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 20, 2008

Clinical Investiation

To validate the method, healthy volunteers underwent 6-18F-fluorodopamine scanning of the head, thorax, and abdomen, with or without treatment with desipramine to block sympathoneural uptake of catecholamines. 13N-Ammonia scanning was used to address possible group differences in 6-18F-fluorodopamine delivery by blood perfusion. Results: Desipramine treatment was associated with decreased 6-18F-fluorodopamine–derived radioactivity in the heart, renal cortex, and thyroid gland but not in the liver, spleen, renal pelvis, or salivary glands. Both the PD+OH group and the PAF group had decreased 6-18F-fluorodopamine–derived radioactivity in the heart (P <> (P = 0.02 and P = 0.005, respectively). The PD+OH group also had decreased radioactivity in the thyroid gland (P = 0.01). Neither group had decreased radioactivity in the other organs, after correction for 13N-ammonia–derived radioactivity. Conclusion: 6-18F-Fluorodopamine scanning visualizes sympathetic innervation in the heart, renal cortex, and thyroid gland. Both PD+OH and PAF involve decreased noradrenergic innervation that is most prominent in the heart but is also detectable in extracardiac organs.
Dnyanesh N. Tipre, MPharm, PhD and David S. Goldstein, MD, PhD

Clinical Neurocardiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland

JNM 2005 46