases, often linked to specific gene mutations.

Treatment Approaches

The primary goal of treatment is a flexible, plantigrade, and pain-free foot that enables normal gait. Early treatment is critical as untreated congenital vertical talus leads to pain, calluses, impaired function, and disability.

Nonsurgical Management

• Serial stretching and casting: Early casting is used to gradually stretch the contracted tissues and restore alignment. The “reverse Ponseti” method (similar to clubfoot treatment) is commonly employed, aiming to stretch the foot into plantarflexion and adduction.
• Physical therapy: Adjunctive stretching may help maintain correction.

Surgical Management

Surgery is considered if casting fails or if the deformity is detected late.

• Minimally invasive approaches: Percutaneous Achilles tenotomy, open reduction of the talonavicular joint, with pin fixation and soft tissue releases, now offer high rates of correction with less morbidity.
• Extensive surgical soft tissue release: Previously common but now largely supplanted by minimal procedures due to complications like stiffness, wound problems, and under/overcorrection.

Postoperative care includes immobilization in a cast and subsequent use of braces or orthotic footwear to maintain correction.

Prognosis

With early and appropriate intervention, the long-term prognosis is generally favorable; most children achieve a pain-free, plantigrade, and functional foot. Delayed diagnosis or suboptimal treatment may result in persistent deformity, pain, mobility limitations, and permanent disability.

Advances and Future Directions

Contemporary management continues to evolve, prioritizing less invasive techniques and earlier interventions. Genetic research is expanding, with identification of at-risk families and syndromic patterns facilitating early recognition.

Congenital vertical talus is a rare, often challenging foot deformity present at birth, necessitating early and accurate diagnosis for best outcomes. Advances in both genetic understanding and treatment paradigms have enabled more effective, less morbid interventions. Recognizing associations with other disorders is vital, as congenital vertical talus may herald broader systemic pathology. Future research will likely yield further insights into both pathogenesis and optimal, patient-friendly therapies.

Clubfoot, medically known as congenital talipes equinovarus (CTEV), is a common congenital deformity of the foot present at birth. It is characterized by the foot being twisted inward and downward, causing an abnormal positioning where the sole faces somewhat medially and the front of the foot points downward. This condition affects approximately 1 in every 1,000 newborns globally, with about half of the cases involving both feet. It is one of the most common musculoskeletal birth defects worldwide and has a higher prevalence in boys than girls, with a male-to-female ratio of roughly 2:1.

Anatomy and Pathophysiology

In a normally developed foot, the tendons—the connective tissues that attach muscles to bones—maintain balance and positioning by pulling at specific angles. In clubfoot, the tendons on the inside and back of the foot are shorter and tighter than usual. This abnormal shortening leads to the foot being drawn inward (adducted) and downward (equinus), with the heel turned inward (varus). The deformity typically has four main components:

• Midfoot cavus: an exaggerated arch of the foot,
• Forefoot adductus: inward deviation of the front of the foot,
• Heel or hindfoot varus: inward tilting of the heel,
• Hindfoot equinus: downward pointed foot caused by tight Achilles tendon.​

Because of these deformities, the foot appears rotated and fixed in an abnormal position that cannot be corrected by simple manipulation. Children with untreated clubfoot often walk on the outer edge or top of the foot, which causes pain, skin sores (calluses), and difficulties with footwear and mobility later in life.

Types and Classification

Clubfoot is generally classified into two categories:

1. Idiopathic Clubfoot (Isolated Clubfoot): This is the most common type, accounting for about 80% of cases. It occurs without any other associated abnormalities or neuromuscular disorders. Idiopathic clubfoot is considered a multifactorial condition resulting from a complex interplay of genetic, environmental, vascular, and positional factors during fetal development.
2. Non-Isolated (Secondary or Syndromic) Clubfoot: This form, comprising about 20% of cases, occurs alongside other medical conditions such as spina bifida, arthrogryposis (joint contractures), or muscular dystrophy. This type is often more rigid and resistant to treatment and may require longer and more intensive management, including multiple surgeries.

Causes and Risk Factors

The exact cause of clubfoot remains uncertain despite decades of research. Both genetic and environmental factors are believed to contribute:

• Genetic predisposition: Studies show familial tendencies, where having a first-degree relative with clubfoot increases the risk by 25%, and identical twins show a 33% concordance rate. However, no single gene mutation has been conclusively identified.
• Environmental factors: These include maternal smoking, maternal diabetes, alcohol consumption during pregnancy, and unusual intrauterine positioning or physical constraints (e.g., a small uterus or oligohydramnios). Seasonal variations affecting maternal temperature during fetal development have also been suggested.
• Mechanical factors: In some cases classified as extrinsic clubfoot, physical compression during pregnancy may lead to milder, more supple deformities.

Overall, the leading theory is that clubfoot results from disruption in the development or functioning of muscles, tendons, and bones in the lower leg and foot during early pregnancy, leading to joint contractures and deformities.

Diagnosis

Clubfoot is most commonly diagnosed at birth by visual and physical examination of the infant’s feet, revealing the characteristic inward twist and rigidity. Affected feet often have a deep crease on the sole and a smaller calf muscle on the affected side due to muscle underdevelopment. The deformity may be unilateral or bilateral.

Prenatal diagnosis via ultrasound is possible, typically around the 20-week anatomy scan, allowing early planning for treatment at birth. Early identification is important because timely management significantly improves outcomes.

Symptoms and Presentation

The classic signs of clubfoot include:

• Feet turned inward and downward,
• Stiffness and rigidity of the foot with limited range of motion,
• Smaller foot size on the affected side,
• Underdeveloped calf muscles,
• Heel turned inward and possible deep creases on the inner sole.

Affected children, without treatment, develop walking difficulties such as walking on the side or top of the foot, leading to pain, skin breakdown, and impaired mobility

Treatment

Clubfoot requires intervention to correct the deformity, as it does not improve spontaneously. The goal of treatment is to enable normal walking without pain or difficulty wearing regular shoes.

Non-surgical Treatment

The Ponseti method is the gold standard for clubfoot correction, especially effective when started shortly after birth:

• Serial casting: Gentle manipulation and weekly casting to gradually stretch the foot and reposition bones and tendons.
• Achilles tendon lengthening: A minor outpatient procedure (tenotomy) frequently performed near the end of the casting phase to lengthen the tight heel cord.
• Bracing: After correction, a foot abduction brace is worn to maintain the correction and prevent relapse, usually for several years or until the child walks independently.

The Ponseti method has a very high success rate worldwide, particularly when started early.

Surgical Treatment

Surgery may be necessary in more severe or resistant cases, or when treatment begins late. Surgical options involve releasing tight tendons and ligaments, repositioning bones, and lengthening muscles. While surgery can provide correction, it carries risks such as stiffness and weakness if overdone. Therefore, surgery is usually reserved for cases where conservative treatment fails.

Prognosis and Long-Term Outcome

When clubfoot is treated early and effectively, children can expect to lead active, normal lives with well-aligned, functional feet. Untreated clubfoot results in lifelong disabilities, including pain, difficulty walking, and inability to wear normal shoes. Treatment outcome depends on severity, timing, and adherence to bracing protocols post-correction.

Even in cases with associated neuromuscular disorders, ongoing orthopedic care can improve mobility and quality of life.

Global Perspective

Clubfoot disproportionately affects low- and middle-income countries, where access to early diagnosis and treatment may be limited. Worldwide efforts by orthopedic organizations and charities focus on training healthcare providers in the Ponseti method and increasing treatment accessibility to reduce disability from untreated clubfoot.

Calcaneal apophysitis, also known as Sever’s disease, is a prevalent cause of heel pain in children and adolescents, particularly those engaged in athletic activity. It represents a temporary yet painful inflammation of the growth plate in the calcaneus (heel bone) before skeletal maturity. The condition typically occurs during periods of rapid growth and resolves after the apophysis fuses with the main body of the calcaneus once ossification completes.

Anatomy and Pathophysiology

The calcaneus is the largest tarsal bone in the foot and develops from two ossification centers: the primary center appears at birth, and the secondary, called the calcaneal apophysis, emerges between ages 5 and 8, fusing around puberty (approximately ages 13–15). The apophysis serves as a site of attachment for the Achilles tendon, which connects the calf muscles to the heel. Continuous traction by the Achilles tendon during growth spurts, especially when the calf muscles do not elongate proportionally, exerts stress on the physes, leading to microtrauma, inflammation, and ultimately pain.

This traction-induced inflammation is the hallmark of calcaneal apophysitis. The condition is distinct from adult heel pain, which is more commonly due to plantar fasciitis; in children, the pain stems from the growing, still-cartilaginous apophysis, making it susceptible to repetitive stresses and excessive strain.

Epidemiology

Calcaneal apophysitis is among the most frequent causes of heel pain in the pediatric and adolescent age groups, predominantly affecting individuals between 8 and 15 years old. It tends to occur more often in physically active children participating in running or jumping sports, such as soccer, basketball, track, and gymnastics. Both genders are affected, though some studies report a slightly higher prevalence among males, likely due to greater participation in high-impact activities.

Bilateral involvement occurs in up to 60% of patients, highlighting the role of symmetrical, repeated loading on both feet. The condition’s onset often coincides with seasonal sports or periods of increased training intensity, further supporting its association with mechanical overuse.

Etiology and Risk Factors

The primary cause of calcaneal apophysitis is repetitive microtrauma to the heel’s growth plate due to excessive traction forces from the Achilles tendon. Contributing factors include:

• Rapid growth spurts leading to tight calf muscles and reduced Achilles tendon flexibility.
• Poorly cushioned or inappropriate footwear, especially flat or “negative-heeled” shoes such as soccer cleats.
• High levels of physical activity without adequate rest or recovery.
• Abnormal body mechanics such as overpronation or unequal leg length.

Other predisposing factors may include obesity and hard playing surfaces, both of which amplify ground reaction forces transmitted through the heel.

Clinical Presentation

Children with calcaneal apophysitis typically report heel pain that worsens during and immediately after physical activity and improves with rest. The pain is localized to the posterior aspect of the heel, near the insertion of the Achilles tendon. It may cause limping or tiptoe walking as compensatory behaviors to reduce discomfort.

Unlike infections or fractures, the heel is usually not visibly swollen or red. Direct palpation or medial-lateral compression of the posterior heel elicits tenderness, which is a diagnostic hallmark. The pain may radiate to the sides or base of the heel but should not extend into the arch or toes.

Diagnosis

Diagnosis is primarily clinical and relies on a thorough history and physical examination. Radiographs are rarely necessary unless to rule out other conditions such as fractures, osteomyelitis, or bone cysts. When imaging is performed, X-rays can show irregularity or fragmentation of the apophysis, findings that can also appear in normal development. Magnetic resonance imaging (MRI) or ultrasound may demonstrate bone marrow edema or apophyseal widening but are reserved for atypical or severe cases.

Differential Diagnosis

Conditions that should be considered include:

• Achilles tendinopathy or bursitis
• Calcaneal stress fracture
• Retrocalcaneal bursitis
• Tarsal coalition
• Plantar fasciitis (rare in children)

A careful clinical assessment and consideration of age, activity level, and symptom characteristics help differentiate these conditions.

Management

Treatment of calcaneal apophysitis is conservative and focuses on symptom relief, reduction of inflammation, and activity modification. Key components include:

• Activity modification: Limiting running and jumping activities until symptoms subside.
• Stretching and strengthening exercises: Especially for the Achilles tendon and gastrocnemius-soleus muscle group, helping to reduce traction on the apophysis.
• Orthotic support: Using heel cups or heel lifts to reduce pressure and absorb shock.
• Footwear: Ensuring properly cushioned, supportive shoes with an elevated heel. Avoiding flat, rigid shoes or cleats.
• Pain management: Application of ice and use of nonsteroidal anti-inflammatory drugs (NSAIDs) as needed for pain control.
• Immobilization: In severe cases, short-term casting or walking boots may be required to alleviate stress on the heel.

Most patients experience complete resolution within weeks to months once the stress on the apophysis is minimized. Importantly, the condition is self-limiting and does not cause lasting anatomical damage once skeletal maturity is reached.​

Prognosis and Prevention

The prognosis for calcaneal apophysitis is excellent. Symptoms typically resolve with conservative management and cessation of growth-related stress on the heel. Recurrence can occur if children return to high-impact activities prematurely or neglect stretching routines. Preventive strategies include regular calf and Achilles tendon stretching, wearing supportive shoes, and gradually increasing sports intensity during seasons of rapid growth.

Emerging Perspectives

Recent clinical studies emphasize the importance of early recognition and multimodal management of the condition. Ultrasound imaging provides a non-invasive means to assess apophyseal changes, and newer orthotic designs aim to optimize heel support and load distribution. Sports medicine specialists increasingly advocate for educational interventions for parents, coaches, and young athletes to promote awareness about footwear selection, stretching, and training schedules.

Calcaneal apophysitis, or Sever’s disease, represents an overuse injury of the heel’s growth plate that arises during childhood and early adolescence. It is a benign and self-limited condition driven by biomechanical stress and growth-related factors. Recognizing the signs early and instituting appropriate conservative management can effectively relieve pain and prevent recurrence. As children mature, the apophysis fuses with the main body of the calcaneus, eliminating future susceptibility. The key lies in balancing physical activity, employing proper footwear, and addressing biomechanical risks — ensuring young athletes maintain both long-term foot health and ongoing participation in sports.

Toe walking, characterized by walking on the balls of the feet with little or no contact between the heels and the ground, is a notable gait pattern observed in children with autism spectrum disorder (ASD). While toe walking can be seen in young children during stages of normal gait development, its persistence beyond early childhood is often associated with underlying neurological or developmental conditions, most prominently autism.

Prevalence and Significance

Persistent toe walking is considerably more frequent among children with autism than in neurotypical peers. Large-scale research has documented that approximately 9% of autistic children demonstrate continued toe walking, compared to less than 0.5% of typically developing children. Other studies suggest a prevalence ranging from 6–20%, with some reports citing even higher rates depending on the age group and clinical setting. This makes autistic children roughly eight times more likely to toe walk than those without ASD. Nevertheless, it is crucial to clarify that not all children who toe walk are autistic, and toe walking itself is not exclusive to autism.

Potential Causes of Toe Walking in Autism

The underlying reasons for toe walking in autism are multifactorial and remain incompletely understood. Sensory processing differences, especially involving the vestibular system, are strongly implicated. The vestibular system provides critical feedback for balance, spatial orientation, and movement. A dysfunctional vestibular system—a common finding in ASD—may disrupt balance and motor planning, prompting toe walking as an adaptive or compensatory response.

• Many autistic individuals have heightened or lowered sensitivity to sensory input, leading them to seek out or avoid certain sensations.
• Toe walking may serve to decrease sensory input from the ground (in sensory-avoidant individuals) or stimulate proprioceptive and vestibular feedback (in sensory-seeking individuals).
• Some children with ASD also exhibit increased muscle tone or subtle dystonia, potentially contributing to the sustained toe-walking posture.
• Delays or differences in motor development and motor planning are also considered relevant factors contributing to this gait pattern in autism.

Clinical Considerations and Developmental Impact

Toe walking in the context of autism can persist through adolescence and even adulthood for some individuals, rather than being a temporary developmental phase. If left unaddressed, chronic toe walking may lead to secondary issues such as shortened Achilles tendons, tight calf muscles, altered foot and ankle biomechanics, and discomfort or pain during activity.

While toe walking alone is not diagnostic of autism, its presence—especially when paired with developmental delays, language difficulties, or social communication deficits—should prompt further evaluation. Early identification allows for timely intervention, potentially preventing longer-term musculoskeletal complications.

Treatment Approaches

Management of toe walking in autistic individuals is multidisciplinary, typically involving occupational therapy, physical therapy, and sensory integration therapy. The specific approach is tailored to the underlying contributing factors and may include:

• Occupational therapy: Focuses on enhancing body awareness, coordination, and sensory processing, which can help normalize gait patterns.
• Physical therapy: Includes gait training, balance activities, muscle stretching, and strengthening, aiming to restore ankle flexibility and encourage heel contact during walking.
• Sensory Integration Therapy: Addresses abnormal sensory processing, especially targeting the vestibular and proprioceptive systems with specific exercises and activities.
• Innovative approaches: The “Cast and Go” protocol (which combines botulinum toxin injections, orthopedic casting, and rehabilitation) has shown promise in correcting persistent toe walking by allowing gradual elongation of the Achilles tendon and retraining walking patterns. Botulinum toxin injections alone, aimed at reducing calf muscle tightness, may be added if spasticity or muscular contraction is a significant factor.
• Assistive devices: In some cases, orthoses or splints may be recommended to help maintain proper foot posture and aid in retraining a normal gait.

Prognosis

Prognosis varies widely. Some autistic individuals may outgrow toe walking with therapy and supportive measures, while others may continue to walk on their toes into adulthood, especially if underlying sensory processing challenges remain significant. Regular monitoring and individualized intervention maximize the potential for a positive outcome.

Toe walking is a distinctive gait pattern commonly observed in children with autism, with rates far exceeding those in the general pediatric population. Its causes are complex, rooted in differences in sensory processing, motor planning, and muscle tone regulation. While toe walking is not unique to autism, its persistence warrants comprehensive assessment and often multidisciplinary intervention. Early recognition and tailored therapy can help alleviate physical complications and promote better motor development for autistic individuals who toe walk.