Facioscapulohumeral muscular dystrophy

Overview

Facioscapulohumeral muscular dystrophy (FSHD) is the third most common inherited muscular dystrophy, with autosomal dominant inheritance and a unique genetic mechanism: aberrant DUX4 expression due to D4Z4 repeat contraction on chromosome 4q35, requiring a permissive 4qA haplotype.

Presentation

Characteristic descending pattern: face and shoulder girdle first, then upper arms, then lower limbs (foot drop), then pelvic girdle in advanced disease.

Facial weakness - lagophthalmos, inability to whistle, horizontal smile; often first symptom but unnoticed
Scapular winging - most striking sign; inability to elevate arms above head
'Popeye arm' - prominent deltoid with wasted biceps/triceps (deltoid relatively spared)
Foot drop - tibialis anterior weakness; often asymmetric
Positive Beevor sign - umbilicus moves upward on neck flexion/partial sit-up; lower abdominals weaker than upper; highly specific for FSHD
Sensorineural hearing loss - high-frequency; extramuscular feature, commoner with early-onset disease
Coats-like retinal vasculopathy - typically subclinical; risk of exudative detachment if untreated; associated with severe/infantile-onset FSHD
💡
FSHD does NOT cause cardiomyopathy - this distinguishes it from Duchenne, Becker, Emery-Dreifuss, and myotonic dystrophy. Routine cardiac screening is not required.

Investigations

🥇 First-line

Serum CK - mildly elevated (2-5x ULN) or normal; markedly elevated CK should prompt reconsideration of diagnosis
EMG - myopathic pattern; nerve conduction studies normal (confirms primary muscle disorder)

🏆 Gold standard

Genetic testing - Southern blot to quantify D4Z4 repeats on chromosome 4q35 with 4qA haplotype confirmation; <10 D4Z4 units on permissive 4qA allele is diagnostic for FSHD1

🥈 Second-line

Muscle MRI - fatty infiltration in periscapular, facial, and lower limb muscles; maps disease extent
Muscle biopsy - non-specific myopathic/inflammatory changes; only if genetic result uncertain

Differential diagnosis

Key differentials
ConditionDistinguishing features
Myotonic dystrophy type 1Myotonia, cataracts, frontal balding, cardiac conduction defects
LGMDProximal limb weakness without facial involvement; genetic panel distinguishes
Polymyositis/dermatomyositisMarkedly elevated CK, inflammatory infiltrate on biopsy, rash in dermatomyositis
SMAEMG shows denervation (neurogenic), not myopathic pattern

Management

No approved disease-modifying treatment. Management is MDT-based and function-focused.

🥇 First-line

Physiotherapy and aerobic/strength exercise - slows functional decline; avoid eccentric overload exercise
Ankle-foot orthoses (AFOs) - for foot drop to reduce falls
Scapular fixation (scapulodesis) - surgical option in selected patients with significant winging; improves shoulder abduction
Ophthalmology surveillance - laser photocoagulation if active Coats-like retinal disease

🥈 Second-line

Pain management - NSAIDs, amitriptyline or pregabalin depending on pain character
Respiratory support - spirometry in non-ambulant patients; non-invasive ventilation (NIV) if FVC falls significantly

Prognosis and complications

Near-normal lifespan; majority remain ambulant; ~20% become wheelchair-dependent
Prognosis inversely correlates with D4Z4 repeat length - shorter repeats (1-3 units) = earlier onset, more severe disease, more extramuscular features
Infantile-onset FSHD - very short D4Z4 arrays; facial diplegia in infancy, severe winging, higher rate of hearing loss and Coats-like retinopathy
Respiratory failure - uncommon; most patients do not develop clinically significant compromise
📌
Genetic counselling is essential for all patients - autosomal dominant with 50% transmission risk to offspring. De novo mutations account for ~30% of FSHD1 cases.