nerve damage causes an inflammatory response

Damage to peripheral nerves often results in pain and hyperalgesia. We suggest that nerve damage causes an inflammatory response in which cells associated with the nerve release inflammatory mediators such as
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

Chronic bilateral postganglionic sympathectomy (4-6 weeks duration) caused a drastic reduction in the capacity of the gland to secrete saliva in response to parasympathetic stimulation, reaching only one-third of that from normal animals. The initial output of amylase was greater than in normal animals but the total output was similar. The control unstimulated sympathectomized glands appeared similar morphologically to normal resting glands. However, on the parasympathetically stimulated side, besides the usual amount of acinar degranulation, there was also a conspicuous development of acinar vacuolation, not seen in the other groups of animals.

http://jp.physoc.org/content/403/1/105.abstract

PARAPLEGIA AS A COMPLICATION OF SYMPATHECTOMY FOR HYPERTENSION

Six years ago we encountered paraplegia as a postoperative complication in a patient who had undergone thoraco-lumbar 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:

March 1954 - Volume 139 - Issue 3 - ppg 330-334

Effect of sympathectomy on the expression of NMDA receptors in the spinal cord

The expression of NMDA receptors in the intermediolateral (IML) region of the upper thoracic spinal cord, was studied in 3 week old rats. The effect of section of the cervical sympathetic nerve on neuronal cell number and receptor expression was examined up to two weeks after the operation. Age-matched sham-operated and unoperated animals were used as controls. It was shown using quantitative autoradiography with the NMDA receptor antagonist [(3)H]MK-801 (dizocilpine maleate), that there was a marked downregulation of receptors in all groups of animals, beginning at approximately 4 weeks of age. However after sympathectomy, which resulted in the death of 44% of neurones in the IML by 7 days, there was a significant increase in receptor density per neurone compared to sham-operated controls. In the control animals there was a significant increase in the Kd value of the binding between 21 and 24 days after birth indicating an increased expression of a low affinity receptor, but no such increase was seen after axotomy. The results are consistent with two populations of NMDA receptors being transiently expressed in the IML in developing animals, and the higher affinity receptor being down-regulated between 4 and 5 weeks of age. The presence of the high affinity receptor subtype may predispose neurones to die after axotomy.
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

www.springerlink.com/index/M21M2612N2147011.pdf

A correlation of the findings of cytoarchitectonics and sympathectomy with fiber degeneration folowing dorsal rhizotomy

Autonomic neurons in the spinal cord of the rhesus monkey: A correlation of the findings of cytoarchitectonics and sympathectomy with fiber degeneration following dorsal rhizotomy

http://www3.interscience.wiley.com/journal/109712470/abstract

R-R variations, a test of autonomic dysfunction

Patients with symptoms of autonomic failure showed smaller variations than those without such symptoms.

Acta Neurologica Scandinavica

http://www3.interscience.wiley.com/journal/121523081/abstract?CRETRY=1&SRETRY=0