Complications are more common than previously thought

Need for more careful alternative to sympathectomy. Complications following surgery for palmar sweating are more common than previously thought

Meyerson B.
http://www.ncbi.nlm.nih.gov/pubmed/10093434

complications are frequent

Postoperative complications are frequent after surgery for palmar sweating and facial redness. Effects of the treatment must be considered with regard to the risk of side-effects

Lakartidningen. 2001 Apr 11;98(15):1764-5.
http://www.ncbi.nlm.nih.gov/pubmed/11374001

Neuroendocrine regulation of autoimmune/inflammatory disease

Interactions between the immune and nervous systems play an important role in modulating host
susceptibility and resistance to inflammatory disease. Neuroendocrine regulation of inflammatory and immune responses and disease occurs at multiple levels: systemically, through the anti-inflammatory action of glucocorticoids released via hypothalamic-pituitary-adrenal axis stimulation; regionally, through production of glucocorticoids within and sympathetic innervation of immune organs such as the thymus; locally, at sites of inflammation. Estrogens also play an important role in immune modulation, and contribute to the approximately 2- to 10-fold higher incidence of autoimmune/inflammatory diseases seen in females of all mammalian species. During inflammation, cytokines from the periphery activate the central nervous system through multiple routes. This results in stimulation of the hypothalamic-pituitary-adrenal axis which, in turn through the immunosuppressive effects of the glucocorticoids, generally inhibits inflammation. Recent studies indicate that physiological levels of glucocorticoids are immunomodulatory rather than solely immunosuppressive, causing a shift in patterns of cytokine production from a TH1- to a TH2-type pattern. Interruptions of this loop at any level and through multiple mechanisms, whether genetic, or through surgical or pharmacological interventions, can render an inflammatory resistant host susceptible to inflammatory disease.
Over-activation of this axis, as occurs during stress, can also affect severity of infectious disease
through the immunosuppressive effects of the glucocorticoids. These interactions have been clearly
demonstrated in many animal models, across species, strains and diseases, and are also relevant to
human inflammatory, autoimmune and allergic illnesses, including rheumatoid arthritis, systemic lupus erythematosus, Sjogren's syndrome, allergic asthma and atopic skin disease. While many genes and environmental factors contribute to susceptibility and resistance to autoimmune/inflammatory diseases, a full understanding of the molecular effects on immune responses of combinations of neuropeptides, neurohormones and neurotransmitters at all levels has opened up new therapeutic approaches and are essential for the design of future therapies based on such principles.
J Endocrinol. 2001 Jun;169(3):429-35

Parry-Romberg syndrome and sympathectomy-a coincidence?

Parry-Romberg syndrome is a clinical entity consisting of progressive hemifacial atrophy appearing at a young age. Animal studies indicate that sympathectomy can produce hemifacial atrophy. To our knowledge, this is the first report of a patient with a possible association between Parry-Romberg syndrome and thoracoscopic sympathectomy.

Cutis. 2004 May;73(5):343-4, 346.

http://www.ncbi.nlm.nih.gov/pubmed/15186051

Overall, gustatory sweating occurred in 32% of patients

Gustatory sweating is a frequent side effect after thoracoscopic sympathectomy. This is the first study to report that its incidence is significantly related to the extent of sympathectomy or the location of primary hyperhidrosis. Although there is no pathophysiologic explanation of gustatory sweating, these findings should be considered before planning thoracoscopic sympathectomy and patients should be thoroughly informed.

Ann Thorac Surg. 2006 Mar;81(3):1047.

http://www.ncbi.nlm.nih.gov/pubmed/16488719

Hyperhidrosis versus compensatory sweating: is it a treatment benefit or a risk of a new problem?

http://www.ncbi.nlm.nih.gov/pubmed/17952340

Breast enlargement after thoracoscopic sympathectomy

http://www.ncbi.nlm.nih.gov/pubmed/18403276

Side-effects of Sympathectomy treated with further surgical procedure and botox

Compensatory hyperhidrosis: a consequence of truncal sympathectomy treated by video assisted application of botulinum toxin and reoperation.

Surgical management of primary hyperhidrosis by upper dorsal sympathectomy is the treatment of choice for intractable hyperhidrosis, however, paradoxically it may be followed by troublesome compensatory hyperhidrosis in a significant number of patients.

We report for the first time the successful treatment of a patient who developed compensatory hyperhidrosis following sympathectomy using video assisted extension of the sympathectomy by application of botulinum toxin (BTX-A).

http://www.ncbi.nlm.nih.gov/pubmed/18450468

Sympathicotomy affects cutaneous blood flow, temperature, and sympathicus-mediated reflexes

To study the sympathetically mediated effects of transthoracic endoscopic sympathicotomy (TES) in the treatment of severe primary palmar hyperhidrosis. MATERIALS AND METHODS: The effects of TES, on sympathetic ganglia at the thoracic level of 2-3, finger blood flow, temperature, and on heat and cold provocation were investigated. Middle cerebral artery (MCA) blood flow velocities were studied by transcranial Doppler. RESULTS: The finger blood flow increased by about 700% after TES and finger temperature by 7.0 +/- 0.5 degrees C. Several autonomic reflexes were dramatically affected. A finger pulp-shrinking test showed a major decrease after surgery. MCA mean blood flow velocities were not affected by TES. CONCLUSIONS: Besides the high success rate of good clinical effect of TES on palmar hyperhidrosis, major effects on local blood flow and temperature are elicited by TES. Complex autonomic reflexes are also affected. The patient should be completely informed before surgery of the side effects elicited by TES.

http://www.ncbi.nlm.nih.gov/pubmed/18540897

Treatment required to treat side-effects of the treatment for palmar hyperhidrosis?

An alternative treatment option for compensatory hyperhidrosis after endoscopic thoracic sympathectomy

http://www.ncbi.nlm.nih.gov/pubmed/20028410

Morphofunctional changes in the myocardium following sympathectomy and their role in the development of sudden death

A comprehensive study revealed 2 main stages in the sympahtectomy caused by reserpine. In the early stages, the functional and metabolic changes in the heart muscle are caused by a dramatic reduction in the activity of the sympathoadrenal system with a relatively preserved structure of the myocardium. The second stage of the sympathectomy is marked by demonstrable morphological and metabolic abnormalities in the myocardium, thereby leading to the occurrence of irreversible fibrillation or hte heart ventricles.
Vestn Akad Med Nauk SSSR. 1984;(2):80-5.

Morphofunctional changes in the myocardium following sympathectomy and their role in the development of sudden death from ventricular fibrillation
[Article in Russian]
Beskrovnova NN, Makarychev VA, Kiseleva ZM, Legon'kaia, Zhuchkova NI.
PMID: 6711115 [PubMed - indexed for MEDLINE]

Sympathectomy affects the function of the Hypothalamus

Sympathectomy at the T2 level would block the afferent projection negative feedback to the hypothalamus, since it would section practically all afferent pathways, and would favor CH appearance at the periphery, due to the continuous efferent projections from the hypothalamus. Sympathectomy below this level would section a smaller number of afferent pathways, avoiding the feedback blockage and decreasing CH.

By understanding that CH is a result of a lack of negative feedback to the hypothalamus after sympathectomy, we found out that this side effect is more pronounced when sympathectomy is performed on the T2 ganglion, where there is greater convergence of afferent pathways to the hypothalamus. However, when the sympathectomy is more caudal, the adverse effect is less pronounced.^(13,14)

J. bras. pneumol. vol.34 no.11 São Paulo Nov. 2008

doi: 10.1590/S1806-37132008001100013

decrease of hyperhidrosis in the zones regulated by mental or emotional stimuli

Redistribution of perspiration as reported by the patients comprised significant reductions in palmar and axillary hyperhidrosis, and an increase in the zone of the trunk and popliteal region. The incidence of plantar anhydrosis and plantar hypohidrosis was 30.3% and 20.7%, respectively (p < 0.001). Conclusions: EBTS is followed by redistribution of body perspiration, with, and important, plantar anhydrosis and hypohidrosis. Although EBTS is the standard treatment for palmar primary hyperhidrosis, we must continue studying baseline sympathetic activity in patients affected by primary hyperhidrosis and the neuroanatomy of the sympathetic system to understand the redistribution of sweating and decrease of hyperhidrosis in the zones regulated by mental or emotional stimuli.
European Journal of Cardio-Thoracic Surgery, Volume 36, Issue 2, August 2009, Pages 360-363

Recurrent sweating occurred in 17.6% of patients

The overall mean patient satisfaction rate was 78%, with a median 80% improvement on a visual analog scale from 0% (poor) to 100% (excellent). Overall, 88 patients (96.7%) developed compensatory hyperhidrosis, with the mean initial occurrence at 8.2 weeks. The symptoms of compensatory hyperhidrosis progressively worsened to the maximum degree within another 2 weeks after onset (mean 10.3 ± 1.83 weeks). In 19 patients (21.6%), symptoms of compensatory hyperhidrosis improved spontaneously within 3 months after sympathectomy (mean 13.3 weeks). Postoperative compensatory hyperhidrosis occurred in 71.4% of patients within the 1st year. Recurrent sweating occurred in only 17.6% of patients. None of these patients required repeated operation. The earliest onset of recurrent sweating was noted at 2 weeks postoperatively by three patients, and the mean initial postoperative reccurrence was 32.7 weeks after surgery.
http://thejns.org/doi/abs/10.3171/spi.2005.2.2.0151

Young woman dies after a 'routine' operation

A 'fit and healthy' young woman was left brain dead after a pioneering operation to reduce her excessive sweating went catastrophically wrong, a medical panel has heard.

Louise Field, 27, suffered severe brain damage when doctors accidentally punctured her lung and pumped gas into her stomach, the General Medical Council heard. She died two days later.

Mr Ormiston accidentally punctured her lung during the procedure, causing her oxygen levels to dip fatally. Dr Yanny allegedly failed to tackle the situation properly as the GMC hearing was told he “knew, or ought to have known” that brain damage was inevitable as he pumped Louise full of drugs to try to reverse the condition.

When the young Midland woman was rushed to another hospital, it was claimed Dr Yanny gave no indication she might have neurological problems – likely to have been caused due to a lack of oxygen.

He was also accused of failing to inform the specialist registrar at Hemel Hempstead General Hospital about drugs given, or even provide a simple anaesthetic chart.

Mr Ormiston admitted making inaccurate records after the operation and was slammed by the GMC panel for “significant departures from good medical practice”.

But he was still cleared of serious misconduct and it was decided that his fitness to practise was not impaired.

Dr Yanny managed to keep his job after offering a series of “undertakings”.

http://www.sundaymercury.net/news/midlands-news/2010/06/20/newport-parents-speak-about-tragic-loss-of-beautiful-daughter-66331-26685674/2/

results of ETS deteriorate and compensatory sweating does not improve with time

Our findings indicate that results of ETS deteriorate and compensatory sweating does not improve with time. It is mandatory to inform patients of the potential long-term adverse effects before surgery.
10-YEAR FOLLOW-UP OF ENDOSCOPIC THORACIC SYMPATHECTOMY
G. Somuncuoglu, T. Walles, V. Steger, S. Veit, G. Friedel
Schillerhoehe Hospital, Gerlingen, Germany
2008;7:147-200 Interact CardioVasc Thorac Surg

hand, which may become hyperkeratotic, with fissuring and scaling

Sympathectomy for palmar hyperhidrosis is effective, but has risks associated with surgery and a permanent non-sweating hand, which may become hyperkeratotic, with fissuring and scaling.

The autonomic nervous system: an introduction to basic and clinical concepts

By Otto Appenzeller, Emilio Oribe

Post-sympathectomy neuralgia: hypotheses on peripheral and central neuronal mechanisms

Post-sympathectomy neuralgia is proposed here to be a complex neuropathic and central deafferentation/reafferentation syndrome dependent on: (a) the transection, during sympathectomy, of paraspinal somatic and visceral afferent axons within the sympathetic trunk; (b) the subsequent cell death of many of the axotomized afferent neurons, resulting in central deafferentation; and (c) the persistent sensitization of spinal nociceptive neurons by painful conditions present prior to sympathectomy. Viscerosomatic convergence, collateral sprouting of afferents, and mechanisms associated with sympathetically maintained pain are all proposed to be important to the development of the syndrome.

Author Keywords: Deafferentation; Central sensitization; Viscero-somatic convergence; Ectopic discharge; Sympathetically maintained pain

Pain
Volume 64, Issue 1, January 1996, Pages 1-9

Ectopic discharge in injured nerves: comparison of trigeminal and somatic afferent

Brain Research
Volume 579, Issue 1, 1 May 1992, Pages 148-151

Autonomic neuropathy simulating the effects of sympathectomy

Odel, H. M., Roth, G. M., and Keating, F. R., Jr. (1955). Autonomic
neuropathy simulating the effects of sympathectomy as a
complication of diabetes mellitus. Diabetes, 4, 92-98.

Sympathectomy limits blood flow to a vital organ like the brain

1. Acta Physiol Scand. 2000 Sep;170(1):33-8.

Middle cerebral artery blood velocity during exercise with beta-1 adrenergic and unilateral stellate ganglion blockade in humans.

Ide K, Boushel R, Sørensen HM, Fernandes A, Cai Y, Pott F, Secher NH.

Department of Anaesthesia, The Copenhagen Muscle Research Centre, University of Copenhagen, Rigshospitalet, Denmark.

A reduced ability to increase cardiac output (CO) during exercise limits blood flow by vasoconstriction even in active skeletal muscle. Such a flow limitation may also take place in the brain as an increase in the transcranial Doppler determined middle cerebral artery blood velocity (MCA V(mean)) is attenuated during cycling with beta-1 adrenergic blockade and in patients with heart insufficiency. We studied whether sympathetic blockade at the level of the neck (0.1% lidocaine; 8 mL; n=8) affects the attenuated exercise - MCA V(mean following cardio-selective beta-1 adrenergic blockade (0.15 mg kg(-1) metoprolol
i.v.) during cycling. Cardiac output determined by indocyanine green dye dilution, heart rate (HR), mean arterial pressure (MAP) and MCA V(mean) were obtained during moderate intensity cycling before and after pharmacological intervention. During control cycling the right and left MCA V(mean) increased to the same extent (11.4 1.9 vs. 11.1 1.9 cm s(-1)). With the
pharmacological intervention the exercise CO (10 1 vs. 12 1 L min(-1); n=5), HR (115 4 vs. 134 4 beats min(-1)) and delta MCA V(mean) (8.7 2.2 vs. 11.4 1.9 cm s(-1) were reduced, and MAP was increased (100 5 vs. 86 2 mmHg; P < 0.05).

However, sympathetic blockade at the level of the neck eliminated the beta-1 blockade induced attenuation in delta MCA V(mean) (10.2 2.5 cm s(-1)). These results indicate that a reduced ability to increase CO during exercise limits blood flow to a vital organ like the brain and that this flow limitation is likely to be by way of the sympathetic nervous system.

PMID: 10971220 [PubMed - indexed for MEDLINE]

Elective surgery described as complicated and dangerous, or experimental

If the Japanese were guilty of running germ warfare tests elsewhere on American POWs, they were guilty of conducting surgical experiments at Itchioka. "Burning Feet," as my father had learned, was treated simply by improving the diet. But one patient suffering from it was forced by a Japanese doctor to submit to an abdominal sympathectomy, a complicated and dangerous operation. As my father wrote in his notes at the time:

The value of these operations for this condition was highly questionable even on theoretical grounds. In effect, Lt. Nisura (the Japanese surgeon) was using these patients as guinea pigs. The operation on____, without consent, and over the objection of Dr. Jackson (the attending physician), which resulted directly in___'s death, constitutes even in its most favorable light—manslaughter.

http://www.vqronline.org/articles/1990/autumn/glusman-heroes-sons/

Surgery for hyperhidrosis abolished 6-sulphatoxymelatonin excretion

The amount of 6-sulphatoxymelatonin, the chief metabolite of melatonin, in the urine was measured in nine patients, who were subjected to bilateral sympathectomy at the second thoracic ganglionic level for treatment of hyperhidrosis of the palms.
All patients showed before surgery a normal 6-sulphatoxymelatonin excretion with a peak in the excretion during the night time. After the sympathectomy, the high night time excretion was clearly abolished in five patients but remained high in four patients. This indicates that the segmental locations of the preganglionic sympathetic perikarya in the spinal cord, stimulating the melatonin secretion in the pineal gland in humans, vary between individuals. An increase in daytime melatonin excretion was observed in the patients responding to the sympathectomy with an abolished 6-sulphatoxymelatonin rhythm. This increase could indicate that the final sympathetic neurons innervating the pineal gland might have a both stimulatory and inhibitory function.
Molecular and Cellular Endocrinology
Volume 252, Issues 1-2, 27 June 2006, Pages 40-45

Parallels between effects of spinal cord injury and sympathectomy on cardiac function

Cardiac dysfunctions are common complications following SCI. Cardiovascular disturbances are the leading causes of morbidity and mortality in both acute and chronic stages of SCI. We reviewed epidemiology of cardiac disturbances after SCI, and neuroanatomy and pathophysiology of autonomic nervous system, sympathetic and parasympathetic. SCI causes disruption of descendent pathways from central control centers to spinal sympathetic neurons, originating into intermediolateral nuclei of T1-L2 spinal cord segments. Loss of supraspinal control over sympathetic nervous system results in reduced overall sympathetic activity below the level of injury and unopposed parasympathetic outflow through intact vagal nerve. SCI associates significant cardiac dysfunction. Impairment of autonomic nervous control system, mostly in patients with cervical or high thoracic SCI, causes cardiac dysrrhythmias, especially bradycardia and, rarely, cardiac arrest, or tachyarrhytmias and hypotension. Specific complication dependent on the period of time after trauma like spinal shock and autonomic dysreflexia are also reviewed. Spinal shock occurs during the acute phase following SCI and is a transitory suspension of function and reflexes below the level of the injury. Neurogenic shock, part of spinal shock, consists of severe bradycardia and hypotension. Autonomic dysreflexia appears during the chronic phase, after spinal shock resolution, and it is a life-threatening syndrome of massive imbalanced reflex sympathetic discharge occurring in patients with SCI above the splanchnic sympathetic outflow (T5-T6). Besides all this, additional cardiac complications, such as cardiac deconditioning and coronary heart disease may also occur.
http://www.ncbi.nlm.nih.gov/pubmed/20108532


Neurogenic shock is shock caused by the sudden loss of the autonomic nervous system signals to the smooth muscle in vessel walls. This can result from severe central nervous system (brain and spinal cord) damage. With the sudden loss of background sympathetic stimulation, the vessels suddenly relax resulting in a sudden decrease in peripheral vascular resistance (vasodilation)^[1] and decreased blood pressure.

Signs and symptoms

• hypotension
• bradycardia
• warm, dry extremities
• peripheral vasodilation
• venous pooling
• Poikilothermia
• Priapism Due to PNS stimulation
• decreased cardiac output (with cervical or high thoracic injury)

Mayo Clinic investigates the same disorder as the one resulting from the elective surgical sympathectomy

Autoimmune autonomic ganglionopathy is characterized by impairment of multiple autonomic domains of which sudomotor function is among the most common. Many patients with this disorder have difficulties with thermoregulation and anhidrosis.

Sudomotor dysfunction in autoimmune autonomic ganglionopathy

http://www.ncbi.nlm.nih.gov/pubmed/19884578

Other alternative more selective methods, rather than cutting the main trunk should be studied

Compensatory sweating remains the most common, and most disabling complication of video-assisted thoracoscopic sympathectomy. Other alternative more selective methods, rather than cutting the main trunk should be studied thoroughly to assess their efficacy in reducing the complication of compensatory sweating.
http://www.ncbi.nlm.nih.gov/pubmed/18521466

Evidence: sympathectomy created imbalance of autonomic activity and functional changes of the intrathoracic organs

Surgical thoracic sympathectomy such as ESD or heart transplantation can result in an imbalance between the sympathetic and parasympathetic activities and result in functional changes
in the intrathoracic organs.
Therefore, the procedures affecting sympathetic nerve functions, such as epidural anesthesia, ESD, and heart transplantation, may cause an imbalance between sympathetic and parasympa-
thetic activities (1, 6, 16, 17). Recently, it has been reported that ESD results in functional changes of the intrathoracic organs.


In conclusion, our study demonstrated that ESD adversely affected lung function early after surgery and the BHR was affected by an imbalance of autonomic activity created by bilateral ESD in patients with primary focal hyperhidrosis.
Journal of Asthma, 46:276–279, 2009

sympathectomy significantly increased the ratio of patients exhibiting a positive response to methacholine

Of 46 patients who had a negative result for methacholine challenge preoperatively, 12 (26%) became positive after surgery. In terms of the level of sympathectomy, T3 sympathectomy significantly increased the ratio of patients exhibiting a positive response to methacholine (from 19% to 34%, respectively) (p < 0.005).
Conclusions. Thoracic sympathectomy can adversely affect lung function early after surgery, although the clinical significance is uncertain. It may also exert an influence on the development of bronchial hyperresponsiveness, especially when performed at the T3 level.
Journal of Asthma, 46:276–279, 2009

Compensatory Hyperhidrosis is a result of a lack of negative feedback to the hypothalamus after sympathectomy

"CH (compensatory hyperhidrosis) is a result of a lack of negative feedback to the hypothalamus after sympathectomy"

J. bras. pneumol. vol.34 no.11 São Paulo Nov. 2008

The authors of the article consider this to be more evident after T2 sympathectomy, but members of this forum (http://etsandreversals.yuku.com/directory) who have had the surgery performed at a lower level(s) have also experienced thermoregulatory dysfunction and severe/disabling lower body hyperhidrosis.
The article is important because it states clearly that sympathectomy will change the function of the hypothalamus, - part of the brain responsible for much more than thermoregulation. It also refers to the abnormal sweating as hyperhidrosis, indicating that it will be more that what the body needs for thermoregulation.

"The hypothalamus affects the endocrine system and governs emotional behavior, such as anger and sexual activity. Most of the hypothalamic hormones generated are distributed to the pituitary via the hypophyseal portal system.^[10] The hypothalamus maintains homeostasis; this includes a regulation of blood pressure, heart rate, and temperature."
http://en.wikipedia.org/wiki/Hypothalamus

When you sign the 'informed consent' document, you are not told that the surgeon is going to interfere with the system that maintains the body's homeostasis, and that loss of homeostasis leads to pathology. If you are not told this by your surgeon, then he/she is withholding information that would allow you to understand the nature and scope of the irreversible procedure your are agreeing to.
You are also told that the amount of sweat you will have on other parts of the body after surgery equals the amount of sweat on the palms before surgery. There is not truth to this claim, and no surgeon can substantiate this. The doctors KNOW that this is a lie, yet they tell this to the patients in order to make the surgery appear as a simple and safe and ...predictable.

If you have a procedure that is distinctly different than what you agreed to, your consent based on the information provided by your surgeon is void, meaning that you can argue your case in court that the procedure was performed WITHOUT consent, which constitutes 'trespass to a person' and battery. In this case (if you win), the court can bring a much harsher sentence on the (fraudulent) surgeon, and can award exemplary/aggravated damages in addition to your loss of earnings etc.

"The High Court (of Australia) has said that the question of choice on the part of the patient is meaningless, unless he or she is provided with the information to make a reasoned decision." (Oxford Journal of Legal Studies, Vol. 15, No 1 1995)

Cutaneous vasodilator responses induced by activation of hypothalamic heat loss mechanisms are completely abolished by sympathectomy

http://www3.interscience.wiley.com/journal/121531565/abstract

Effects of Sympathectomy on the mean decrease in HBF (Hypothalamic blood flow)

Intrahypothalamic injection of 0.1 mug of tyramine caused a mean decrease in HBF of 15.6 ml/100 g per min (P less than 0.001). This effect of intrahypothalamic injection of tyramine was abolished by bilateral cervical sympathectomy but not by chemical sympathectomy of the upper brainstem. These results support the idea that local CBF, at least in the hypothalamus, is mediated by two distinct pathways. The first consists of the sympathetic nerves which arise in the cervical ganglia, and which activate intrahypothalamic alpha-receptors to cause constriction. The second is an entirely intracerebral noradrenergic pathway which stimulates beta-receptors to cause vasodilation.
http://circres.ahajournals.org/cgi/content/abstract/circresaha;38/3/140
Circulation Research, Vol 38, 140-145, Copyright © 1976 by American Heart Association

Cervical sympathectomy inhibits axonal transport of gonadotropin-releasing hormone during continuous exposure to light in male rats

Considering the action of colchicine, which inhibits axonal transport, it is suggested that cervical sympathectomy also inhibits axonal transports of GnRH between the GnRH neurons and the median eminence during continuous exposure to light.
http://www.springerlink.com/content/q261272138632p52/

T2 procedure results in a complete sympathectomy

Sympathectomy of the upper extremity. Evidence that only the second dorsal ganglion need be removed for complete sympathectomy.

Hyndman OR,Wolkin J

Arch Surg. 1942 45:145–155

Sympathectomy and parasympathectomy leads to the hyperfunction of the serotoninergic system and pathology

We studied the balance of activity of sympathetic, parasympathetic, and serotoninergic divisions of the autonomic nervous system in the regulation of the heart function in rabbits. High activities of the sympathetic and parasympathetic system are associated with antagonistic interactions between them. Moderation of activity of these systems could be accompanied by activation of the serotoninergic system. Physiological sympathectomy and parasympathectomy lead to hyperfunction of the serotoninergic system and pathology.
Bulletin of Experimental Biology and Medicine, Vol. 140, No. 5, 2005 PHYSIOLOGY

Disturbances in brain serotonergic systems result in a range of phenotypes such as depression, suicide and anxiety disorders.
http://www.biomedcentral.com/1471-2202/10/50

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.