Abstract
The most important complication of spinal cord lesions above T6 level is the phenomenon of Autonomic Hyperreflexia (AH). Symptoms and signs of AH result from the predominant parasympathetic excitation above the level of injury, and sympathetic excitation below the level of injury. Various noxious and nonnoxious stimuli below the level of injury can thus trigger off a mass autonomic response. The main triggering factor of AH is related with the urinary tract. The main treatment of AH is removal of the triggering factors. The development of intraoperative AH and hypertension can be prevented either by general anesthesia, which blunts autonomic reflexes, or regional anesthesia (spinal or epidural), which blocks afferent and autonomic efferent neural impulses.
Highlights
The most important complication of spinal cord lesions above T6 level is the phenomenon of Autonomic Hyperreflexia (AH)
The Autonomic Hyperreflexia (AH) was first described in 1860 by Hilton [1] and the neuro-anatomical pathway was suggested by Kurnick in 1956 [2]
AH is developed in patients after severe spinal cord injury (SCI) above T6 level as a result of exaggerated spinal sympathetic excitation
Summary
AH is initiated by afferent impulses reaching the isolated spinal cord below the level of the spinal cord damage. The reason that AH is a feature of lesions at the T6 level or above is related with splanchnic circulation response to this sympathetic overactivity The latter activity below the injury level results a splanchnic and peripheral vasoconstriction and causes hypertension. Cord damage at T6 level or above is accompanied by increased secretion of adrenal medullary cathecholamines suggesting adrenaline implication in the development of the hyperreflexic responses as well as activation of adrenal sympathetic preganglionic neurons by visceral afferences leading to severe AH. Bors and French [9] reported that the greatest responses were produced by stimuli with the most caudal root levels below the region of SCI This explains why pelvic visceral stimulation is the most commonly implicated [1,7,10,11]. During surgery under general anesthesia, various tiggers can precipitate AH, such as tracheal intubation or extubation, pain and other surgical stimuli [4,5,7]
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