Changes in hemodynamics of the carotid and middle cerebral arteries before and after endoscopic sympathectomy in patients with palmar hyperhidrosis

There was a significant reduction in diastolic pressure after T-2 sympathectomy (p = 0.003), but not in systolic pressure or heart rate. The vessel diameter was increased after sympathectomy in the left CAs and right CCA. The T-2 sympathectomy led to significant elevation of blood flow volume and Rl in the left CCA. ICA, and ECA (p < 0.05). The authors found significant increases in maximum flow velocity and RI in the left MCA (p < 0.05). Conclusions. Patients who underwent T-2 sympathectomy demonstrated a significant increase in blood flow volume and flow velocities of the CAs and MCA, especially on the left side. Asymmetry of sympathetic influence on the hemodynamics of the CAs and MCA was noted.
Journal of neurosurgery
1999, vol. 90, no3, pp. 463-467 (38 ref.)

Ultrastructural changes in the nerves innervating the cerebral artery after sympathectomy

http://www.springerlink.com/content/l7213648355u2088/

surgical sympathectomy produces hypersensitivity of the vessels.

Scand J Work En viron Health 13 (1987) 3 1 3 - 3 1 6

Depression of Endothelial Nitric Oxide Synthase

but Increased Expression of Endothelin-1 Immunoreactivity in Rat Thoracic Aortic Endothelium Associated With Long-term, but Not Short-term, Sympathectomy.

Original Contribution

Circulation Research. 79(2):317-323, August 1996.
Aliev, Gjumrakch; Ralevic, Vera; Burnstock, Geoffrey

Denervation supersensitivity in the denervated heart

The guanethidine sympathectomy in 4- and 8-week old white rats increased cardiac sensitivity to acetylcholine. An increase of sensitivity to adrenaline was observed in 8 to 20 weeks of postnatal period. The significance of the changes of extracardiac effects and the cardiac sensitivity to acetylcholine and adrenaline for its chronotropic control in sympathectomized 10-14 week old rats is discussed.
http://www.ncbi.nlm.nih.gov/pubmed/3569584

Indeed, local sympathectomy influences specific responses in immune organs.

Brain Research
Volume 888, Issue 2, 12 January 2001, Pages 227-234

Lumbar sympathectomy, which interferes with the sympathetic nerve supply to the colon

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

By Otto Appenzeller, Emilio Oribe
Elsevier Health Sciences, 1997

absent sympathetic skin responses post ETS

Compared with the presympathectomy rate, the rate of absent SSR (sympathetic skin responses) also significantly increased after sympathectomy: from 20 to 76% after electrical stimulation and 36 to 64% after deep inspiration stimulation, respectively (p <>

CONCLUSIONS: In contrast to compensatory sweating in other parts of the body after T2-3 sympathetomy, improvement: in plantar sweating was shown in 72% and worsened symptoms in 6% of patients. The intraoperative plantar skin temperature change and perioperative SSR demonstrated a correlation between these changes.

http://www.ncbi.nlm.nih.gov/pubmed/11453433

A sympathectomy does not cure hyperhidrosis

A sympathectomy does not cure hyperhidrosis. It does not leave a person "free of hyperhidrosis". The best that can be said is that is stops all sweating in one large area of the body, and makes the other part of the body sweat a lot more.

http://editthis.info/corposcindosis/Brat_Dialog

experts agree that sympathectomy, like the other nerve-cutting operations, is getting out of hand

Sympathectomy, cutting of the sympathetic nerves, is causing the most violent arguments of all. The operation is now prescribed for a wide variety of ailments, from excessive sweating to high blood pressure. Nobody knows how many thousands of sympathectomies surgeons perform each year; there are an estimated 1,000 in Manhattan alone. Admittedly the operation is a life-saver in many cases of gangrene, angina pectoris, hypertension. But some sympathectomies may make men sterile. And because a sympathectomy reduces pain, some doctors consider it insidiously dangerous, e.g., a patient could have a perforating ulcer without pain. The experts agree that sympathectomy, like the other nerve-cutting operations, is getting out of hand.
Time Magazine,
Monday, Jun. 30, 1947 Losing Nerves

The anterior rami of the spinal nerves between the C4 and T2 innervate the skin of the upper limb

The area of skin supplied by one spinal nerve is known as dermatome. A knowledge of segmental innervation of the skin enables one to determine the level of injury to the spinal cord. It is also essential in the conduction and interpretation of the physical examination of a patient.
A lesion of a spinal nerve manifests itself as a motor or sensory disturbance along it's distribution.

Human Anatomy:Volume I: Upper Limb And Thorax, 2008

The T1 and T2 segments innervate the head and neck; T2 through T6 segments, the upper extremities and thoracic viscera

Basic neurosciences with clinical applications
By Eduardo E. Benarroch, Elsevier Health Sciences, 2006

discrepancies in denervation of the SNS

Surgical extirpation of portions of the sympathetic nervous system frequently fails to produce precisely that permanent peripheral denervation which is to be expected from text-book diagrams of the anatomical arrangement of the system.
The discrepancies are not uncommon even when the surgical technique is above suspiciion. They can in part, of course, be attributed to variations in the detailed anatomy of the sympathetic trunks or in the pattern of distribution of the branches and communications of these trunks. Such atypical arrangements in the autonomic nervous system are frequent. Thus, for example, during careful dissection of the cadaver, with all the relationships exposed, the correct identification of a particular paravertebral sympathetic ganglion can be very difficult; in the depths of a surgical incision, it is often impossible. But, even when the possibility of the usual anatomical anomalies of the sympathetic nervous system has been excluded, persistence of autonomic activity in unexpected areas may, and in certain regions always does, follow operative removal of parts of the system which should have caused complete sympathetic paralysis in the are or region concerned.
Intermediate sympathetic ganglia, J. D. Boyd, Univ. of Cambridge

• Oxford Journals
• Medicine
• British Medical Bulletin, Vol. 13 No. 3
  

Primer on the autonomic nervous system

Hyperthermia, heat intolerance, heat prostration and heat stroke may occur with widespread failure of thermoregulatory sweating, whereas local skin trophic changes occur with chronic postganglionic sudomotor neuropathy.

Primer on the autonomic nervous system, By David Robertson, Academic Press, 2004

more liable to develop reflex bronchospasm under light levels of anesthesia after ETS

Thus, patients with essential hyperhidrosis who have undergone bilateral thoracic sympathectomy, may be more liable to develop reflex bronchospasm under light levels of anesthesia.
CAN J ANESTH 2005 52:9

depletion of brain noradrenaline levels caueses a disturbance in cerebral microvasculatur tone

Chemical sympathectomy with six-hydroxydopamine leads to marked noradrenaline denervation in the nucleus ceruleus-innervated areas (Jonnson 1983) and to a decrease in noradrenaline levels measured in the cerebral cortex (Onesti et al. 1989).
Rats were subjected to chemical sympathectomy by stereotactic injection of 6-hydroxydopamine into the lateral ventricle. A hypertensive condition at a mean arterial pressure of about 160mm Hg was maintained for 1 hour by intravenous phenylephedrine. Compared with a control group CBF increased, cerebral autoregulation was impaired and specific gravity of the cerebral tissue revealed cerebral oedema. It was suggested that depletion of brain noradrenaline levels caueses a disturbance in cerebral microvasculatur tone and renders the cerebral blood vessels more vulnerable to hypertension (Kobayashi et al. 1991).

Topics in Neuroanaesthesia and Intensive Care

Experimental and Clinical Studies upon Cerebral Circulation, Metabolism and Intracranial Pressure

Cold, Georg E., Dahl, Bent L. 2002, XIV, 416 p., Hardcover ISBN: 978-3-540-41871-9

Effect of adrenalectomy or sympathectomy on spinal cord blood flow

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

http://ajpheart.physiology.org/cgi/content/abstract/260/3/H827
Am J Physiol Heart Circ Physiol 260: H827-H831, 1991;

Alterations in cytokine and antibody production following chemical sympathectomy

The Journal of Immunology, Vol 155, Issue 10 4613-4620, Copyright © 1995 by American Association of Immunologists

acinar degranulation following sympathectomy

Chronic bilateral postganglionic sympathectomy (4-6 weeks duration) caused a drastic reduction in the capacity of the gland to secrete saliva in response to parasympathetic stimulation, reaching only one-third of that from normal animals. The initial output of amylase was greater than in normal animals but the total output was similar. The control unstimulated sympathectomized glands appeared similar morphologically to normal resting glands. However, on the parasympathetically stimulated side, besides the usual amount of acinar degranulation, there was also a conspicuous development of acinar vacuolation, not seen in the other groups of animals.
September 1, 1988 The Journal of Physiology, 403, 105-116.

Elective treatment for sweaty palms is classified as psychosurgery

ETS can alter many bodily functions, including sweating , heart rate , heart stroke volume , blood
pressure , thyroid , baroreflex , lung volume , pupil dilation, skin temperature, goose bumps and
other aspects of the autonomic nervous system . It can diminish the body's physical reaction to
exercise and/or strong emotion, and thus is considered psychiatric surgery. In rare cases sexual
function or digestion may be modified as well.
LVHyperhidrosis.com
Aury Nagy MD

Catecholamine sensitivity of cat leg vessels after sympathectomy

Am J Physiol 212: 466-471, 1967;

Differences in the injury/sprouting response

While increased hilar and decreased distal NA innervation in arthritic rats was strikingly similar to that of non-arthritic 6-OHDA-treated rats, there were differences in splenic compartments innervated by sympathetic nerves between these groups. In 6-OHDA-treated rats, NA nerves re-innervated splenic compartments normally innervated by sympathetic nerves. In arthritic rats, sympathetic nerves returned to normally innervated splenic compartments, but also abundantly innervated red pulp. These findings suggest that splenic sympathetic nerves undergo a disease-associated injury/sprouting response with disease development that alters the normal pattern and distribution of NA innervation. The altered sympathetic innervation pattern is likely to change NA signaling to immune cell targets, which could exert long-term regulatory influences on initiation, maintenance, and resolution of immune responses that impact disease pathology.
Brain, Behavior & Immunity; Feb2009, Vol. 23 Issue 2, p276-285, 10p

Phantom sweating occurs frequently after sympathectomy

To describe the biology of phantom sweating, a novel autonomic neuropathy symptom, based on a description of a patient with a small fiber and autonomic neuropathy. Clinical and laboratory assessments. Evidence of a generalized small fiber and autonomic neuropathy. Phantom sweating occurs frequently after sympathectomy but has not been reported previously in patients with a somatosensory or autonomic neuropathy. We suggest that this symptom is an autonomic paresthesia.
Clinical Autonomic Research; Dec2008, Vol. 18 Issue 6, p352-354, 3p,

Similar pathological effects of sympathectomy and hypercholesterolemia on arterial smooth muscle cells and fibroblasts

In a previous study, we showed that after sympathectomy, the femoral (FA) but not the basilar (BA) artery from non-pathological rabbits manifests migration of adventitial fibroblasts (FBs) into the media and loss of medial smooth muscle cells (SMCs). The aim of the present study was to verify whether similar behaviour of arteries occurred in the pathological context of atherosclerosis. Thus, similar experiments were conducted on hypercholesterolemic rabbits, which were chemically sympathectomized with 6-hydroxydopamine (n=4) or treated with vehicle for control (n=5). Cross-sections of BA and FA were immunolabelled for five markers of phenotypic modulation of vascular SMCs and FBs: vimentin, desmin, α-smooth muscle actin, β-isoform of actin, and h-caldesmon and examined using a confocal microscope. Also, 3D images were constructed and morphometric analysis performed using image analysis software. Both intact and sympathectomized BA and FA developed atherosclerotic plaques, but the thickening of the intima was more advanced in sympathectomized animals, as judged by increased plaque frequency and by the phenotypic modulation of SMCs in the intima. Our results show that in the media of FAs hypercholesterolemia induces changes similar to those observed in sympathectomized rabbits in non-pathological conditions, i.e., migration of adventitial FBs to the media and loss of medial SMCs. These latter changes, which can be ascribed to pathological events, were accentuated after sympathectomy in the hypercholesterolemic rabbits. The present study reveals that pathological events, including migration and phenotypic modulation of vascular FBs and loss of SMCs, may be under the influence of sympathetic nerves. [Copyright &y& Elsevier]

Orthostatic syncope can occur after a spinal cord injury or sympathectomy

Neurocardiogenic syncope is also referred to as vasovagal, vasodepressor, neurally mediated, and reflex syncope. As the name implies, neurocardiogenic syncope involves the interaction of various autonomic nervous system reflexes, the central nervous system, and the cardiovascular system..sup.1,4,12-14 The Bezold-Harisch reflex is cited as the mechanism responsible for vasovagal syncope and has two components. There is "cardio-inhibitory syncope" due to a vagal (parasympathetic) mediated reflex causing bradycardia or even asystole, plus "vasodepressor syncope" from withdrawal of sympathetic input leading to a drop in PVR with venous pooling in the periphery leading to hypotension.

Vasovagal syncope can occur in heart transplant patients, suggesting that the Bezold-Harisch reflex or vagal stimulation plus sympathetic withdrawal as the only factor may be a somewhat simplistic explanation, and that other variables may also play a role.

Although there are many causes of cardiovascular syncope, the final common mechanism is a decrease in cardiac output causing a decrease in cerebral perfusion.
Orthostatic syncope can occur after a spinal cord injury or sympathectomy, which eliminates
the vasopressor reflexes, and in patients on certain medications, commonly antihypertensive and
vasodilator drugs.
http://www.thefreelibrary.com/Syncope+in+Pediatric+Patients-a0217945432

neuralgia is a severe complication since pain can be permanent

The rate of morbidity reported in the literature for lumbar sympathectomy is low. However, post-operative neuralgia is a severe complication since pain can be permanent, severe, and incapacitating. Relief of pain by traditional means is ofter hazardous and symptoms may persist.

Between March and October 1986, 33 consecutive patients underwent unilateral lumbar sympahtectomy in the Thoracic and Cardiovascular Surgical Unit of the Catholic University in Louvain, Belgium. Ten patients experienced post-sympathectomy neuralgia.

Doppler studies and thermography were used to assess the efficacy of the operation in improving arterial supply to the lower limb on the side of sympathectomy. In all ten cases, neuralgia appeared between the ninth and 30th postoperative days, with mean of 16 days.

http://www.springerlink.com/content/q04711t06j164206/

Effects of sympathectomy on skin and muscle microcirculation during dorsal column stimulation

A cold test with monitoring of cold-induced changes in peripheral blood flow was used to assess the completeness of the sympathectomy. The preoperative cold test induced a reciprocal response, vasoconstriction in the skin and vasodilation in muscle. DCS with clinical parameters did not produce this reciprocity in the control and sham-operated rats, but induced a vasodilation in both skin and muscle. After complete sympathectomy, defined as postoperative disappearance of the vasomotor responses to cold, the vasodilation in skin and muscle in response to DCS was abolished; however, the vasodilatory response to high-intensity stimulation (approximately 10 times the motor threshold) was not affected. Incomplete sympathetic denervation in some animals resulted in partial preservation of a vasodilatory response to DCS.
http://www.ncbi.nlm.nih.gov/pubmed/1758600

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

sympathectomy syndrome:

A traumatic sympathectomy occurs below the level of the spinal cord lesion with the risk of hypotension secondary to arteriolar and venular vasodilation. Injuries at or above T6 are particularly associated with hypotension, as the sympathetic outflow to splanchnic vascular beds is lost. Bradycardia will occur if the lesion is higher that the sympathetic cardioaccelerator fibers (T1-T4), with the parasympathetic cranial outflow being preserved. A complete cervical cord injury produces a total sympahtectomy and therefore hypotesion will be more marked.

Injuries to the sympathetic chain may result in retrograde ejaculation (in males) or a sympathectomy syndrome with disturbed capability for vasoconstriction. This may result in the feeling of a hot (ipsilateral) or cold (contralateral) leg or foot, respectively. (p. 358)

Spinal disorders: fundamentals of diagnosis and treatment

By Norbert Boos, Max Aebi
Springer 2008

animals that underwent late sympathectomy had significantly increased arthritis scores compared with controls

Arthritis & Rheumatism; Apr2005, Vol. 52 Issue 4, p1305-1313, 9p

Immunoglobulin producing cells in the rat dental pulp after unilateral sympathectomy

Recent studies show that sympathetic nerves participate in immunomodulation. We investigated the effects of unilateral sympathectomy on recruitment of cells expressing kappa and lambda (κ and λ) light chains in the rat dental pulp. Superior cervical ganglion was removed in experimental rats (n=10) while control rats (n=8) received sham surgery. Following perfusion 18 days later, mandibular jaws were processed for immunohistochemistry and electron microscopy. Sympathectomy results in recruitment of cells expressing κ and λ light chains into the dental pulp (P=0.005). Electron microscopy revealed these cells to be mainly plasma cells and Mott cells. We conclude that neural imbalance caused by unilateral sympathectomy recruits immunoglobulin producing cells in the dental pulp. Our results are in agreement with a model of immune regulation in which the sympathetic nervous system exerts a tonic regulatory effect over lymphocyte proliferation and migration.
Neuroscience
Volume 136, Issue 2, 2005, Pages 571-577

Recurrence

Postoperative satisfaction degree is high but decreases over time owing to the appearance of recurrence.
European Journal of Cardio-Thoracic Surgery; Sep2008, Vol. 34 Issue 3, p514-519, 6p

paraplegia as a postoperative complication

SIX YEARS AGO we encountered paraplegia as a postoperative complication in a patient who had undergone thoraco-lumbar sympathectomy for hypertension. Such a phenomenon was unique in our experience.
After a search of the literature and a number of informal inquiries among our colleagues, we were surprised to find that such an occurrence is not as unusual as we had believed. Bassett, in 1948,1 reporting on his experience with sympathectomy in the treatment of hypertension, stated: 'We
have had four cases of thrombosis of the anterior spinal artery with resultant permanent residual ischemic myelitis.
Poppen, in a personal communication, has stated that, although this complication has not
occurred in his own experienoe, three cases have been brought to his attention in which
paraplegia followed thoraco-lumbar sympathectomy for hypertension. Therefore, we have knowledge of eight cases in which such a catastrophe followed an elective operation which has enjoyed wide usageduring the past decade.
Annals of Surgery, M a r c h, 1 9 5 4

Spinal Cord Infarction caused by sympathectomy

Uncommon causes include decompression sickness, which has a predilection for spinal ischemic damage; complications of abdominal surgery, particularly sympathectomy; circulatory failure as a result of cardiac arrest or prolonged hypotension; and vascular steal in the presence of an arteriovenous malformation.

Author: Thomas F Scott, MD, Professor, Program Director, Department of Neurology, Drexel University College of Medicine; Director, Allegheny MS Treatment Center
Contributor Information and Disclosures

Updated: Aug 21, 2009

cerebral edema is worsened by sympathectomy, which causes increased cerebral blood flow

Although excessive SNS activity may be globally harmful, catecholamines and sympathetic nerves may also have organ-protective effects via reflex arteriolar constriction, which may protect the capillaries of the brain and kidney from surges in SBP. A baroprotective role of cerebral sympathetic nerves was uncovered by Heistad et al., who unilaterally denervated the cerebral vasculature in stroke-prone rats and found that fatal stroke occurred rapidly in the hemisphere ipsilateral to the sympathetic denervation. In the syndrome of malignant hypertension, cerebral edema is worsened by sympathectomy, which causes increased cerebral blood flow.

Role of hte Hypothalamus in Integration of behavior and Cardiovascular Responses (p. 60)

Hypertension: a companion to Brenner and Rector's the kidney

By Suzanne Oparil, Michael A. Weber
Elsevier Health Sciences, 2005 - Medical - 872 pages

depletion of brain noradrenaline levels causes a disturbance in cerebral microvascular tone

A hypertensive condition at a mean arterial pressure of about 160 mm Hg was maintained for 1 hour by intravenous infusion of phenylephrine. In the 6-hydroxydopamine-treated group, CBF increased significantly after the elevation of systemic blood pressure compared with that in the control group, and cerebral autoregulation was impaired. After a 1-hour study, the specific gravity of the cerebral tissue in the treated group significantly decreased; electron microscopic studies at that time revealed brain edema.
It is suggested that depletion of brain noradrenaline levels causes a disturbance in cerebral microvascular tone and renders the cerebral blood vessels more vulnerable to hypertension.

Journal of Neurosurgery, December 1991 Volume 75, Number 6

Unilateral removal of the superior cervical ganglion (SCG) results in the reinnervation of the denervated cerebral vessels by sprouting nerves

Chemical sympathectomy of the mature rat rather than the neonate also leads to sensory hyperinnervation, although there are a few differences. In the lung, sympahtectomy induces a marked increase in CGRP-immunoreactive nerve density around the ariways, blood vessels, and also in the vicinity of the neuroepithelial bodies of the pulmonary epithelium.

Following transection of the preganglionic autonomic nerves or in spinal cord injury, there are marked changes in the nerves that remain. Such changes can be manifested not only as nerve growth and changes in neurotransmitter expression, but remarkably, in reorganization of nerve pathways and their function.

Since sprouting is a common response of the nerves that remain following nerve injury, the close association of the different divisions of the autonomic nervous system in the pelvic region opens up the possibility for new connections to form new pathways. Spinal cord injury can unmask spinal reflexes that are normally inhibited by input from higher centers in the brain.

Handbook of the autonomic nervous system in health and disease

By Liana Bolis, J. Licinio, Stefano Govoni
Informa Health Care, 2003 - Medical - 677 pages

adverse cardiac and cerebral intraoperative events secondary to hypoxia from presumed hypoventilation

The thoracoscopic sympathectomy procedure requires several anesthetic considerations that include an anesthesiologist and operating room staff familiar with thoracic endoscopy. Double-lumen endotracheal tube placement is needed for ventilation of the contralateral lung and active deflation of the ipsilateral lung. Care must be taken to ensure adequate inflation of the lung on the operated side before proceeding to the contralateral side because there have been both published and anecdotal reports of adverse cardiac and cerebral intraoperative events secondary to hypoxia from presumed hypoventilation.
The choice whether to use carbon dioxide insufflation versus ambient pressure coupled with lung deflation and a fan refractor is surgeon specific. There are case reports of intraoperative cardiac arrest requiring resuscitation when carbon dioxide insufflation was used, with speculation that an increased mediastinal or intrathoracic pressure resulted in a decreased stroke volume and subsequent arrhytmia.

Neurosurgical operative atlas: Spine and peripheral nerves

By Christopher E. Wolfla, Daniel K. Resnick
Thieme, 2007 - Medical - 424 pages

alterations in the three-phase bone scan in acute CRPS are similar to those resulting from sympathectomy

There is only limited evidence regarding the efficacy of thoracoscopic or surgical sympathectomy. Four studies reported partial long-lasting benefits in CRPS types 1 and 2.

Postoperatively, no vasoconstriction due to deep inspiration (vasoconstrictor reflex) could be elicited at the affected extremity, indicatin complete sympathetic denervation. Additionally the temperature at the affected hand increased. After 4 weeks, skin temperature decreased, without signs of reinnervation. This denervation supersensitivity was associated with recurrence of pain and is thought to rely on a vascular supersensitivity to could and circulating catecholamines.

Interestingly, alterations in the three-phase bone scan in acute CRPS are similar to those resulting from sympathectomy without being related to the success of the intervention. (p.370)

The neurological basis of pain

By Marco Pappagallo
McGraw-Hill Professional, 2005 - Medical - 673 pages

sympathectomy per se may sensitize peripheral nociceptors and lead to neuralgia

Interestingly, while is used for the treatment of some chronic pain conditions, sympathectomy per se may sensitize peripheral nociceptors to circulating norephinephrine, and this sensitization may lead to post-sympathectomy neuralgia. (p.287)

Peripheral Receptor Targets for Analgesia: Novel Approaches to Pain Management

By Brian E. Cairns
John Wiley and Sons, 2009 - Medical

Compensatory hyperhidrosis reported in 0% to 74.5% of cases

Compensatory hyperhidrosis is the most common and unpredictable side effect of thoracoscopic sympathectomy and is reported to occur in 0% to 74.5% of cases. (p.555)

Wesley S. Moore, Samuel S. Ahn

Elsevier Health Sciences, 2001

cerebral edema following CO2 insufflation

Death after thoracoscopic sympathectomy has been reported, secondary to cerebral edema, when CO2 insufflation has been employed. Another patient in this series sustained severe neurological dysfunction, secondary to cerebral edema. The development of cerebral edema after thoracoscopic sympathectomy is attributable to gas insufflation, which is not required and should be avoided. Major vascular injury during thoracoscopic sympathectomy has also been reported, and this complication should be completely avoidable. Chylothorax after sympathectomy has also been described and is related to division of accessory ducts rather than injury to the thoracic duct.
The most common complications of sympathectomy are related to manipulation of the autonomic nervous system.

Injury to the stellate ganglion is caused by mechanical or thermal damage to T1 during dissection. In order to prevent this injury, precise identification of ribs 1-4 is required prior to dissection of the sympathetic ganglion at T2; no dissection is performed above this level. Furthermore, excessive nerve traction is avoided during dissection. Finally, the use of bipolar cautery or ultrasonic dissection will prevent current diffusion to the stellate ganglion.
Neuralgia along the ulnar aspect of the upper limb may occur after sympathectomy, which usually resolves within 6 weeks. (p.250)

Complications in cardiothoracic surgery: avoidance and treatment

By Alex G. Little

Wiley-Blackwell, 2004 - Medical - 454 pages

"Sympathectomy is another animal."

Sympathectomy. This is a radical, now-controversial approach to blocking pain, and it includes extremely high risks for additional tissue damage and spread of RSD. (p.40)

Sympathectomy also potentially precludes future new treatments from working. (p.41)

A recent review article by (Johns Hopkins Hospital anesthesiologist and medical school professor) Srinivasa Raja covering all previous articles on sympathectomy showed that 10 percent of sympathectomies done for various reasons have complications. The complication rate for sympathectomy done to treat neuropathic (i.e., RSD) pain is 30 percent. A lot of these people can have a return of pain, and if they do, you can no longer do a sympathetic block to get rid of it. Then you have got these people in terrible pain that you cannot treat. And so, in my book, surgical sympathectomy is out. (p.81)

Positive Options for Reflex Sympathetic Dystrophy (RSD):

Elena Juris

6 Reviews

Hunter House, 2004

Post-Sympathectomy pain (neuralgia)

Post-Sympathectomy pain (neuralgia) is a potential complication of all types of sympathectomy. Post-Sympathectomy pain is typically proximal to the original pain (e.g. proximal means that the pain may appear for the first time in the groin or buttock region for sympathectomy of the lower extremity and pain in the chest wall region for sympathectomy of the upper extremity).

Textbook of orthopedics and trauma

GS Kulkarni

Jaypee Brothers Publishers, 2008 - Medical

Sympathectomy considered a last resort or end-of-the-road treatment

Surgical sympathectomy has been advocated for patients who do not get permanent pain relief from blocks and is somewhat of a last resort or end-of-the-road treatment. (p.469)

Skeletal trauma: basic science, management, and reconstruction, Volume 1

Elsevier Health Sciences, 2003 - 2768 pages
By Bruce D. Browner

lung and nerve problems

Even with newer endoscopic techniques, the complications can include excessive sweating in other parts of the body and lung and nerve problems. As many of these complications are serious and not reversible, this option is rarely used, and then only as a last resort.
http://awurl.com/4CZkP4bNh
Medical Author: Alan Rockoff, MD
Medical Editor: Frederick Hecht, MD, FAAP, FACMG
Medical Reviewer: Melissa Conrad Stöppler, MD

Horner syndrome continues to occur in about 5% to 10% of cases after upper thoracic sympathectomy for palmar or axillary sympatholysis

http://jtcs.ctsnetjournals.org/cgi/content/full/124/3/636

Cutaneous innervation in man before and after lumbar sympathectomy: Evidence for interruption of both sensory and vasomotor nerve fibres

	Coventry, Brendon John Walsh, J. A.
Citation:	ANZ Journal of Surgery, 2003; 73 (1-2):14-18
Publisher:	Blackwell Science Asia
Issue Date:	2003
ISSN:	1445-1433

Sympathectomy at the T2 level would block the afferent projection negative feedback to the hypothalamus

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

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

Jornal Brasileiro de Pneumologia

Print version ISSN 1806-3713

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

Direct hypothalamo-autonomic connections.

Brain Res. 1976 Nov 26;117(2):305-12. http://www.ncbi.nlm.nih.gov/pubmed/62600

Effects of sympathicolysis on bronchial responsiveness to histamine: implications of the autonomic imbalance

Respirology. 1996 Sep;1(3):195-9.
Effects of thoracoscopic upper dorsal sympathicolysis for essential hyperhidrosis on bronchial responsiveness to histamine: implications on the autonomic imbalance theory of asthma.
http://www.ncbi.nlm.nih.gov/pubmed/9424396

TES is not as minor a procedure as usually asserted

Although morbidity was low, significant complications of TES (Thoracic endoscopic sympathectomy) occurred. Patients should be clearly warned that TES is not as minor a procedure as usually asserted. Complications as well as adverse effects should be considered when discussing this surgical indication.
Ann Thorac Surg 71(4):1116-9 (2001)

bradycardia as likely, and compensatory sweating as obligatory after Sympathectomy

Clin Auton Res. 2003 Dec;13 Suppl 1:I36-9.

Related Articles, Links

Sequelae of endoscopic sympathetic block.

Schick CH, Horbach T.

Dept. of Surgery, University of Erlangen-Nürnberg, Krankenhausstrasse 12, 91054, Erlangen, Germany. schick@hyperhidrosis.de

Endoscopic sympathetic block as a treatment for primary hyperhidrosis is associated with certain sequelae. The reported occurrence of side effects still varies in the literature. As the majority of patients describe sequelae after sympathetic surgery, the frequency and importance of these persisting changes are still underestimated. Patient's informed consent should include and define side effects like gustatory sweating, olfactory sweating and bradycardia as likely, and compensatory sweating as obligatory.

An assessment of plantar hyperhidrosis after endoscopic thoracic sympathicolysis

EBTS is followed by redistribution of body perspiration, with, and important, plantar anhydrosis and hypohidrosis. Although EBTS is the standard treatment for palmar primary hyperhidrosis, we must continue studying baseline sympathetic activity in patients affected by primary hyperhidrosis and the neuroanatomy of the sympathetic system to understand the redistribution of sweating and decrease of hyperhidrosis in the zones regulated by mental or emotional stimuli.
http://www.ncbi.nlm.nih.gov/pubmed/19410478

Eur J Cardiothorac Surg. 2009 Aug;36(2):360-3. Epub 2009 May 1.

Parry-Romberg syndrome and sympathectomy--a coincidence?

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

Cutis. 2004 May;73(5):343-4, 346.

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

Overall, gustatory sweating occurred in 32% of patients

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

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

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

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

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

Breast enlargement after thoracoscopic sympathectomy

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

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

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

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

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

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

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

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

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

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

An alternative treatment option for compensatory hyperhidrosis after endoscopic thoracic sympathectomy

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

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

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

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

Sympathectomy affects the function of the Hypothalamus

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

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

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

doi: 10.1590/S1806-37132008001100013

Morphofunctional changes in the myocardium following sympathectomy

Vestn Akad Med Nauk SSSR. 1984;(2):80-5.
Morphofunctional changes in the myocardium following sympathectomy and their role in the development of sudden death from ventricular fibrillation

Beskrovnova NN, Makarychev VA, Kiseleva ZM, Legon'kaia, Zhuchkova NI.
PMID: 6711115 [PubMed - indexed for MEDLINE]

Complications are more common than previously thought

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

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

complications are frequent

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

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

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

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

Recurrent sweating occurred in 17.6% of patients

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

Young woman dies after a 'routine' operation

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

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

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

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

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

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

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

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

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

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

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

hand, which may become hyperkeratotic, with fissuring and scaling

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

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

By Otto Appenzeller, Emilio Oribe

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

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

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

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

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

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

Autonomic neuropathy simulating the effects of sympathectomy

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

Sympathectomy limits blood flow to a vital organ like the brain

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

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

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

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

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

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

http://www.ncbi.nlm.nih.gov/pubmed/10971220

Cardiac failure and ischaemic heart disease patients receive standard of care cardiac beta(1)-adrenergic blockade medication. Such medication reduces cardiac output and cerebral blood flow.

http://www.ncbi.nlm.nih.gov/pubmed/17506866

Surgery for hyperhidrosis abolished 6-sulphatoxymelatonin excretion

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

Since melatonin, the hormone secreted from the pineal gland has a remarkable anti-oxidant property and whose rate of production declines with increase in age, has prompted many to suggest that this hormone plays a crucial role in the genesis of neurodegenerative diseases. Melatonin cannot only scavenges oxygen free radicals like super oxide radical (O2-), hydroxyl radical (*OH), peroxyl radical (LOO*) and peroxynitrite anion (ONOO-), but can also enhance the antioxidative potential of the cell by stimulating the synthesis of antioxidative enzymes like super oxide dismutase (SOD), glutathione peroxidase (GPX), and also the enzymes that are involved in the synthesis of glutathione. In many instances, melatonin increases the expression of m RNA's of the antioxidative enzymes. Melatonin administration has been shown to be effective in counteracting the neurodegenerative conditions both in experimental models of neurodegenerative diseases and in patients suffering from such diseases. A disturbance of melatonin rhythm and secretion also has been noted in patients suffering from certain neurodegenerative diseases. From all these, it is evident that melatonin has a neuroprotective role.
http://www.curehunter.com/public/pubmed12587715.do

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

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


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

Signs and symptoms

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

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

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

Sudomotor dysfunction in autoimmune autonomic ganglionopathy

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

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

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

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

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


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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

T2 procedure results in a complete sympathectomy

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

Hyndman OR,Wolkin J

Arch Surg. 1942 45:145–155

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

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

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

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

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

Long-term cardiopulmonary function after thoracic sympathectomy

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

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

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

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

Data show that the nervous and immune systems communicate with one another to maintain immune homeostasis. Activated immune cells secrete cytokines that influence central nervous system activity, which in turn, activates output through the peripheral nervous system to regulate the level of immune cell activity and the subsequent magnitude of an immune response. In this review, we will focus our presentation and discussion on the findings that indicate a regulatory role for the peripheral sympathetic nervous system in modulating the level of cytokine and antibody produced during an immune response. Data will be discussed from studies involving the stimulation of the ß₂ adrenergic receptor expressed on CD4⁺ T cells and B cells by norepinephrine or selective agonists. We will also discuss how dysregulation of this line of communication between the nervous and immune systems might contribute to disease development and progression.
http://www.jleukbio.org/cgi/content/abstract/79/6/1093

Alterations in cytokine and antibody production following chemical sympathectomy

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

cytokines mediate and control immune and inflammatory responses

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

Denervation resulted in increased production of tumor necrosis factor-α

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

Tumor necrosis factor-a induces oligodendrocytes apoptosis

Tumor necrosis factor-a induces oligodendrocytes apoptosis, and is known to stimulate the hydrolysis of sphingomyelin to form the lipid mediator, ceramide.
http://www.springerlink.com/content/mu032lj427l85701/

Oligodendrocyte apoptosis and primary demyelination

We demonstrate that local production of TNF (tumor necrosis factor) by central nervous system glia potently and selectively induces oligodendrocyte apoptosis and myelin vacuolation in the context of an intact blood-brain barrier and absence of immune cell infiltration into the central nervous system parenchyma. Interestingly, primary demyelination then develops in a classical manner in the presence of large numbers of recruited phagocytic macrophages, possibly the result of concomitant pro-inflammatory effects of TNF in the central nervous system, and lesions progress into acute or chronic MS-type plaques with axonal damage, focal blood-brain barrier disruption, and considerable oligodendrocyte loss. Both the cytotoxic and inflammatory effects of TNF were abrogated in mice genetically deficient for the p55TNF receptor demonstrating a dominant role for p55TNF receptor-signaling pathways in TNF-mediated pathology.
http://www.ncbi.nlm.nih.gov/pubmed/9736029

Sympathectomy induces adrenergic excitability of cutaneous C-fiber nociceptors

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

nerve damage causes an inflammatory response

Damage to peripheral nerves often results in pain and hyperalgesia. We suggest that nerve damage causes an inflammatory response in which cells associated with the nerve release inflammatory mediators such as
eicosanoids; these mediators may contribute to the hyperalgesia which results from nerve injury. The cell types most likely to be responsible include macrophages and postganglionic sympathetic neurones.
http://www.springerlink.com/content/pjh3832058475340/
D. J. Tracey1 J. S. Walker1
School of Anatomy, University of New South Wales, 2052 Sydney, NSW, Australia

The brain and the immune system are the two major adaptive systems of the body. During an immune response the brain and the immune system “talk to each other” and this process is essential for maintaininghomeostasis. Two major pathway systems are involved in this cross-talk: the hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic nervous system (SNS). This overview focuses on the role of SNS in neuroimmune interactions, an area that has received much less attention than the role of HPA axis. Evidence accumulated over the last 20 years suggests that norepinephrine (NE) fulfills the criteria for neurotransmitter/neuromodulator in lymphoid organs.
http://pharmrev.aspetjournals.org/content/52/4/595.abstract

The effects of atropine and chronic sympathectomy on maximal parasympathetic stimulation of parotid saliva in rats

Chronic bilateral postganglionic sympathectomy (4-6 weeks duration) caused a drastic reduction in the capacity of the gland to secrete saliva in response to parasympathetic stimulation, reaching only one-third of that from normal animals. The initial output of amylase was greater than in normal animals but the total output was similar. The control unstimulated sympathectomized glands appeared similar morphologically to normal resting glands. However, on the parasympathetically stimulated side, besides the usual amount of acinar degranulation, there was also a conspicuous development of acinar vacuolation, not seen in the other groups of animals.

http://jp.physoc.org/content/403/1/105.abstract

PARAPLEGIA AS A COMPLICATION OF SYMPATHECTOMY FOR HYPERTENSION

Six years ago we encountered paraplegia as a postoperative complication in a patient who had undergone thoraco-lumbar sympathectomy for hypertension.
After a search of the literature and a number of of informal inquiries among our colleagues, we were surprised to find that such an occurrence is not as unusual as we had believed. Bassett, in 1948, reporting on his experience with sympathectomy in the treatment of hypertension, stated:"we have had four cases of thrombosis of the anterior spinal artery with resultant permanent residual ischemic myelitis." Poppen, in a personal communication, has stated that, although this complication has not occurred in his own experience, three cases have been brought to his attention in which paraplegia followed thoraco-lumbar sympathectomy for hypertension. Therefore, we have knowledge of eight cases in which a catastrophe followed an elective operation which has enjoyed wide usage during the past decade.

Annals of Surgery:

March 1954 - Volume 139 - Issue 3 - ppg 330-334

Effect of sympathectomy on the expression of NMDA receptors in the spinal cord

The expression of NMDA receptors in the intermediolateral (IML) region of the upper thoracic spinal cord, was studied in 3 week old rats. The effect of section of the cervical sympathetic nerve on neuronal cell number and receptor expression was examined up to two weeks after the operation. Age-matched sham-operated and unoperated animals were used as controls. It was shown using quantitative autoradiography with the NMDA receptor antagonist [(3)H]MK-801 (dizocilpine maleate), that there was a marked downregulation of receptors in all groups of animals, beginning at approximately 4 weeks of age. However after sympathectomy, which resulted in the death of 44% of neurones in the IML by 7 days, there was a significant increase in receptor density per neurone compared to sham-operated controls. In the control animals there was a significant increase in the Kd value of the binding between 21 and 24 days after birth indicating an increased expression of a low affinity receptor, but no such increase was seen after axotomy. The results are consistent with two populations of NMDA receptors being transiently expressed in the IML in developing animals, and the higher affinity receptor being down-regulated between 4 and 5 weeks of age. The presence of the high affinity receptor subtype may predispose neurones to die after axotomy.
J Neurol Sci (1999) 169: 156-60.
http://www.ionchannels.org/showabstract.php?pmid=10540025

signs of degeneration can already be recog- nized in the myelinated as well as in the unmyelinated axons. 48 h after sympathectomy

www.springerlink.com/index/M21M2612N2147011.pdf

A correlation of the findings of cytoarchitectonics and sympathectomy with fiber degeneration folowing dorsal rhizotomy

Autonomic neurons in the spinal cord of the rhesus monkey: A correlation of the findings of cytoarchitectonics and sympathectomy with fiber degeneration following dorsal rhizotomy

http://www3.interscience.wiley.com/journal/109712470/abstract

R-R variations, a test of autonomic dysfunction

Patients with symptoms of autonomic failure showed smaller variations than those without such symptoms.

Acta Neurologica Scandinavica

http://www3.interscience.wiley.com/journal/121523081/abstract?CRETRY=1&SRETRY=0