The amount of compensatory sweating depends on the patient, the damage that the white rami communicans incurs, and the amount of cell body reorganization in the spinal cord after surgery.
Other potential complications include inadequate resection of the ganglia, gustatory sweating, pneumothorax, cardiac dysfunction, post-operative pain, and finally Horner’s syndrome secondary to resection of the stellate ganglion.
www.ubcmj.com/pdf/ubcmj_2_1_2010_24-29.pdf

After severing the cervical sympathetic trunk, the cells of the cervical sympathetic ganglion undergo transneuronic degeneration
After severing the sympathetic trunk, the cells of its origin undergo complete disintegration within a year.
http://onlinelibrary.wiley.com/doi/10.1111/j.1439-0442.1967.tb00255.x/abstract

Saturday, June 20, 2009

blockade of the sympathetic nervous system substantially degrades ligament

THE PERIPHERAL NERVOUS SYSTEM (PNS) has three primary functions: 1) relaying sensorimotor information to and from the central nervous system; 2) controlling local blood flow; and 3) influencing inflammatory, proliferative, and reparative processes in injured tissue. In the PNS, neurogenic factors, such as neuropeptides and neurotransmitters, are chemical agents that mediate these functions (35). These factors can influence PNS-related actions by modulating immune cell responses, cytokine response, and local blood flow (5, 35). Although neurogenic factors are released from stimulated nerve endings, their actions are not restricted to the point of stimulation (10). For example, the autonomic neuropeptides vasoactive intestinal peptide (VIP) and neuropeptide Y (NPY) can have angiogenic, vasoregulatory, and cell proliferative actions hours to days after release from nerve endings (35, 44). In addition, Ackermann et al. (1) recently reported a role for peripheral neuropeptides in healing of tendon tissue. The above observations make it likely that these neurogenic factors play an important role in tissue homeostasis.

Clinically, chemical inhibition of the PNS is used to manage joint pain. Chemical blockade of the sympathetic nervous system is often accomplished through the administration of guanethidine. Guanethidine blocks the release and subsequent reuptake of norepinephrine (NE) (a major sympathetic neurotransmitter) in patients with osteoarthritis, rheumatoid arthritis, and reflex sympathetic dystrophy (12, 13, 24, 38, 40). This treatment, while effective in relieving pain, may have undesirable effects on connective tissues, because it alters the normal concentration of neurogenic factors.

Growing anatomic and physiological evidence suggest that the PNS is important to ligament and joint homeostasis.
Denervation of peripheral nerves leads to decreased healing of the MCL and promotes the onset of osteoarthritis (22, 34). Partial injury to the MCL can lead to increases in vascular volume, a factor that is largely controlled by ligament innervation (7). During periods of chronic overuse or disuse, homeostatic changes can be detrimental to the structural integrity of ligaments. Although the above evidence suggests that peripheral nerves play an essential role in ligament homeostasis, few studies exist that directly investigate this role.

J Appl Physiol 96: 711-718, 2004