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

Monday, July 20, 2009

The angina-relieving effects of sympathetic blockade

In the 1930's it was recognised by neurosurgeons performing destructive sympathectomies for angina pectoris that local anaesthetic infiltration around the stellate ganglion often resulted in pain relief outlasting the duration of action of the local anaesthetic drug13. This observation has been more recently confirmed14, and is currently (June 1999) the subject of a large scale randomised double-blind placebo-controlled trial funded by the British Heart Foundation.

The pathogenesis of angina and myocardial infarction pain involves the activation of the afferent sympathetic pathway. A frequent and important consequence of pain (especially when severe) is the `flight or fight' response through activation of sympathetic efferents. The clinical image of the patient with an acute myocardial infarction (cold, clammy, sweaty, anxious, tachycardic) is secondary to this adrenergic activation. Therefore, angina might be regarded as the sensory component of a positive feedback loop, which cannot under these circumstances be conceived as resulting in benefit, and which may be considered to be a maladaption.

The angina-relieving effects of sympathetic blockade might be due to interference with this maladaptive feedback loop, in a similar manner to the way in which adenosine interrupts a re-entrant tachycardia. If such a loop exists, it may partly explain chronic refractory angina and the fact that temporary interruption of this pathway has a prolonged effect on pain14. Beneficial amelioration of angina can be achieved with repeated blocks14. There does not appear to be any predictability in the length of time a patient remains pain-free after successive blocks.

http://www.angina.org/source/pro/symp_block.htm