A patient with a complete cord lesion at T6 develops spastic paraplegia and exaggerated deep tendon reflexes below the lesion after the initial spinal shock phase. The return of hyperreflexia is best explained by:

• A Denervation supersensitivity of spinal interneurons and alpha motor neurons; upregulation of glutamate receptors combined with loss of descending inhibitory control ✓
• B Regeneration of corticospinal tract axons through the lesion restoring partial voluntary control
• C Collateral sprouting of sensory afferents that produces an anatomically amplified reflex arc
• D Increased tonic activity of gamma motor neurons driving spindle sensitivity via intact spinoreticular pathways

Explanation

After spinal shock resolves (days to weeks), the isolated spinal cord below the lesion shows increased excitability. Loss of descending inhibitory (corticospinal, reticulospinal, vestibulospinal) inputs combined with denervation supersensitivity — upregulation of glutamate and monoamine receptors on motor neurons and interneurons — leads to hyperreflexia and spasticity. Increased stretch reflex gain results from enhanced alpha motor neuron responses to Ia afferent input. The descending tracts do not regenerate in the adult CNS. Collateral sprouting contributes to some phenomena but is not the primary mechanism for early spasticity.

Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.

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Written and medically reviewed by the StethoPrep medical team.