Reflexes in Myasthenia Gravis
Deep tendon reflexes are characteristically normal and preserved in myasthenia gravis, which is a critical distinguishing feature from other neuromuscular disorders.
Key Reflex Characteristics
Reflexes remain intact throughout the disease course in myasthenia gravis, regardless of the severity of muscle weakness 1, 2. This is because the pathology affects the postsynaptic neuromuscular junction (specifically acetylcholine receptors), not the reflex arc itself 2, 3.
Distinguishing Features from Other Neuromuscular Conditions
The preservation of normal reflexes helps differentiate myasthenia gravis from:
- Guillain-Barré syndrome: characterized by decreased or absent reflexes in most patients at presentation and almost all patients at nadir 4, 5
- Other peripheral neuropathies: typically show diminished or absent reflexes 6
- Motor neuron diseases: may show hyperreflexia or hyporeflexia depending on upper vs. lower motor neuron involvement 1
Clinical Examination Pearls
When examining a patient with suspected myasthenia gravis, you should find:
- Normal deep tendon reflexes despite significant muscle weakness 1
- Normal sensation throughout 1
- Absence of autonomic symptoms (unlike Guillain-Barré syndrome which can have dysautonomia) 1
- No fasciculations (unlike motor neuron disease) 1
- Worsening weakness with repetitive motion (fatigability) 7, 3
Common Diagnostic Pitfalls
Do not dismiss myasthenia gravis because reflexes are normal - this is actually an expected finding and supports the diagnosis when combined with fatigable weakness 1. The presence of normal reflexes in a patient with significant muscle weakness should raise suspicion for a neuromuscular junction disorder rather than a neuropathy or myopathy 1.
Pupils are typically not affected in myasthenia gravis, though rare cases may show impaired or slow pupillary responses 6. This contrasts with certain autonomic neuropathies where pupillary dysfunction is more common 6.
Clinical Implications
The preservation of reflexes in myasthenia gravis reflects the specific pathophysiology: autoantibodies target postsynaptic acetylcholine receptors (80-85% of cases), muscle-specific kinase (5-8%), or other neuromuscular junction proteins, but the reflex arc remains functionally intact 2, 3. This allows the monosynaptic stretch reflex to function normally even when voluntary muscle contraction is severely impaired 2.