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Spinal Muscular Atrophy

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Spinal Muscular Atrophy

Comprehensive guide to Spinal Muscular Atrophy (SMA), covering classification, orthopaedic manifestations, and management including scoliosis and hip dysplasia.

complete
Updated: 2026-01-02
High Yield Overview

Spinal Muscular Atrophy

Progressive Motor Neuron Disease

SMN1 Gene MutationGenetics
Autosomal RecessiveInheritance
1 in 10,000Incidence
100% in Type I/IIScoliosis

SMA Classification

Type I (Werdnig-Hoffmann)
PatternOnset less than 6 months. Never sits.
TreatmentSupportive. Gene therapy.
Type II
PatternOnset 6-18 months. Sits but never walks.
TreatmentSupportive. Scoliosis surgery common.
Type III (Kugelberg-Welander)
PatternOnset greater than 18 months. Walks.
TreatmentVariable progression.
Type IV
PatternAdult onset.
TreatmentMild, slowly progressive.

Critical Must-Knows

  • SMN1 Gene: Survival motor neuron gene mutation.
  • Four Types: Based on age of onset and motor milestones.
  • Scoliosis: Universal in Type I/II, common in Type III.
  • New Therapies: Gene therapy and antisense oligonucleotides.
  • Respiratory Care: Primary cause of mortality.

Examiner's Pearls

  • "
    Know the SMA types and motor milestones
  • "
    Scoliosis is nearly universal
  • "
    Gene therapy has changed prognosis
  • "
    Respiratory failure is the main cause of death

Gene Therapy Era

New disease-modifying therapies have dramatically changed the prognosis for SMA.

  • Nusinersen (Spinraza): Antisense oligonucleotide. Intrathecal. Increases SMN2 expression.
  • Onasemnogene (Zolgensma): Gene therapy. Single IV dose. Replaces SMN1.
  • Early treatment (before symptom onset) leads to best outcomes.
  • Orthopaedic manifestations may still occur but are less severe with early treatment.

SMA Types

TypeOnsetMotor MilestonesPrognosis
Less than 6 monthsNever sitsDeath by 2 years without treatment
6-18 monthsSits, never walksSurvives to adulthood with support
Greater than 18 monthsWalks (may lose ability)Normal or near-normal lifespan
Adult onsetWalksMild, slowly progressive
Mnemonic

SMA Types

I
Infant
Never sits (Werdnig-Hoffmann)
II
Intermediate
Sits, never walks
III
Late
Walks (Kugelberg-Welander)
IV
Adult
Adult onset, mild

Memory Hook:I-II-III-IV: Infant, Intermediate, Late, Adult.

Mnemonic

Orthopaedic Issues

S
Scoliosis
Nearly universal
H
Hip Dysplasia
Common in Type I/II
C
Contractures
Hips, knees, ankles

Memory Hook:SHC - Scoliosis, Hips, Contractures.

Mnemonic

Treatment Principles

R
Respiratory
Primary focus
S
Scoliosis
Bracing then surgery
G
Gene Therapy
Disease-modifying

Memory Hook:RSG - Respiratory, Scoliosis, Gene therapy.

Overview/Epidemiology

Spinal Muscular Atrophy (SMA) is a progressive neuromuscular disorder.

  • Genetics: Autosomal recessive. Mutation/deletion in SMN1 (Survival Motor Neuron 1) gene on chromosome 5q.
  • Incidence: 1 in 10,000 live births. Carrier frequency 1 in 50.
  • Pathophysiology: Degeneration of anterior horn cells in the spinal cord leads to progressive weakness.
  • Historical Significance: Leading genetic cause of infant death (prior to gene therapy).

Pathophysiology

Spinal Cord Pathology

  • Anterior horn cells (lower motor neurons) degenerate.
  • Results in denervation of skeletal muscles.
  • Proximal muscles affected more than distal.
  • Lower limbs typically weaker than upper limbs.

Why Scoliosis Develops

  • Trunk muscle weakness leads to spinal collapse.
  • Gravity + asymmetric weakness = progressive curve.
  • Usually thoracolumbar, long sweeping C-curve.
  • Pelvic obliquity is common.

Classification Systems

SMA Type I (Werdnig-Hoffmann Disease)

  • Onset: Birth to 6 months.
  • Motor Milestones: Never achieves sitting.
  • Features: Severe hypotonia, frog-leg posture, paradoxical breathing.
  • Prognosis: Without treatment, death by age 2 (respiratory failure).
  • With Gene Therapy: Dramatically improved survival.

SMA Type II (Intermediate)

  • Onset: 6-18 months.
  • Motor Milestones: Achieves sitting, never walks independently.
  • Features: Proximal weakness, tremor (minipolymyoclonus), scoliosis (100%).
  • Prognosis: Survive into adulthood with respiratory support.

SMA Type III (Kugelberg-Welander)

  • Onset: After 18 months (typically 2-17 years).
  • Motor Milestones: Achieves walking (may lose ability later).
  • Features: Proximal weakness, waddling gait, Gowers' sign.
  • Prognosis: Normal or near-normal lifespan.

SMA Type IV (Adult Onset)

  • Onset: Adulthood.
  • Motor Milestones: Walks.
  • Features: Mild, slowly progressive weakness.
  • Prognosis: Normal lifespan.

Clinical Assessment

History:

  • Age of symptom onset.
  • Motor milestones achieved and lost.
  • Family history.
  • Respiratory status.

Physical Exam:

  1. Hypotonia: Floppy infant (Type I).
  2. Weakness: Proximal greater than distal. Symmetric.
  3. Reflexes: Absent or diminished.
  4. Fasciculations: Tongue fasciculations are characteristic.
  5. Spine: Assess for scoliosis.
  6. Hips: Assess for dysplasia, contractures.

Investigations

Genetic Testing:

  • SMN1 gene deletion/mutation: Confirmatory.
  • SMN2 copy number: Prognostic (more copies = milder phenotype).

EMG/Nerve Conduction:

  • Denervation pattern (rarely needed now with genetic testing).

Pulmonary Function:

  • FVC (forced vital capacity) monitoring.

Imaging:

  • Spine X-ray: Scoliosis assessment.
  • Hip X-ray: Dysplasia, subluxation.

Management Algorithm

Medical Management

  • Gene Therapy (Onasemnogene/Zolgensma): Single IV dose in infants.
  • Nusinersen (Spinraza): Intrathecal injections every 4 months.
  • Risdiplam (Evrysdi): Oral SMN2 splicing modifier.
  • Respiratory Support: BiPAP, cough assist, suctioning.
  • Nutritional Support: Gastrostomy if swallowing impaired.

Orthopaedic Management

  • Scoliosis:
    • Bracing: Supportive (does not prevent progression). Allows optimal positioning.
    • Surgery: Posterior spinal fusion when curve greater than 40-50 degrees and FVC allows.
  • Hip Dysplasia:
    • Observation if asymptomatic (many do not cause issues).
    • Surgery rarely indicated.
  • Contractures:
    • Stretching, physiotherapy.
    • Splinting/bracing.
    • Soft tissue releases if interfering with function.

Surgical Techniques

Posterior Spinal Fusion

Indications: Progressive scoliosis greater than 40-50 degrees with adequate pulmonary function.

Technique: Posterior approach. Long fusion from upper thoracic to pelvis (typically T2-pelvis). Pelvic fixation (iliac screws or S2-alar-iliac screws) is essential due to pelvic obliquity. Use of hybrid constructs or all-screw constructs.

Considerations: High perioperative risk due to respiratory compromise. Anesthesia team experienced in neuromuscular scoliosis is essential.

Growing Rods / MAGEC

Indications: Young children with early-onset scoliosis who need growth preservation.

Technique: Magnetically controlled growing rods (MAGEC) allow non-invasive lengthening. Fixed proximally and distally with periodic lengthening.

Considerations: Limited by progression and pulmonary status. Definitive fusion eventually needed.

Complications

ComplicationContextManagement
Respiratory FailurePrimary cause of deathBiPAP, ventilation, cough assist
Progressive ScoliosisUniversal in Type I/IIBracing, surgery
Hip DysplasiaCommon in Type I/IIUsually observation
ContracturesHips, knees, feetStretching, splinting, releases
Perioperative ComplicationsHigh risk for scoliosis surgeryExperienced team, ICU care

Postoperative Care

  • ICU Admission: For scoliosis surgery.
  • Respiratory: May require prolonged ventilation.
  • Mobilization: Early sitting in wheelchair.
  • Pain Management: Multimodal.
  • Long-Term: Bracing discontinued after fusion. Ongoing respiratory and nutritional support.

Outcomes/Prognosis

  • Type I (Untreated): Death by 2 years.
  • Type I (Gene Therapy): Many achieving motor milestones, survival dramatically improved.
  • Type II: Survive to adulthood with respiratory support.
  • Type III/IV: Normal or near-normal lifespan.
  • Scoliosis Surgery: Improves sitting balance, quality of life, may improve respiratory function.

Evidence Base

Level II
📚 Mendell et al
Key Findings:
  • Onasemnogene (gene therapy) trial
  • Dramatic improvement in survival and motor function
  • Best outcomes with early treatment
Clinical Implication: Gene therapy is disease-modifying.
Source: NEJM 2017

Level II
📚 Finkel et al
Key Findings:
  • Nusinersen in infantile-onset SMA
  • Improved motor function and survival
  • Intrathecal administration effective
Clinical Implication: Antisense oligonucleotides are effective.
Source: NEJM 2017

Level IV
📚 Oskoui et al
Key Findings:
  • Natural history of SMA
  • SMN2 copy number correlates with severity
  • Baseline for new therapies
Clinical Implication: SMN2 copies are prognostic.
Source: Neurology 2007

Level IV
📚 Apkon et al
Key Findings:
  • Scoliosis in SMA Type II
  • 100% develop scoliosis
  • Posterior spinal fusion improves sitting
Clinical Implication: Scoliosis surgery is beneficial.
Source: J Pediatr Orthop 2003

Level IV
📚 Chua et al
Key Findings:
  • Perioperative complications in neuromuscular scoliosis
  • High complication rate in SMA
  • Experienced team essential
Clinical Implication: High-risk surgery requires specialized care.
Source: Spine 2015

Viva Scenarios

Practice these scenarios to excel in your viva examination

VIVA SCENARIOStandard

The Infant with SMA Type I and Scoliosis

EXAMINER

"8-month-old with confirmed SMA Type I. Has received gene therapy. Now developing thoracolumbar scoliosis of 30 degrees."

EXCEPTIONAL ANSWER

This child has benefited from gene therapy but is still at risk for orthopaedic complications. At 30 degrees, I would observe closely. Bracing (TLSO) can be considered for positioning but is unlikely to prevent progression. Given the young age, if the curve progresses rapidly, **growing rod constructs (e.g., MAGEC)** may be considered to allow continued growth. However, any surgery has high perioperative risk. Close collaboration with neurology and respiratory teams is essential. I would monitor closely with serial X-rays every 4-6 months.

KEY POINTS TO SCORE
Gene therapy has changed prognosis
Scoliosis still develops
Growing rods may be needed
COMMON TRAPS
✗Ignoring scoliosis progression
✗Rushing to fusion in a young child
LIKELY FOLLOW-UPS
"At what curve magnitude would you consider surgery?"
VIVA SCENARIOStandard

The Adolescent with SMA Type II and Severe Scoliosis

EXAMINER

"14-year-old with SMA Type II. Wheelchair-dependent. Thoracolumbar scoliosis of 80 degrees with pelvic obliquity. FVC 35%."

EXCEPTIONAL ANSWER

This is a challenging case. The scoliosis is severe and the pulmonary function is significantly impaired. However, surgery may still be beneficial. I would assess sitting balance and quality of life. Preoperative optimization with the respiratory team (BiPAP optimization, cough assist) is critical. Surgery: **Posterior spinal fusion from T2 to pelvis** with pelvic fixation (S2-alar-iliac or iliac screws). Expect prolonged ICU stay and potential need for postoperative ventilation. The goal is improved sitting balance and halting curve progression. I would ensure informed consent reflects the high perioperative risk.

KEY POINTS TO SCORE
High-risk surgery
Pelvic fixation essential
Preoperative respiratory optimization
COMMON TRAPS
✗Refusing surgery due to low FVC
✗Not including pelvis in fusion
LIKELY FOLLOW-UPS
"What is the threshold FVC for safe surgery?"
VIVA SCENARIOStandard

Hip Dysplasia in SMA

EXAMINER

"Same patient also has bilateral hip subluxation on X-ray. Is this an indication for surgery?"

EXCEPTIONAL ANSWER

In SMA, **hip dysplasia is common but surgery is rarely indicated**. The hips are often asymptomatic even when subluxated. Surgery (reconstruction) has high failure rates in this population and the functional gains are minimal since the patient is not walking. I would observe and manage with seating adaptations if there is discomfort. Pain is rare but if present, salvage options like proximal femoral resection may be considered. I would not pursue reconstructive surgery.

KEY POINTS TO SCORE
Hip surgery rarely indicated in SMA
High failure rate, minimal functional benefit
Seating adaptations for comfort
COMMON TRAPS
✗Performing hip reconstruction surgery
✗Over-treating asymptomatic hips
LIKELY FOLLOW-UPS
"What are the seating adaptations?"

MCQ Practice Points

Genetics MCQ

Q: What gene is mutated in SMA? A: SMN1 (Survival Motor Neuron 1) on chromosome 5q.

Classification MCQ

Q: A child who can sit but never walks has which SMA type? A: Type II.

Prognosis MCQ

Q: What correlates with disease severity? A: SMN2 copy number - more copies = milder phenotype.

Treatment MCQ

Q: What is the mechanism of nusinersen (Spinraza)? A: Antisense oligonucleotide that increases SMN2 expression.

Scoliosis Surgery

Q: What is the extent of fusion in SMA scoliosis surgery? A: T2 to pelvis with pelvic fixation (S2-alar-iliac or iliac screws).

Hip Management

Q: How should hip dysplasia in SMA be managed? A: Observation - surgery rarely indicated due to high failure rate and minimal functional benefit.

Australian Context

  • Newborn Screening: SMA is now included in newborn screening in some Australian states.
  • PBS Access: Gene therapy (Zolgensma) and nusinersen (Spinraza) are PBS-listed with criteria.
  • Multidisciplinary Care: Managed in specialized neuromuscular clinics (e.g., Royal Children's Hospital, Westmead).
  • Scoliosis Surgery: Performed at tertiary pediatric spine centers.

SPINAL MUSCULAR ATROPHY

High-Yield Exam Summary

GENETICS

  • •SMN1 Mutation
  • •Autosomal Recessive
  • •SMN2 Copies = Prognosis
  • •Chromosome 5q

TYPES

  • •I: Never sits
  • •II: Sits, never walks
  • •III: Walks
  • •IV: Adult onset

ORTHO ISSUES

  • •Scoliosis (universal)
  • •Hip Dysplasia
  • •Contractures
  • •Pelvic Obliquity

SCOLIOSIS SURGERY

  • •T2 to Pelvis Fusion
  • •Pelvic Fixation Essential
  • •High Perioperative Risk
  • •ICU Postop Care

MEDICAL THERAPY

  • •Onasemnogene (Gene Therapy)
  • •Nusinersen (Intrathecal)
  • •Risdiplam (Oral)
  • •Early Treatment Best

EXAM PEARLS

  • •Tongue Fasciculations
  • •100% Scoliosis in Type I/II
  • •Hip Surgery Rarely Indicated
  • •FVC Monitoring Critical

Self-Assessment Quiz

Differential Diagnosis

Similar Neuromuscular Conditions:

  • Duchenne Muscular Dystrophy: X-linked, CK elevated, dystrophin gene mutation.
  • Congenital Myopathies: Various types, muscle biopsy diagnostic.
  • Spinal Cord Lesions: MRI differentiates.
  • Metabolic Myopathies: Specific enzyme deficiencies.

Key Differentiators for SMA:

  • Genetic testing (SMN1 mutation) is confirmatory.
  • Tongue fasciculations are characteristic.
  • Normal CK (or mildly elevated).
  • Reflexes absent/diminished.

Additional Quiz Questions

Quick Stats
Reading Time42 min
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