Segmental spinal sympathetic machinery: Implications for autonomic dysreflexia

The sympathetic nervous system has a critical role in maintenance of arterial blood pressure; regulation of regional blood flow; thermoregulation; and integrated response to exercise, disturbances in homeostasis, and external stressors. Together with the parasympathetic system, the sympathetic output participates in control of pupillary, gastrointestinal, bladder, and sexual organ function. The sympathetic preganglionic neurons (SPNs) form distinct functional subunits that initiate patterns of responses via their excitatory inputs to sympathetic ganglion neurons or the adrenal medulla. The SPNs are functionally heterogeneous and their electrophysiologic activity is regulated by descending inputs largely from the brainstem and hypothalamus, primary afferents from somatic or visceral receptors, and activity of local excitatory or inhibitory interneurons. Following complete spinal cord injury (SCI), typically above the T5 segmental level and interrupting the descending input to the segmental spinal sympathetic apparatus, there are plastic changes in the local circuitry controlling the SPNs. As a consequence, segmental somatic or visceral stimuli trigger excessive unpatterned sympathetic activity referred to as autonomic dysreflexia. In addition to preventing triggering stimuli, elucidation of these segmental pathophysiologic mechanisms may provide a rationale for management of this potentially life-threatening condition. There are comprehensive reviews on the properties and inputs of the SPNs and the pathophysiologic mechanisms of autonomic dysreflexia.1–5

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