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

Sunday, April 27, 2008

the sympathetic nervous system regulates the clinical and pathological manifestations of experimental autoimmune encephalomyelitis (EAE)

Neuropeptide Y (NPY) suppresses experimental autoimmune encephalomyelitis: NPY1 receptor-specific inhibition of autoreactive Th1 responses in vivo.
Sammy Bedoui, Sachiko Miyake, Youwei Lin, Katsuichi Miyamoto, Shinji Oki, Noriyuki Kawamura, Annette Beck-Sickinger, Stephan von Hörsten, Takashi Yamamura
Department of Immunology, National Institute of Neuroscience, NCNP, Ogawahigashi, Kodaira, Tokyo, Japan.
Prior studies have revealed that the sympathetic nervous system regulates the clinical and pathological manifestations of experimental autoimmune encephalomyelitis (EAE), an autoimmune disease model mediated by Th1 T cells. Although the regulatory role of catecholamines has been indicated in the previous works, it remained possible that other sympathetic neurotransmitters like neuropeptide Y (NPY) may also be involved in the regulation of EAE. Here we examined the effect of NPY and NPY receptor subtype-specific compounds on EAE, actively induced with myelin oligodendrocyte glycoprotein 35-55 in C57BL/6 mice. Our results revealed that exogenous NPY as well as NPY Y(1) receptor agonists significantly inhibited the induction of EAE, whereas a Y(5) receptor agonist or a combined treatment of NPY with a Y(1) receptor antagonist did not inhibit signs of EAE. These results indicate that the suppression of EAE by NPY is mediated via Y(1) receptors. Furthermore, treatment with the Y(1) receptor antagonist induced a significantly earlier onset of EAE, indicating a protective role of endogenous NPY in the induction phase of EAE. We also revealed a significant inhibition of myelin oligodendrocyte glycoprotein 35-55-specific Th1 response as well as a Th2 bias of the autoimmune T cells in mice treated with the Y(1) receptor agonist. Ex vivo analysis further demonstrated that autoimmune T cells are directly affected by NPY via Y(1) receptors. Taken together, we conclude that NPY is a potent immunomodulator involved in the regulation of the Th1-mediated autoimmune disease EAE.

J. Immunol. 2003 Oct 1;171 (7):3451-8 14500640 (P,S,E,B) Cited:3