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

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