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Muscular Dystrophy

Duchenne Care UK Clinical recommendations for Duchenne muscular dystrophy care. Published: 2018

Muscular dystrophy UK Becker Muscular Dystrophy (BMD). Last reviewed: Feb 2025.

Muscular Dystrophy

Muscular dystrophy is an umbrella term for a group of inherited muscle disorders causing progressive muscle weakness. This article focuses on Duchenne muscular dystrophy (DMD) and Becker muscular dystrophy (BMD), the main dystrophinopathies that are most important and most commonly examined at a non-specialist level.

Causes and Pathophysiology

Both DMD and BMD are genetic conditions caused by mutations in the DMD gene (which encodes dystrophin, a cytoskeletal protein important for muscle fibre stability)

  • Inheritance pattern: X-linked recessive
  • DMD: more severe, as mutations result in absolute deficiency of functional dystrophin
  • BMD: less severe, as mutations usually result in a relative deficiency of dystrophin

As DMD and BMD are X-linked recessive conditions, they predominantly affect males.

  • Carrier females are usually asymptomatic or mildly affected, but may develop cardiac involvement
  • A carrier mother has a 50% chance of passing the mutation to each son, who would be affected, and a 50% chance of passing it to each daughter, who would become a carrier
  • An affected father passes the mutation to all daughters, who become carriers, but not to sons

Affected male = mutation is on the X chromosome from the maternal side or from a new mutation (de novo). Not father-to-son transmission.

Clinical Features

DMD features:

Body system Clinical features
Musculoskeletal Hallmark: progressive bilateral, symmetrical muscle weakness

  • Typically begins in the proximal lower limb (pelvis)
  • Progresses to affect the distal lower limb and upper body

Motor signs are typically noticed before 5 y/o

  • Motor delay (not walking by 16-18 months)
  • Difficulty walking and/or climbing stairs
  • Abnormal gait
    • Waddling gait
    • Toe walking
  • Frequent falls
  • Hypotonia
  • Calf pseudohypertrophy
  • Gower’s sign: patient uses their hands to “walk up” their legs when rising from the floor, due to proximal muscle weakness affecting the hips and thighs

Patients often lose the ability to walk around age 10-12 y/o

Increased risk of:

  • Scoliosis
  • Joint contractures
  • Osteoporosis and fractures (from both DMD itself and as a result of steroids)
Cardiovascular
  • Dilated cardiomyopathy
  • Arrhythmias
Respiratory Respiratory muscle weakness causes breathing problems

  • ↓ Lung function
  • Weak cough (→ recurrent chest infections)
  • Sleep apnoea
  • Nocturnal hypoventilation
  • Risk of respiratory failure
GI and nutritional
  • Dysphagia
  • Gastroparesis
  • GORD
  • Constipation

Obesity can occur due to reduced mobility / steroids; or undernutrition can occur due to dysphagia / feeding difficulty

Neurodevelopmental and psychosocial
  • Cognitive delay
  • Learning and attention issues
  • Speech delay
  • Higher risk of behavioural and emotional conditions (e.g. autism, ADHD, OCD, anxiety)
Life expectancy Most individuals now live into their 30s and beyond

Most common cause of death: cardiac or respiratory failure

BMD presents similarly to DMD but with the following differences:

  • BMD is less severe than DMD
  • Onset in later childhood (~5-15 y/o)
  • Slowly progressive
  • Typically do NOT reduce life expectancy

Investigation and Diagnosis

Standard work-up for ALL patients:

  • 1st line: serum creatine kinase (↑ creatine kinase is seen in DMD and BMD due to muscle breakdown)
  • Confirmatory test: genetic testing to detect mutations in the dystrophin gene (DMD gene)

If genetic testing is -ve and clinical suspicion of DMD / BMD remains → muscle biopsy

  • Immunohistochemistry to demonstrate complete absence of dystrophin protein (DMD) or deficiency in dystrophin protein (BMD)

Management

Both DMD and BMD require an MDT management approach.

Duchenne Muscular Dystrophy (DMD)

Mainstay of treatment: glucocorticoids (prednisolone or deflazacort)

  • Steroids are disease-modifying as they slow the disease progression
  • Steroids also delay loss of walking ability and help preserve upper limb strength and respiratory function

Other aspects of management:

  • Daily home stretching programme + use of ankle-foot orthoses to prevent contracture development
  • ACE inhibitors should be initiated by 10 y/o even if asymptomatic due to the risk of developing DCM
  • Steroids often cause impaired growth, delayed puberty, severe osteoporosis
    • Testosterone replacement for males >14 y/o with delayed puberty
    • IV bisphosphonates for moderate to severe vertebral and long bone fractures
  • GI and nutrition
    • A dietitian should manage calorie and fluid intake
    • When the patient can no longer maintain adequate nutrition or hydration orally → gastrostomy feeding tube

Ongoing surveillance and monitoring

  • ECG and echo – due to the risk of DCM (most important)
  • Lung function test (specifically FVC)
  • Spinal and MSK monitoring (for scoliosis and contracture detection)
  • Bone health assessment (DEXA, assessment of calcium and vitamin D intake, spine X-rays to detect asymptomatic vertebral compression fractures) – risk of osteoporosis and fractures is high due to steroid use
  • Routine mental health and quality of life screening at each clinic visit

Depolarising muscle relaxants (e.g. suxamethonium) and inhalation anaesthetics are contraindicated as they can trigger fatal rhabdomyolysis and hyperkalaemia.

Becker Muscular Dystrophy (BMD)

Unlike DMD, corticosteroids are not routinely used as disease-modifying therapy in BMD.

Otherwise, the general management principles are similar to DMD (see above).

References

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