Immunology · Year 2 · from Immunology

Case 3: Myasthenia Gravis

Patient Demographics

  • Age: 32 years old
  • Sex: Female
  • Ethnicity: Asian

Chief Complaint

Double vision and difficulty chewing for 2 months

History of Present Illness

A 32-year-old woman presents with intermittent double vision (diplopia) and difficulty chewing tough foods that has progressed over 2 months. She first noticed drooping of her eyelids (ptosis) in the evening after long days at work, which initially improved after rest. Over time, she developed horizontal diplopia and her jaw feels "tired" after eating. She denies limb weakness, difficulty breathing, or swallowing problems. Symptoms consistently worsen throughout the day and improve after rest.

Past Medical History

  • Graves disease diagnosed 3 years ago (treated with radioiodine ablation)
  • Currently on levothyroxine

Physical Examination

  • General: Alert woman, appears comfortable
  • Vital Signs: Normal
  • HEENT: Bilateral ptosis, worse on right; positive fatigue test (ptosis worsens with sustained upgaze); diplopia on lateral gaze
  • Cranial nerves: Otherwise intact; no facial weakness; voice normal
  • Neck: Well-healed thyroidectomy scar
  • Motor: 5/5 strength in all extremities; no fatigability with repetitive testing
  • Sensory: Intact
  • Reflexes: 2+ throughout, symmetric

Diagnostic Testing

TestResultReference Range
Acetylcholine receptor antibodies18.5 nmol/L<0.4 nmol/L
Anti-MuSK antibodiesNegativeNegative
TSH2.1 mIU/L0.4-4.0 mIU/L
Repetitive nerve stimulation>10% decrement<10% decrement
CT chest3 cm anterior mediastinal massNormal

Diagnosis

Myasthenia Gravis (MG) with thymoma, ocular-predominant with bulbar involvement

Discussion

Myasthenia gravis is an antibody-mediated autoimmune disorder targeting the neuromuscular junction:

Immunopathogenesis:

  • Anti-AChR antibodies (present in 85% of generalized MG) cause:
  • Accelerated receptor internalization and degradation
  • Complement-mediated destruction of postsynaptic membrane
  • Direct blockade of acetylcholine binding
  • Anti-MuSK antibodies (5-8%) cause impaired AChR clustering
  • Results in reduced safety factor at neuromuscular junction

This patient demonstrates classic features:

  • Fatigable weakness: Worse with use, improves with rest
  • Diurnal variation: Worse as day progresses
  • Preferential ocular/bulbar involvement: Ptosis, diplopia, jaw fatigue
  • Association with other autoimmune disease: Graves disease

Thymoma and MG:

  • Thymic abnormalities in 75% of MG patients
  • Thymoma in 10-15% (requires surgical resection)
  • Thymic hyperplasia in 60-65%
  • Thymectomy improves outcomes even without thymoma

MG classification by affected muscle groups:

ClassDescription
IOcular only
IIMild generalized
IIIModerate generalized
IVSevere generalized
VRequiring intubation

Treatment

  1. Symptomatic: Pyridostigmine (acetylcholinesterase inhibitor)
  2. Immunosuppression: Prednisone, azathioprine, or mycophenolate for generalized disease
  3. Thymectomy: Indicated for thymoma (mandatory) and non-thymoma MG under age 65
  4. Crisis management: IVIG or plasmapheresis for myasthenic crisis
  5. Monitor for respiratory compromise: Forced vital capacity
  6. Avoid medications that worsen MG: Aminoglycosides, beta-blockers, quinolones, magnesium

Myasthenic crisis warning signs: Dyspnea, weak cough, difficulty swallowing secretions

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