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, October 26, 2008

Abnormalities in autonomic cardiovascular control can impair blood supply to the brain

Abnormalities in autonomic cardiovascular control can impair blood supply to the brain and produce syncope in two different disorders: autonomic failure and neurally mediated syncope. In autonomic failure, sympathetic efferent activity is chronically impaired so that vasoconstriction is deficient, upon standing blood pressure always falls (i.e., orthostatic hypotension), and syncope or presyncope occurs. Conversely, in neurally mediated syncope, the failure of sympathetic efferent casoconstrictor traffic (and hypotension) occurs episodically and in response to a trigger. Between syncopal episodes, patients with neurally mediated syncope have normal blood pressure and orthostatic tolerance. This article reviews the characteristics of autonomic failure and describes in more detail the pathophysiology, diagnosis, and treatment of neurally mediated syncope.

Neurally Mediated Syncope and Syncope Due to Autonomic Failure: Differences and Similarities.

Review Articles

Journal of Clinical Neurophysiology. Neurocardiogenic Syncope. 14(3):183-196, May 1997.
Kaufmann, Horacio

Cannon phenomenon after sympathectomy

Sympathectomy in such cases causes classic Cannon phenomenon. This physiological phenomenon refers to the fact that the end organ that is controlled by sympathetic fibers will become uninhibited in it's chemical dysfunction. As a result, even though the sympathetic nerve fibers are not contributing to acetylcholine or norepinephrine secretion at the area of nerve damage, the partially damaged sensory nerves become uninhibited with resultant increase pain input.

In patients who have had sympathectomy, thermography shows an increase iof temperature in the focus of ephatic nerve damage (Cannon phenomenon) with secondary increase of pain and discomfort.

Chronic Pain: Reflex Sympathetic Dystrophy : Prevention and Management
By Hooshang Hooshmand
Published by CRC Press, 1993