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

Thursday, September 4, 2008

Headache Following Cervical Sympathectomy - Harvard Medical School

Headache Following Cervical Sympathectomy and Results of a Blood Flow Study in the Cat
Egilius L. H. Spierings, MD, PhD
Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass.
Address all correspondence to Dr. Egilius L. H. Spierings, 25 Walnut Street, Suite 102, Wellesley Hills, MA 02481-2106.

Background.—A patient developed severe, continuous, unilateral headache that was "vascular" in nature, following cervical sympathectomy.

Objective.—To determine the changes in cranial blood flow in the cat following lesioning and stimulation of the cervical sympathetic nerve.

Method.—Carotid blood flow was determined by electromagnetic flowmetry and its tissue distribution by intra-arterial injection of 15-μm radioactive microspheres.

Results.—Following sympathetic lesioning, an increase in carotid blood flow was observed and reversed with stimulation. The distribution of carotid blood flow changed for the brain only, maintaining relatively constant tissue perfusion.

Conclusion.—An increase in cerebral blood flow could not have accounted for the sympathectomy-induced headache. Dilation of major cerebral arteries and cranial noncerebral vasodilation probably constitutes its mechanism.

Accepted for publication October 6, 2002