decreased conditioning-related activity in insula and amygdala in patients with autonomic denervation

The degree to which perceptual awareness of threat stimuli and bodily states of arousal modulates neural activity associated with fear conditioning is unknown. We used functional magnetic neuroimaging (fMRI) to study healthy subjects and patients with peripheral autonomic denervation to examine how the expression of conditioning-related activity is modulated by stimulus awareness and autonomic arousal. In controls, enhanced amygdala activity was evident during conditioning to both "seen" (unmasked) and "unseen" (backward masked) stimuli, whereas insula activity was modulated by perceptual awareness of a threat stimulus. Absent peripheral autonomic arousal, in patients with autonomic denervation, was associated with decreased conditioning-related activity in insula and amygdala. The findings indicate that the expression of conditioning-related neural activity is modulated by both awareness and representations of bodily states of autonomic arousal.
http://www.ncbi.nlm.nih.gov/pubmed/11856537

Effect of sympathectomy on mechanical properties of common carotid and femoral arteries

Compared with the intact animals, sympathectomized rats showed a marked increase in arterial distensibility over the entire systolic-diastolic pressure range. When quantified by the area under the distensibility-pressure curve, the increase was 59% and 62% for the common carotid and femoral arteries, respectively (P<.01 for both). In the femoral but not in the common carotid artery, sympathectomy was accompanied also by an increase in arterial diameter (+18%, P<.05 versus intact). Therefore, in the anesthetized normotensive rat, sympathetic activity exerts a tonic restraint on large-artery distensibility. This restraint is pronounced in elastic vessels and even more pronounced in muscle-type vessels.
http://www.ncbi.nlm.nih.gov/pubmed/9369260

Effects of endoscopic sympathicotomy in carotid and vertebral arteries in the surgical treatment of primary hyperhidrosis

Analyze, in patients with primary hyperhidrosis (PH) who was undergone to videothoracoscopic sympathicotomy, the degree of vascular denervation after surgical transection of the thoracic sympathetic chain by measuring ultrasonografic parameters in carotid and vertebral arteries.

METHODS:

Twenty-four patients with PH underwent forty-eight endoscopic thoracic sympathicotomy and were evaluated by duplex eco-Doppler measuring systolic peak velocity (SPV), diastolic peak velocity (DPV), pulsatility index (PI) and resistivity index (RI) in bilateral common, internal and external carotids, besides bilateral vertebral arteries. The exams were performed before operations and a month later. Wilcoxon test was used to analyse the differences between the variables before and after the sympatholisis.

RESULTS:

T3 sympathicotomy segment was the most frequent transection done (95.83%), as only ablation (25%) or in association with T4 (62.50%) or with T2 (8.33%). It was observed increase in RI and PI of the common carotid artery (p < 0.05). The DPV of internal carotid artery decreased in both sides (p < 0.05). The SPV and the DPV of the right and left vertebral arteries also increased (p < 0.05). Asymmetric findings were observed so that, arteries of the right side were the most frequently affected.

CONCLUSIONS:

Hemodynamic changes in vertebral and carotid arteries were observed after sympathicotomy for PH. SPV was the most often altered parameter, mostly in the right side arteries, meaning significant asymmetric changes in carotid and vertebral vessels. Therefore, the research findings deserve further investigations to observe if they have clinical inferences.

http://www.ncbi.nlm.nih.gov/pubmed/16186983

most experts do not recommend ETS for the treatment of hyperhidrosis

http://www.sweathelp.org/English/PFF_Treatment_Surgery.asp

sweating from these areas could be under cortical control, separate from the hypothalamic centers involved in thermoregulation

Compensatory hyperhidrosis is excessive sweating of the abdomen, chest, back, thighs, and face,[6,72] usually in response to increased temperature.[46] This is the most common complication following ETS, reported to occur at an average rate of about 60%, with a range of 3% to 98%.[46] Higher rates have been reported from countries with warmer climates, such as in Asia and the Middle East.[46,82] The sweating can be severe for 10% to 40% of patients.[10] Although it has been written that compensatory sweating diminishes with time, several series have documented continued symptoms with longer-term follow-up.[46] In one series of 270 patients followed for a mean of 15 years postsympathectomy, 67% still complained of compensatory sweating, and overall satisfaction fell from an initial level of 96% to 67%.[55] It is possible that patients begin to notice compensatory sweating some time after ETS, as they are initially more aware of the marked reduction of their primary hyperhidrosis.[46] The mechanism for compensatory sweating is unclear; the most likely explanation is that sweating in the trunk increases to compensate for the lack of sweating from the denervated areas in order to maintain thermoregulation.[82] The occurrence of decreased sweating in other areas not innervated by the ganglia treated by ETS suggests that the response to ETS is more complex. The soles are the most common area with decreased sweating post-ETS, and, along with the axillae and palms, sweating from these areas could be under cortical control, separate from the hypothalamic centers involved in thermoregulation.[72] It has also been proposed that ganglion destruction affects axons of neurons in the interomediolateral spinal cord, which could lead to cell death or re-organization, changing the control of the sympathetic system by the spinal cord and higher, leading to increased sympathetic tone in the other body areas not treated by ETS.[10]  http://www.sweathelp.org/English/HCP_Treatment_ETS_Surgery_Complications.asp?printfriendly=true

the decrease in CBF induced by chronic sympathectomy cannot be attributed to the development of hypersensitivity

Thus the decrease in CBF induced by chronic sympathectomy cannot be attributed to the development of hypersensitivity to catecholamines. This decrease remained stable whatever the value of resting flow and was maintained under anesthesia. It is concluded that, as in the peripheral circulation, chronic sympathectomy affects the equilibrium of the vascular smooth muscle fibers, but that circulating amines play no compensatory role in the cerebral circulation because of the blood-brain barrier.
http://www.sciencedirect.com/science/article/pii/0006899385902434

Sympathectomy - a surgically induced neuropathy

"Vascular and neural diseases are closely related and intertwined. Blood vessels depend on normal nerve function, and nerves depend on adequate blood flow. The first pathological change in the microvasculature is vasoconstriction. As the disease progresses, neuronal dysfunction correlates closely with the development of vascular abnormalities, such as capillary basement membrane thickening and endothelial hyperplasia, which contribute to diminished oxygen tension and hypoxia."
http://en.wikipedia.org/wiki/Diabetic_neuropathy


Sympathectomy results in vascular abnormalities, loss of vasoconstriction, capillary basement thickening and endothelial hyperplasia...

Swelling and oedema associated with the interruption of preganglionic sympathetic tract

Swelling and oedema is often observed in patients with Raynaud's disease or causalgia after acute interruption of post-ganglionic sympathetic fibres such as a wide-spread sympathectomy. Complete sympathetic block dilates vein and capillary and increases peripheral pooling, which raises hydrostatic the shins and feet (fig 2), constipation and abdominal distention, and dysuria were observed. Oedema was not noted in the hands or face. There were no signs or abnormal laboratory data suggesting heart failure, renal failure, liver dysfunction, thyroid dysfunction or local inflammation. Venography of the left leg did not show obstruction in the deep veins. 

We showed that the preganglionic sympathetic tract in the spinal cord was often disturbed in patients with multiple sclerosis with myelopathy.' Most patients with complete transection of the spinal cord due to injury showed swelling of the lower limbs or oedema, but they gradually subsided within several months even without restoration of somatic function. Probably some compensatory mechanism improves the hydrostatic condition in the chronic stage and explains why oedema is not noted in patients with chronic autonomic failure syndrome. 

Journal ofNeurology, Neurosurgery, and Psychiatry 1992;55:232-239
http://jnnp.bmj.com/content/55/3/232.1.full.pdf 

The indications for neurolytic or surgical sympathectomy are uncertain

The indications for neurolytic or surgical sympathectomy are uncertain. There is no clear correlation between the degree or duration of pain relief and the actual period of sympathetic blockade and the same patient may show variable responses on different occasionsv (Loh et al 1980). Some patients demonstrate unexpected responses such as contralateral or delayed blocks and some are made worse (Purcell-Jones &Justins 1988, Evans et al 1980, Kleiman 1954)

http://www.springerlink.com/content/7013w45630522h6k/
and
http://ceaccp.oxfordjournals.org/content/10/3/88.full

Sympathectomy causes depigmentation of the skin

In this article, 2 patients were submitted to video-assisted thoracoscopic sympathectomy, and after approximately 8 months they noticed depigmentation of the region corresponding to the blockage of sympathetic stimulus. This fact could be explained by the possible effect of the nervous system on the melanocytes of human skin. 

Sympathectomy? 

Skin Depigmentation: Could it Be a Complication Caused by Thoracic 

 2009;88:42-43 Ann Thorac Surg 

http://ats.ctsnetjournals.org/cgi/reprint/88/4/e42.pdf 

platelet aggregation significantly lower after sympathectomy

It was shown that platelet aggregation in partially (with stellate ganglia containing 25% neurons of normal amount) and completely (0,5% neurons) sympathectomized rats was significantly lower than in intact animals. Concurrently the blood coagulation system of sympathectomized rats was hyperactive. The reasons for sympathectomy-induced changes seems likely to be elevated adrenalin blood concentration in such rats.
http://www.ncbi.nlm.nih.gov/pubmed/7388153

Hyperhidrosis is not caused by 'overactivity' of the sympathetic nervous system

At the high-frequency band (0.15-0.5 Hz), which represents parasympathetic cardiac innervation, an interaction of type and position influencing spectral power was detected. Our highly interesting findings indicate that primary focal hyperhidrosis is based on a much more complex autonomic dysfunction than generalised sympathetic overactivity and seems to involve the parasympathetic nervous system as well.
Eur Neurol 2000;44:112-116 (DOI: 10.1159/000008207)

the sympathetic block, regularly extends six or more spinal segments above the level of sensory block

Chamberlain et al, using a very sensible technique with thermographic imaging, showed that the sympathetic block, at least partial, regularly extends six or more spinal segments above the level of sensory block [8].


Therefore, it seems that a partial sympathetic blockage exists on substantial area over and under of the level of somatic block. In fact, preganglionic sympathetic fibers, once they quit the dura, enter the paravertebral sympathetic chain. From there, these fibers can ascend or descend, synapsing with up to 18 postganglionic fibers, which may project to dermatomes well above and below the spinal segment from which they originated [9].

Bradycardia associated with spinal block is usually light, and contributes modestly to the drop of blood pressure. Rarely, bradycardia is associated with cardiac collapse. Traditional explanation of this bradycardia originating from a spinal anesthesia is the blockage of cardiac accelerator sympathetic nerves (T1-4). Many studies showed than the incidence and the severity of bradycardia is not related to the height of the sensory block.

Onset time of the bradycardia has poor relation with the timing of the spinal block [10]. Carpenter, in a prospective study on 1000 patients under spinal block., showed that bradycardia occured in 13% (heart rate < 50/min) with an onset time of 47 min (range from1 to 204).

There is a pulse rate paradoxical response to movement of the operation table. Under a spinal or epidural anesthesia, when one lift patient head, blood pressure decreases caused by pooling of the venous blood. But in place of a reflex tachycardia mediated by baroreceptors, there is a paradoxical bradycardia. Interestingly, in situation associated with severe reduction of venous return, paradoxical bradycardia can be seen even in the absence of sympathetic block.

There is similarities between hypotension related to bradycardia of the spinal anesthesia and vasovagal reaction. Vasovagal shock is characterized by hypotension and bradycardia, and can progress to syncope. It has a central or a peripheral etiology.

Because of their rare occurrence, almost all studies on cardiac arrest during spinal anesthesia are retrospective, therefore limited in their ability to identify variables and incidents of such events.

Caplan [14] in 1988 has identified 14 cases of sudden cardiac arrest on patients in good health and undergoing minor surgical procedures. None of these patients had unusually high block, nor received badly inadequate resuscitative care. Despite all this, only 8 of 14 patients survived, and only one survivors had acceptable neurological functions Retrospectively, respiratory insufficiency was suspected, secondary to a strong sedation, as the main etiology of the cardiac arrest. Even a complete sympathectomy leaves a good arterial vascular tone, but in presence of hypoxia and acidosis can lead to a fall in arterial tone, to an exaggerated decrease in blood pressure and cardiac collapse. Early sympathetic responses to hypoxia, which are tachycardia and vasoconstriction, are almost severely blunt by spinal anesthesia [15].

Mackey reported 3 cases of severe bradycardia during spinal anesthesia in the absence of hypoxia and strong sedation [16]. He concludes that severe bradycardya was caused by a drop in venous return triggering Bezold-Jarisch reflex which in presence of sympathetic block led to exaggerated bradycardia, hypotension and arrest.

http://www.esra-learning.com/site/generalites/pathology/b_haemodynamic.htm

Gustatory sweating is a frequent side effect of sympathectomy

The Annals of Thoracic Surgery
Volume 81, Issue 3, March 2006, Pages 1043-1047
http://www.sciencedirect.com/science/article/pii/S0003497505017571

Post-sympathectomy pain and changes in sensory neuropeptides

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

sensory abnormalities, abnormal body sweating, and pathologic gustatory sweating

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

Recurrent sweating occurred in 17.6% of patients

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

Post-sympathectomy neuralgia

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

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

Neuroma following Sympathectomy

The authors conclude recomemnding the application of clips and if the syndrome nevertheless appears novocaine infiltration of the upper end of the sympathetic chain. The authors are convinced that the theory of Hermann and Cooley about neuroma formation at the ends of the sympathetic chain after resection of a segment is true.
http://www.revangiol.com/sec/resumen.php?or=web&i=e&id=227082.
Traumatic neuroma follows different forms of nerve injury (often as a result of surgery). They occur at the end of injured nerve fibres as a form of ineffective, unregulated nerve regeneration; it occurs most commonly near a scar, either superficially (skin, subcutaneous fat) or deep (e.g., after acholecystectomy). They are often very painful. It is also known as "pseudoneuroma".

bone atrophy on the side of the sympathectomy

localized alopecia, corneal ulceration, keratitis, strabismus, enophthalmos, ocular atrophy, hemifacial atrophy and slight bone atrophy on the side of the sympathectomy were observed

http://www.ncbi.nlm.nih.gov/pubmed/1962072

Autonomic Neuropathy Differential Diagnoses

Differentials 

Aromatic L-amino acid decarboxylase deficiency 

Autonomic dysreflexia syndrome in spinal injuries. 

Dopamine beta-hydroxylase deficiency 

Multiple System Atrophy 

Parkinson Disease 

Parkinson-Plus Syndromes 

Progressive Supranuclear Palsy 

Pure Autonomic Failure 

Surgical sympathectomy 

Syphilis (tabes dorsalis) 

Vagotomy 

http://emedicine.medscape.com/article/1173756-differential

Skin depigmentation: could it be a complication caused by thoracic sympathectomy?

http://www.ncbi.nlm.nih.gov/pubmed/19766777

Patients need to be carefully counselled before committing to sympathectomy

However 43 patients (93%) suffered with compensatory sweating, of these 27 had to change clothes more than once daily. Compensatory sweating was graded as severe in 18 and incapacitating in 2. Of note only 5 patients noticed an improvement in the compensatory sweating over time. Only 26 (56%) would recommend thoracoscopic sympathectomy to others with hyperhydrosis.

CONCLUSION:

Thoracoscopic sympathectomy is effective in the treatment of hyperhydrosis. However compensatory sweating seems unavoidable and infrequently improves with time. Patients need to be carefully counselled before committing to surgery.

http://www.ncbi.nlm.nih.gov/pubmed/21539945

RA, lupus and other connective tissue disorders may have abnormalities of sympathetic postganglionic function

Rheumatoid arthritis, systemic lupus erythematosus, and other connective tissue disorders may have abnormalities of sympathetic postganglionic function. Some of these patients may have autoantibodies to ganglionic acetylcholine receptors. Autoimmune thyroiditis, as with chronic thyroiditis and Hashimoto thyroiditis, can be associated with some features of Sjögren syndrome such as xerostomia. Patients with systemic sclerosis and mixed connective tissue disorder may have abnormalities of autonomic functioning of esophageal motor activity.
http://www.emedicine.com/NEURO/topic720.htm

Regional sympathectomy leads to qualitative alterations in localized bone modeling and remodeling

http://www.ncbi.nlm.nih.gov/pubmed/8723974

Depressed heart rate variability has independent prognostic value in patients with chronic heart failure; spectral analysis identifies an increased risk for sudden death in these patients

http://www.ncbi.nlm.nih.gov/pubmed/10681488

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

The baroreceptor reflex is only a short-term regulator of blood pressure because the receptors adapt by raising the threshold and lowering discharge rate.
8. Describe the reflex compensations when someone suddenly stands up from a supine position. What would happen in a patient who just had a sympathectomy?

Sudden standing causes pooling of blood in the leg veins. This results in decreased venous return to the heart, which leads to decreased cardiac output (Frank-Starling mechanism), which leads to decreased MAP. This decrease in MAP is detected by the carotid sinus baroreceptors, which relay a message to the medullary cardiovascular control center, which increases sympathetic outflow and decreases parasympathetic outflow, this causes:

* An increase in HR and myocardial contractility, tending to restore cardiac output.
* Vasoconstriction in skeletal musculature, skin, kidneys and gut, reducing blood flow to these organs and increasing TPR.
* Venoconstriction decreasing capacitance and increasing venous return

A patient with a sympathectomy would experience what's referred to as orthostatic hypotension (which might lead to syncope). Orthostatic hypotension is a decrease in arterial pressure when going from supine to a standing position. A person with a normal baroreceptor mechanism will try to restore MAP. In a person who had a sympathectomy, the sympathetic component of the baroreceptor mechanism is absent.

Heart Physiology II

M.A.S.T.E.R. Learning Program, UC Davis School of Medicine, Sacramento, CA 95817 
Date Revised: Jan 16, 2002
Revised by: Gordon Li and Carolyn Nguyen

blunted hypoxic pulmonary vasoconstriction due to partial interruption of the sympathetic nerve supply to the lung by bilateral thoracic sympathectomy

Anaesth Intensive Care. 2003 Oct;31(5):581-3.

Orthodeoxia--an uncommon presentation following bilateral thoracic sympathectomy.

van Heerden PV, Cameron PD, Karanovic A, Goodman MA.

Source

Departments of Intensive Care and Vascular Surgery, Sir Charles Gairdner Hospital, Pharmacology Unit, School of Medicine and Pharmacology, University of Western Australia, Perth, Western Australia.

Abstract

We present a case of orthodeoxia (postural hypoxaemia) which resulted from a combination of lung collapse/consolidation and blunted hypoxic pulmonary vasoconstriction due to partial interruption of the sympathetic nerve supply to the lung by bilateral thoracic sympathectomy.

http://www.ncbi.nlm.nih.gov/pubmed/14601286

Bezold-Jarisch Reflex and Sympathectomy

Much attention has been focused on the Bezold-Jarisch Reflex as the cause of sudden acute bradycardia during spinal or epidural anesthesia. The basis of this reflex is a decrease in stretch tension on mechanoreceptors located in the left ventricle. A sudden empty left ventricle triggers this paradoxical reflex which resulst in increased parasympathetic activity. Sympathetic output is also inhabited. Anything that decreases left ventricular end-diastolic volume suddenly, such as spinal anesthesia may rigger his reflex.

   By contrast, bradycardia that is slow on onset, developing after administration of spinal anesthesia, has been recognized and attributed to decreased activity of the cardioaccelerator nerves to the heart. This is a different phenomenon than the sudden bradycardia or asystole in the patient presented above. Complete sympathectomy of the heart itself reduces heart rate by about 20%.

Complications of regional anesthesia

Brendan T. Finucane

Springer, 2007 - 506 pages

An unopposed vagal tone secondary to sympathectomy

1.) An unopposed vagal tone secondary to sympathectomy. This sympathectomy occurs 2-6 dermatomes higher than sensory block, so that a sensory block of T6 can conceivably inhibit all of the sympathetic innervation to the heart.

2.) The Bezold-Jarisch reflex – which may be widely under appreciated phenomenon. You’ll be surprised how many clinicians are not well versed in this essential physiology.

Sympathectomy → reductions in venous tone → profound decreased venous return. This activates mechanoreceptors embedded within the walls of the myocardium → stimulating vagal afferents → vasomotor center of medulla → increased vagal tone to the heart, thus slowing or stopping the heart entirely to allow enough filling time to generate an effective stroke volume. 
http://allnurses.com/certified-registered-nurse/sympathectomies-and-atropine-124910.html

A drastic reduction in tissue noradrenaline, adrenaline, and dopamine levels occurred after sympathectomy

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

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

A depression in the heart rate and decrease in response to stress is expected to some degree in all patients after sympathectomy

A depression in the heart rate with resultant drop in the heart rate product and decrease in response to stress is expected to some degree in all patients. Some series have described this finding in most patients, whereas others report at least a 10% drop in heart rate in all patients. This is a possible major cause for postoperative dysfunction and should be cautiously sought after. Patients with resting heart rate that is below 50 to 60 beats/min should undergo electrocardiography. It is recommended that if the heart rate is low on a subsequent electrocardiogram as well, that a tilt test should be performed to exclude patients in whom there is an inordinately high risk of postoperative bradycardia.

In conclusion, thoracoscopic sympathectomy can be done as an outpatient procedure safely and efficiently. Debate continues about the correct transection levels, but at this time there is a consensus that division or clipping is equal to resection. Although the procedure has several severe side effects, they are rare. The predominant complication remains compensatory sweating, which may occur regardless of the level transected or the indication. Future clinical trials should compare some of the different techniques to achieve a global consensus of the surgical approach.

http://ats.ctsnetjournals.org/cgi/content/full/85/2/S764

The biology and control of surface overhealing

Lesions of “surface overhealing” include keloid, hypertrophic scar, and burn scar. All are characterized by overabundant collagen deposition. The biology of these lesions is reviewed, suggesting that abnormal collagen metabolism results from alterations in the inflammatory/immune response. Practical and theoretical treatment plans are outlined based on methods that alter collagen metabolism, the inflammatory/immune system or rely on physical alterations (surgery, pressure).
http://www.springerlink.com/content/3g2mr5r32m438125/

mechanisms of the post-sympathectomy syndrome and of the action of these drugs are uncertain

Fifty-six consecutive patients who subsequently underwent ninety-six lumbar sympathectomies were studied prospectively with regard to the development of postoperative pain. Pain after operation was observed in thirty-four extremities by twenty-five of the patients (35 per cent). It began abruptly an average of twelve days after operation and was often accentuated nocturnally. The pain was almost always described as a deep, dull ache and persisted two to three weeks before spontaneously remitting. Postsympathectomy pain of such severity that parenteral narcotics afforded no relief developed in two of these fifty-six patients and in nine additional patients. Treatment with carbamazepine produced dramatic reduction in the intensity of pain in seven of these nine patients within twenty-four hours after the institution of therapy. Two patients were given intravenous diphenylhydantoin and both experienced immediate relief of pain. The mechanisms of the syndrome and of the action of these drugs are uncertain.
http://www.sciencedirect.com/science/article/pii/0002961074902384

post-sympathectomy syndrome

Sympathectomy. Some patients with CRPS have good pain relief from sympathetic nerve blocks, but the pain relief does not last long. For these patients, doctors might suggest a sympathectomy (killing the sympathetic nerves leading to the painful body part, either by using surgery or chemicals). Some patients get longer pain relief after the sympathectomy, but others do not. Also, there is the slight chance that patients who get a sympathectomy for CRPS of the leg might develop a new pain syndrome, called post-sympathectomy syndrome. 

http://www.stoppain.org/pain_medicine/content/chronicpain/crps.asp