The stretch reflex (myotatic reflex) is a monosynaptic reflex arc. A patient with an upper motor neuron lesion at T8 shows hyperreflexia of knee and ankle jerks. The mechanism of hyperreflexia after UMN lesion is:

• A Release from descending facilitatory inhibition that normally suppresses Ia afferent synaptic efficacy at the anterior horn cell
• B Increased sensitivity of muscle spindles due to descending gamma motor neuron activation unchecked by cortical control
• C Loss of descending inhibitory (especially corticospinal and reticulospinal) inputs normally controlling the excitability of Ia afferents and alpha motor neurons, plus loss of supraspinal inhibitory presynaptic control; spinal reflexes are released from supraspinal inhibition ✓
• D Proliferation of new synapses on alpha motor neurons from sprouting Ia afferents

Explanation

After an upper motor neuron (corticospinal, reticulospinal) lesion, the spinal cord below the lesion loses descending inhibitory control over the stretch reflex arc. Normally, descending pathways (especially reticulospinal tracts) tonically inhibit both alpha motor neurons and provide presynaptic inhibition of Ia afferent terminals in the spinal cord. Loss of this inhibitory tone releases the stretch reflex from supraspinal control, resulting in hyperreflexia. Additionally, gamma motor neurons, which set muscle spindle sensitivity, are released from normal descending modulation, further increasing spindle afferent activity. This explains the classical UMN syndrome: hyperreflexia, spasticity, clonus, Babinski sign, with preserved or increased muscle bulk (unlike LMN lesion causing hyporeflexia, flaccid paralysis, denervation atrophy).

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

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