http://www.ncbi.nlm.nih.gov/pubmed/10577971
dysregulation between the nervous and immune systems might contribute to disease development and progression
http://www.jleukbio.org/cgi/content/abstract/79/6/1093
Alterations in cytokine and antibody production following chemical sympathectomy
http://www.jimmunol.org/cgi/content/abstract/155/10/4613
cytokines mediate and control immune and inflammatory responses
http://www.ncbi.nlm.nih.gov/pubmed/16166805
Denervation resulted in increased production of tumor necrosis factor-α
linkinghub.elsevier.com/retrieve/pii/S0889159100906184
Tumor necrosis factor-a induces oligodendrocytes apoptosis
http://www.springerlink.com/content/mu032lj427l85701/
Oligodendrocyte apoptosis and primary demyelination
We demonstrate that local production of TNF (tumor necrosis factor) by central nervous system glia potently and selectively induces oligodendrocyte apoptosis and myelin vacuolation in the context of an intact blood-brain barrier and absence of immune cell infiltration into the central nervous system parenchyma. Interestingly, primary demyelination then develops in a classical manner in the presence of large numbers of recruited phagocytic macrophages, possibly the result of concomitant pro-inflammatory effects of TNF in the central nervous system, and lesions progress into acute or chronic MS-type plaques with axonal damage, focal blood-brain barrier disruption, and considerable oligodendrocyte loss. Both the cytotoxic and inflammatory effects of TNF were abrogated in mice genetically deficient for the p55TNF receptor demonstrating a dominant role for p55TNF receptor-signaling pathways in TNF-mediated pathology.
http://www.ncbi.nlm.nih.gov/pubmed/9736029
Sympathectomy induces adrenergic excitability of cutaneous C-fiber nociceptors
nerve damage causes an inflammatory response
eicosanoids; these mediators may contribute to the hyperalgesia which results from nerve injury. The cell types most likely to be responsible include macrophages and postganglionic sympathetic neurones.
http://www.springerlink.com/content/pjh3832058475340/
D. J. Tracey1 J. S. Walker1
School of Anatomy, University of New South Wales, 2052 Sydney, NSW, Australia
The brain and the immune system are the two major adaptive systems of the body. During an immune response the brain and the immune system “talk to each other” and this process is essential for maintaininghomeostasis. Two major pathway systems are involved in this cross-talk: the hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic nervous system (SNS). This overview focuses on the role of SNS in neuroimmune interactions, an area that has received much less attention than the role of HPA axis. Evidence accumulated over the last 20 years suggests that norepinephrine (NE) fulfills the criteria for neurotransmitter/neuromodulator in lymphoid organs.
http://pharmrev.aspetjournals.org/content/52/4/595.abstract
The effects of atropine and chronic sympathectomy on maximal parasympathetic stimulation of parotid saliva in rats
http://jp.physoc.org/content/403/1/105.abstract
PARAPLEGIA AS A COMPLICATION OF SYMPATHECTOMY FOR HYPERTENSION
After a search of the literature and a number of of informal inquiries among our colleagues, we were surprised to find that such an occurrence is not as unusual as we had believed. Bassett, in 1948, reporting on his experience with sympathectomy in the treatment of hypertension, stated:"we have had four cases of thrombosis of the anterior spinal artery with resultant permanent residual ischemic myelitis." Poppen, in a personal communication, has stated that, although this complication has not occurred in his own experience, three cases have been brought to his attention in which paraplegia followed thoraco-lumbar sympathectomy for hypertension. Therefore, we have knowledge of eight cases in which a catastrophe followed an elective operation which has enjoyed wide usage during the past decade.
Annals of Surgery:
Effect of sympathectomy on the expression of NMDA receptors in the spinal cord
J Neurol Sci (1999) 169: 156-60.
http://www.ionchannels.org/showabstract.php?pmid=10540025
signs of degeneration can already be recog- nized in the myelinated as well as in the unmyelinated axons. 48 h after sympathectomy
A correlation of the findings of cytoarchitectonics and sympathectomy with fiber degeneration folowing dorsal rhizotomy
http://www3.interscience.wiley.com/journal/109712470/abstract
R-R variations, a test of autonomic dysfunction
Acta Neurologica Scandinavica
http://www3.interscience.wiley.com/journal/121523081/abstract?CRETRY=1&SRETRY=0
Risk of bradycardia after endoscopic electrocautery of the upper thoracic sympathetic ganglia
http://www.ncbi.nlm.nih.gov/pubmed/10885235
the most pronounced feature is a mental change
Sympathectomy in Relation to Meniere's Disease, Nerve Deafness
and Tinnitus. A Report on 110 Cases
By E. R. GARNETT PASSE, F.R.C.S., F.A.C.S.
1952, Vol. 42, No. 1-2, Pages 133-151