Autonomic dysreflexia
[6] Hypertension in AD may result in mild symptoms, such as sweating above the lesion level, goosebumps, blurred vision, or headache.
[7] Severe symptoms may result in life-threatening complications including seizure, intracranial bleeds (stroke), myocardial infarction, and retinal detachment.
[9] The noxious stimuli activate a sympathetic surge that travels through intact peripheral nerves, resulting in systemic vasoconstriction below the level of the spinal cord lesion.
However, the parasympathetic signal is unable to transmit below the level of the spinal cord lesion to reduce elevated blood pressure.
[10] This can result in bradycardia, tachycardia, vasodilation, flushing, pupillary constriction and nasal stuffiness above the spinal lesion.
This entails sitting the patient upright, removing any constrictive clothing (including abdominal binders and support stockings), and rechecking blood pressure often.
[8] If systolic blood pressure remains elevated (over 150 mm Hg) after these steps, fast-acting short-duration antihypertensives are considered,[13] while other inciting causes must be investigated for the symptoms to resolve.
An elevation of 20 mm Hg over baseline systolic blood pressure, with a potential source below the neurological level of injury, meets the current definition of dysreflexia.
Complications of severe acute hypertension can include seizures, pulmonary edema, myocardial infarction, or cerebral hemorrhage.
[16] The first episode of autonomic dysreflexia may occur weeks to years after the spinal cord injury takes place.
In the absence of clear triggering factors, recurrent episodes of AD can be important signs that there is an underlying pathology in a patient that has not yet been discovered.
[11] The supraspinal neurons act on the SPN and its tonic firing by modulating its action on the peripheral sympathetic chain ganglia and the adrenal medulla.
[11][21] In a patient with a spinal cord lesion, the descending autonomic pathways that are responsible for the supraspinal communication with the SPN are interrupted.
This parasympathetic signal is unable to transmit below the level of the spinal cord lesion and there is a heightened sympathetic response.
[25] An essential step to diagnosing AD is careful monitoring of blood pressure and other vital sign changes.
If the noxious stimuli cannot be identified or the systolic blood pressure remains above 150 mmHg, then pharmacologic treatment may be needed.
[30] If the episode of AD is triggered by bowel or bladder irritants, topical analgesics such as lidocaine and bupivacaine are commonly used.
Mortality is rare with AD, but morbidities such as stroke, retinal hemorrhage, and pulmonary edema if left untreated can be quite severe.
Overall, the goal of these research projects involves minimizing complications that result from late detection of autonomic dysreflexia.
Some research is aimed at investigating the use of non-invasive sensors to track nerve activity to detect signs of AD.
[35] Results from a study showed that AI can serve as another non-invasive tool in combination with sensors that track nerve activity.
While it is understood that spinal cord injury results in inhibited parasympathetic surges and a heightened sympathetic response that can lead to AD, other details are yet to be defined.
