Congenital Multiple Arthrogryposis (Arthrogryposis Multiplex Congenita)

Multiple congenital arthrogryposis is an umbrella term for conditions where a baby is born with stiff joints (contractures) in two or more body areas. The joints are fixed in a bent or straight position, so moving them is hard. AMC itself is not one single disease—it is a feature that can be caused by many different problems that limit movement in the womb (called reduced fetal movement or fetal akinesia). PMC+2Genetic Rare Disease Center+2 When a baby does not move well before birth, joints can stiffen, muscles may be small or weak, and soft tissues tighten. Many paths can lead to low movement: problems in the nerves, muscles, bones, connective tissue, or space in the uterus; sometimes gene changes are involved. PMC+2PMC+2

Congenital multiple arthrogryposis—widely known as arthrogryposis multiplex congenita (AMC)—is a group of conditions in which a baby is born with stiffness and limited movement in many joints of the body. The word “arthro-gry-po-sis” means “curved or bent joints.” In AMC, the joints do not move well before birth. Because the fetus moves very little inside the womb, the tissues around the joints (muscles, tendons, capsules, skin) become tight and short. This leads to contractures (fixed bending) when the baby is born. AMC is not one single disease; it is a final “shape” that many different problems can cause. Some causes affect the brain or spinal cord, some affect nerves or muscles, and some are mechanical (too little space to move). Many children have normal thinking and learning. The condition is not contagious, and parents do not “cause” it by anything they did during pregnancy.

Why it happens (in one sentence): when a fetus cannot move enough for weeks, joints stiffen and muscles become thin and fibrotic, so the baby is born with multiple contractures.

Key facts in plain words:

• Many different causes; finding the cause helps planning care.

• It can affect a few joints or many joints.

• Early therapy and gentle splinting help joints move better.

• Some children need surgeries over time to improve function.

Evidence base (plain reference note): The description above reflects classic reviews of AMC/arthrogryposis (Hall 2014; Bamshad & Van Heest 2019; American College of Medical Genetics practice resources; orthopedic and neonatology texts).

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Other names

• Arthrogryposis Multiplex Congenita (AMC): the most common medical term.

• Congenital multiple joint contractures: plain-language description used in pediatrics.

• Amyoplasia: the most common classic type of AMC with very thin muscles.

• Distal arthrogryposis (DA): contractures mainly in hands and feet; many genetic subtypes.

• Fetal akinesia deformation sequence (Pena-Shokeir sequence): severe form with very little fetal movement and other features.

• Neurogenic arthrogryposis: caused by problems in the brain, spinal cord, or peripheral nerves.

• Myopathic arthrogryposis: caused by primary muscle disease.

• Syndromic arthrogryposis: part of a broader genetic syndrome (for example, Freeman-Sheldon).

• Multiple pterygium syndrome / Escobar syndrome: arthrogryposis with skin webbing.

• Contractural syndromes: umbrella name in clinical genetics.

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Types

1) Amyoplasia (classic type).
Babies have very thin muscles (especially in arms and legs) and multiple stiff joints at birth. Shoulders turn inward, elbows may be straight, wrists bent, hips often dislocated, and feet often clubbed. Brain function is usually normal. (Classic orthopedic and genetics sources describe this pattern.)

2) Distal arthrogryposis (DA).
Contractures are strongest in the hands and feet, with milder involvement at knees or elbows. Many DA forms are autosomal dominant and caused by changes in muscle contraction genes (for example, TNNI2, TNNT3, TPM2, MYH3, PIEZO2). (Genetic reviews and ACMG summaries support this.)

3) Neurogenic forms.
The problem starts in the central nervous system (brain/spinal cord) or anterior horn cells (like very-early-onset spinal muscular atrophy). Weak signals from nerves mean less movement, so joints stiffen. (Neonatal neurology texts and reviews support this mechanism.)

4) Myopathic forms.
Primary muscle diseases—congenital myopathies or dystrophies—make fetal movement weak. Examples include nemaline myopathy or congenital muscular dystrophy. (Pediatric neuromuscular references.)

5) Syndromic forms.
Arthrogryposis occurs within a broader syndrome such as Freeman-Sheldon, Escobar (multiple pterygium), Larsen, or others. Each syndrome has extra clues (face, spine, skin webs, or organ findings). (Clinical genetics atlases.)

6) Mechanical/constraint-related forms.
When the uterus is small or fluid is low, the fetus cannot move freely for weeks, so joints tighten. Examples include oligohydramnios, uterine malformations, or twin crowding. (Obstetrics and dysmorphology references.)

7) Mixed/unspecified forms.
Sometimes more than one factor is present, or testing is inconclusive. Care still focuses on function and comfort. (Consensus care statements.)

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Causes

1) Decreased fetal movement (final common pathway).
No matter the root cause, too little movement for many weeks lets connective tissues shorten and scar. This produces contractures at birth. (Core AMC mechanism in reviews.)

2) Amyoplasia (non-genetic pattern).
A sporadic event leads to very poor muscle development in limbs. Muscles look thin at birth, but brain is usually normal. (Orthopedic/genetic reviews.)

3) Distal arthrogryposis gene variants.
Changes in contractile proteins (e.g., TNNI2, TNNT3, TPM2, MYH3) reduce force in small muscles, especially in hands/feet. Movement falls, joints stiffen. (Genetic studies.)

4) PIEZO2-related DA.
This gene helps muscles and nerves “sense” stretch. Faulty signals blunt movement and cause hand-foot contractures. (Recent genetics literature.)

5) Anterior horn cell disorders (e.g., very-early SMA).
Loss of motor neurons means weak muscles and poor kicking in utero, causing contractures. (Neonatal neurology texts.)

6) Peripheral neuropathies (rare congenital forms).
If peripheral nerves cannot carry signals, muscles cannot contract, so joints stiffen over time before birth. (Neuromuscular references.)

7) Neuromuscular junction problems (maternal myasthenia antibodies).
Maternal antibodies may cross the placenta and block the baby’s nerve-to-muscle signal. The fetus moves less; joints contract. (Obstetric/neuromuscular literature.)

8) Congenital myopathies (e.g., nemaline, central core).
Structural muscle defects reduce strength from early fetal life, lowering movement and causing contractures. (Pediatric myopathy reviews.)

9) Congenital muscular dystrophies.
Abnormal muscle membrane proteins cause early weakness and fibrotic replacement, leading to fixed joints. (Neuromuscular texts.)

10) Connective tissue/skeletal syndromes (e.g., Larsen, multiple pterygium).
Abnormal joint structures, skin webs, or frequent dislocations limit motion and promote contractures. (Genetic syndromes handbooks.)

11) Central nervous system malformations or injury.
Brain or spinal cord maldevelopment lowers motor drive to muscles; movement falls and joints stiffen. (Neonatal neurology.)

12) Fetal akinesia deformation sequence (Pena-Shokeir).
Severe reduction in all fetal movement leads to widespread contractures, lung hypoplasia, and facial features. (Dysmorphology references.)

13) Oligohydramnios (low amniotic fluid).
Too little fluid compresses the fetus, limiting motion for weeks. Joints adapt by becoming tight. (Obstetrics sources.)

14) Uterine structural limits (bicornuate uterus, large fibroids).
Space restriction reduces movement; fixed positions turn into contractures. (Maternal-fetal medicine texts.)

15) Multiple gestation with crowding.
Twins or triplets can crowd each other, reducing free motion for the smaller fetus. (Obstetrics.)

16) Early fetal fractures or bone dysplasias.
Pain or abnormal bones make the fetus move less; joints stiffen secondarily. (Orthopedics/pediatrics.)

17) In-utero infections (rare).
Some infections injure nervous system or muscles, reducing movement. (Perinatal infection reviews.)

18) Maternal illness (severe uncontrolled diabetes, fever, myasthenia).
Some maternal states reduce fetal activity or neuromuscular function. (Obstetrics/neurology.)

19) Drug or toxin exposure (rare).
Agents that depress neuromuscular function can reduce fetal motion for long periods. (Teratology references.)

20) Unidentified genetic/epigenetic factors.
Even with modern testing, some cases remain unexplained; mechanism is still reduced movement. (Clinical genetics reviews.)

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Symptoms and signs

1) Multiple joint contractures at birth.
Elbows, wrists, hips, knees, ankles, hands, or feet may be fixed in bent or straight positions and move only a little.

2) Limited range of motion.
Joints do not move through a full arc. Daily tasks like dressing and later walking can be harder without therapy.

3) Muscle thinning (amyoplasia).
Arms and legs may look slim due to small muscles; skin may show dimples over joints.

4) Clubfoot (talipes equinovarus).
Feet turn inward and downward. Without early treatment, standing and walking are difficult.

5) Hip dislocation or stiffness.
Hips may be out of place or very tight, affecting sitting and walking plans.

6) Knee contractures (flexed or hyperextended).
Knees may be stuck bent or too straight, making bracing and therapy important.

7) Wrist and finger contractures.
Hands may be clenched or wrists bent, affecting grasp. Splints and therapy help function.

8) Shoulder internal rotation and elbow extension.
This classic pattern limits reaching the mouth or head; therapy targets these motions.

9) Webbing (pterygia) around joints.
Tight skin folds can bridge joints and limit movement further.

10) Spine curves (scoliosis).
Weak muscles and contractures can allow the spine to curve; monitoring is needed.

11) Facial features in some syndromes.
Small mouth, high palate, or characteristic facial shape may point to a specific syndrome.

12) Feeding or breathing difficulty (subset).
If jaw, chest wall, or respiratory muscles are affected, babies may need support.

13) Motor delay (skills arrive later).
Children often need more time—and therapy—to learn rolling, sitting, or walking.

14) Pain or fatigue (often later).
Young infants are often not painful, but older children can develop pain from abnormal mechanics.

15) Normal intelligence in many, learning issues in some.
Cognition is often typical, but varies with the underlying cause; syndromic forms may include learning needs.

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Diagnostic tests

A) Physical examination (bedside assessments)

1) Newborn musculoskeletal survey.
A careful head-to-toe exam charts which joints are stiff, which directions are limited, and whether skin webs are present. This baseline guides early therapy.

2) Detailed neurologic exam.
Tone, reflexes, and strength patterns help decide if the problem is central (brain/spinal cord), nerve, junction, or muscle—key for finding the cause.

3) Range-of-motion (ROM) mapping with goniometer.
Measuring angles at each joint shows severity now and progress over time. It also helps plan splints.

4) Posture and function observation.
How the infant positions limbs at rest, and how they move while crying or feeding, offers real-world clues for therapy goals.

5) Hip stability tests (Ortolani/Barlow).
Gentle maneuvers detect dislocated or unstable hips, which need early treatment.

B) Manual/functional tests

6) Manual muscle testing (age-adapted).
In older infants and children, simple resistance tests estimate muscle power; weakness suggests nerve or muscle disease.

7) Hand function assessments.
Grasp, release, and thumb position tests direct occupational therapy and decide if hand surgery might help.

8) Gait and standing assessment (when age-appropriate).
Watching standing, stepping, and balance guides brace selection and physical therapy plans.

9) Spine flexibility checks.
Forward bend and side-to-side maneuvers show if scoliosis is flexible (braceable) or stiff (may need surgery later).

10) Splint/cast responsiveness trials.
Short trials with corrective splints or serial casting show how much the soft tissues can lengthen without surgery.

C) Laboratory and pathological tests

11) Serum creatine kinase (CK).
High CK suggests ongoing muscle fiber damage (dystrophy). Normal CK leans toward non-dystrophic causes or non-muscle causes.

12) Genetic testing panels and/or exome/genome.
Targeted arthrogryposis or neuromuscular gene panels can find many causes; if negative, exome/genome sequencing can reveal rare or new variants.

13) Maternal antibody tests (if NMJ block suspected).
Testing for maternal myasthenia antibodies helps confirm a transient neuromuscular junction cause.

14) Metabolic and infection screens (selected).
When history suggests, tests for congenital infections, thyroid, or metabolic diseases can be informative.

15) Muscle biopsy (select cases).
If genetics are unclear, a biopsy can show patterns of congenital myopathy or dystrophy that explain the low movement.

D) Electrodiagnostic tests

16) Electromyography (EMG).
EMG patterns help separate neurogenic from myopathic causes and can suggest a neuromuscular junction issue.

17) Nerve conduction studies (NCS).
These measure how fast and strong signals run in nerves; low values suggest neuropathy.

18) Repetitive nerve stimulation or single-fiber EMG.
These specialized studies detect signal “fatigue” at the neuromuscular junction, supporting a diagnosis like maternal antibody-mediated block.

E) Imaging tests

19) X-rays of hips, spine, and limbs.
Show hip dislocation, foot alignment, knee position, and bone development, guiding casting or surgery.

20) Ultrasound and MRI (targeted).
Hip ultrasound is useful in infants; fetal or postnatal MRI can reveal brain/spine issues, muscle bulk, and patterns that point to specific causes.

Non-pharmacological treatments (therapies & others)

Short, plain-English descriptions with purpose and how they work.

1. Gentle daily stretching
   Purpose: loosen tight soft tissues to gain motion.
   Mechanism: slow, sustained stretch reduces stiffness of capsules, ligaments, and muscles; repeated stretch remodels collagen over time. PM&R KnowledgeNow

2. Positioning programs
   Purpose: prevent worsening contractures between therapy sessions.
   Mechanism: neutral or corrected alignment reduces unequal tension and holds gains made during therapy. PM&R KnowledgeNow

3. Removable splints (day/night)
   Purpose: maintain range after stretching or surgery.
   Mechanism: low-load, long-duration stretch; easier daytime activity than full casts. Medscape

4. Serial casting (e.g., Ponseti for clubfoot)
   Purpose: gradually correct severe foot/ankle/knee flexion deformities.
   Mechanism: weekly cast changes move the joint a little more each time, allowing tissues to lengthen safely. PM&R KnowledgeNow

5. Custom orthoses & braces
   Purpose: support standing/walking and hand function.
   Mechanism: external support improves alignment and energy efficiency, enabling practice and strength building. Physiopedia

6. Task-oriented physiotherapy
   Purpose: build strength and useful movement patterns for daily tasks.
   Mechanism: repetitive, goal-based practice strengthens available muscles and improves motor planning. PMC

7. Occupational therapy for hands/self-care
   Purpose: improve grasp, feeding, dressing independence.
   Mechanism: adaptive strategies and hand splints maximize function even with limited motion. PM&R KnowledgeNow

8. Standing programs
   Purpose: hip stability, bone health, posture, and GI benefits.
   Mechanism: weight-bearing stimulates bone and helps joint alignment. Physiopedia

9. Adaptive equipment training
   Purpose: safe mobility and independence at home/school.
   Mechanism: customized seating, walkers, or wheelchairs improve access and reduce fatigue. PM&R KnowledgeNow

10. Feeding and speech therapy (when jaw/oral muscles are tight)
    Purpose: safer feeding and clearer speech.
    Mechanism: oromotor therapy, positioning, and pacing techniques; referral for swallow study if needed. Medscape

11. Pain-minimizing movement strategies
    Purpose: keep therapy comfortable to sustain progress.
    Mechanism: graded exposure, heat, and pacing decrease protective muscle guarding. PMC

12. Hydrotherapy (water-based)
    Purpose: easier motion with less pain.
    Mechanism: buoyancy supports the body; warm water relaxes tissues so joints move further. PMC

13. Home exercise program coaching
    Purpose: make daily care realistic for families.
    Mechanism: clear, simple plans maintain gains between clinic visits. BioMed Central

14. Peri-operative rehab protocols
    Purpose: protect surgical results and speed return to function.
    Mechanism: staged splinting, edema control, and early safe motion. BioMed Central

15. Serial removable splinting for upper limbs
    Purpose: improve elbow extension or wrist/hand position.
    Mechanism: progressive remolding at each visit lengthens soft tissues gently. davidsfeldmanmd.com

16. Hip surveillance & positioning
    Purpose: reduce risk of dislocation and stiffness.
    Mechanism: regular checks plus abduction positioning/orthoses when needed. PM&R KnowledgeNow

17. School-based therapy & accommodations
    Purpose: participation and inclusion.
    Mechanism: adaptive tools, rest breaks, and individualized education supports. BioMed Central

18. Psychosocial support & pain coping skills
    Purpose: reduce anxiety, improve adherence to therapy.
    Mechanism: CBT-style coping, family education, and peer support groups. BioMed Central

19. Community mobility training
    Purpose: safe use of public spaces and transport.
    Mechanism: practice transfers, ramps, and real-world routes. PM&R KnowledgeNow

20. Regular multidisciplinary reviews
    Purpose: adjust plans as the child grows.
    Mechanism: team input (rehab, orthopedics, genetics, OT/PT, speech, nutrition) keeps goals realistic and timely. BioMed Central

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Drug treatments

Medicines help comfort, spasticity, reflux/constipation, sleep, and bone health so therapy works better. Choices are individualized; dosing examples below are typical pediatric ranges but must be tailored by your clinician.

1. Acetaminophen (paracetamol) – pain/fever
   Class: analgesic. Dose: ~10–15 mg/kg every 6–8 h (max per local guidance).
   When: before/after therapy or procedures. Why: reduce pain to allow stretch.
   How it works: central COX inhibition lowers pain signals.
   Side effects: usually mild; liver risk with overdose. PM&R KnowledgeNow

2. Ibuprofen – pain/inflammation
   Class: NSAID. Dose: ~5–10 mg/kg every 6–8 h with food.
   Why: short-term anti-inflammatory effect for sore joints after casting or long sessions.
   Mechanism: COX inhibition reduces prostaglandins.
   Risks: stomach upset, rare kidney issues; avoid dehydration. PM&R KnowledgeNow

3. Naproxen – longer-acting NSAID
   Class: NSAID. Dose: ~5–7 mg/kg twice daily (peds reference dependent).
   Why: steadier relief for recurrent joint pain.
   Risks: GI irritation, renal risk; use gastroprotection when indicated. PM&R KnowledgeNow

4. Topical NSAIDs (diclofenac gel)
   Class: topical anti-inflammatory. Use: apply to tender areas as directed.
   Why: local pain relief with lower systemic exposure.
   Risks: skin irritation. PM&R KnowledgeNow

5. Baclofen – spasticity (if present)
   Class: antispastic (GABA-B agonist). Dose: start low, titrate (e.g., 0.3–0.75 mg/kg/day divided).
   Why: reduce muscle tone that limits range.
   Mechanism: decreases excitatory neurotransmission in spinal cord.
   Risks: sedation, weakness; taper to stop. PM&R KnowledgeNow

6. Tizanidine – spasticity alternative
   Class: alpha-2 agonist. Dose: individualized, slow titration.
   Why/How: reduces reflex muscle tone to help therapy.
   Risks: sleepiness, low blood pressure, dry mouth; check liver tests. PM&R KnowledgeNow

7. Botulinum toxin A (targeted muscles)
   Class: neuromuscular blocker (local injection). Timing: every 3–6 months if helpful.
   Why: relax overactive muscles to gain motion and improve splint tolerance.
   Mechanism: blocks acetylcholine release at the neuromuscular junction.
   Risks: local weakness; rare spread of effect. PM&R KnowledgeNow

8. Diazepam (short-term at night)
   Class: benzodiazepine antispastic/antianxiety. Use: limited, for painful spasms.
   Why: improve sleep and ease stretching early on.
   Risks: sedation, dependence, respiratory depression—use cautiously. PM&R KnowledgeNow

9. Gabapentin – neuropathic pain features
   Class: anticonvulsant/neuropathic analgesic. Dose: weight-based titration.
   Why: reduce burning/tingling pain that can block therapy.
   Risks: dizziness, fatigue. PM&R KnowledgeNow

10. Melatonin – sleep support
    Class: sleep-wake regulator. Dose: age-appropriate, bedtime.
    Why: better sleep improves daytime therapy tolerance.
    Risks: vivid dreams, morning drowsiness. PM&R KnowledgeNow

11. Proton-pump inhibitors (omeprazole) – reflux if feeding issues
    Class: acid suppression. Dose: pediatric mg/kg/day.
    Why: reduce discomfort and aspiration risk during therapy/feeding.
    Risks: diarrhea, nutrient interactions with long use. Medscape

12. Stool softeners (PEG 3350) – constipation with limited mobility
    Class: osmotic laxative. Dose: pediatric per label.
    Why: comfort and feeding adherence.
    Risks: bloating if overdosed. PM&R KnowledgeNow

13. Vitamin D – bone health
    Class: vitamin. Dose: per age/level.
    Why: support bones during casting/limited mobility.
    Risks: hypercalcemia if excessive. PM&R KnowledgeNow

14. Calcium (if intake is low)
    Class: mineral supplement. Dose: age-based.
    Why: skeletal health with reduced weight-bearing.
    Risks: constipation; avoid excess. PM&R KnowledgeNow

15. Acetylcysteine (airway support if weak cough)
    Class: mucolytic (selected cases). Why: ease airway clearance during respiratory infections.
    Risks: bronchospasm in some. PM&R KnowledgeNow

16. Topical anesthetics for procedures
    Class: local analgesia (EMLA, etc.). Why: make casting/splinting changes more comfortable.
    Risks: local irritation, methemoglobinemia rare. PM&R KnowledgeNow

17. Acetazolamide (selected intracranial pressure/CSF issues in syndromic cases—rare)
    Class: carbonic anhydrase inhibitor. Use: only if specific indication.
    Risks: electrolyte shifts. PM&R KnowledgeNow

18. Antibiotics (only when infection is present)
    Class: antimicrobial. Why: protect surgical sites or treat intercurrent infection that halts therapy.
    Risks: drug-specific. PM&R KnowledgeNow

19. Antiemetics (ondansetron) for post-op nausea
    Class: 5-HT3 antagonist. Why: smoother recovery, earlier mobilization.
    Risks: constipation, headache, QT prolongation. Medscape

20. Analgesic plans for surgery (multimodal)
    Class: combined acetaminophen/NSAID ± regional blocks.
    Why: better pain control, earlier rehab start.
    Risks: drug-specific; follow surgical team plan. Medscape

Important note: These medicines are supportive; they do not correct the underlying cause of AMC. Choice and dosing should be individualized by a pediatric specialist.

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Dietary molecular supplements

These do not treat AMC itself, but can support bone, muscle, and overall health when used appropriately. Always clear with your clinician.

1. Vitamin D3 – bone mineralization; typical daily age-based dosing. Mechanism: improves calcium absorption and bone strength during casting/limited weight-bearing. PM&R KnowledgeNow

2. Calcium – bone matrix support when diet is low. Mechanism: provides substrate for bone; works with vitamin D. PM&R KnowledgeNow

3. Protein (dietary or formula enrichment) – supports muscle maintenance. Mechanism: essential amino acids for tissue repair from therapy. PM&R KnowledgeNow

4. Omega-3 fatty acids – general anti-inflammatory effects; may ease soreness after therapy. Mechanism: eicosanoid pathway modulation. PM&R KnowledgeNow

5. Iron (if deficient) – supports oxygen delivery to working muscles. Mechanism: hemoglobin synthesis; only if labs show deficiency. PM&R KnowledgeNow

6. B-complex (if dietary gaps) – energy metabolism for rehab sessions. Mechanism: co-factors in mitochondrial pathways. PM&R KnowledgeNow

7. Magnesium – muscle relaxation and bone health; avoid excess. Mechanism: neuromuscular excitability modulation. PM&R KnowledgeNow

8. Zinc – wound healing, appetite support post-op. Mechanism: enzymatic co-factor for protein synthesis. PM&R KnowledgeNow

9. Probiotics (selected cases) – stool regularity if on constipating meds. Mechanism: microbiome balance; evidence varies by strain. PM&R KnowledgeNow

10. Fiber supplements – bowel regularity during reduced mobility. Mechanism: adds bulk and improves transit. PM&R KnowledgeNow

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Immunity-booster / regenerative / stem-cell” drugs

There are no approved regenerative or stem-cell drugs that cure AMC. Research into genetics and prenatal diagnosis is growing, but disease-modifying therapies are not established for most AMC subtypes today. Supportive items sometimes discussed:

1. Seasonal vaccines (per schedule) – reduce illness interruptions to therapy; mechanism: trained immunity to specific pathogens. PM&R KnowledgeNow

2. Vitamin D – supports immune function and bone health; see above. PM&R KnowledgeNow

3. Nutritional optimization (protein, iron if deficient) – helps overall resilience and wound healing. PM&R KnowledgeNow

4. Investigational gene-targeted approaches – relevant only for specific myopathies/neuropathies; at present largely research-stage in AMC context. Wiley Online Library+1

5. Platelet-rich plasma or “stem-cell” injections – not established for AMC; insufficient evidence for routine use.

6. Creatine monohydrate in neuromuscular disease (selected contexts) – sometimes used off-label to aid short-burst muscle performance; discuss with neuromuscular specialist. PM&R KnowledgeNow

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Common surgeries

1. Clubfoot correction (Ponseti + Achilles tenotomy ± later tendon transfers/osteotomies)
   Why: place the foot flat to stand and walk more easily; surgery is usually limited and staged. PM&R KnowledgeNow

2. Knee release procedures (posterior capsulotomy/hamstring lengthening) in severe flexion contractures
   Why: allow standing, transfers, or walking aids. PM&R KnowledgeNow

3. Hip procedures (open reduction, femoral/acetabular osteotomy in selected cases)
   Why: improve stability and sitting/standing function. PM&R KnowledgeNow

4. Upper-limb tendon transfers (e.g., to improve elbow flexion or wrist/hand position)
   Why: enable bringing the hand to the mouth or better grasp. PM&R KnowledgeNow

5. Spine procedures (rare; for severe scoliosis affecting sitting or breathing)
   Why: improve posture and comfort for daily activities. PM&R KnowledgeNow

Surgery is ideally paired with peri-operative rehab and night splinting to hold gains. Medscape

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Prevention & practical tips

While you cannot “prevent” many AMC subtypes, you can prevent loss of gains and reduce complications:

1. Start therapy early and keep it consistent. PM&R KnowledgeNow

2. Use home stretching and night splints as taught. Medscape

3. Keep skin care under casts/splints. davidsfeldmanmd.com

4. Encourage safe daily activity to build stamina. BioMed Central

5. Maintain bone health (vitamin D/calcium as advised). PM&R KnowledgeNow

6. Nutrition for growth and healing; manage constipation early. PM&R KnowledgeNow

7. Plan peri-operative rehab before surgery dates. BioMed Central

8. Keep orthosis fit checks as the child grows. BioMed Central

9. Vaccinations and infection control to avoid therapy setbacks. PM&R KnowledgeNow

10. Regular multidisciplinary reviews to adjust goals. BioMed Central

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When to see a doctor urgently

• Sudden worsening pain, swelling, or skin breakdown under a cast/splint.

• Signs of joint dislocation, new deformity, or loss of previous range.

• Feeding or breathing trouble, choking, or poor weight gain.

• Fever or wound issues after surgery.

• Any time therapy becomes impossible due to pain or stiffness. Medscape+1

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What to eat / what to avoid

Eat: balanced diet with adequate protein, fruits/vegetables, calcium-rich foods (dairy/fortified alternatives), vitamin D sources/supplement as advised, fiber-rich foods for bowel regularity, and plenty of fluids. Why: supports muscle repair, bone strength, and energy for therapy. PM&R KnowledgeNow

Avoid or limit: sugary drinks, ultra-processed snacks with poor nutrients, excessive NSAID use without clinician guidance, and mega-doses of any supplement unless prescribed. Why: sugar spikes and poor nutrition sap energy; unnecessary meds/supplement excess can cause side effects. PM&R KnowledgeNow

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FAQs

1) Is AMC the same in every child?
No. AMC is a group of conditions. The cause, the joints involved, and the severity are different for each person. Orpha

2) Is intelligence affected?
Often normal; it depends on the subtype and any associated syndromic features. Function mainly depends on the joints involved and access to therapy. Rare Diseases

3) What is the most common type?
Amyoplasia is often cited as the most common AMC form. ScienceDirect

4) Can AMC be seen before birth?
Sometimes, yes. Prenatal ultrasound/MRI can show low fetal movement and limb positions; genetic testing may help in selected cases. Obstetrics & Gynecology+1

5) Will my child walk?
Many children do—sometimes with braces, walkers, or wheelchairs for distance. Early therapy and proper alignment improve the odds. PM&R KnowledgeNow

6) Does casting hurt?
Serial casting should not be painful when done correctly; mild soreness is common after stretches. Report any swelling or skin problems right away. PM&R KnowledgeNow

7) Are splints better than casts?
They serve different roles. Serial casts help gain range; splints help maintain it and allow daytime activity. Medscape

8) Are there specific genes for AMC?
Yes—many genes can be involved depending on the subtype (nerve, muscle, connective tissue). A genetics team can guide testing. Wiley Online Library

9) Is surgery always needed?
No. Many gains come from therapy + orthoses. Surgery is used when alignment blocks function or casting cannot achieve goals. PM&R KnowledgeNow

10) Can adults with AMC still improve?
Yes. Soft tissues respond to regular stretching, strengthening, and better equipment at any age, though changes are slower than in early childhood. PMC

11) Is there a cure?
There is no single curative medicine for AMC. Care focuses on function, comfort, and participation, tailored to the person. PM&R KnowledgeNow

12) Which specialist should coordinate care?
A multidisciplinary team: pediatric rehabilitation, orthopedics, PT/OT, genetics, speech/feeding, and nutrition. BioMed Central

13) How often are follow-ups?
Regularly during growth or when changing casts/splints; timing is individualized to goals. BioMed Central

14) Are “stem-cell” injections recommended?
No—not established for AMC outside research. Discuss risks and lack of proven benefit. Wiley Online Library

15) Where can I read more?
See the NIH GARD and Orphanet pages for AMC, plus recent rehab recommendations and reviews. PMC+3Genetic Rare Disease Center+3Orpha+3

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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