Congenital Arthromyodysplasia

“Congenital arthromyodysplasia” is an old medical label that appeared in mid-20th-century rheumatology papers. It described babies born with stiff, bent joints and reduced muscle bulk that made the joints hard to move. Today, most experts place these babies under the broader, modern umbrella arthrogryposis multiplex congenita (AMC)—a descriptive term for multiple joint contractures present at birth due to very low fetal movement from many possible causes. In simple words: the joints are “stuck” or tight at birth because the muscles, nerves, or connective tissues did not develop or work normally in the womb, so the baby couldn’t move enough before birth. Genetic Rare Disease Center+3PMC+3Arthritis & Rheumatology+3

Congenital arthromyodysplasia describes babies born with stiff joints and weak or small muscles because the joints and muscles did not form normally in the womb. The stiffness is called contracture—a joint that stays stuck in a bent or straight position and does not move well. Many body areas can be affected, like shoulders, elbows, hands, hips, knees, and feet. The condition is usually non-progressive (it does not keep getting worse), but children need early therapy to improve movement, function, and daily life. Doctors often group these cases under arthrogryposis multiplex congenita (AMC), which means contractures in two or more body regions at birth. PMC+3Genetic Rare Disease Center+3Johns Hopkins Medicine+3

Other names

Because “congenital arthromyodysplasia” is historical, you will find more information under these names:

• Arthrogryposis multiplex congenita (AMC)

• Arthrogryposis (general term)

• Amyoplasia (the most common classic pattern of AMC with severe muscle underdevelopment)

• Distal arthrogryposis (hands/feet more involved)

• Syndromic arthrogryposis (when joint contractures are part of a broader genetic syndrome)

• Fetal akinesia sequence (severe spectrum related to very little fetal movement)
  All of these share the core feature of multiple congenital joint contractures. PMC+2PMC+2

Types

Doctors no longer use a single, narrow box for this condition. Instead, they classify AMC by pattern and cause:

1. Amyoplasia type – severe, symmetric contractures in arms and legs, with weak or absent muscles. Children often have normal thinking and learning but need long-term therapy and sometimes surgery to improve movement. PMC

2. Distal arthrogryposis – mainly hands and feet are tight. Many forms are genetic and run in families. PMC

3. Syndromic arthrogryposis – joint contractures happen with other problems (brain, spine, heart, lungs, skin, or skeleton) as part of a named syndrome. PMC

4. By body system involved – neurological (brain/spinal cord), neuromuscular (nerves/muscles), connective-tissue (tendons/capsules), or extrinsic (uterine space/placenta limiting movement). This “cause-based” view helps plan tests and treatment. Merck Manuals+1

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Causes

Anything that prevents normal fetal movement can lead to joint contractures. Causes are often grouped as intrinsic (inside the baby) and extrinsic (outside pressures in the womb).

Intrinsic (inside the baby):

1. Brain or spinal cord conditions. If the motor system cannot send strong signals to move, joints stay still and become tight. PMC

2. Peripheral nerve problems. Damaged or undeveloped nerves cannot activate muscles to move joints. PMC

3. Primary muscle disorders (myopathies, muscular dystrophies). Weak or poorly formed muscles can’t move the joints, so connective tissue tightens around them. PMC

4. Motor neuron disorders (e.g., some spinal muscular atrophy forms). Fewer working motor neurons mean less movement in the womb. PMC

5. Connective-tissue disorders. Abnormal tendons, ligaments, or joint capsules restrict motion and form contractures. PMC

6. Gene variants in contractile proteins (e.g., MYH3, MYH8, TPM2, TNNT3). These can cause distal arthrogryposis patterns by changing how muscles contract. Wikipedia

7. Chromosomal conditions (e.g., trisomy 18). Whole-chromosome changes can reduce movement and cause contractures as part of a syndrome. Cleveland Clinic

8. Mitochondrial disorders. Low cellular energy limits sustained fetal movement. Wikipedia

9. Maternal antibodies affecting fetal neuromuscular transmission (rare). If the baby’s receptors are blocked, muscles do not work well in utero. Wikipedia

10. Vascular disruption inside the fetus. Poor blood flow to muscles/joints leads to scarring and stiffness. Wikipedia

Extrinsic (outside the baby):

11. Oligohydramnios (low amniotic fluid). Less fluid = less room to move; joints stay in one position and stiffen. Wikipedia

12. Uterine constraint (very little space). Multiple pregnancy, uterine malformations, or large fibroids can keep limbs bent and still. Wikipedia

13. Placental problems. Poor placental function reduces oxygen/nutrients, lowering movement. Wikipedia

14. Amniotic band sequence. Bands can trap or tether limbs, restricting motion and causing deformities. PMC

15. Maternal fever or hyperthermia during key stages can disturb fetal tissues and movement. Wikipedia

16. Maternal viral infections (for example, Zika). Some infections impair the fetal brain or nerves, lowering movement. Wikipedia

17. Maternal illnesses that limit fetal movement (e.g., severe myasthenia gravis affecting the fetus). Wikipedia

18. Drugs/toxins that depress fetal movement (varies by exposure and timing). PMC

19. Long-term fetal immobilization (any reason). Joints that don’t move become tight and fibrotic. Wikipedia

20. Combination of factors. Many babies have more than one contributor; a mixed cause is common and requires broad evaluation. PMC

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Symptoms and everyday signs

1. Stiff, bent joints at birth in more than one body region (the hallmark). Parents see joints that won’t fully straighten or bend. Merck Manuals+1

2. Limited range of motion. Attempts to move the limb meet resistance. Gentle stretching helps, but range is still short at first. Merck Manuals

3. Clubfoot or vertical talus (foot fixed in a twisted position). Wikipedia

4. Hip issues (flexion/abduction contractures or dislocation). Wikipedia

5. Elbow extension and forearm pronation that make feeding and reaching hard. Wikipedia

6. Wrist bent toward the palm and toward the ulna; fingers may be flexed; thumb in palm. Wikipedia

7. Shoulders turned inward and hard to lift. Wikipedia

8. Knee flexion or extension contractures that limit standing or walking early on. Wikipedia

9. Spine curves (scoliosis) in some children. Wikipedia

10. Noticeably small or weak muscles (amyoplasia) around tight joints. PMC

11. Delayed motor milestones (rolling, sitting, walking), mostly due to stiffness—not necessarily learning issues. Wikipedia

12. Normal intelligence in many children with classic amyoplasia; learning differences depend on the underlying cause. Wikipedia

13. Feeding or speech difficulties if jaw/face or trunk muscles are affected; therapy helps skill building. Merck Manuals

14. Breathing or chest wall problems in severe cases with thoracic involvement. PMC

15. Activity-related pain or fatigue around tight joints; improves with therapy, splints, and good positioning. Merck Manuals

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Diagnostic tests

A) Physical examination (at the bedside)

1. Global joint check. The clinician inspects posture, limb position, and fixed deformities, then compares sides to map which joints are involved. This baseline guides therapy plans. Merck Manuals

2. Range-of-motion (ROM) assessment. Gentle movement of each joint shows how far it can go; repeated over time to track progress with therapy. Merck Manuals

3. Neurological exam. Reflexes, tone, and sensation are checked to see if the problem is mainly brain/spinal cord, nerves, or muscles. PMC

4. Muscle bulk and strength check. Noting thin or fibrous muscles suggests amyoplasia or a primary myopathy and directs the next tests. PMC

5. Spine, chest, and hip stability. The examiner screens for scoliosis and hip dislocation because they change therapy and casting plans. Wikipedia

B) “Manual” functional testing (simple tools at the visit)

6. Goniometry. A handheld angle gauge measures exact degrees of joint movement to set goals for stretching and splinting. Merck Manuals

7. Manual muscle testing. The clinician grades strength against gentle resistance to see which muscles can be trained and which need support. Merck Manuals

8. Joint stability and provocation maneuvers. Gentle tests look for hip instability, foot rigidity, or tendon tightness that may need casting or surgery. Merck Manuals

9. Functional skills observation. Watching feeding, rolling, sitting, or grasping helps tailor occupational/physical therapy goals. Merck Manuals

C) Laboratory and pathological tests

10. Creatine kinase (CK). High CK hints at a muscle breakdown/myopathy; normal CK leans toward neurogenic or connective-tissue causes. Merck Manuals

11. Genetic testing panels/exome. Looks for known gene changes linked to distal arthrogryposis and syndromic forms; results shape counseling and prognosis. PMC

12. Chromosomal microarray (± karyotype). Detects gains/losses linked with syndromes such as trisomy 18. Genetic Rare Disease Center

13. Maternal antibody testing (e.g., anti-acetylcholine receptor) if fetal neuromuscular transmission is suspected. Wikipedia

14. Infection serology (e.g., Zika/TORCH when relevant). Targets extrinsic infectious causes that reduce fetal movement. Wikipedia

15. Muscle biopsy (select cases). Microscopy can distinguish neurogenic from myopathic patterns when genetics is unrevealing. PMC

D) Electrodiagnostic tests

16. Electromyography (EMG). Measures electrical activity in muscles to separate nerve vs muscle problems and to map which muscles are recruitable with therapy. PMC

17. Nerve conduction studies (NCS). Check the speed/strength of signals in peripheral nerves; abnormal results point to neuropathic causes. PMC

E) Imaging tests

18. Prenatal ultrasound (and sometimes 4D ultrasound). Low fetal movement and fixed limb positions can be seen before birth; this allows early counseling and planning. Wikipedia

19. X-rays of limbs and hips. Show bone alignment, dislocations, and the rigidity of feet; essential for casting or surgical planning. Merck Manuals

20. MRI (fetal or postnatal) of brain/spine and involved limbs. Detects central nervous system causes, spinal abnormalities, or muscle replacement by fat/fibrosis. PMC

Non-pharmacological treatments

1. Early physiotherapy & stretching
   Gentle, frequent stretching keeps joints from getting stiffer and helps lengthen tight muscles and tendons. Purpose: improve range, prevent deformity, support milestones. Mechanism: repeated slow stretch remodels collagen and reduces contracture over time. BioMed Central

2. Positioning & splinting
   Night splints, serial casts, and daytime positioning keep joints in better alignment during growth. Purpose: maintain gains after therapy. Mechanism: low-load, long-duration stretch promotes tissue lengthening. Johns Hopkins Medicine

3. Serial casting (e.g., for clubfoot)
   Casts applied and changed every 1–2 weeks gradually correct foot position. Purpose: avoid or minimize surgery. Mechanism: incremental correction while tissues are most adaptable. Johns Hopkins Medicine

4. Occupational therapy (OT) for function
   OT teaches everyday skills—dressing, feeding, writing—using adapted methods and tools. Purpose: independence. Mechanism: task-specific practice builds motor learning and compensatory strategies. Johns Hopkins Medicine

5. Orthoses (AFOs, hand splints)
   Braces support weak muscles, align joints, and aid standing/walking. Purpose: mobility, safety. Mechanism: external stabilization improves lever arms and reduces energy cost. Johns Hopkins Medicine

6. Adaptive equipment & seating
   Custom chairs, standing frames, and mobility devices help posture and participation. Purpose: reduce fatigue and contracture risk. Mechanism: optimized biomechanics distribute pressure and maintain alignment. PM&R KnowledgeNow

7. Constraint-induced and bimanual training (upper limb)
   Focused use of the weaker arm or coordinated two-hand tasks. Purpose: better reach and grasp. Mechanism: neuroplasticity via high-repetition, task-oriented practice. BioMed Central

8. Hydrotherapy (water-based exercise)
   Warm water reduces joint load and pain, allowing fuller motion and practice. Purpose: flexibility and strength with comfort. Mechanism: buoyancy and warmth lower resistance and spasm. PM&R KnowledgeNow

9. Strengthening programs
   Gentle, progressive strengthening for underused muscles around stabilized joints. Purpose: function, endurance. Mechanism: muscle adaptation with safe loads improves torque across stiff joints. BioMed Central

10. Gait training & mobility skills
    Practice with walkers, crutches, or wheelchairs as needed. Purpose: safe, efficient community mobility. Mechanism: motor learning and orthotic alignment reduce compensations. PM&R KnowledgeNow

11. Serial night stretching protocols
    Home routines that pair heat, gentle stretch, and splints. Purpose: maintain therapy gains. Mechanism: prolonged low-intensity stretch remodels connective tissue. Johns Hopkins Medicine

12. Fine-motor retraining
    Activities for grasp, release, and handwriting aids. Purpose: school readiness. Mechanism: repetitive task practice with adaptive grips builds efficiency. Johns Hopkins Medicine

13. Pain-minimizing body mechanics education
    Training families in handling and daily care without over-stress. Purpose: prevent overuse pain. Mechanism: ergonomics and pacing reduce joint strain. PM&R KnowledgeNow

14. School-based therapy & IEP planning
    Coordinated services in school to support access and learning. Purpose: participation. Mechanism: environmental and curricular adaptations. PM&R KnowledgeNow

15. Home exercise program (HEP) coaching
    Simple daily plans parents can do safely. Purpose: consistency. Mechanism: frequent low-dose therapy preserves motion. BioMed Central

16. Serial tone-management strategies (non-drug)
    Heat, slow stretch, positioning to reduce reflex stiffness. Purpose: easier movement. Mechanism: modulates reflex arcs and viscoelastic resistance. PM&R KnowledgeNow

17. Myofascial release & soft-tissue mobilization
    Hands-on techniques to free tight tissues. Purpose: decrease resistance to stretch. Mechanism: alters fascia glide and pain perception. BioMed Central

18. Parent training & motivational coaching
    Teach safe techniques and set goals families can sustain. Purpose: carryover at home. Mechanism: self-efficacy improves adherence and outcomes. BioMed Central

19. Peer support & psychosocial care
    Support groups and counseling for child and family. Purpose: resilience and engagement. Mechanism: reduces stress barriers to therapy. Johns Hopkins Medicine

20. Transition-to-adulthood planning
    Plan for college/work mobility, self-care, and equipment upgrades. Purpose: lifelong independence. Mechanism: anticipatory guidance prevents setbacks. PM&R KnowledgeNow

Note: A 2025 consensus stresses early, family-centered, goal-oriented rehabilitation, while also acknowledging the evidence base is still limited and personalized care is important. BioMed Central

Drug treatments

(AMC/arthrodysplasia have no single “curative” drug; medicines target pain, spasm, sleep, bone health, etc. Always prescribe individually.) Johns Hopkins Medicine

1. Acetaminophen (paracetamol) — Analgesic/antipyretic
   Dose/time: weight-based, given in divided doses. Purpose: mild pain to help tolerate therapy. Mechanism: central COX modulation. Side effects: generally well tolerated; watch total daily dose for liver safety. Merck Manuals

2. NSAIDs (e.g., ibuprofen, naproxen) — Non-steroidal anti-inflammatory
   Purpose: reduce pain/inflammation from soft-tissue stress and casting. Mechanism: COX inhibition. Risks: stomach upset, rare kidney effects—use pediatric dosing and food. Merck Manuals

3. Topical NSAIDs (diclofenac gel)
   Purpose: focal joint/soft-tissue pain with fewer systemic effects. Mechanism: local COX inhibition. Risks: mild skin irritation. Merck Manuals

4. Gabapentin — Neuromodulator for neuropathic pain
   Purpose: burning or nerve-type pain after surgery or bracing. Mechanism: α2δ calcium channel modulation. Risks: sedation, dizziness—start low. Johns Hopkins Medicine

5. Baclofen (oral) — Antispasticity
   Purpose: reduce reflex stiffness where co-existing spasticity is present. Mechanism: GABA-B agonist decreases spinal reflexes. Risks: drowsiness, weakness; taper to avoid withdrawal. PM&R KnowledgeNow

6. Diazepam (night dosing in select cases)
   Purpose: short-term muscle relaxation for painful spasms or post-op. Mechanism: GABA-A facilitation. Risks: sedation, dependence—use sparingly. PM&R KnowledgeNow

7. Botulinum toxin injections (targeted)
   Purpose: reduce over-active opposing muscles to allow stretching/positioning. Mechanism: blocks acetylcholine release at neuromuscular junction. Risks: local weakness; needs expert dosing. PM&R KnowledgeNow

8. Bisphosphonates (in special cases of low bone density)
   Purpose: protect bones if mobility is very limited. Mechanism: inhibits osteoclasts. Risks: hypocalcemia, bone pain; specialist use only. Johns Hopkins Medicine

9. Vitamin D & Calcium (see supplements below for dosing)
   Purpose: bone health during growth and casting periods. Mechanism: supports mineralization. Risks: hypercalcemia if overdosed. Merck Manuals

10. Melatonin (sleep support)
    Purpose: improve sleep when nighttime splints/casts disrupt rest. Mechanism: circadian rhythm support. Risks: morning sleepiness in some. Merck Manuals

11. Acetazolamide (rare, for episodic edema with casting)
    Purpose: reduce fluid retention if it limits brace wear. Mechanism: carbonic anhydrase inhibition diuresis. Risks: electrolyte changes—specialist decision. Merck Manuals

12. Short-course opioids (post-op only)
    Purpose: acute surgical pain control. Mechanism: μ-opioid receptor agonism. Risks: constipation, sedation; short duration only with taper plan. Merck Manuals

13. Topical anesthetics (EMLA) for procedures
    Purpose: ease pain of injections, blood draws. Mechanism: local sodium channel block. Risks: skin irritation. Merck Manuals

14. Antiemetics (ondansetron) peri-operatively
    Purpose: reduce nausea after anesthesia/casting procedures. Mechanism: 5-HT3 antagonism. Risks: constipation, headache. Merck Manuals

15. Antibiotics (standard indications only)
    Purpose: treat infections (e.g., post-op wound). Mechanism: pathogen-specific. Risks: drug-specific. Merck Manuals

16. Proton-pump inhibitors/H2 blockers (if NSAID-related dyspepsia)
    Purpose: stomach protection. Mechanism: acid suppression. Risks: nutrient malabsorption long-term—use only when indicated. Merck Manuals

17. Laxatives/stool softeners (when on opioids or reduced mobility)
    Purpose: prevent constipation. Mechanism: osmotic or stimulant action. Risks: cramps (stimulants), electrolyte changes if overused. Merck Manuals

18. Antispasmodic alternatives (tizanidine)
    Purpose: reduce spasm where baclofen not tolerated. Mechanism: α2-agonist reduces motor neuron firing. Risks: sedation, liver enzymes. PM&R KnowledgeNow

19. Topical heat/analgesic balms (adjunct, non-drug OTCs)
    Purpose: comfort before stretching. Mechanism: counter-irritation/vasodilation. Risks: skin irritation. Johns Hopkins Medicine

20. Allergy-safe skin care with braces/casts
    Purpose: prevent dermatitis under orthoses. Mechanism: barrier creams, careful hygiene. Risks: product-specific. Johns Hopkins Medicine

These medications are supportive; the cornerstone remains rehabilitation, orthoses, and selected surgeries. Individual pediatric and rehab specialists tailor choices. BioMed Central

Dietary molecular supplements

(Always coordinate with your clinician; doses are pediatric/individualized.)

1. Vitamin D3 — helps bone strength during growth and limited mobility; dose per levels and age. Mechanism: improves calcium absorption and mineralization. Merck Manuals

2. Calcium — pairs with vitamin D for bone health; avoid excess. Mechanism: bone matrix mineral supply. Merck Manuals

3. Protein (whey or food-first) — supports muscle recovery from therapy. Mechanism: amino acids for muscle protein synthesis. Johns Hopkins Medicine

4. Omega-3 fatty acids — may reduce inflammation and aid joint comfort. Mechanism: eicosanoid modulation. Merck Manuals

5. Magnesium — supports muscle relaxation and nerve function. Mechanism: cofactor in neuromuscular transmission. Merck Manuals

6. Multivitamin (age-appropriate) — covers gaps in picky eating. Mechanism: micronutrient sufficiency. Merck Manuals

7. Iron (if deficient) — for energy and development; test first. Mechanism: hemoglobin and mitochondrial enzymes. Merck Manuals

8. Vitamin C — supports collagen formation in connective tissue. Mechanism: cofactor for prolyl/lysyl hydroxylase. Merck Manuals

9. Zinc — growth and wound healing after procedures. Mechanism: enzyme cofactor, DNA synthesis. Merck Manuals

10. Probiotics (select cases) — may help bowel habits with low mobility/opioids. Mechanism: microbiome modulation. Merck Manuals

Immunity-booster / regenerative / stem-cell drugs

There is no proven curative stem-cell or “regenerative drug” therapy for AMC/arthrodysplasia at this time. Care focuses on rehab, orthoses, and targeted surgery. Below are contexts you might hear about, with caution. BioMed Central+1

1. Standard childhood vaccinations (not a drug for AMC, but essential) — protect from infections that could set back therapy. Mechanism: immune memory. Dose: per national schedule. Merck Manuals

2. Vitamin D (see above) — supports bone/immune health; not disease-modifying. Mechanism: immune modulation/mineralization. Merck Manuals

3. Omega-3s — general anti-inflammatory support; adjunct only. Mechanism: lipid mediator balance. Merck Manuals

4. Experimental cell therapies — not standard of care; risks and unknown benefit in AMC. Mechanism: theoretical tissue repair. Use: research settings only. BioMed Central

5. Platelet-rich plasma (PRP) — no good pediatric evidence for AMC contractures. Use: not recommended outside research. BioMed Central

6. Anabolic agents (off-label) — not appropriate for children unless specialist-led for another indication. Mechanism: protein synthesis. Risk: growth/endocrine effects. Merck Manuals

Surgeries

1. Ponseti clubfoot correction (with or without tenotomy) — serial casts and tiny heel-cord cut if needed; why: to align the foot for standing/walking. Johns Hopkins Medicine

2. Soft-tissue releases (capsulotomy/tenotomy) — carefully lengthen tight capsules or tendons; why: increase range for function and brace wear. Johns Hopkins Medicine

3. Tendon transfers — move a functioning tendon to help a weak motion (e.g., wrist extension); why: improve reach/grasp. Johns Hopkins Medicine

4. Osteotomies (bone realignment) — correct bony angles that block motion; why: better joint mechanics and gait. Merck Manuals

5. External fixation/gradual correction — frame-based slow stretch and alignment; why: complex multi-plane deformity correction with control. Merck Manuals

Preventions

1. Early therapy start to prevent worsening stiffness. BioMed Central

2. Daily gentle stretches to keep gains. Johns Hopkins Medicine

3. Night splints/positioning to hold corrected range. Johns Hopkins Medicine

4. Safe skin care under braces/casts to prevent sores. Johns Hopkins Medicine

5. Nutrition for growth (protein, vitamin D, calcium). Merck Manuals

6. Bone-health monitoring in low-mobility kids. Johns Hopkins Medicine

7. Regular equipment checks to adjust fit as the child grows. PM&R KnowledgeNow

8. Infection prevention (vaccines, hand hygiene) to avoid therapy interruptions. Merck Manuals

9. Caregiver training to use correct handling and avoid forced positions. BioMed Central

10. Mental-health and school supports to sustain participation. PM&R KnowledgeNow

When to see doctors

See your pediatrician/rehab team if you notice new swelling, redness, fever, sudden pain, skin breakdown under a brace/cast, loss of function, or equipment that no longer fits. Plan regular reviews with pediatric orthopedics and physiatry/therapy to adjust splints, exercises, and goals as your child grows. Pre-surgery and post-surgery checks are essential to maintain gains. Johns Hopkins Medicine

What to eat and what to avoid

Eat: protein-rich foods (eggs, fish, beans), dairy or fortified alternatives (calcium), fruit/veg for vitamins C and K, whole grains for energy, and fluids/fiber to prevent constipation (especially after surgery or with low mobility). Avoid/limit: sugary drinks, ultra-processed snacks, excess salt, and very low-calorie “tea-and-toast” patterns that miss protein/micronutrients. Supplements (like vitamin D, calcium, omega-3) are adjuncts, not replacements, and should fit lab levels and age. Merck Manuals

Frequently Asked Questions

1. Is this progressive?
   Usually non-progressive; joints don’t get “worse” by disease itself, but can stiffen without therapy. Wikipedia

2. Is intelligence affected?
   Often normal, especially in amyoplasia; depends on associated syndromes. Wikipedia

3. Can my child walk?
   Many do, with therapy, orthoses, and sometimes surgery; it depends on which joints are involved. Johns Hopkins Medicine

4. Is there a cure?
   No single curative pill or shot; best results come from early, steady rehab and targeted surgery. BioMed Central

5. What causes it?
   Anything that reduces fetal movement; sometimes genetic, sometimes not found. Genetic Rare Disease Center

6. Will more children in the family have it?
   Risk varies; some cases are genetic. Genetics consult can help. Genetic Rare Disease Center

7. What’s the role of splints?
   They hold gains after stretching/casting and prevent relapse. Johns Hopkins Medicine

8. Do we need surgery?
   Sometimes—especially for feet, elbows, or knees that block function after therapy. Johns Hopkins Medicine

9. Are stem cells helpful?
   Not recommended outside research; no proven benefit in AMC. BioMed Central

10. Which specialist should lead care?
    A multidisciplinary team: pediatric rehab (PM&R), orthopedics, PT/OT, genetics, pediatrics. PM&R KnowledgeNow

11. How often is therapy needed?
    Early and consistent; frequency changes with goals and growth stages. BioMed Central

12. Can therapy start in infancy?
    Yes—the earlier, the better. BioMed Central

13. Will pain be constant?
    Many children have manageable pain; good positioning, braces, and exercise help a lot. Johns Hopkins Medicine

14. Can school support my child?
    Yes—IEPs/adaptations and therapy at school support full participation. PM&R KnowledgeNow

15. Where can I read reliable information?
    NORD, NIH GARD, Cleveland Clinic, PM&R KnowledgeNow, and Merck Manuals are trustworthy starting points. Merck Manuals+4Rare Diseases +4Genetic Rare Disease Center+4

Disclaimer: Each person’s journey is unique, treatment plan, life style, food habit, hormonal condition, immune system, chronic disease condition, geological location, weather and previous medical  history is also unique. So always seek the best advice from a qualified medical professional or health care provider before trying any treatments to ensure to find out the best plan for you. This guide is for general information and educational purposes only. Regular check-ups and awareness can help to manage and prevent complications associated with these diseases conditions. If you or someone are suffering from this disease condition bookmark this website or share with someone who might find it useful! Boost your knowledge and stay ahead in your health journey. We always try to ensure that the content is regularly updated to reflect the latest medical research and treatment options. Thank you for giving your valuable time to read the article.

The article is written by Team RxHarun and reviewed by the Rx Editorial Board Members

Last Updated: September 23, 2025.

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