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, April 19, 2008

The effect of noradrenaline, angiotensin II and vasopressin on blood flow and sensitivity to heat in capsaicin-treated skin

Peter D. Drummond1 Contact Information

(1) Psychology Department, Murdoch University, 6150, Western Australia, Australia

Received: 10 June 1997 Accepted: 16 October 1997

Abstract The effect of iontophoretically applied noradrenaline, angiotensin II and vasopressin on blood flow and sensitivity to heat was investigated in the capsaicin-treated forearms of 52 healthy volunteers. Non-specific effects of a 4-min saline iontophoresis were investigated in another 19 subjects. Pretreatment with phentolamine inhibited vasoconstriction and thermal hyperalgesia to noradrenaline, indicating that agr-adrenoceptors mediated these responses. The intensity of thermal hyperalgesia differed significantly across the following treatments: saline (heat pain threshold 1.1°C lower than at control sites), angiotensin II (3.4°C), noradrenaline (6.4°C), and vasopressin (9.0°C). Decreases in skin blood flow were significantly greater after the iontophoresis of noradrenaline (65% reduction from baseline) and vasopressin (68%) than after the iontophoresis of angiotensin II (45%). In contrast to the other two drugs, angiotensin II induced thermal hyperalgesia in proportion to the intensity of vasoconstriction. The findings suggest that iontophoretic currents induce minor non-specific thermal hyperalgesia. Angiotensin II appears to increase sensitivity to heat by an ischaemic mechanism, whereas an additional non-vascular influence contributes to thermal hyperalgesia induced by noradrenalinge and vasopressin. These mechanisms could contribute to hyperalgesia in chronic inflammatory or neuropathic pain syndromes. Clin Auton Res 8:87–93 © 1998 Lippincott-Raven Publishers