Autonomic dysreflexia (AD) is a potential medical emergency classically characterized by uncontrolled hypertension and bradycardia, although tachycardia is known to commonly occur. AD occurs most often in individuals with spinal cord injuries with lesions at or above the T6 spinal cord level, although it has been reported in patients with lesions as low as T10. Guillain–Barré syndrome may also cause autonomic dysreflexia.The uncontrolled hypertension in AD may result in mild symptoms, such as sweating above the lesion level, goosebumps, blurred vision, or headache; However, severe hypertension may result in potentially life-threatening complications including seizure, intracranial bleed, or retinal detachment.AD is triggered by either noxious or non-noxious stimuli, resulting in sympathetic stimulation and hyperactivity. The most common causes include bladder or bowel over-distension, from urinary retention and fecal compaction, respectively. The resulting sympathetic surge transmits through intact peripheral nerves, resulting in systemic vasoconstriction below the level of the spinal cord lesion. The peripheral arterial vasoconstriction and hypertension activates the baroreceptors, resulting in a parasympathetic surge originating in the central nervous system to inhibit the sympathetic outflow; however, the parasympathetic signal is unable to transmit below the level of the spinal cord lesion.
As a result, non-noxious trigger factors remain undetected, prolonging an episode of AD. They concluded that when deducing the potential causes of AD it is important to consider non-noxious sources of stimulation in addition to noxious triggers. Current assessment of autonomic dysreflexia in patients with known causative factors include palpation of the bladder and bowel and can also include bladder scan. Mechanism
Supraspinal vasomotor neurons send projections to the intermediolateral cell column, which is composed of sympathetic preganglionic neurons (SPN) through the T1-L2 segments. The supraspinal neurons act on the SPN and its tonic firing, modulating its action on the peripheral sympathetic chain ganglia and the adrenal medulla. The sympathetic ganglia act directly on the blood vessels they innervate throughout the body, controlling vessel diameter and resistance, while the adrenal medulla indirectly controls the same action through the release of epinephrine and norepinephrine. The descending autonomic pathways, which are responsible for the supraspinal communication with the SPN, are interrupted resulting in decreased sympathetic outflow below the level of the injury. In this circumstance, the SPN is controlled only by spinal influences. The first couple of weeks after a spinal injury, the decreased sympathetic outflow causes reduced blood pressure and sympathetic reflex. Eventually, synaptic reorganization and plasticity of SPN develops into an overly sensitive state, which results in abnormal reflex activation of SPN due to afferent stimuli, such as bowel or bladder distension. Reflex activation results in systemic vasoconstriction below the spinal cord disruption.