The peripheral arterial vasoconstriction and hypertension activates the baroreceptors, resulting in a parasympathetic surge originating in the central nervous system, which inhibits the sympathetic outflow; however, the parasympathetic signal is unable to transmit below the level of the spinal cord lesion. This results in vasodilation, flushing, pupillary constriction and nasal stuffiness above the spinal lesion, while theres piloerection, pale and cool skin below the lesion due to the prevailing sympathetic outflow. The reason this issue is much more prominent for lesions at or above the T6 level is because the Splanchnic nerves emerge from the T5 level and below. Loss of brains control over T6 and below causes splanchnic arteries to reflexively vasoconstrict and since the Splanchnic arteries are the bodys largest reservoir for circulating blood, their vasocontriction dramatically affects the blood pressure of the body. Diagnosis
The symptoms are usually not subtle, although asymptomatic events have been documented. Autonomic dysreflexia differs from autonomic instability, the various modest cardiac and neurological changes that accompany a spinal cord injury, including bradycardia, orthostatic hypotension, and ambient temperature intolerance. In autonomic dysreflexia, patients will experience hypertension, sweating, spasms (sometimes severe spasms) and erythema (more likely in upper extremities) and may experience headaches and blurred vision. Mortality is rare with AD, but morbidity such as stroke, retinal hemorrhage and pulmonary edema if left untreated can be quite severe. Older patients with very incomplete spinal cord injuries and systolic hypertension without symptoms are usually experiencing essential hypertension, not autonomic dysreflexia.
Additional organs that may be affected include the kidneys and retinas of the eyes. Causes
The first episode of autonomic dysreflexia may occur weeks to years after spinal cord injury takes place, but most people at risk (80%) develop their first episode within the first year after injury. Early AD tends to be associated with less severe increases in blood pressure.One common causative factor may be an undetected urinary tract infection. The difficulty in assessing this may be complicated with the usage of indwelling or suprapubic catheters. Other causes include medication side effects and various disease processes. The use of stimulants such as cocaine and amphetamines which can result in urinary retention, and the use of CNS depressants and other psychoactive drugs can also lead to urinary retention and constipation thus leading to autonomic dysreflexia when in use over an extended period of time. Pain
Current scientific literature suggests that noxious (painful) stimuli are the primary initiators of AD. (Note: Not all noxious stimuli will cause AD. Some otherwise severe noxious stimuli in unaffected people, e.g. broken bones, may not result in AD, and may in fact even go unnoticed.) However, different studies have found that activation of pain receptors in muscle and skin below the lesion in spinal cord injured individuals did not trigger AD. These studies suggests that not all noxious stimuli are reliable triggers of AD, and because non-noxious stimuli can also trigger AD, attribution of an episode of AD to noxious stimuli may cause clinicians to overlook underlying non-noxious triggers.