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

side effects, ranging from trivial to devastating

There seem to be no controlled studies demonstrating efficacy of neurolytic sympathetic blocks. Possible side effects, ranging from trivial to devastating, are of even greater importance with these more permanent procedures—painful sequelae may include phe-
nol or alcohol neuritis and postsympathectomy pain (sympathalgia), which can also occur after surgical sympathectomy.

The involvement of the sympathetic nervous system in causalgia and reflex sympathetic dystrophy, which for ms the rationale for treatment by sympathetic interruption, has been questioned, and the issues discussed here raise further questions. Contrary to predictions from experimental data, interrupting the sympathetic nervous system in practice seems futile for obtaining long term relief of pain in many if not most of these patients. How to identify the minority of patients whose pain might respond to these procedures is the next task, but fresh approaches to management are also required.

G D Schott Consultant neurologist
Interrupting the sympathetic outflow in causalgia and reflex sympathetic dystrophy - A futile procedure for many patients
The National Hospital for Neurology and Neurosurgery, London
1998;316;789-790 BMJ

20% of patients attending chronic pain clinics implicated surgery as one of the causes of their chronic pain

Chronic pain after surgery has until recently been a neglected topic. The extent of the problem first came to light in a survey of patients attending pain clinics in Scotland and the north of England.¹⁷ This survey showed that about 20% of patients attending chronic pain clinics implicated surgery as one of the causes of their chronic pain and, in about half of these, it was the sole cause. An extensive literature search failed to produce any references on the general topic of chronic pain after surgery. There were, however, almost 400 references on chronic pain after specific operations, such as mastectomy, cholecystectomy and thoracotomy. The information from this literature search formed the basis of a chapter, entitled ‘Chronic postsurgical pain’,³³ in Epidemiology of Pain, edited by I. K. Crombie and published by the IASP Press in 1999.
http://bja.oxfordjournals.org/cgi/content/full/87/1/88?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=sympathectomy&searchid=1&FIRSTINDEX=20&resourcetype=HWCIT

Blood diverted from muscle to skin after sympathectomy

However, the clinical results of both surgical and neurolityc sympathectomy are uncertain. Indeed these procedures lead to a redistribution of the blood flow in the lower limbs from the muscle to the skin, with a concomitant fall of the regional resistance, mainly in undamaged vessels. The blood flow will be diverted into this part of the vascular tree, so that a
"stealing" of the blood flow may occur.
Vito A. Peduto, Giancarlo Boero, Antonio Marchi, Riccardo Tani
Bilateral extensive skin necrosis of the lower limbs following prolonged epidural blockade
Anaesthesia 1976; 31: 1068-75.

excessive intracranial hypertension following sympathectomy

Increase in Kaolin-Induced Intracranial Hypertension after Decentralization of the Superior Cervical Sympathetic Ganglia in Rabbits

In fact, most of the animals in this group died in the course of the experiment, due to the excessive intracranial hypertension which was more than a tenfold increase compared to normal rabbits. It is suggested that the increased VFP following sympathetic denervation is a result of increased cerebral blood volume (vasodilation) together with increased production of cerebrospinal fluid (loss of inhibitory adrenergic nerve activity in the choroid plexuses).

L. Edvinsson, K.C. Nielsen, C. Owman, K.A. West

Departments of Histology and Neurosurgery A, University of Lund, Lund, and Neurosurgical Clinic, University Hospital, Umeå

Address of Corresponding Author

Eur Neurol 1974;11:296-303 (DOI: 10.1159/000114327)

http://content.karger.com/ProdukteDB/produkte.asp?Aktion=ShowPDF&ArtikelNr=114327&Ausgabe=234447&ProduktNr=223840&filename=114327.pdf

inflammation and pain in teeth

Unilateral sympathectomy induced a significant increase in cell density both in the inflamed and in the uninflamed dental pulp bilaterally. Our results demonstrate, for the first time, a trophic effect of the sympathetic nerves on cells in the dental pulp, indicating that an imbalance of sympathetic nerves may induce inflammation and pain in teeth.
Received 7 July 2000; accepted 8 January 2001. ;

Available online 4 March 2002.

http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6WFG-458NJTW-2R&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=3f63f4106e411d92b1ce5168c2b07fde

Circulatory changes in the blood flow in the human skin and muscle following sympathectomy.

J Physiol. 1951 Sep ;115 (1):9p-10p 14889441 (P,S,G,E,B)

http://lib.bioinfo.pl/pmid:14887106

[My paper

Observations on dye excretion through synovial membrane after lumbosacral sympathectomy and circulatory obstruction.

[My paper] K K CHENG

Q J Exp Psychol. 1949 Jun ;35 (2):135-43 18135572 (P,S,G,E,B)

Influence of sympathectomy in humans on the rhythmicity of 6-sulphatoxymelatonin urinary excretion - effect on pineal gland

Morten Møller, Ole Osgaard, Michael Grønbech-Jensen

Inst. Med. Anatomy, University of Copenhagen, Panum Institute, Blegdamsvej 3, DK-2200 Copenhagen, Denmark.

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.

http://lib.bioinfo.pl/pmid:16647807

Mol Cell Endocrinol. 2006 Apr 27; : 16647807 (P,S,G,E,B,D)

Sympathectomy decreases and adrenergic stimulation increases the release of tissue plasminogen activator (t-PA) from blood vessels: Functional evidence for a neurologic regulation of plasmin production within vessel walls and other tissue matrices

Journal of Neuroscience Research

Published Online: 25 Aug 1999
http://www3.interscience.wiley.com/journal/63500193/abstract?CRETRY=1&SRETRY=0

Effect of cardiac catecholamine depletion through sympathectomy on spontaneous ventricular fibrillation during induced hypothermia in cats

Cellular and Molecular Life Sciences (CMLS)
Volume 24, Number 12 / December, 1968
SpringerLink DateFriday, September 30, 2005
http://www.springerlink.com/content/k391462541tk34x3/

Sympathectomy for Jervell and Lange-Nielsen syndrome

Jervell and Lange-Nielsen syndrome: neurologic and cardiologic evaluation - An indication for cervicothoracic sympathectomy

Authors: Ilhan A.¹; Tuncer C.; Komsuoglu S.S.; Kali S.

Source: Pediatric Neurology, Volume 21, Number 5, November 1999 , pp. 809-813(5)

http://www.ingentaconnect.com/content/els/08878994/1999/00000021/00000005/art00100;jsessionid=4g96ls07h8ihb.alexandra?format=print

What is Jervell and Lange-Nielsen syndrome?

Jervell and Lange-Nielsen syndrome is a condition that causes profound hearing loss from birth and a disruption of the heart's normal rhythm (arrhythmia). This disorder is a form of long QT syndrome, which is a heart condition that causes the heart (cardiac) muscle to take longer than usual to recharge between beats. Beginning in early childhood, the irregular heartbeats increase the risk of fainting (syncope) and sudden death.
http://ghr.nlm.nih.gov/condition=jervellandlangenielsensyndrome

After sympathectomy, all other options are made ineffective

The relapse of Raynaud's phenomenon after surgically sufficient sympathectomy could not be treated by reserpine or alfa-adrenergic receptor blockers in two patients in whom this was tried.
http://www.ncbi.nlm.nih.gov/pubmed/6941602?dopt=Abstract
Acta Chir Scand Suppl. 1980;502:57-62.

Ultrastructural changes in the nerves innervating the cerebral artery after sympathectomy

Volume 109, Number 4 / December,1970
http://www.springerlink.com/content/l7213648355u2088/

Cold Hypersensitivity after Sympathectomy for Raynaud's Disease

Two patients with socially handicapping Raynaud's disease underwent bilateral upper thoracic sympathectomy. One to two days after the operation, both developed local hypersensitivity to cold in the form of a rebound. The cold hypersensitivity persisted in one of the patients, although complete degeneration of vasoconstrictor fibres was proven by absence of the sympathetic veno-arteriolar reflex after sympathectomy. Pre-operative sympathetic blockade could not predict the outcome of sympathectomy.
Scandinavian Cardiovascular Journal, Volume 14, Issue 1 1980 , pages 109 - 111

Information provided to patients regarding side-effects

Mia: The information on the different websites shows great variation in what is disclosed to patients. The full impact of the surgery is never fully explained, but there is indication that some of the surgeons allow more information to appear. The question is: how they narrate this information?! Several of the ETS surgeons list more negative side-effects but they immediately discredit the information as a hearsay, never proven and unscientific. This way they covered the bases without frightening away the patient. Keep in mind, it is an elective surgery.


So far over 70 surgeons (esp. those who are the best known in the field and published the most) have been approached with the request to put a link to this BLOG on their information sheet/website, so that patients are aware of the potential risks associated with sympathectomy and can make an INFORMED decision. So far NONE of the surgeons agreed to do so, even though the material published here is from the medical journals already published.


List of complications from a transcript: Court of Appeals of Texas,San Antonio 2008,
Vaughan v. Nielson

(The highlighted side-effects are rarely disclosed by surgeons)


Possible perforation of breast implants if present

Sensitive Pleurae (chest lining sensitivity) limiting exercise

Horners Syndrome occurrence rate 0.3%

Heat intolerance

Pneumothorax (collapsed lung)

Bleeding

Postop Neuralgia and parasthesias are uncommon

Possible hair loss

Bradycardia (slow heart rate) possibly requiring a pacemaker (SIC!)

Subcutaneous emphysema

Possible conversion to open thoracotomy

Possible recurrence of symptoms

http://209.85.173.132/search?q=cache:WSfz4lbpQ1EJ:lawandmedicine.law.miami.edu/wp-content/uploads/2008/09/vaughan_nielson.doc+%22split+body+syndrome%22&hl=en&ct=clnk&cd=3&gl=us&client=safari