Extensive surgery or burning causes nerve scaring, which may behave like epilepsy of the autonomous nervous system

Extensive surgery or burning causes nerve scaring, which may behave like epilepsy of the autonomous nervous system and cause the well known devastating side effects.
http://sympathectomy.info/

Long-term cardiopulmonary function after thoracic sympathectomy

These evaluations were performed again 1 year after the procedure to assess the long-term effects of sympathectomy.
Lung function tests revealed a significant decrease in forced expiratory volume in 1 second (FEV1) and forced expiratory flow between 25% and 75% of vital capacity (FEF25%–75%) in both groups (FEV1 of −6.3% and FEF25%–75% of −9.1% in the conventional thoracic sympathectomy group and FEV1 of −3.5% and FEF25%–75% of −12.3% in the simplified thoracic sympathectomy group). Dlco and heart rate at rest and maximal values after exercise were also significantly reduced in both groups (Dlco of −4.2%, Dlco corrected by alveolar volume of −6.1%, resting heart rate of −11.8 beats/min, and maximal heart rate of −9.5 beats/min in the conventional thoracic sympathectomy group and Dlco of −3.9%, Dlco corrected by alveolar volume of −5.2%, resting heart rate of −10.7 beats/min, and maximal heart rate of −17.6 beats/min in the simplified thoracic sympathectomy group). Airway resistance increased significantly in the group of patients undergoing conventional thoracic sympathectomy (+13%).
http://www.jtcvsonline.org/article/PIIS0022522309007569/abstract?rss=yes

TNF at a site of immunological injury may lead to chronic activation of innate immune cells and to chronic inflammatory responses

There is now good evidence to demonstrate that aberrations in tumour necrosis factor (TNF) production in vivo may be either pathogenic or protective and several plausible mechanisms may explain these contrasting activities. According to the classic pro-inflammatory scenario, failure to regulate the production of TNF at a site of immunological injury may lead to chronic activation of innate immune cells and to chronic inflammatory responses, which may consequently lead to organ specific inflammatory pathology and tissue damage.
http://www.ncbi.nlm.nih.gov/pubmed/10577971

dysregulation between the nervous and immune systems might contribute to disease development and progression

Data show that the nervous and immune systems communicate with one another to maintain immune homeostasis. Activated immune cells secrete cytokines that influence central nervous system activity, which in turn, activates output through the peripheral nervous system to regulate the level of immune cell activity and the subsequent magnitude of an immune response. In this review, we will focus our presentation and discussion on the findings that indicate a regulatory role for the peripheral sympathetic nervous system in modulating the level of cytokine and antibody produced during an immune response. Data will be discussed from studies involving the stimulation of the ß₂ adrenergic receptor expressed on CD4⁺ T cells and B cells by norepinephrine or selective agonists. We will also discuss how dysregulation of this line of communication 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

It is becoming clear that immune responses are subject to modulation by the sympathetic nervous system. We examined the effect of chemical sympathectomy (to ablate peripheral sympathetic nerve fibers) on cytokine and Ab production in two strains of mice that are known to differ in their response to a variety of pathogens and in the dominant types of cytokines produced. C57Bl/6J mice produce a strong cell- mediated response, characterized by production of IL-2 and IFN-gamma, whereas BALB/cJ have a dominant humoral response, with production of IL- 4 and IL-10. Animals were denervated by injection with 6- hydroxydopamine and immunized with keyhole limpet hemocyanin, and spleens were removed at various times after immunization. Denervation significantly increased the keyhole-limpet-hemocyanin-stimulated in vitro proliferation and IL-2 and IL-4 production by splenocytes from both strains.
http://www.jimmunol.org/cgi/content/abstract/155/10/4613

cytokines mediate and control immune and inflammatory responses

Under certain conditions, however, stress hormones may actually facilitate inflammation through induction of interleukin (IL)-1, IL-6, IL-8, IL-18, tumor necrosis factor-alpha and C-reactive protein production and through activation of the corticotropin-releasing hormone/substance P-histamine axis. Thus, a dysfunctional neuroendocrine-immune interface associated with abnormalities of the 'systemic anti-inflammatory feedback' and/or 'hyperactivity' of the local pro-inflammatory factors may play a role in the pathogenesis of atopic/allergic and autoimmune diseases, obesity, depression, and atherosclerosis. These abnormalities and the failure of the adaptive systems to resolve inflammation affect the well-being of the individual, including behavioral parameters, quality of life and sleep, as well as indices of metabolic and cardiovascular health.
http://www.ncbi.nlm.nih.gov/pubmed/16166805

Denervation resulted in increased production of tumor necrosis factor-α

by TA Callahan - 2002
linkinghub.elsevier.com/retrieve/pii/S0889159100906184

Tumor necrosis factor-a induces oligodendrocytes apoptosis

Tumor necrosis factor-a induces oligodendrocytes apoptosis, and is known to stimulate the hydrolysis of sphingomyelin to form the lipid mediator, ceramide.
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

1: J Neurophysiol. 1996 Jan;75(1):514-7.

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

Risk of bradycardia after endoscopic electrocautery of the upper thoracic sympathetic ganglia

We evaluated risk of bradycardia after endoscopic electrocautery of the upper thoracic sympathetic ganglia (ETS). Enrolled in this study were 24 patients. Bradycardia, defined as heart rate below 50 beats per min continuing for more than 5 min, was found in 12 patients (50%). All patients were divided into two groups; bradycardia group and non-bradycardia group. Age, sex, region of electrocautery, fentanyl dosage, and operation time were not different between the two groups. Power spectral analysis of heart rate variability revealed that sympathetic activity decreased after ETS. Multivariate analysis indicates that postoperative-minimal heart rate depends upon preoperative heart rate at rest. We conclude that careful monitoring after ETS is necessary in a patient with heart rate below 60 bpm preoperatively.
http://www.ncbi.nlm.nih.gov/pubmed/10885235