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 13, 2008

reduced antibody responses to T-dependent antigens

It has been exhaustively demonstrated that the regions in which lymphocytes T cells reside, and through which they recirculate, receive direct sympathetic neural input. Therefore, the immune system can be considered “hard-wired” to the brain. Chemical sympathectomy of adult mice resulted in reduced antibody responses to T-dependent antigens. The interaction between sympathetic NA nerve fibers and cells of the immune system has been shown through the distribution of tyrosine hydrolase (TH+) nerve fibers among lymphocytes and macrophages in lymphoid organs, the expression of adrenoceptors on cells of the immune system, and the immunomodulatory effects of NA. In old rats, a conspicuous decline in NA innervation and NA contents is observed in the splenic white pulp as well as in the cell bodies in superior celiac-mesenteric ganglia that provide preganglionic sympathetic innervation to the spleen (Arnason, 1993; Carlson, Fox et al., 1997; Madden. Felten et al., 1994a; Roszman and Carlson, 1991). Paralleling these alterations in sympathetic NA neuronal activity is an age-related loss of T cell mediated immune responses, including reduced T cell proliferation and IL-2 production by antigen- and mitogen-stimulated lymphocytes. Treatment of these rats with drugs inducing noradrenergic regeneration and re-innervation reverted the rats’ immune abnormalities (Tang, Shankar et al., 1999; Thyaga-Rajan, Madden et al., 1999). Noradrenergic innervation of the spleen is responsible for a significant increase of gamma-interferon, IL-2 and tumor necrosis factor alpha, the three Th-1 cytokines, and a lowering of IL-4, IL-5 and IL-10 (TH-2 cytokines) production (Carlson, Fox et al., 1997; Madden, Moynihan et al., 1994b; Spengler, Allen et al., 1990). Other evidence showed that elevated plasma NA concentrations increased the level of Th-1 cytokines (Kappel, Poulsen et al., 1998; Ross, Williams et al., 1987). These and other findings demonstrate that the noradrenergic innervation of bone marrow is functionally dynamic and is responsive to central activation. Furthermore, these results lend credence to the premise that neural mechanisms participate in regulating lymphopoietic cellular events.

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