The amount of compensatory sweating depends on the patient, the damage that the white rami communicans incurs, and the amount of cell body reorganization in the spinal cord after surgery.
Other potential complications include inadequate resection of the ganglia, gustatory sweating, pneumothorax, cardiac dysfunction, post-operative pain, and finally Horner’s syndrome secondary to resection of the stellate ganglion.
www.ubcmj.com/pdf/ubcmj_2_1_2010_24-29.pdf

After severing the cervical sympathetic trunk, the cells of the cervical sympathetic ganglion undergo transneuronic degeneration
After severing the sympathetic trunk, the cells of its origin undergo complete disintegration within a year.
http://onlinelibrary.wiley.com/doi/10.1111/j.1439-0442.1967.tb00255.x/abstract

Thursday, December 18, 2008

EFFECTS OF SYMPATHECTOMY ON catecholamine concentrations ...

Effects of surgical sympathectomy on catecholamine concentrations ...

completely depleted from the pineal gland. These results. suggest that NE in the pineal gland ... amine declines following sympathectomy. Bjrrklund et al. 4 ...
www.springerlink.com/index/QP13674817684227.pdf - Similar pages - Note this
More results from www.springerlink.com »

CARDIOVASCULAR CHANGES POST SYMPATHECTOMY

Short- and Long-term Effects
Pulse rates taken at rest and after effort were significantly
lower than those taken after operation, and the blood pressure
response to exercise was blunted. ECG tracings showed a sig-
nificant change in the electrical frontal plane axis and shortening
of the QTc interval.

Tel-Hashomer, and Tel Aviv University Sackler Medical
School, Tel Aviv, Israel, and the National Heart,
Lung, Blood Institute, National Institutes of Health,t Bethesda, Maryland

SYMPATHECTOMY CAUSES PARTIAL AUTONOMIC FAILURE

NIH Book: Sympathectomy is "Neurocardiologic Disorder"

SURGICALLY INDUCED autonomic disfunction

HEAT STROKE AFTER SYMPATHECTOMY

As you - I mean your body - will have no control over thermoregulation, and you will not be able to cool off from your head (the top of your head gets rid of 40% of your body's heat, but it will be unable to do so. Completely!), even small exertion will cause a major drain on your system. Effectively you will be cut into two separate bodies: the top part of the body will be in constant hyperthermia - overheating your brain..., and the lower part from the shoulders down in constant hypothermia. One hot the other always cold, because of the changes in the circulation, and the thermoregualtory dysfunction. Your head will not know how hot your body is, as the signals from the body going to the brain are cut. The adipose tissue has been denervated, so it will not be able to send 'reading' the body's temperature ..or to send signals... Because your head is constantly hot, it thinks, asumes, that your body is as hot as the head (would make sense....but not any more), so it goes into overdrive to cool off where it can, to sweat where it can: from the shoulders or nipple line - again - depending on the level where the sympathetic chain was cut. On the shoulders up, neck and face you will not sweat any more, - this condition is called anhidrosis, - your skin will become dry, brittle, flaky, eliminating the skins natural cleansing process, that happens through sweating. It will also affect the circulation of the scull and the hair growth. There have been reports of the changes in hair colour, in fact becoming ..grey following sympathectomy. Hair loss has been also reported.
The surgery is also performed in cases where they have to do skin grafting, in order to reduce the immune responses of the skin, so it will not reject the new skin. It will make your skin more vulnerable and prone to infections. In general it will change your body's immune responses and make you more vulnerable to certain diseases and conditions. Arthritis is one of them.

bioinfo.pl
Ann Thorac Surg. 2007 Sep ;84 (3):1025-7 17720429
Is previous thoracic sympathectomy a risk factor for exertional heat stroke?
Alan D L Sihoe , Raymond W T Liu , Alex K L Lee , Chak-Wah Lam , Lik-Cheung Cheng
We report the case of a physically fit young man who presented with severe, life-threatening heat
stroke after running a 10 km road race. He had previously received bilateral thoracic
sympathectomy for axillary hyperhidrosis at another hospital, and was known to have upper body
and limb anhidrosis. Thoracic sympathectomy can result in reduced sweating and disturbed
peripheral vascular and heart rate responses. Patients should be warned that these mechanisms may play a role in the development of exertional heat stroke.

SYMPATHECTOMY and the drugs you should not take

VISKEN®
(pindolol)

INTERACTIONS

Potentiation of the antihypertensive effect occurs with ganglionic or peripheral adrenergic
blocking drugs and in the post-sympathectomy patient (see “PRECAUTIONS”). Calcium
antagonists and antiarrhythmics (see “WARNINGS”).

SYMPATHECTOMY causing damage

The damage to the sympathetic ganglia, be it in the form of sympathectomy, chemical sympathectomy, and radiofrequency (all of these sympathectomies are cardinal sins), or repetitive stellate ganglion blocks are damaging (causing "Virtual Sympathectomy") and can complicate the chronic CRPS pain further rather than helping the patient.

SYMPATHECTOMY IS A FAILURE

CRC Press, Boca Raton, Florida

H. Hooshmand, M.D.

CAUSE OF FAILURE AFTER SYMPATHECTOMY

1. Sympathectomy is analogous to the act of killing the messenger. The sympathetic nervous system has the critical job of properly controlling and preserving the circulation in different parts of the body, especially in the extremities. By paralyzing the system, the extremity will be more apt to have disturbance of circulation and is left unprotected from fluctuation in circulation.

Sympathectomy is similar to permanently removing the central heat and air-conditioning system and never replacing it because of malfunction.

Sympathectomy permanently damages the temperature regulatory system. The reason sympathectomy does not cause side effects other than ineffective control of pain as well as impotence and orthostatic hypotension is because it is invariably partial and incomplete.
4. Usually the patients that end up needing sympathectomy are the ones who suffer from ephaptic dystrophy. Sympathectomy in such cases cause a classic Cannon phenomenon. This physiological phenomenon refers to the fact that the end organ that is controlled by sympathetic nerve fibers will become uninhibited in its chemical dysfunction. As a result, even though the sympathetic fibers are not contributing to acetylcholine or become uninhibited with resultant increase of pain input.

In diabetic neuropathy RSD, sympathectomy dramatically relieves the pain for the first 1 to 3 years. Then deafferentation can Cannon phenomenon set in. As a result, invariably by the second to fifth year the patient ends up with a lot more pain. Sympathetic blocks repeated every 6 to 12 months yield similar results.
In patients who have had sympathectomy, thermography shows an increase of temperature in the focus of ephaptic nerve damage (Cannon phenomenon) with secondary increase of pain and discomfort.

http://www.rsdrx.com/sympathectomy_failure.htm

SYMPATHECTOMY IS AN EXPERIMENT

Article
Sympathectomy as an experiment in human physiology
J. Paterson Ross
Surgical Professorial Unit, St. Bartholomew's Hospital
A Hunterian Lecture delivered at the Royal College of Surgeons, February 3, 1933.
ABSTRACT

(P.S.: It is still an experiment! There has been no objective trial or study into the effectiveness, safety and efficiacy of the procedure. No real long-term study into the effects of the surgery. There has been one study that reported that 25% of the patients operated for palmar HH said that their original condition returned within 5 years. Remember? Nerves regenerate. The sympathetic chain does not. You might end up with the return of your original symptoms, plus the many adverse effects of the surgery (decreased heart rate, lung function, abolished homeostasis, inability to maintain the correct bloodpressure, high plasma NOREPHRINE, that has been associated with joint inflammation, arthritis, also: 95 % of the patients who underwent Sympathectomy ended up with Sclerosis within 6 years!!!, irrespective of the fact if they had diabetes or not, etc etc. )

article - cerebral damage, sympathectomy

Complications of endoscopic sympathectomy
Alan E. P. Cameron
Abstract
Four cases are presented in which complications occurred during or after thoracic endoscopic
sympathectomy (TES). In one patient inappropriate TES resulted in disabling hyperhidrosis. In one
patient laceration of the subclavian artery required major surgery. In two cases intraoperative
cerebral damage occurred. Training in TES is essential.
Copyright © 1998 Taylor and Francis

sympathectomy interrupts neural messages to many different organs, glands and muscles

Acquired cardiovascular disease following Sympathectomy

We found statistically significant differences (P < .05) in both time and frequency domains. Parameters that evaluate global cardiac autonomic activity (total power, SD of normal R-R intervals, SD of average normal R-R intervals) and vagal activity (rhythm corresponding to percentage of normal R-R intervals with cycle greater than 50 ms relative to previous interval, square root of mean squared differences of successive normal R-R intervals, high-frequency power, high-frequency power in normalized units) were statistically significantly increased after sympathectomy. Low-frequency power in normalized units, reflecting sympathetic activity, was statistically significantly decreased after sympathectomy. Low-/high-frequency power ratio also showed a significant decrease, indicating relative decrease in sympathetic activity and increase in vagal activity.

The Journal of Thoracic and Cardiovascular Surgery
Volume 137, Issue 3, March 2009, Pages 664-669

decreased conditioning-related activity in insula and amygdala after autonomic denervation

The degree to which perceptual awareness of threat stimuli and bodily states of arousal modulates neural activity associated with fear conditioning is unknown. We used functional magnetic neuroimaging (fMRI) to study healthy subjects and patients with peripheral autonomic denervation to examine how the expression of conditioning-related activity is modulated by stimulus awareness and autonomic arousal. In controls, enhanced amygdala activity was evident during conditioning to both "seen" (unmasked) and "unseen" (backward masked) stimuli, whereas insula activity was modulated by perceptual awareness of a threat stimulus. Absent peripheral autonomic arousal, in patients with autonomic denervation, was associated with decreased conditioning-related activity in insula and amygdala. The findings indicate that the expression of conditioning-related neural activity is modulated by both awareness and representations of bodily states of autonomic arousal.

http://www.ncbi.nlm.nih.gov/pubmed/11856537

Surgical and chemical sympathectomy can alter cellular proliferation

Surgical denervation and chemical sympathectomy can alter cellular proliferation, B- and T-cell responsiveness and lymphocyte migration in lymphoid organs [17].

In vitro studies have shown that neuropeptides can have numerous effects, either inhibiting or stimulating the proliferation, differentiation and functions of immune cells [19]* Development of systemic lupus erythematosus in mice is associated with alteration of neuropeptide concentrations in inﬂamed kidneys and immunoregulatory organs

Neuroscience Letters 248 (1998) 97– 100

Cell body reorganization in the spinal cord after elective surgery to treat sweaty palms

The amount of compensatory sweating depends on the patient, the damage that the white rami communicans incurs, and the amount of cell body reorganization in the spinal cord after surgery.

Other potential complications include inadequate resection of the ganglia, gustatory sweating, pneumothorax, cardiac dysfunction, post-operative pain, and finally Horner’s syndrome secondary to resection of the stellate ganglion.
www.ubcmj.com/pdf/ubcmj_2_1_2010_24-29.pdf

After severing the cervical sympathetic trunk, the cells of the cervical sympathetic ganglion undergo transneuronic degeneration
After severing the sympathetic trunk, the cells of its origin undergo complete disintegration within a year.
http://onlinelibrary.wiley.com/doi/10.1111/j.1439-0442.1967.tb00255.x/abstract

Spinal cord infarction occurring during thoraco-lumbar sympathectomy
J Neurol Neurosurg Psychiatry 1963;26:418-421 doi:10.1136/jnnp.26.5.418

Retrograde Changes in the Nervous System Following Unilateral Sympathectomy

In consequence of right-sided smpathectomy at the level of C5 it was found that in the sheep the cervical sympathetic trunk contains nerve fibres which proceed from cells situated in the first four segments of the thoracic part of the spinal cord and in the stellate ganglion. These fibres are about 85 per cent of all fibres of the sympathetic trunk.
http://onlinelibrary.wiley.com/doi/10.1111/j.1439-0442.1967.tb00255.x/abstract

Segmental myoclonus was associated with thoracic sympathectomy

Spinal myoclonus was associated with laminectomy, remote effect of cancer, spinal cord injury, post-operative pseudomeningocele, laparotomy, thoracic sympathectomy, poliomyelitis, herpes myelitis, lumbosacral radiculopathy, spinal extradural block, and myelopathy due to demyelination, electrical injury, acquired immunodeficiency syndrome, and cervical spondylosis.

http://www.ncbi.nlm.nih.gov/pubmed/3753263

Spinal myoclonus is typically associated with a localized area of damaged tissue (focal lesion). The injured area may include direct damage of the spinal cord or may cause abnormal changes in the function of the spinal cord.

http://www.wemove.org/myo/myo_pc.html

Spinal myoclonus following a peripheral nerve injury: a case report

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2526081/

cross-inhibitory control of various afferent in the spinal cord

In conclusion, our results suggest that cross-inhibitory control by various afferents in the spinal cord may exist in the feet as well as in the contralateral hand. The release of cross-inhibitory control by T3 sympathicotomy results in vasoconstriction and a decrease of skin temperature on the contralateral hand and the feet.

The basic neuronal network for this reciprocal organization is probably located in the spinal level (15). Therefore, the reduction in the contralateral skin temperature may be explained by cross-inhibitory control of various afferent in the spinal cord.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2722005/

Contralateral temperature changes of the finger surface during video endoscopic sympathectomy for palmar hyperhidrosis
http://www.ncbi.nlm.nih.gov/pubmed/8832515

Spinal Ischemic Stroke from complications of abdominal surgery, esp. sympathectomy

Viktor’s Notes℠ for the Neurosurgery Resident
Please visit website at www.NeurosurgeryResident.net
Updated: April 17, 2010

painful vasospastic condition in the right arm following surgical sympathectomy on the left side

decline in external heart work due to sympathectomy both at rest and under exercise

Hemodynamic changes in vertebral and carotid arteries were observed after sympathicotomy for PH

ATELECTASIS IS A COMMON PULMONARY COMPLICATION FOLLOWING THORACIC AND UPPER ABDOMINAL PROCEDURES

General anesthesia and surgical manipulation lead to atelectasis by causing diaphragmatic dysfunction and diminished surfactant activity. The atelectasis is typically basilar and segmental in distribution. After induction of anesthesia, atelectasis increases from 1 to 11% of total lung volume. End-expiratory lung volume is also found to be decreased.

Postoperative atelectasis is extremely common. Lobar atelectasis is also common. The incidence and prevalence of this disorder are not well documented.

http://emedicine.medscape.com/article/296468-overview#a0104

Atelectasis occurs regularly after induction of general anesthesia, persists postoperatively, and may contribute to significant postoperative morbidity and additional health care costs. Laparoscopic surgery has been reported to be associated with an increased incidence of postoperative atelectasis.

Anesth Analg 2009; 109:1511-1516

RESPONSE TO SYMPATHETIC BLOCKADE DEPENDS ON THE DEGREE OF SYMPATHETIC TONE BEFORE THE BLOCK

Denervation of preganglionic cardiac accelerator fibres leaving the cord at T1-T5 results in minimal vasodilatory consequences. Changes however in heart rate, left ventricular function and myocardial oxygen demand may occur due to high thoracic epidural blockade and are discussed below.

The major determinant of heart rate is the balance between sympathetic and parasympathetic systems with the latter predominating. A high thoracic epidural anaesthesia (TEA) covering the cardiac segments (T1-T4) produces small but significant reductions in heart rate4-8. During cardiac sympathetic denervation, parasympathetic cardiovascular responses, including those involved in baroreflexes, may dominate.

Individual cardiovascular response to different levels of sympathetic blockade varies widely, depending on the degree of sympathetic tone before the block.
Anaesth Intensive Care 2000; 28: 620-635
B. T. VEERING*, M. J. COUSINS†
Department of Anesthesiology, Leiden University Medical Center, Leiden, The Netherlands and Department of Anaesthesia and
Pain Management, University of Sydney, Royal North Shore Hospital, Sydney, New South Wales

limited sympathectomy does not reduce postoperative compensatory sweating

On univariate and multivariate analysis, the extent of denervation was not associated with the occurrence or the severity of compensatory sweating.

Compensatory sweating and temporary relief/recurrence were equally considered to be the main causes of dissatisfaction. CONCLUSION: Compensatory sweating was the most common long-term complication of thoracodorsal sympathectomy for primary hyperhidrosis. Its incidence and severity were not associated with the extent of sympathectomy.

http://www.ncbi.nlm.nih.gov/pubmed/12514588

cervical sympathectomy is a psychosurgery

Effects of upper abdominal sympathectomy on gastric acid, serum gastrin, and catecholamines

Selective upper abdominal sympathectomy increased basal acid output in rats but was without effect on stimulated acid output, serum gastrin concentration, and gastric mucosal histidine decarboxylase activity. The sympathectomy was verified by fluorescence histochemistry and determination of tissue catecholamines. A drastic reduction in tissue noradrenaline, adrenaline, and dopamine levels occurred after sympathectomy, and fluorescence microscopy showed a complete loss of adrenergic nerve fibers. Vagotomy reduced catecholamine levels in the stomach wall by 50% but did not affect the catecholamine content in the pancreas and small bowel. Surprisingly, combined vagotomy and upper abdominal sympathectomy resulted in lower catecholamine levels than sympathectomy alone in extragastric but not in gastric tissues.

http://www.ncbi.nlm.nih.gov/pubmed/6515311

our ignorance of the mechanisms of primary hyperhidrosis and of the effect of sympathetic ablation

Muliptle organ failure as a consequence of elective sympathectomy

In the post-sympathectomy patient, the abnormalsympathetic skin response may lead to peripheral vascular failureor the reduced cardiac chronotropic response may impair thebody’s capacity to compensate for shock. These may havecontributed to the rapid development of shock and severe multipleorgan dysfunction syndrome in this patient.
He had multiple organ dysfunction syndrome develop, with severerenal and hepatic failure, grade II hepatic encephalopathy,and disseminated intravascular coagulation. He responded remarkablywell to aggressive supportive measures including forced alkalinediuresis, and he was eventually discharged home after 1 month. The patient was previously a healthy, physically fit, nonsmoker.He worked as a body building trainer and led an active, sportylifestyle. The only significant medical history was that hehad received thoracic sympathectomy for axillary hyperhidrosis4 years ago at another hospital.

http://ats.ctsnetjournals.org/cgi/content/full/84/3/1025

the muscles that are supplied by these nerves shorten and tighten

This now well-established but generally under-appreciated principle of physiology is aptly known as 'Cannon's Law of Denervation Supersensitivity'. It describes the wide ranging effects of the complete loss of nerve inputs to a variety of bodily structures under experimental conditions. One of the many responses to nerves that are sick or dysfunctional (now termed Disuse Supersensitivity) is that the muscles that are supplied by these nerves shorten and tighten (due to the supersensitivity of both the muscle's specialized stretch receptors and motor nerve-muscle junctions), resulting not only in muscle spasm and stiffness which limit flexibility, but a whole sequence of pain compounding reactions. The two earliest are that localized taut bands of muscle fibers begin to compress the small specialized pain sensing (and now extra-sensitive) nerve fibers within the muscle (known as myofascial tender or trigger points) causing type 1 pain, and the compressed muscles do not allow proper blood flow in, or waste products to be removed. This leads to a build up of lactic acid, which further enhances the perception of pain through type 2 pain mechanisms. Continued and prolonged muscle shortening or contracture gradually leads to increased mechanical tension on the muscle's tendonous attachments to bone, causing all of the various tendonitis (types 1 & 2 pain) syndromes throughout the body. The end result is a truly vicious snowballing cycle of pain, with the muscle shortening further increasing pressure on the nerves.

www.northwestims.com/faq-4.html

Cannon's law of denervation tells us that if a post-ganglionic neurone has it's pre-ganglionic input removed, then it will become super-sensitive to the normal neurotransmitters that mediate that pre-ganglionic input. There is a variety of reasons for this, including up-regulation of receptors for the neurotransmitter(s), post-receptor effects, and impaired removal of neurotransmitters from the synapse

www.anaesthetist.com/anaes/patient/ans/

Most authors do not describe clinically significant capsular adhesions as a predominant finding in the chronic phase of this condition. Instead, pathologic data confirm an active process of hyperplastic fibroplasia and excessive type III collagen secretion that lead to soft-tissue contractures of the aforementioned structures (ie, the coracohumeral ligament, soft tissues of rotator interval, the subscapularis muscle, the subacromial bursae). However, these findings were observed in surgical patients who had severe and late-phase disease and cannot be applied to early phases of the disease.

From the chromosomal, cytochemical, and histologic points of view, the soft-tissue contractures are identical to those seen in a Dupuytren contracture of the hand. These contractures result in the classic progressive loss of ROM of the glenohumeral joint, which affects external rotation and abduction, then flexion, adduction, and extension (in descending order of severity). Despite these histopathologic similarities, the favorable and regressive outcome of adhesive capsulitis differs from the unfavorable and progressive outcome of Dupuytren disease.

http://emedicine.medscape.com/article/326828-overview#a0104

The courts have become the sole policing body for the medical profession

Major lawsuits, with the major judgments that go with them, may not completely keep negligent physicians from practicing, but they are the one way that currently exists to deter these individuals from practicing their inept brand of medicine. "

Over the years, we have given a lot of thought to why the medical profession adheres to this code of silence. What is it about this profession that causes it to protect its own at the expense of the public?"

Harvey F. Wachsman: Lethal Medicine

Publisher: Henry Holt & Co

All patients except one suffered from compensatory sweating

Complications in patients with palmar hyperhidrosis treated with transthoracic endoscopicsympathectomy.

Neurosurgery. 1997 Jul ;41 (1):110-3; discussion 113-5 9218302

OBJECTIVE: To assess the complications in a group of patients with palmar hyperhidrosis treated with transthoracic endoscopic sympathectomy. The extraordinarily high incidence of postoperative compensatory hyperhidrosis in our series is stressed and explained. METHODS: The retrospective study included chart reviews and outpatient assessments. Seventy-two patients underwent T2 or T2-T3 endoscopic sympathectomy for primary palmar hyperhidrosis. Patients' hyperhidrosis severity, precipitating factors, postoperative complications, surgical results, and satisfaction were assessed. Severity of palmar hyperhidrosis and compensatory hyperhidrosis was classified by two grading scales. RESULTS: The success rate ofsympathectomy was 93%. All patients except one suffered from compensatory sweating,which was the main cause of patients' dissatisfaction postoperatively. Seventeen percent of the patients (12 of 72 patients) experienced new symptoms of gustatory sweating (facial sweating associated with eating). Twenty-one patients experienced other complications, including pneumothorax, Horner's syndrome,nasal obstruction, and intercostal neuralgia.

'Emotional' sweating regulated by neocortex and limbic cortex

Careful observations showed that the forearm sweating responded diversely to various mental stimuli, unlike the palmar sweating whose response was always an increase. Mental arithmetic, mental testing and physical exercise caused an immediate increase in the palmar sweating but often elicited a transient decrease in the forearm sweating, whereas pain, noise, and emotional stimuli consistently provoked an increase of sweating on the forearm as well as on the palm. These observations suggest that the activities of higher centers, presumably involving neocortex and limbic cortex, exert various influences on the central mechanisms of palmar and generalized sweating.
Jpn J Physiol. 1975;25(4):525-36.
http://www.ncbi.nlm.nih.gov/pubmed/1206808

Very severe discomfort following sympathectomy with alarming frequency and intensity

a reduction of the muscular tone and to a secondary neurovascular disorder after sympathectomy

Neuroma following nerve injury/surgery

When a nerve is cut, the piece of nerve that is beyond the cut point eventually dies, however, its Schwann cells, the cells that encircle the nerve fibers remain for a much longer time. These Schwann cells secrete a chemical messenger known as nerve growth factor that tells the cut end of nerve where to grow back. So the cut end of nerve will send out multiple sprouts in the direction of the nerve growth factor, however, these sprouts do not go out in an orderly manner, instead they grow out in all directions and eventually cluster and form a knot of nerve fibers. This eventually leads to the formation of a TRUE neuroma or a END BULB or STUMP neuroma.

www.tarsaltunnelcenter.com/assets/recurrent.shtml

hyperhidrosis is not related with social phobia or personality disorder

The total reward dependence and persistence scores were significantly higher in hyperhidrosis patients. The fear of uncertainty in the harm avoidance scale was found to be significantly greater in hyperhidrosis patients. Regarding character dimensions, the total score in each of the subscales self-directedness, cooperativeness and self-transcendence was found to be higher in hyperhidrosis patients. Conclusion: The higher scores of all subscales of character dimensions in hyperhidrosis patients suggest that hyperhidrosis is not related with social phobia or personality disorder.

http://www.online.karger.com/ProdukteDB/produkte.asp?Aktion=ShowFulltext&ArtikelNr=99589&Ausgabe=232867&ProduktNr=224164

Use of stellate ganglion block for the treatment of psychiatric and behavioral disorders

The present invention is directed to a method for the treatment of a patient suffering from psychiatric and behavioral disorders, including post partum depression, post traumatic stress disorder, compulsive smoking, attention deficit hyperactivity disorder, gambling addiction, comprising the step of administering a stellate ganglion block to the patient to alleviate the symptoms. The stellate ganglion block may be followed by a sympathectomy to provide permanent relief.

United States Patent 20070135871

Kind Code: A1

http://www.freepatentsonline.com/y2007/0135871.html

slowing of the heart rate usually occurs on the second to fourth day after sympathectomy

The rate fell to a level between 40 and 6o per minute, the maximal slowing usually occurring on the second to fourth day after operation. Consistent slowing of the rate was not observed after a unilateral thoracic sympathectomy of either side. While there was some recovery from the maximum bradycardia with the passage of time in most patients, relatively slow resting cardiac rates and failure of tachycardia to develop with postural hypotension or exercise persisted in all patients.

Skoog's12 work has shown that there are marked differences in the number and precise location of the accessory ganglion cells in the cervical region in different patients and on the two sides in the same patient.
Annals of Surgery, 1949 October, Volume 130 Number 4

Receptor hypersensitivity is a common problem

Because of their size and location, injuries to the sympathetic ganglia or chain is rarely indicated or performed. Receptor hypersensitivity is a common problem after significant sympathetic injury, including clammy hands, erythema, and allodynia. When sympathetic nerves regenerate, they may establish aberrant connections to sensory receptors, muscles, or other sympathetics receptors; this may lead to an over-response or abnormal response.
http://wiki.cns.org/wiki/index.php/Injury,_Sympathetic_Nerve

he could not be thrilled in the sympathectomized half of his body

Sweet* has reported the case of a very intelligent patient, the dean of a graduate school, who after a unilateral sympathectomy to treat his upper limb hyperhidrosis, found that his previous and customary sensation of shivering while listening to a stirring passage of music occurred in only one side and he could not be thrilled in the sympathectomized half of his body. These cases were interesting because emotions are usually experienced in a rather diffuse and bilateral fashion unless innervation has been specifically interrupted. (p.134.)
Jose M.R. Delgado, M.D.
Physical control of the mind,
Harper Torchbooks, Harper & Row Publishers, 1971

*Sweet, W.H. Participant in "Brain Stimulation in Behaving Subjects". Neurosciences Research Program Workshop. Dec. 1966

Permanent thermoregulatory dysfunction after ETS

What you see here is not a result of the surgery gone wrong, this is the inevitable consequence of cutting/clamping the sympathetic chain, independently of skill of the surgeon, experience of the surgeon, T2, or T3, T4, or method used. Once the communication is disrupted, (and it happens with the clamping as well), it will disable the body's thermoregulation and will cause malfunctioning of the sympathetic nervous system. This damage is permanent and irreversible. There has been no controlled clinical trial into the effects of this surgery on humans or its safety, but it is still used for many conditions: angina pectoris, to lower blood pressure, to treat migraine, to reduce pain in cancer patients, to reduce immuneresponses after skin transplant, to treat various cancers in the oral cavity, and among many: to treat anxiety disorders, schizophrenia, and phobias. Every drug introduced into the market has to go through rigorous testing procedures before approval. This does not apply to surgeries. It is left to the surgeons to decide whether they offer sympathectomy or not. It is not based on scientific evidence and research but 'opinion' and business plan. Patients are rarely followed up and if they are, the questions asked are limited. Patient complaints about unexpected symptoms are dismissed as imagined - until you speak to someone who has an understanding of the ANS.

denervation supersensitivity of alpha recepors following sympathectomy

There is, however, considerable risk of developing a post-sympathectomy pain syndrome that may be the result of a denervation supersensitivity of alpha receptors.
www.mc.vanderbilt.edu/.../Complex%20Regional%20Pain%20Syndrome-1...

Paradoxically it has been suggested that in some cases there may be abnormal vasoconstriction rather than the expected vasodilatation after sympathectomy.
ats.ctsnetjournals.org/cgi/content/full/84

complex alterations of vascular reactivity

In conclusion, we showed that sympathectomy produces complex alterations of vascular reactivity both in vivo and in isolated vessels, which shift the balance of the sensitivity of the vessel between vasoconstrictor and vasodilating agents towards an increased constriction. These results are unlikely to simply reflect denervation supersensitivity; their underlying receptor, post-receptor and/or contractile mechanisms are yet to be identified. Journal of Hypertension. 18(8):1041-1049, August 2000.

Haematological changes during stress abolished by sympathectomy

http://www3.interscience.wiley.com/journal/120731423/abstract

Receptor hypersensitivity is a common problem

causes of autonomic dysfunction - sympathectomy

The finger wrinkling response is abolished by upper thoracic sympathectomy. The test is also abnormal in some patients with diabetic autonomic dysfunction, the Guillan-Barre syndrome and other peripheral sympathetic dysfunction in limbs. (p.46)

Other causes of autonomic dysfunction without neurological signs include medications, acute autonomic failure, endocrine disease, surgical sympathectomy . (p.100)

Disorders of the Autonomic Nervous System

By David Robertson, Italo Biaggioni

Edition: illustrated

Published by Informa Health Care, 1995

ISBN 3718651467, 9783718651467

A depression in the heart rate and decrease in response to stress is expected

decreased conditioning-related activity in insula and amygdala after autonomic denervation

http://www.ncbi.nlm.nih.gov/pubmed/11856537

the primary event of gustatory sweating is a degeneration of the cervical sympathetic neurons

The development of gustatory sweating after cervical sympathectomy can only be explained if one is to admit that the primary event of gustatory sweating is a degeneration of the cervical sympathetic neurons. The initial event is the loss of postganglionic sympathetic neurons and the resulting denervation of the corresponding facial sweat glands. Regeneration of parasympathetic fibers, within the degenerating sympathetic neurilemmal sheets, is a secondary event although it accounts for the observed symptoms.

Salivary gland disorders

Eugene N. Myers, Robert L. Ferris

Springer, 2007 - Medical - 517 pages

International systematic reviews of ETS surgery warn of insuffiecient evidence on ETS

Australian Review of ETS surgery

"A lack of high quality randomised trial evidence on ETS means that it is difficult to make a judgment on the safety and effectiveness of this technique. There is potentially a number of safety issues associated with this procedure. ASERNIP-s suggests that a full systematic review including all available comparative and case series information, together with clinical inpuut, should be undertaken to provide up-to-date and comprehensive assessment of the safety and effectiveness of ETS." (ASERNIP-s Report No. 71, August 2009)

Australian Review of ETS surgery - 2001

The four case series were not critically appraised because they are prone to bias and have significant methodological problems. These studies represent level IV evidence according to the NHMRC criteria and one should not draw firm conclusions from their findings.

To date, the benefits or side effects associated with endoscopic thoracic sympathectomy for treating facial blushing have not been properly evaluated and reported.

Further research using a well-designed controlled trial is warranted to assess the efficacy of endoscopic thoracic sympathectomy for treating facial blushing.

Centre for Clinical Effectiveness - Monash

Swedish Review

Finnish Review

UK Review of ETS surgery

We did not identify any controlled trials or cohort studies. The
evidence about effectiveness, based on three case series, was
therefore very limited. The main weakness of these studies was their lack of a comparison group and their resulting inability to exclude a placebo response to surgery. In addition, the methods of assessing outcome were poorly described and not validated, and the range of outcomes assessed was limited. The studies provided very limited evidence that sympathectomy improves blushing. Side effects were common.
London: Bazian Ltd (Editors), Wessex Institute for Health Research and Development, University of Southampton 2003: 11

Wiley & Sons, Inc, news release - 2004

"Lifestyle" surgical procedure carries unrecognized risk of complications.”
Hoboken, NJ: John Wiley & Sons, Inc, British Journal of Surgery, Feb 5, 2004

"Sympathectomy is a technique about which we have limited knowledge, applied to disorders about which we have little understanding." Harald Breivik Professor og avdelingsoverlege Anestesiavdelingen, Rikshospitalet http://www.pfizer.no/templates/Page____886.aspx

The aim of the present prospective study was to confirm that a significant impairment of the heart rate to workload relationship was consistently observed following unilateral and/or bilateral (sympathectomy) surgery. Eur J Cardiothorac Surg 2001;20:1095-1100 http://ejcts.ctsnetjourna...i/content/full/20/6/1095

The authors found that the incidence of hypotension was a function of the level of sympathetic denervation, occurring in 60% of patients with a T7 sympathectomy, and in 100% of patient with a T4 or higher level of sympathectomy.
(p 226)

"Inappropriate" bradycardia (i.e. "normal" HR in face of ↓MAP with sensory level T3-T4)
Peripheral vasodilation should evoke an ↑ HR. But ↓ venous return → ↑vagal tone, so HR remains at preblock rate but is "inappropriately" slow.

Central neuraxial anesthesia-induced sympathectomy leads to peripheral vasodilation, reduced preload, and subsequently decreased cardiac output. The incidence and extent of hypotension depends on the height of the block, the patient's position, and whether appropriate measures were instituted prophylactically to minimize hypotension.

After thoracoscopic sympathectomy for hyperhidrosis, very severe discomfort and hyperhidrosis in the neighboring non-sympathectomized regions occurred with alarming frequency and intensity.
(p.879)

Cousins and Bridenbaugh's Neural Blockade in Clinical Anesthesia and Pain Medicine by Michael J Cousins, Phillip O Bridenbaugh, Daniel B Carr, and Terese T Horlocker

Wolters Kluwer Health
Edition: 4 - 2008

Clinical Anesthesiology By G. Edward Morgan, Maged S. Mikhail, Michael J. Murray
McGraw-Hill, Edition: 3, 2002

“cervical sympathectomy isolates all these sympathetic ganglion cells from the central nervous system and prevents them from responding to reflex or emotional changes in the central nervous system." Cunningham's Manual of Practical Anatomy: Volume III: Head, Neck and Brain, 1986

ETS is a surgical procedure for hand sweating and blushing. This is achieved by cutting the sympathetic chain, resulting in autonomic dysfunction and the inability to sweat on the upper body. But it does more than that.
“cervical sympathectomy isolates all these sympathetic ganglion cells from the central nervous system and prevents them from responding to reflex or emotional changes in the central nervous system."
Cunningham's Manual of Practical Anatomy: Volume lll: Head, Neck and Brain, 1986

disturbed peripheral vascular and heart rate responses after sympathectomy

Denervation supersensitivity leads to Raynaud's Disease

$Denervation supersensitivity leads to Raynaud\$
Cannon and his colleagues showed in the 1930s that section and subsequent degeneration of the sympathetic nerves led to a marked supersensitivity of the sturcture to exogenous catecholamines. The increase in sensitivity ranged from 10-to 100-fold in different tissues, such as the spleen on section of the splenic nerves, or the nictitating membrane on section of the postganglionic cervical sympathetic nerve or the heart on removal of the stellate ganglion. In smooth muscle the increase in sensitivity is mostly explained by the associated loss of neuronal re-uptake of noradrenaline, with only a lesser role for the increase in receptor numbers. Mechanisms of Drug Action on the Nervous System by Ronald W. Ryall, Cambridge University Press, 1989

Changes in Electrophysiology following sympathectomy

Sympathectomised dogs presented significant increases in: basic sinus period, sino-atrial conduction time (SACT), AH and HV intervals of the His bundle electrogram, atrial functional (AFRP) and effective (AERP) refractory periods, atrio-ventricular node functional (AVNFRP) and effective (AVNERP) refractory periods, ventricular functional (VFRP) and effective (EVRP) refractory periods and atrial (AMAP) and ventricular (VMAP) monophasic action potential durations. Corrected sinus recovery time (CSRT) was not affected by chemical sympathectomy. Neither was the atrial ERP/MAP duration ratio. This new form of sympathectomy affects all the levels of the cardiac conduction system. Such results are in accordance with those obtained with surgical sympathectomy or the use of beta-blocking agents.

DIANE GODIN*, CLAUDE GUIMOND{dagger}, RÉGINALD A NADEAU{ddagger} and A ROBERT LEBLANC§

Cardiovascular Research 1982 16(9):524-529;
© 1982 by European Society of Cardiology

Cardiovascular collapse caused by carbon dioxide insufflation during sympathectomy

Carbon dioxide insufflation into the pleural space during one-lung anaesthesia for thoracoscopic surgery is used in some centres to improve surgical access, even though this practice has been associated with well-described cardiovascular compromise. The present report is of a 35-year-old woman undergoing thoracoscopic left dorsal sympathectomy for hyperhidrosis. During one-lung anaesthesia the insufflation of carbon dioxide into the non-ventilated hemithorax for approximately 60 seconds, using a pressure-limited gas inflow, was accompanied by profound bradycardia and hypotension that resolved promptly with the release of the gas.
Australian Society of Anaesthetists 2002

Sympathetic regulation of the cerebral circulation by the carotid chemoreceptor reflex

After bilateral cervical sympathectomy (n = 9), carotid chemoreceptor reflex stimulation induced significantly different (P less than 0.01) effects on cerebral blood flow, which rose by 42 +/- 8%, and cerebral vascular resistance, which did not change.
In "sham" dogs, the repeat response to carotid chemoreceptor stimulation also induced significantly different effects from those in dogs with sympathectomy. Thus, in the conscious dog, stimulation of the carotid chemoreceptor reflex elicits significant sympathetically mediated vasoconstriction in cerebral vessels.
Am J Physiol Heart Circ Physiol 238: H594-H598, 1980;

Effect of adrenalectomy or sympathectomy on spinal cord blood flow

We conclude that adrenalectomy near-totally ablates the hypothermia-associated increase in RSCBF (regional spinal cord blood flow) measured in intact rats and that abdominal sympathectomy totally ablates it. This evidence complements morphological evidence for adrenergic innervation of the spinal cord vasculature.

Heart and Circulatory Physiology, Vol 260, Issue 3 827-H831, Copyright © 1991 by American Physiological Society

A. Iwai, W. W. Monafo and S. G. Eliasson
Department of Surgery, Washington University School of Medicine, St. Louis, Missouri 63110.

Sympathectomy induced adrenal hypertropy

Journal of Hypertension. 17(7):933-940, July 1999.
Qiua, Jingxin 1; Nelsona, Sharon H. 1; Spethb, Robert C. 2; Wanga, Donna H. 1,3

Objective: Previous studies indicate that the adrenal gland plays a compensatory role in the maintenance of blood pressure in chemically sympathectomized rats. However, the mechanisms responsible for compensatory adrenal responses are poorly understood. This study examined the regulation of adrenal growth and type 1A, 1B, and type 2 angiotensin II (Ang II) receptor (AT1A, AT1B and AT2) expression in the adrenal gland induced by sympathectomy.

Denervation supersensitivity leads to Raynaud's Disease

Changes in Electrophysiology following sympathectomy

Cardiovascular collapse caused by carbon dioxide insufflation during sympathectomy

Sympathetic regulation of the cerebral circulation by the carotid chemoreceptor reflex

Effect of adrenalectomy or sympathectomy on spinal cord blood flow

Sympathectomy induced adrenal hypertropy

Journal of Hypertension. 17(7):933-940, July 1999.
Qiua, Jingxin 1; Nelsona, Sharon H. 1; Spethb, Robert C. 2; Wanga, Donna H. 1,3

Sympathectomy supressed baroreflex control of heart rate

Loss of Baroreflex = aberrant blood pressure

Sympathectomy can be considered a psychiatric surgery

Circadian Rhythm eliminated by Sympathectomy

The abrupt increase and decrease in BP observed at the time when the lighting conditions are changed are eliminated by chemical sympathectomy

The disruption of the baroreflex selectively eliminatesthe circadian rhythm of BP, and the circadian rhythms of BP andHR are modulated by the autonomic nervous system in rats. The circadianrhythms of BP and HR are regulated by different mechanisms involvingthe autonomic nervous system.
(Circulation. 1997;96:1667-1674.)
© 1997 American Heart Association, Inc.

retarded adaptation of hemodynamics to a sudden start of exercise following sympathectomy

The exercise capacity and the increase of coronary and systemic hemodynamics under treadmill exercise were studied in 5 dogs, chemically sympathectomized with 6-hydroxy-dopamine.

Completeness of adrenergic denervation was verified by stimulation of the right stellate ganglion, by intravenous administration of tyramine, and by demonstration of supersensitivity to exogenous norepinephrine.

These dogs demonstrated a retarded adaptation of hemodynamics to a sudden start of exercise. A fall in mean arterial pressure below 45 mmHg within 10 to 15 sec lead to collapse.
steady state attainment of hemodynamic parameters was considerably delayed.

E. Bassenge¹, J. Holtz¹, W. v. Restorff¹ and K. Oversohl¹

Received: 18 April 1973

Things you might want to know about ETS:

What is ETS or Sympathectomy?

If you do a quick search on google because you want to find a solution for your sweaty palms, or do not want to blush every time someone looks at you, you will be flooded by all the information from the surgeons offering this procedure. If you only read these and do not have a medical background, you might fall for their statements and think to yourself: well, isn't medical science wonderful?!
You make your booking with one of the surgeons who will charm you and soon you are being wheeled in for the surgery with the promise from the surgeon, that it will change your life. You don't even know how true that is, until you wake up.
Here you will find the other side of the sales pitch and some answers to just how your life will never be the same.

Thermoregulatory Disfunction - Severe CS as the result of the elective surgery.

Note the sharp divisive line on chest: top anhidrosis, the body is unable to sweat and dissipate heat through shoulders, arms and head. 40% of heat is released from top of the head. This function of the thermoregulation is disabled for patients undergoing the selective surgery. Below the level of the T2 cut - Pathological sweating that requires complete change of clothes several times during the day. CS is not just thermoregulatory. It can be triggered by stress, in cold/winter conditions. All this as a result of an elective cosmetic surgery. The result is necessary consequence of disrupting the sympathetic chain and is independent of expertise or experience of the surgeon performing the procedure. Post ETS sweating can not be predicted. Sweating patterns prior to surgery are no relevant. There is no difference in gender or weight when it comes to CS. Some websites promoting the procedure will claim that CS diminished over time. The mechanism of CS is not understood and has not been investigated. In some cases it can take years to develop. Patients who are happy with the initial result of the surgery might deteriorate with the outcome and side-effects becoming worse.

ETS Surgery