Sympathetic Nerve Block

Excerpt

The sympathetic autonomic nervous system (SANS) is spatially and pathophysiologically related to both acute and chronic pain. Acute generalized sympathetic activation, as occurs with the stress response, can temporarily increase the nociceptive threshold via a combination of neural and endocrine effects. Given its trophic and immunomodulatory function, the SANS can exert pro-inflammatory and pro-nociceptive effects, particularly at the tissue level. Blocking regional sympathetic efferent activity can indirectly relieve ischemic pain. Similarly, a regional blockade of sympathetic activity can directly interrupt the nociceptive transmission of pain from internal organs, as most general afferent visceral fibers travel with sympathetic nerves. The SANS may pathologically evolve into a major contributor of pain (“sympathetically mediated pain”), as occurs in the case of complex regional pain syndrome (CRPS).

Selective interventional blockade of sympathetic pathways is commonly used to treat ischemic pain or sympathetically mediated pain. Most large sympathetic ganglia and plexi are anatomically separate from somatic nerves in prevertebral and paravertebral regions, and thus are readily accessible to percutaneous interruption. When indicated, sympathetic blocks can provide significant analgesia without causing somatic sensory deficits; but blockade of visceral sympathetic outflow will shift the homeostatic balance in the target region toward parasympathetic prevalence, with corresponding physiologic effects.