A patient with a complete spinal cord lesion at T10 develops autonomic dysreflexia after the period of spinal shock. This is characterized by sudden hypertension triggered by a noxious stimulus below the lesion. The mechanism involves:

• A Loss of cardiac vagal tone causing reflex tachycardia and increased cardiac output
• B Excessive adrenal epinephrine release due to de-afferentation supersensitivity
• C Upregulation of alpha-2 adrenergic receptors on vascular smooth muscle enhancing sensitivity
• D Uninhibited spinal sympathetic reflexes below the lesion causing massive vasoconstriction without supraspinal inhibition ✓

Explanation

After spinal shock resolves, spinal interneuronal circuits below the lesion reorganize. A noxious stimulus below the lesion (e.g., bladder distension, fecal impaction) activates spinal sympathetic reflexes, causing massive splanchnic and peripheral vasoconstriction. Normally, descending inhibitory signals from the hypothalamus and brainstem modulate these reflexes; with a complete cord lesion, this supraspinal inhibition is absent. Baroreceptors detect the hypertension and attempt to compensate by increasing vagal tone (bradycardia) and inhibiting sympathetics above the lesion, but the isolated spinal cord below continues its sympathetic discharge.

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

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Written and medically reviewed by the StethoPrep medical team.