A patient with a spinal cord injury at T10 shows absent voluntary movement and sensation below the lesion, but has exaggerated deep tendon reflexes in both legs one month after injury. Which mechanism explains the DTR hyperreflexia?
- A Loss of descending excitatory pathways reduces reflex arc activity, but Ia afferents upregulate
- B Peripheral nerve axons regenerate faster below the injury, enhancing Ia afferent signaling
- C Interruption of descending corticospinal and reticulospinal inhibitory pathways releases alpha motor neurons from supraspinal control ✓
- D Gamma motor neuron activity is permanently increased by the spinal shock recovery phase
Explanation
After the initial period of spinal shock (flaccid paralysis), recovery reveals hyperreflexia due to release of segmental reflex arcs from descending corticospinal and reticulospinal inhibition. These supraspinal tracts normally modulate alpha and gamma motor neuron excitability; their interruption disinhibits the stretch reflex circuitry, resulting in hyperreflexia, clonus, and extensor plantar responses—hallmarks of upper motor neuron lesions.
Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.
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