Chemical sympathectomy-induced changes in TH-, VIP-, and CGRP-immunoreactive fibers

Journal of Cellular Physiology

Volume 194 Issue 3, Pages 341 - 348

Published Online: 10 Jan 2003

http://www3.interscience.wiley.com/journal/102523100/abstract

Heat loss due to sympathectomy-induced vasodilation

Hypothermia (a decrease in core temperature) is common in patients undergoing surgery with epidural anesthesia an is thought to result from heat loss to the cold environment due to sympathectomy-induced vasodilation.
Sympathectomy-induced vasodilation produced central hypothermia via net convection of the heat from the warmer central to cooler peripheral tissues. The net effect is an increase in peripheral tissue temperature at the expense of decreased central temperature.

Neural Blockade in Clinical Anesthesia and Management of Pain

By Michael J. Cousins, Phillip O. Bridenbaugh

Contributor Michael J. Cousins

Published by Lippincott Williams & Wilkins, 1997

p. 277

Hyperpigmentation after sympathectomy

Clin Exp Dermatol. 1980 Sep;5(3):349-50.
Samuel C, Bird DR, Burton JL.

Disabling Orthostatic Hypotension Caused by Sympathectomies for Hyperhidrosis

Syncope Cases

Published Online: 16 Nov 2007

Editor(s): Roberto Garc�a-Civera, Gonzalo Bar�n-Esquivias, Jean-Jacques Blanc, Michele Brignole, Angel Moya i Mitjans, Ricardo Ruiz-Granell, Wouter Wieling

Print ISBN: 9781405151092 Online ISBN: 9780470995013

Copyright © 2006 by Blackwell Publishing

http://www3.interscience.wiley.com/cgi-bin/summary/116842153/SUMMARY

A mismatch between intravascular volume and the required cardiac output on standing up is the most common cause of orthostatic hypotension. In a small minority of cases, however, orthostatic hypotension is not caused by volume depletion, but by impairment of the autonomic reflexes required to maintain blood pressure in the upright position. This disorder is known as autonomic failure.

In patients with autonomic failure, orthostatic hypotension is caused by an impaired capacity of sympathetic nerves to increase vascular resistance. Downward pooling of venous blood and a consequent reduction in stroke volume and cardiac output lead to the orthostatic fall in arterial pressure.

Adrenal Insufficiency after sympathectomy

A Study of Adrenal Insufficiency After Treatment of Hypertension by Bilateral Sympathectomy Plus Unilateral Adrenalectomy

Chapter Author: P. Etienne-Martin

http://www3.interscience.wiley.com/cgi-bin/summary/119228241/SUMMARY

Copyright © 1954 Ciba Foundation

Structural changes of arteries after sympathectomy

The findings indicate that in renal hypertensive rats structural changes of both large arteries and veins may develop in the absence of an intact sympathoadrenergic system.

Effect of sympathectomy on arterial and venous changes in renal hypertensive rats

G. Simon
Am J Physiol Heart Circ Physiol 241: H449-H454, 1981;

The place of sympathectomy in the treatment of young married women

J Obstet Gynaecol Br Emp. 1954 Dec;61(6):797-803.

Related Articles, Links

GRANT TP.

The obstetrical future of woman having undergoing lumbodorsal sympathectomy for hypertension

Presse Med. 1953 Feb 21;61(12):227-9.
MILLIEZ P, FRITEL D.

PET Imaging of Oxidative Metabolism Abnormalities in Sympathetically Denervated Myocardium

The average percentage of the left ventricle denervated in the group I animals was 13.1% ±7.3%.
Significant reductions in oxidative metabolism were observed in the sympathectomized tissue both at 2 and 8 wk after surgery (22% and 15% reductions, respectively).

Gary D. Hutchins, Timothy Chen, Kathy A. Carlson, Richard L. Fain, Wendy Winkle, Triad Vavrek, Bruce H. Mock
and Douglas P. Zipes
J NucÃ-Med 1999; 40:846-853

hypersensitization of adenoreceptors in the sympathectomized area

Radiofrequency neurolysis (RFN) is becoming a popular method of sympathectomy among pain specialists. The advantages of RFN over chemical and surgical sympathectomy are decrease incidence of neuritis, avoidance of tinitus, blindness and urethral stricture that can occur with chemical sympathectomy, amelioration of anesthetic and surgical risks and early ambulation of the patient. The reasons for the failure of sympathectomy are incomplete sympathectomy, extensive interconnection of chains of sympathectomy ganglia cause rerouting of sympathetic impulse after removal of short chain of ganglia, and hypersensitization of adenoreceptors in the sympathectomized area.

Meraj Siddiqui, Shazia Siddiqui, J. Sue Ranasinghe & Fred Furgang: Complex Regional Pain Syndrome: A Clinical Review: Pain, Symptom Control and Palliative Care. 2001; Volume 2, Number 1.

http://ispub.com/IJPSP/2/1/8541

cardiovascular adjustment to exercise and sympathectomy

Mean arterial pressure and total peripheral resistance were significantly reduced at rest and during steady state of exercise as compared to controls prior to sympathectomy identical vO₂, whereas CO remained unchanged.

The significant fall in left circumflex coronary flow was proportional to the decline in external heart work due to sympathectomy both at rest and under exercise.

http://www.springerlink.com/content/k2n6j4555g16x773/

Coronary blood flow reduced by 50% after sympathectomy

However, at each level of exercise, mean coronary flow in sympathectomized ventricles was reduced by about 50% compared to control values. The slopes of coronary flow on pressure-rate product and tension-time index were also reduced. No difference in left ventricular oxygen extraction between control and sympathectomized hearts were observed. Thus, chronic ventricular sympathectomy altered the relationships between coronary flow and oxygen consumption, on the one hand, and ventricular oxygen-dependent performance and whole-body exercise level, on the other hand.
Med Sci Sports Exerc. 1988 Apr;20(2):126-35.
http://www.ncbi.nlm.nih.gov/pubmed/3367747

Sympathectomy impaired the PTH response to hypocalcaemia

Clinical Physiology and Functional Imaging

Volume 10 Issue 1, Pages 37 - 53
Published Online: 28 Jun 2008

surgical sympathectomy is known to induce resorption within mandibular and auditory bulla bone

Bone destruction causes hearing loss in various middle ear disorders. The mechanisms of such pathological remodeling are unknown.
Unilateral surgical sympathectomy is known to induce resorption within mandibular and auditory bulla bone. Explanation of the cause of this effect, however, may be confounded by hemodynamic changes induced by hemicranial sympathectomy and by uncertainty as to the neuroanatomical origins of sympathetic fibers.
Ann Otol Rhinol Laryngol. 1999 Nov;108(11 Pt 1):1078-87.
http://www.ncbi.nlm.nih.gov/pubmed/10579236

Changes in Parathyroid Hormone and Calcium Levels after Superior Cervical Ganglionectomy of Rats

Changes in Parathyroid Hormone and Calcium Levels after Superior Cervical Ganglionectomy of Rats

23-26 h after SCGx there is a significant impairment of homeostatic iPTH responses to low Ca levels which can be overcome by suitable Ca stimulus; (3) circulating catecholamines may affect denervated parathyroid cells, as revealed by the changes in serum iPTH and Ca elicited by - and -adrenoceptor-blocker treatment of SCGx rats.

Daniel P. Cardinali, Marta G. Ladizesky

Vol. 40, No. 4, 1985

Amygdala and aversive conditioning

Lesioned rats and controls were again tested for aversive conditioning to explicit and contextual cues. Rats with cell body lesions of the hippocampus showed normal suppression of drinking in the presence of the conditioned stimulus, but were severely impaired in choosing the safe environment based on contextual cues alone. These results suggest a double dissociation of the effects of amygdala and hippocampal damage on fear conditioning to explicit and contextual cues.

Complementary roles for the amygdala and hippocampus in aversive conditioning to explicit and contextual cues.

[My paper] N R Selden, B J Everitt, L E Jarrard, T W Robbins

Department of Experimental Psychology, University of Cambridge, U.K.

Neuroscience. 1991 ;42:335-50 1832750

Peripheral sympathectomy resulted in 2- to 5-fold increases in NGF protein levels in heart atrium and ventricle

Peripheral sympathectomy carried out in the adult rat resulted in 2- to 5-fold increases in NGF protein levels in heart atrium and ventricle, as well as submandibular gland, with no concomitant increase in NGF mRNA.

Increased beta-nerve growth factor messenger RNA and protein levels in neonatal rat hippocampus following specific cholinergic lesions.

[My paper] S R Whittemore, L Lärkfors, T Ebendal, V R Holets, A Ericsson, H Persson

J Neurosci. 1987 Jan ;7 (1):244-51 3806196

Sympathectomy Attenuates the Maintenance but Not Initiation of L-NAME– Induced Hypertension

We measured intra-arterial pressure in conscious, unrestrained rats with and without guanethidine-induced sympathectomy during varying durations of intravenous N-nitro-L-arginine methyl ester (L-NAME). The major new finding is that sympathectomy had no effect on the hypertensive response to bolus injections of L-NAME but in the same rats it produced a greater than 50% attenuation in the hypertension seen after 6 days of continuous L-NAME (change in mean arterial pressure, 23±4 versus 55±4 mm Hg,
P<.01, sympathectomy versus control). Using 8-hour infusions of L-NAME, we found that 60 minutes was the minimum time required for detecting a sympathectomy-sensitive component of L-NAME–induced hypertension. Furthermore, we demonstrate that the magnitude of this component increases further between 8 hours to 6 days of continuous L-NAME: it accounted for only 18% of the total hypertensive response at 8 hours but 61% after 6 days. From these experiments, we conclude that the importance of the sympathetic system in the pathogenesis of L-NAME–induced hypertension accrues slowly over hours and days, and thus its importance can be overlooked by focusing on the initial phase of the hypertension. (Hypertension. 1997;30[part 1]:64-70.) Sander, Mikael; Hansen, Jim; Victor, Ronald G.

Anti-inflammatory role of the sympathetic nerves

In all layers, Crohn’s disease patients demonstrated a loss of sympathetic nerve fibres. Sprouting of SP⁺ nerve fibres was particularly observed in the mucosa and muscular layer in Crohn’s disease.

http://gut.bmj.com/cgi/content/abstract/57/7/911

In a person who had a sympathectomy, the sympathetic component of the baroreceptor mechanism is absent

A patient with a sympathectomy would experience what's referred to as orthostatic hypotension (which might lead to syncope). Orthostatic hypotension is a decrease in arterial pressure when going from supine to a standing position. A person with a normal baroreceptor mechanism will try to restore MAP. In a person who had a sympathectomy, the sympathetic component of the baroreceptor mechanism is absent.
M.A.S.T.E.R. Learning Program, UC Davis School of Medicine
Date Revised: Jan 16, 2002
Revised by: Gordon Li and Carolyn Nguyen

Sympathectomy causes ejaculatory dysfunction

We conclude that sympathectomy delays the transit of sperm through the cauda epididymidis and produces ejaculatory dysfunction but does not compromise sperm quality in the distal cauda epididymidis.
Biology of Reproduction 59, 897-904 (1998)

http://www.biolreprod.org/cgi/content/full/59/4/897

Sympathectomy reduces catecholamines

Sympathectomy has been used to study the role of the sympathetic nervous system in the control of gastric acid secretion. Conflicting results may reflect differences in the sympathectomy procedures used. In a previous study we showed a reduction of catecholamines by more than 90% in the gut wall of the rat after surgical upper abdominal sympathectomy.
Scand J Gastroenterol. 1985 Dec;20(10):1276-80.
http://www.ncbi.nlm.nih.gov/pubmed/4095497

Informed consent - from the ets forum

Physicians are required to gain informed consent prior to administering a treatment. Informed consent is gained by providing patients with a full accounting of the risks of the treatment as documented in peer-reviewed, published medical/scientific literature.

Your scenario of surgeons being flummoxed by unhappy patients complaining after surgery doesn't hold water. The rules of professional medical ethics require that the treating physician be well versed in the published literature on the treatments he delivers.

There is a mountain of published research (spanning nearly a century) documenting the adverse effects of sympathectomy. There are numerous studies, for example, showing very high rates of severe side effects and studies showing that satisfaction diminishes substantially over the long term.

It is a doctors job to know this stuff and it is their ethical duty to disclose that information to patients.

So, I see the blame thing as pretty cut and dry. Surgeons perfoming sympathectomies routinely withhold information vital to informed consent. Anyone who does objective comparison between what is documented in medical/scientific literature and what is typically disclosed to prospective ETS patients has no choice but reach this conclusion.

And, to make matters worse, many surgeons use testimonials from a hand-selected group of their happiest patients to advocate the surgery. That practice is considered unethical by all medical professional organizations.

http://etsandreversals.yuku.com/directory

Adrenal Tyrosine Hydroxylase: Compensatory Increase in Activity after Chemical Sympathectomy

Destruction of peripheral sympathetic nerve endings with 6-hydroxydopamine causes a disappearance of cardiac tyrosine hydroxylase, accompanied by a twofold increase in adrenal tyrosine hydroxylase and a small increase in phenyl-ethanolanine-N-methyl transferase.
Robert A. Mueller ¹, Hans Thoenen ¹, and Julius Axelrod ¹
Science 31 January 1969:
Vol. 163. no. 3866, pp. 468 - 469
DOI: 10.1126/science.163.3866.468

Cardiac hypertrophy accelerated by left cervical sympathectomy

Cellular and Molecular Life Sciences (CMLS)
Volume 37, Number 7 / July, 1981

Summary Cardiac hypertrophy in spontaneously hypertensive rats was accelerated by denervation of the left cervical sympathetic ganglia. Supersensitivity due to denervation may also exist in cardiac muscles.

This work was supported by a grant of the Ministry of Education for 1980.

Joint inflammation is reduced by dorsal rhizotomy and not by sympathectomy or spinal cord transection

Ann Rheum Dis. 1994 May; 53(5): 309–314.

PMCID: PMC1005329

Joint inflammation is reduced by dorsal rhizotomy and not by sympathectomy or spinal cord transection.

K A Sluka, N B Lawand, and K N Westlund

Marine Biomedical Institute, University of Texas Medical Branch, Galveston 77555-0843
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1005329

NMDA and Sympathectomy

CONCLUSIONS: NMDA receptor is related to the induction and maitenance of neuropatic pain, and sympathetic nervous system has a main role in the already induced neuropathic pain.
The Effects of NMDA Antagonists and Sympathectomy on the c-Fos mRNA Expression in the Neuropathic Rat.
http://www.koreamed.org/SearchBasic.php?DT=1&RID=47481

Role of Dopamine in behavior modulation

These findings support the idea that DA signals errors in expectancy and that DA signaling is necessary for certain behavioral responses to unexpected events.
Behavioural Brain Research
Volume 122, Issue 2, 1 October 2001, Pages 193-199
Mitchell F. Roitman^a, Gertjan van Dijk^b, Todd E. Thiele^c and Ilene L. Bernstein^{, ,}

Sympathectomy eliminates the fight-or flight response and is used as a surgical treatment of anxiety disorders and phobias

What the myriad of anxiety disorders have in common is a state of increased arousal or fear. Anxiety disorders often are conceptualized as an abnormal or exaggerated version of arousal. Much is known about arousal because of decades of study in animals and humans of the so-called fight-or-flight response, which also is referred to as the acute stress response. The acute stress response is critical to understanding the normal response to stressors and has galvanized research, but its limitations for understanding anxiety have come to the forefront in recent years.

Thoracic Sympathectomy In Social Phobia: A Pilot Study

http://www.ispub.com/ostia/index.php?xmlFilePath=journals/ijs/vol7n2/social.xml

Recurrent and enhanced vasoconstrictor function makes Sympathectomy a questionable treatment for vascualr disorders

T2 sympathectomy leads to long-lasting inhibition of palmar sweating, which does not correlate to loss of vasoconstriction. Recurrent and enhanced vasoconstrictor function 3 months following endoscopic sympathetic block has major implications for its use to treat enhanced vasoconstriction.
http://www.neurology.org/cgi/content/abstract/60/11/1770
Neurology 2003;60:1770-1776
© 2003 American Academy of Neurology

Norepinephrine activates pain pathways after nerve injury

According to MedicineNet, RSD involves "irritation and abnormal excitation of nervous tissue, leading to abnormal impulses along nerves that affect blood vessels and skin."

Animal studies indicate that norepinephrine, a catecholamine released from sympathetic nerves, acquires the capacity to activate pain pathways after tissue or nerve injury, resulting in RSD.
http://arthritis.about.com/od/rsd/a/rsd.htm

Autonomic Hyperreflexia is caused by noxious stimulation below the level of the lesion in a patient with a sympathectomy at or above T6

...The efferent sympathetic fibers recover from the initial injury but remain unaffected by central inhibitory input from the brain stem and hypothalamus.
The severity and manifestations of autonomic hyperreflexia are affected by the level of the sympathectomy. With mid-thoracic lesions below the level of cardiac accelerator fibers, hypertension is accompanied by reflex bradycardia transmitted via cardiac accelerator fibers and the vagus. In patients whose sympathectomy is above the level of the thoracic cardiac accelerator fibers, tachycardia may occur because cardiac accelerator fibers become part of the efferent sympathetic activity rather than part of the central inhibitory input from the brain stem and hypothalamus. Arrythmias and occasional heart block may accompany changes in heart rate.
Clinical manifestations of autonomic hyperreflexia include vasodilation, decresed sympathetic activity, and increased vagal activity above the level of the lesion such as nasal congestion, flushing, headache, dyspnea, nausea, and visceral muscle contraction. Vasoconstriction and increased sympathetic activity below the level of the lesion cause vasoconstrictive pallor, sweating, piloerection, and somatic muscle fasciculation. Patients also develop hypertension with headache, blurred vision, myocardial infarction, andretinal, subarachnoid and cerebral hemorrhages that may lead to syncope, convulsion and death.
Handbook of Neuroanesthesia
page 343

By Philippa Newfield, James E. Cottrell

Contributor Philippa Newfield, Stephen Onesti, James E. Cottrell

Published 2006, Lippincott Williams & Wilkins

Sympathectomy suppresses cell-mediated (T helper-1) responses

In vivo, chemical sympathectomy suppresses cell-mediated (T helper-1) responses, and may enhance antibody (T helper-2) responses. Noradrenergic innervation of spleen and lymph nodes is diminished progressively during aging, a time when cell-mediated immune function also is suppressed. In animal models of autoimmune disease, sympathetic innervation is reduced prior to onset of disease symptoms, and chemical sympathectomy can exacerbate disease severity.
Annu Rev Pharmacol Toxicol. 1995;35:417-48.

Substance P has a proinflammatory role

These studies have been carried out in a large number of patients with long-standing autoimmune diseases. It turned out that sympathetic nerve fibers are lost in chronically inflamed tissue, while substance P-positive nerve fibers sprout into the inflamed area.

Brain Behav Immun. 2007 Jul;21(5):528-34. Epub 2007 May 22. Links

http://www.ncbi.nlm.nih.gov/pubmed/17517488?ordinalpos=58&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum

Brain-Adipose tissue cross talk

Local injections of the sensory nerve neurotoxin capsaicin into WAT selectively destroy this innervation. Just as surgical removal of WAT pads triggers compensatory increases in lipid accretion by non-excised WAT depots, capsaicin-induced sensory denervation triggers increases in lipid accretion of non-capsaicin-injected WAT depots, suggesting that these nerves convey about body fat levels to the brain.
Proc Nutr Soc. 2005 Feb;64(1):53-64.
http://www.ncbi.nlm.nih.gov/pubmed/15877923?ordinalpos=21&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSuminformation

risk of vascular insufficieny and subsequent dysfunction of thoracolumbar autonomic outflow to the head and neck

Cadaveric studies of the blood supply to the human cervical sympathetic chain and ganglia are lacking in the English literature. This study seeks to elucidate the gross blood supply of the cervical sympathetic chain so as to avoid surgical disruption of these vessels and thus decrease the risk of vascular insufficieny and subsequent dysfunction of thoracolumbar autonomic outflow to the head and neck.

Conclusions: Although sympathetic injury is a rare consequence of cervical operations, the current data should be useful to the surgeon who operates in the cervical region so as to avoid potential complications from disruption of the primary blood supply of the cervical sympathetic chain and ganglia.
European Journal of Morphology, Volume 40, Issue 5 December 2002 , pages 283 - 288
http://www.informaworld.com/smpp/content~content=a725290831~db=all

Parallels between post sympathectomy symptoms and Spinal Cord Injury symptoms

Autonomic component of spinal cord injury:

Hypotension, Skin Hyperaemia, Bradycardia (unopposed vagatonia), Low body temperature - high skin temperature,

Spinal shock involves loss of sympathetic autonomic function.

Secondary changes:
-Accumulation of extracellular neurotransmitters: Serotonin, Catecholamines, Glutamate are TOXIC to cells
-Free radical accumulation

http://209.85.173.132/search?q=cache:Yir6NMnAPdEJ:www.drramani.com/presentations/Acute_Spinal_Cord_Injury.pdf+compression+of+the+cervical+sympathetic+chain&hl=en&ct=clnk&cd=69&gl=au&client=firefox-a

Sympathetic chain injury called 'complication'. Now this same 'complication' is marketed for people with palmar hyperhidrosis and blushing.

Cervical sympathetic chain injury is a rare complication of surgery for thyroid and parathyroid conditions.
ANZ Journal of Surgery. 74(6):442-445, June 2004.
HARDING, JANE L. MB BS; SYWAK, MARK S. MB BS, FRACS; SIDHU, STAN MB BS, PhD, FRACS; DELBRIDGE, LEIGH W. MD, FRACS

Eye innervation - part of the thermoregulatory system

Our results show that cold thermoreceptors sensitive to small temperature changes are distributed throughout the entire ocular surface, most frequently in the highly vascularized perilimbal episclera, but also in the posterior segment of the eye. Nerve fibers activated by cold had spotlike receptive fields and responded to temperature reductions with a nerve impulse discharge that started as soon as the local temperature began to decline, and increased monotonically in firing frequency in parallel with the decrease in temperature.
http://www.iovs.org/cgi/content/full/44/2/697

Transection of the sympathetic chain

Activating transcription factor 3 immunoreactivity identifies small populations of axotomized neurons in rat cervical sympathetic ganglia after transection of the preganglionic cervical sympathetic trunk.

These data indicate that, after transection of the CST, neuronal labeling in the SCG and MICG is restricted to axotomized neurons but that in addition there is extensive labeling of glial cells associated with anterograde degeneration within the SCG.
http://www.nextbio.com/b/literature/literature.nb?id=17583680&query=Right+cervical+sympathetic+trunk&author=

Selective brain cooling following sympathectomy

We have investigated the role of the sympathetic innervation of the vasculature of the head in the control of selective brain cooling of sheep, during exposure to high and low ambient temperatures and during endotoxin-induced fever. Bilateral removal of the superior cervical ganglia resulted in a significant reduciton of hypothalamic temperture during all procedures. Respiratory rate was also depressed by the sympathectomy, apparently mainly as a result of a decrease in nasal airway patency. Rectal temperature changes after sympathectomy were dependent on the experimental conditions, and the rectal — hypothalamic temperature difference was enhanced during heat exposure and fever. Our results support the contention that sympathetically mediated changes in nasal blood flow and in venous return from the nasal cavity, via the angularis oculi and facial veins, may be involved in the control of selective brain cooling in sheep.

	Pflügers Archiv European Journal of Physiology
Publisher	Springer Berlin / Heidelberg
ISSN	0031-6768 (Print) 1432-2013 (Online)
Issue	Volume 417, Number 4 / December, 1990

various other central physiological and metabolic events in cervical sympathectomized animals

Studies were conducted confirming supersensitivity to catecholamines on intraocular pressure and pupil size following bilateral superior cervical ganglionectomy in rabbits.
At the termination of these studies we examined changes in cyclic adenylic acid and prostaglandin content in jugular vein effluent and various brain and ocular tissues and fluids of the sympathectomized versus control animals. In the blood effluent we found significant elevation of cyclic adenylic acid and significant lowering of prostaglandin F1alpha in the sympathectomized animals. Although we found elevation of prostaglandin in certain tissues of the sympathectomized animals, there were no significant changes in cyclic adenylic acid levels between sympathectomized and control animals in the tissues examined. The findings of prostaglandin (blood and tissue) and cyclic adenylic acid (blood) changes in sympathectomized animals, associated with known changes in intraocular pressure and pupil size (due to catecholamine supersensitivity) must elicit further interest in the correlation and interpretation of various other central physiological and metabolic events in cervical sympathectomized animals.
http://www.ncbi.nlm.nih.gov/pubmed/213796?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_Discovery_RA&linkpos=3&log$=relatedarticles&logdbfrom=pubmed

Sympathectomy can result in Dysautonomia

Dysautonomia is any disease or malfunction of the autonomic nervous system.
In some cases, dysautonomia results in a reduction in the ability of the heart and circulatory system to compensate for changes in posture, such as causing dizziness or fainting when standing or even sitting up. In other cases, inappropriate sinus tachycardia may cause the heart to race for no apparent reason. Other symptoms can include severe migraines, excessive urination.
Causes of dysautonomias are not fully understood, but they are thought to include viral illness, genetic factors, exposure to chemicals, pregnancy, autoimmune disorders, and a physical trauma or injury which damages the autonomic nervous system.^[3]

There is no cure for dysautonomia, medications are used to stablize the condition on a long-term basis.
http://www.reference.com/browse/dysautonomia,+familial

galanin and VIP mRNA after sympathectomy

Large changes in neuronal gene expression occur in adult peripheral neurons after axonal transection. In the rat superior cervical ganglion, for example, neurons that do not normally express vasoactive intestinal peptide (VIP) or galanin do so after postganglionic nerve transection. These effects of axotomy could result from a number of aspects of the surgical procedure. To test the idea that the important variable might be the disconnection of axotomized neuronal cell bodies from their target tissues, we examined the effects of producing such a disconnection by means of the compound 6-hydroxydopamine (6-OHDA), a neurotoxin that causes degeneration of sympathetic varicosities and avoids many of the complications of surgery. Two days after 6-OHDA treatment, VIP and galanin immunoreactivities had increased two- and 40-fold, respectively. Nevertheless, these increases were substantially smaller than the 30- and 300-fold changes seen after surgical axotomy. When expression of VIP and galanin was examined at the mRNA level, however, comparable increases were found after either procedure. The results indicate that chemical destruction of sympathetic varicosities produces an equivalent signal for increasing VIP and galanin mRNA as does axonal transection.

Chemical sympathectomy and postganglionic nerve transection produce similar increases in galanin and VIP mRNA but differ in their effects on peptide content.

H. Hyatt-Sachs, M. Bachoo, R. Schreiber, S. A. Vaccariello, R. E. Zigmond *

Department of Neurosciences, Case Western Reserve University, School of Medicine, Cleveland, Ohio 44106-4975

Received: 9 January 1996; Accepted: 3 April 1996

Journal of Neurobiology

A reduction in heat tolerance after Sympathectomy

Role of splanchnic and lumbar sympathetic nerves in physiologic responses to fever and hypoxia in dogs

W. G. Kubicek ¹, W. F. Geber ¹, J. W. Geiger ¹, and E. A. Johnson ¹
Am J Physiol 196: 685-690, 1959;
The most important function of the splanchnic and lumbar sympathetic nerves was apparently the control of the circulatory system and secondly the partial regulation of blood glucose probably through liberation of epinephrine from the adrenal medulla. A reduction in heat tolerance of the animals was observed after sympathectomy.

DOPAMINE, AROUSAL, CREATIVE DRIVE AND IDEA GENERATION

Dopamine in the mesolimbic pathway increases general arousal and goal directed behaviors and decreases latent inhibition; all three effects increase the creative drive of idea generation. This has led to a three-factor model of creativity involving the frontal lobes, the temporal lobes, and mesolimbic dopamine.^[34]

Behavior disorders

Pharmacological blockade of brain dopamine receptors increases rather than decreases drug-taking behavior. Since blocking dopamine decreases desire, the increase in drug-taking behaviour may be seen as not a chemical desire but as a deeply psychological desire to just 'feel something'.

The effect of reduced DOPAMINE

In humans, however, drugs that reduce dopamine activity (neuroleptics, e.g. some antipsychotics) have been shown to reduce motivation, and to cause anhedonia a.k.a. the inability to experience pleasure.^[13] Selective D2/D3 agonists pramipexole and ropinirole, used to treat Restless legs syndrome, have limited anti-anhedonic properties as measured by the Snaith-Hamilton Pleasure Scale.^[14] (The Snaith-Hamilton-Pleasure-Scale (SHAPS), introduced in English in 1995, assesses self-reported anhedonia in psychiatric patients.)

Additionally, users of stimulants often have depleted dopamine levels after withdrawal from these sometimes addictive substances.

Sociability is also closely tied to dopamine neurotransmission. Low D2 receptor-binding is found in people with social anxiety. Traits common to negative schizophrenia (social withdrawal, apathy, anhedonia) are thought to be related to a hypodopaminergic state in certain areas of the brain.

Abnormalities in dopaminergic neurotransmission have also been demonstrated in painful clinical conditions, including burning mouth syndrome,^[26] fibromyalgia ^{[27] [28]} and restless legs syndrome.^[29]

Salience

Dopamine may also have a role in the salience ('noticeableness') of perceived objects and events, with potentially important stimuli such as: 1) rewarding things or 2) dangerous or threatening things seeming more noticeable or important.^[31] This hypothesis argues that dopamine assists decision-making by influencing the priority, or level of desire, of such stimuli to the person concerned.

Since blocking dopamine decreases desire, the increase in drug-taking behaviour may be seen as not a chemical desire but as a deeply psychological desire to just 'feel something'.

Deficits in dopamine levels are implicated in attention-deficit hyperactivity disorder (ADHD), and stimulant medications used to successfully treat the disorder increase dopamine neurotransmitter levels, leading to decreased symptoms.

Dopamine is reduced by Sympathectomy

Dopamine has many functions in the brain, including important roles in behavior and cognition, motor activity, motivation and reward, inhibition of prolactin production (involved in lactation), sleep, mood, attention, and learning. Dopaminergic neurons (i.e., neurons whose primary neurotransmitter is dopamine) are present chiefly in the ventral tegmental area (VTA) of the midbrain, substantia nigra pars compacta, and arcuate nucleus of the hypothalamus.
In the frontal lobes, dopamine controls the flow of information from other areas of the brain. Dopamine disorders in this region of the brain can cause a decline in neurocognitive functions, especially memory, attention, and problem-solving. Reduced dopamine concentrations in the prefrontal cortex are thought to contribute to attention deficit disorder. It has been found that D1 receptors are responsible for the cognitive-enhancing effects of dopamine.^[7]

Effect of reduced Dopamine

Enlargement of the Breast—A New Side Effect of Transaxillary Cervical Sympathectomy: Case Report

http://ves.sagepub.com/cgi/content/abstract/20/1/50

Breast enlargement after thoracoscopic sympathectomy
http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B7XNJ-4S7S2X0-1&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=3f96573d845688f9c13551c594353d73

Mia: Dopamine is also a neurohormone released by the hypothalamus. Its main function as a hormone is to inhibit the release of prolactin from the anterior lobe of the pituitary.
Prolactin has many effects including regulating lactation, orgasms, and stimulating proliferation of oligodendrocyte precursor cells.
It stimulates the mammary glands to produce milk (lactation): Increased serum concentrations of prolactin during pregnancy cause enlargement of the mammary glands of the breasts.

A comparison is made with the present opinion on activation of parasympathetic and blockade of sympathetic nerves to explain the various symptoms of a cluster attack.

The Involvement of Trigeminal Substance P Neurons in Cluster Headache. An Hypothesis

Jan Erik Hardebo , M.D.

From the Department of Neurology and Department of Histology, University of Lund, Lund, Sweden.

Headache: The Journal of Head and Face Pain

Volume 24 Issue 6, Pages 294 - 304

Published Online: 22 Jun 2005

The present evidence suggests that the tonic discharge of normally functioning sympathetic nerves is capable of facilitating the response to angiotensin and that sympathectomy results in an abolition of this effect.

Effect of Acute Sympathectomy on Responses to Angiotensin and Norepinephrine

B. G. Zimmerman Ph.D.¹
(Circulation Research. 1962;11:780.)
© 1962 American Heart Association, Inc.

Parallels between post sympathectomy patient's symptoms and Chronic Fatigue Syndrome

Dr. Goldstein's CFS/FM protocol revolves around his understanding of these ailments as neurosomatic disorders. In helping to define such disorders, Dr. Goldstein says patients afflicted "do not feel, think, or function properly because the brain does not handle information properly." According to his research, Dr. Goldstein believes brain circuitry and transmittal of data for proper bodily function and health have become altered in conditions like CFS. Further, Dr. Goldstein comments "how the brain, the immune system, and the hormonal system simultaneously regulate the function of each other…is usually 'out of whack' in various ways in patients with neurosomatic disorders."

Dr. Goldstein believes that neurotransmitters, chemical substances that act as information messengers in the brain, are abnormally low in this condition. Norepinephrine and dopamine are two such neurotransmitters lacking in CFS patients. When these are decreased, the brain has difficulty assessing relevance of the numerous messages it constantly receives. Because of this, mentally challenging situations such as taking a test or sensory stimulating situations such as a shopping at a mall can be overwhelming.

Another cause of this easily distractible state is elevated levels of substance P. Substance P is a chemical that transmits pain messages. Overproduction of substance P results in increased sensations of pain.
Article by John W. Addington on Jay A. Goldstein's book:

Betrayal by the Brain: The Neurologic Basis of Chronic Fatigue Syndrome, Fibromyalgia Syndrome, and Related Neural Network Disorders

Published by Haworth Press, 1996

Blockade of the sympathetic nervous system substantially degrades ligament

Kelley W. Dwyer,1,2 Paolo P. Provenzano,1,2 Peter Muir,3 Wilmot B. Valhmu,1 and Ray Vanderby, Jr.1,2
J Appl Physiol 96: 711–718, 2004.

The alpha-adrenergic sensitivity of smooth muscle following sympathectomy

The data obtained suggest alteration of pharmacological characteristics of smooth muscle alpha-adrenoceptors after interruption of the sympathetic nerve.
Fiziol Zh SSSR Im I M Sechenova. 1988 Sep;74(9):1287-93.

CARDIOVASCULAR REACTIVITY AS A MEASURE OF AUTONOMIC OR SYMPATHOADRENAL FUNCTION

http://www.psychosomaticmedicine.org/cgi/content/full/65/1/9

Compensatory sweating occurred in 87% of the patients serious in 36% and incapacitating in 6%)

Ann Thorac Surg. 2004 Nov;78(5):1801-7.

haemodynamic response to cardiac sympathetic denervation corresponded to the efferent effect of beta-receptor blockade

The sympathetic denervated heart showed little chronotropic response to anaesthetic and surgical stimulation. On the contrary, the parasympathetic response was predominant. An episode of severe bradycardia occurred during endotracheal suctioning prior to extubation. The haemodynamic response to cardiac sympathetic denervation corresponded to the efferent effect of beta-receptor blockade.
The haemodynamic effect of thoracoscopic cardiac sympathectomy
Lim-Sim Lee, Chien-Chih Lin, Seok-Mun Ng, Chung-Fai Au

European Journal of Surgery, British Journal of Surgery

Volume 164 Issue S1, Pages 37 - 38, Published Online: 2 Dec 2003

http://www3.interscience.wiley.com/journal/106568649/abstract

orthostatic hypotension increased significantly after ETS

Endoscopic thoracic sympathectomy attenuates reflex tachycardia during head-up tilt in lightly anesthetized patients with essential plamar hyperhidrosis

Journal of Anesthesia
Publisher	Springer Japan
ISSN	0913-8668 (Print) 1438-8359 (Online)
Issue	Volume 16, Number 1 / February, 2002

http://www.springerlink.com/content/dk8tq89wnhq4naqy/
The increase in heart rate in response to HUT (head-up tilt) was significantly reduced after surgery in the ETS group (from 34 ± 18 to 14 ± 11 beats·min⁻¹; P <>−1; P = 0.911). Orthostatic hypertension disappeared completely after ETS (from 5 of 11 to none of 11 patients; P = 0.035), whereas the prevalence of orthostatic hypotension increased significantly after ETS (from 3 of 11 to 9 of 11 patients; P = 0.030). In the control group, the prevalence of neither orthostatic hypertension nor orthostatic hypotension changed after surgery.

Endoscopic thoracic sympathectomy is prohibited for patients under 20 years old in Taiwan

Patients with severe compensatory sweating after ETS must change clothes several times a day (some patients complained that they change as often as 10 times a day), resulting in serious impact on work and social interaction. Patients suffering from such serious side effects in Taiwan have formed a support group based on an Internet discussion forum to request the government to take this problem seriously. Starting in October 2004, The Department of Health, Executive Yuan, Taiwan, has prohibited surgeons from performing this operation on patients under 20 years old. To our knowledge, this type of support group also exists in United States, England, Sweden, Spain and Japan (Table 1).

ETS is a relatively safe and simple procedure. However the side effects are possibly devastating All physicians providing this service and all peoples preparing to undergo this treatment should know this well.
Min-Huei Hsu (10 January 2005)
http://www.cmaj.ca/cgi/eletters/172/1/69#1908

Hperhidrosis is not due to sympathetic overactivity.

Our overall findings suggest that essential hyperhidrosis is a complex autonomic dysfunction rather than sympathetic overactivity, and parasympathetic system seems to be involved in pathogenesis of this disorder.
Dayimi Kaya, M.D.*, Semsettin Karaca, M.D.†, Irfan Barutcu, M.D.‡, Ali Metin Esen, M.D.‡, Mustafa Kulac, M.D.†, and Ozlem Esen, M.D.

Annals of Noninvasive Electrocardiology,

Volume 10 Issue 1, Pages 1 - 6

Published Online: 13 Jan 2005

ANS provides physiological stability

The autonomic nervous system dynamically controls the response of the body to a range of external and internal stimuli, providing physiological stability in the individual. With the progress of information technology, it is now possible to explore the functioning of this system reliably and non-invasively using comprehensive and functional analysis of heart rate variability. This method is already an established tool in cardiology research, and is increasingly being used for a range of clinical applications. This review describes the theoretical basis and practical applications for this emerging technique.

Functional assessment of heart rate variability: physiological basis and practical applications .

International Journal of Cardiology , Volume 84 , Issue 1 , Page 1

J . Pumprla

Copyright © 2003 Elsevier Inc

hyperhidrosis is based on a much more complex autonomic dysfunction than generalised sympathetic overactivity

Our highly interesting findings indicate that primary focal hyperhidrosis is based on a much more complex autonomic dysfunction than generalised sympathetic overactivity and seems to involve the parasympathetic nervous system as well.
Cardiac Autonomic Function in Patients Suffering from Primary Focal Hyperhidrosis
Peter Birner^a, Harald Heinzl^b, Monika Schindl^c, Jiri Pumprla^d, Peter Schnider^a
Eur Neurol 2000;44:112-116

Sympathectomy Suppresses Baroreflex Control of Heart Rate

Endoscopic Thoracic Sympathectomy Suppresses Baroreflex Control of Heart Rate in Patients with Essential Hyperhidrosis
Yurie T. Kawamata, MD*, Tomoyuki Kawamata, MD†, Keiichi Omote, MD†, Eiji Homma, MD*,
Tatsuo Hanzawa, MD*, Toshifumi Kaneko, MD‡, and Akiyoshi Namiki, MD†
(Anesth Analg 2004;98:37–9)


In this study, baroreflex control of HR was completely inhibited in 9 of 21 patients in the depressor test but in only 1 of 19 patients in the pressor test. All patients who showed complete inhibition had received bilateral T2-3 sympathectomy. Responses to decreased blood pressure are mediated by the sympathetic nervous system, whereas responses to increased blood pressure predominantly involve vagal compensation (13). Therefore, it seems that the effects of sympathetic denervation were most prominent in the de-
pressor test after ETS.
The suppression of baroreflex function can be detrimental during anesthetic management. In particular, a poorly preserved baroreflex response to decreasing blood pressure may exaggerate hemodynamic perturbation after a sudden loss of circulating blood volume.
In addition, it is possible that patients who have received ETS will show unexpected HR responses after the administration of a vasopressor or vasodilator. We conclude that baroreflex response as a compensatory function for hemodynamic changes is suppressed in patients who receive ETS.

Increased Lipid Deposits in the Iris following Sympathectomy

• Much interest has focused recently on the important role played by the smooth muscle
cell in the pathogenesis of atherosclerosis. This is because it is the smooth muscle cell of
the intimal and subintimal region which is involved early and to a marked degree by the
lipid deposits.

The eye provides a model system with three unique advantages: (1) the iris is rich in smooth
muscle cells which are well localized; (2) lipid deposits in the eye can be easily seen and their
progression can be followed visually; (3) certain experimental modifications can be readily
introduced into the model system during life. For example, the eye can be sympathetically
denervated. This deprives smooth muscle cells of the levator and iris dilator muscles of locally
released norepinephrine. It is increasingly recognized that norepinephrine exerts a regula-
tory effect on lipid metabolism.
1971;2;23-34 Stroke (Stroke is published by the American Heart Association)
ARMSTRONG JAMES AUSTIN, WILLIAM ROBERTS, HANS NEVILLE and DONALD

Autonomic dysequilibrium leading to obesity

Total chemical sympathectomy in experimental animals results in loss of shivering and nonshivering thermogenesis, and death within a few hours.

Further evidence suggesting that abnormal sympathetic activity may cause pain comes from reports of pain following sympathectomy. This has occurred after stellate ganglion block and lumbar sympathectomy.

A similar reduction of fat mobilization from fat depots occurs after VMH lesions, as after local sympathectomy, suggesting that the sympathetic pathway to the adipose tissue runs through the VMH.
Bray and York hypothesize that the change in energy balance in animals after VMH lesions is a result of autonomic dysequilibrium. The sympathetic outflow is reduced and the parasympathetic outflow increased. This shift in balance results in hyperinsulinemia and altered metabolic pathways leading to obesity. During the digestion and metabolism of a meal, the autonomic nervous system provides important (but not sole) feedback control on satiety.

The Nervous System and Adipose Tissue, By Katharine Dalziel, MD, MBBS, MRCP
Clinics in Dermatology
October-December 1989, Volume 7, Number 4, pages 62-77

Neuroma following Sympathectomy

The authors conclude recomemnding the application of clips and if the syndrome nevertheless appears novocaine infiltration of the upper end of the sympathetic chain. The authors are convinced that the theory of Hermann and Cooley about neuroma formation at the ends of the sympathetic chain after resection of a segment is true.
http://www.revangiol.com/sec/resumen.php?or=web&i=e&id=227082.

Traumatic neuroma follows different forms of nerve injury (often as a result of surgery). They occur at the end of injured nerve fibres as a form of ineffective, unregulated nerve regeneration; it occurs most commonly near a scar, either superficially (skin, subcutaneous fat) or deep (e.g., after a cholecystectomy). They are often very painful. It is also known as "pseudoneuroma".

postsympathectomy syndrome

In both groups two cases of postsympathectomy syndrome were seen, with one leg being colder and dryer than the other.

Clinical Orthopaedics & Related Research. 360:122-126, March 1999.

neuropathic and central deafferentation/reafferentation syndrome

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.

Pain. 1996 Jan;64(1):1-9
http://www.ncbi.nlm.nih.gov/pubmed/8867242?ordinalpos=2&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum

Postsympathectomy pain and changes in sensory neuropeptides

Postsympathectomy limb pain, postsympathectomy parotid pain, and Raeder's paratrigeminal syndrome are pain states associated with the loss of sympathetic fibres and in particular with postganglionic sympathetic lesions. There is a characteristic interval of about 10 days between surgical sympathectomy and onset of pain. It is proposed that this pain in man is correlated with the delayed rise in sensory neuropeptides seen in rodents after sympathectomy. These chemical changes probably reflect the sprouting of sensory fibres and may result from the greater availability of nerve growth factor after sympathectomy. The balance between the sensory and sympathetic innervations of a peripheral organ may be determined by competition for a limited supply of nerve growth factor.
Lancet. 1985 Nov 23;2(8465):1158-60
http://www.ncbi.nlm.nih.gov/pubmed/2414615?dopt=Abstract

sensory abnormalities, abnormal body sweating, and pathologic gustatory sweating

The aim of this study is to describe the incidence and characteristics of pain, sensory abnormalities, abnormal body sweating, and pathologic gustatory sweating in pain patients with persistent post-sympathectomy pain.
Results: Seventeen adults (13 females and 4 males) with a mean age of 37 years (range 25-52) at the time of sympathectomy met the inclusion criteria. Five of the 17 patients experienced temporary pain relief for an average of 4 months (range 2-12 months), 3/17 retained the same pain as before the surgery, 1 patient was cured of her original pain but experienced a new debilitating pain, and 8/17 patients continued to have the same or worse pain in addition to a new or expanded pain. Pathologic gustatory sweating was present in 7/11 patients asked, and abnormal sweating (known as compensatory hyperhidrosis) in 11/13 patients asked. Discussion: The present study does not allow for conclusions about the effectiveness of surgical sympathectomy for neuropathic pain. However, our findings indicate that if the pain persists after the procedure, the complications may be quite serious and at times worse than the problem for which the surgery was originally performed.
The Clinical journal of pain
2003, vol. 19, n^o3, pp. 192-199
http://cat.inist.fr/?aModele=afficheN&cpsidt=14775091

Recurrent sweating occurred in 17.6% of patients

J Neurosurg Spine. 2005 Feb;2(2):151-4.
http://www.ncbi.nlm.nih.gov/pubmed/15739526

Post-sympathectomy the peripheral vascular failure or the reduced cardiac chronotropic response can impair the body’s capacity to compensate for shock

First, the abolition of sweating from the upper body as well as the axillae and both upper limbs may have significantly reduced the capacity of the patient to lose heat through sweating during exercise. Anhidrosis in the head and neck after sympathectomy affects a proportion of patients, but is often neglected in most reports of post-sympathectomy complications [3]. The loss of head and neck sweating in this patient may have further impaired overall heat loss. However we would also note that the degree of heat loss impairment after sympathectomy has never been quantified, and its effect on body temperature during exercise remains to be established.

Second, thoracic sympathectomy has been demonstrated to abolish or alter sympathetic vasoconstrictive responses in the skin, and this may contribute to abnormal peripheral vascular responses to temperature [4]. Paradoxically it has been suggested that in some cases there may be abnormal vasoconstriction rather than the expected vasodilatation after sympathectomy [5]. It is not impossible that such atypical peripheral vascular responses to rising body temperature may have contributed to impaired heat loss during exercise or to an inappropriate response to shock on the development of the heat stroke.
In the post-sympathectomy patient, the abnormal sympathetic skin response may lead to peripheral vascular failure or the reduced cardiac chronotropic response may impair the body’s capacity to compensate for shock. These may have contributed to the rapid development of shock and severe multiple organ dysfunction syndrome in this patient.

Third, it has been shown that thoracic sympathectomy can impair the autonomic nervous system’s increase of the heart rate in response to exercise [6]. Although absolute tachycardia is not eliminated, given the endocrine and paracrine stimuli during exercise, the maximum heart rate reached during exercise has been shown to be significantly reduced after sympathectomy. Thus for a given workload during exercise, there will be a relative bradycardia. This may possibly affect the circulatory system’s ability to convey heat from the body core to the extremities for heat loss.

Is Previous Thoracic Sympathectomy a Risk Factor for Exertional Heat Stroke?

Alan D.L. Sihoe, FRCSEd(CTh)^a,_*, Raymond W.T. Liu, MRCP^b, Alex K.L. Lee, MRCP^b, Chak-Wah Lam, FHKAM^b, Lik-Cheung Cheng, FRCS^a
http://ats.ctsnetjournals.org/cgi/content/full/84/3/1025

Atrial Fibrillation chemically induced

Pituitary adenylate cyclase-activating polypeptide-27 causes a biphasic chronotropic effect and atrial fibrillation in autonomically decentralized, anesthetized dogs.
Author: Hirose, M : Furukawa, Y : Nagashima, Y : Lakhe, M : Chiba, S

J-Pharmacol-Exp-Ther. 1997 Nov; 283(2): 478-87

Effect of local autonomic denervation on in vitro responsiveness of lymphocytes

The results further indicate that an appropriate sympathetic and parasympathetic local environment may be needed for immunomodulation, as well as for cyclosporine activity in lymphoid tissue.
Journal of the Autonomic Nervous System
Volume 62, Issue 3, 17 February 1997, Pages 155-162
http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T05-3PKTG6C-6&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=da81efda6c250763623b89537aed8109

Origins of the sympathetic projections to rat thyroid and parathyroid glands

These results indicate that postganglionic sympathetic perikarya innervating the thyroid-parathyroid territory are located in the middle and/or inferior cervical ganglia and send their axons through the SCG and the external carotid nerve to these glands.
http://lib.bioinfo.pl/pmid:3772028

J Auton Nerv Syst. 1986 Sep ;17 (1):63-70 3772028

stress responses and adrenal sensitivity to ACTH.

Walker CD.
Chemical sympathectomy and maternal separation affect neonatal stress responses and adrenal sensitivity to ACTH.
Am J Physiol Regul Integr Comp Physiol 268: R1281–R1288, 1995.

Decrease in neuronal uptake of noradrenaline

Shibata K, Takei S, Kawai T, Imaizumi Y, and Watanabe M.
Decrease in neuronal uptake of noradrenaline simply explains the supersensitivity
after sympathectomy in the rat iris dilator.
Jpn J Pharmacol 50: 19 –29, 1989.D

Sympathetic nervous system activity in rat thyroid: potential role in goitrogenesis

Unilateral superior cervical ganglion decentralization led to a reduction in thyroid weight, in ¹²⁵I uptake by thyroid tissue, and in TSH-induced stimulation of ¹²⁵I uptake in decentralized hemithyroids. These results suggest that sympathetic activity in thyroid contributes to gland enlargement and may modulate tissue responsiveness to TSH.
Am J Physiol Endocrinol Metab 288: E861-E867, 2005. First published December 7, 2004
http://ajpendo.physiology.org/cgi/content/full/288/5/E861

lack of free noradrenaline after sympathectomy

The similarity of the ultrastructural changes in the light pinealocytes occurring after sympathectomy and after continuous illumination was striking. It is supposed that these changes have a common cause,viz. the lack of free noradrenaline, the pinealotropic neurotransmitter.
Journal of Neural Transmission Volume 36, Numbers 3-4 / September, 1975
http://www.springerlink.com/content/j121443576128248/

SYMPATHETIC REINNERVATION DOES NOT RESTORE NORMAL FUNCTION

SYMPATHETIC REINNERVATION OF THE PINEAL GLAND AFTER
POSTGANGLIONIC NERVE LESION DOES NOT RESTORE NORMAL
PINEAL FUNCTION’
C. W. BOWERS,’ C. BALDWIN, AND R. E. ZIGMOND3
Department of Pharmacology, Harvard Medical School, Boston, Massachusetts 02115
Received October 6, 1983; Revised January 5, 1984; Accepted February 17, 1984

www.jneurosci.org/cgi/reprint/4/8/2010.pdf

Degeneration activity of the pineal gland after sympathetic denervation

The present findings confirm that, in endocrine glands and similarly to other autonomically innervated organs, acute denervation induces degeneration acitivity.
http://www.springerlink.com/content/u573421xk753rk83/

Syncope - neurologic or mechanical causes

among others:
Shy-Drager syndrome
Sympathectomy
Primary autonomic insufficiency
http://www.wrongdiagnosis.com/j/jervell_and_lange_nielsen_syndrome/book-diseases-6a.htm