direct injury to the anatomic structure of the autonomic nervous system in the thoracic cavity, and postthoracotomy pain may contribute independently or in association with each other to the development of these arrhythmias

Anesthesiol Res Pract. 2013;2013:413985. doi: 10.1155/2013/413985. Epub 2013 Oct 23.

Supraventricular arrhythmias after thoracotomy: is there a role for autonomic imbalance?

Vretzakis G1, Simeoforidou M, Stamoulis K, Bareka M.

Author information

Abstract

Supraventricular arrhythmias are common rhythm disturbances following pulmonary surgery. The overall incidence varies between 3.2% and 30% in the literature, while atrial fibrillation is the most common form. These arrhythmias usually have an uneventful clinical course and revert to normal sinus rhythm, usually before patent's discharge from hospital. Their importance lies in the immediate hemodynamic consequences, the potential for systemic embolization and the consequent long-term need for prophylactic drug administration, and the increased cost of hospitalization. Their incidence is probably related to the magnitude of the performed operative procedure, occurring more frequently after pneumonectomy than after lobectomy. Investigators believe that surgical factors (irritation of the atria per se or on the ground of chronic inflammation of aged atria), direct injury to the anatomic structure of the autonomic nervous system in the thoracic cavity, and postthoracotomy pain may contribute independently or in association with each other to the development of these arrhythmias. This review discusses currently available information about the potential mechanisms and risk factors for these rhythm disturbances. The discussion is in particular focused on the role of postoperative pain and its relation to the autonomic imbalance, in an attempt to avoid or minimize discomfort with proper analgesia utilisation.

http://www.ncbi.nlm.nih.gov/pubmed/24235971

Since changes in old age show some similarities with those following chronic sympathectomy,

"For the tracheobronchial tree. surgical (sympathectomy) and chemical (with 6-hydroxydopamine or reserpine) interventions lead to histological disappearance of the NA and NPY." (p.435)

" Prejunctional supersensitivity to norepinephrine after sympathectomy or cocaine treatment." (p. 410)

"Following chronic sympathectomy, substance P expression in presumptive sensory nerves....and NPY-expression in parasympathetic nerves ...to autonomically innervated tissues have both been shown to increase... Experiments using NGF and anti-NGF antibodies (Kessler et al., 1983) have suggested that competition between sympathetic and sensory fibers for target-derived growth factors could explain these apparently compensatory interactions,..." (p. 33)

"Since changes in old age show some similarities with those following chronic sympathectomy, it is tempting to consider whether alterations in one group of nerves in tissues with multiple innervations trigger reciprocal changes in other populations of nerves, perhaps through the mechanism of competition for common, target-produced growth factors. The nature of these changes is such that they could be nonadaptive and even destabilizing of cardiovascular homeostasis. (p. 34) 

Impairment of sympathetic and neural function has been claimed in cholesterol-fed animals (Panek et al., 1985). It has also been suggested that surgical sympathectomy may be useful in controlling atherosclerosis in certain arterial beds (Lichter et al., 1987). Defective cholinergic arteriolar vasodilation has been claimed in atherosclerotic rabbits (Yamamoto et al., 1988) and, in our laboratory, we have recently shown impairment of response to perivascular nerves supplying the mesenteric, hepatic, and ear arteries of Watanabe heritable hyperlipidemic rabbits (Burnstock et al., 1991). 
   Loss of adrenergic innervation has been reported in alcoholism (Low et al., 1975), amyloidosis (Rubenstein et al., 1983), orthostatic hypotension (Bannister et al., 1981), and subarachnoid haemorrhage (Hara and Kobayashi, 1988). Recent evidence shows that there is also a loss of noradrenergic innervation of blood vessels supplying malignant, as compared to benign, human intracranial tumours (Crockard et al., 1987). (p. 14)  

Vascular Innervation and Receptor Mechanisms: New    Perspectives 

Rolf Uddman

Academic Press, 2 Dec 2012 - Medical - 498 pages

Postganglionic sympathetic efferents play a critical role in several types of pathological pain

Postganglionic sympathetic efferents play a critical role in several types of pathological pain (Gibbs et al., 2008; Jänig and McLachlan, 1994; Jänig et al., 1996; Raja, 1995). For example, sympathetic stimulation may excite sensory neurons in animals with inflamed peripheral tissue or after peripheral nerve injury (Devor et al., 1994; Sato and Kumazawa, 1996; Sato and Perl, 1991). Sympathectomy relieves hyperalgesic and allodynic behaviors in several pathological pain models (Kim et al., 1993; Kinnman and Levine, 1995; Malmberg and Basbaum, 1998). Clinical observations and experimental studies suggest that a crosstalk between sympathetic efferents and sensitized primary afferent nociceptors is produced by the release of norepinephrine, adenosine 5′-triphosphate (ATP) and/or neuropeptide Y from sympathetic efferents onto dorsal root ganglion (DRG) neurons (Chung et al., 1996; Devor et al., 1994), at the site of nerve injury (Devor and Seltzer, 1999) and in the skin (Lin et al., 2003,2004; Sato and Perl, 1991).

Many studies reveal that neurogenic inflammation and the resulting pain induced by intradermal injection of capsaicin (CAP) are sympathetically dependent (Coderre et al., 1989; Lin et al., 2003,2004; Ren et al., 2005,2006). Activation of transient receptor potential vanilloid-1 (TRPV1) receptors in primary afferent nociceptive neurons and their axons evoked by CAP injection produces an efferent function that initiates neurogenic inflammation (Kessler et al., 1999; Szolcsanyi, 1996,2004) by the release of neuropeptides from the nociceptors (Garcia-Nicas et al., 2001; Li et al., 2008; Lin et al., 2007). We proposed in our previous studies that neurogenic inflammation is likely to be sympathetically-mediated by influencing the sensitivity of primary afferent nociceptive neurons and/or their terminals (Ren et al., 2005,2006). However, no direct evidence has so far been provided to show if this process is done by modulation of TRPV1receptors.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2824038/

Exp Neurol. Author manuscript; available in PMC Mar 1, 2011.

Published in final edited form as:

Exp Neurol. Mar 2010; 222(1): 93–107.

Published online Dec 28, 2009. doi:  10.1016/j.expneurol.2009.12.011

sympathectomy leads to fluctuation of vasoconstriction alternated with vasodilation in an unstable fashion. Following sympathectomy the involved extremity shows regional hyper - and hypothermia

"To quote Nashold, referring to sympathectomy, "Ill- advised surgery may tend to magnify the entire symptom complex"(38). Sympathectomy is aimed at achieving vasodilation. The neurovascular instability (vacillation and instability of vasoconstrictive function), leads to fluctuation of vasoconstriction alternated with vasodilation in an unstable fashion (39). Following sympathectomy the involved extremity shows regional hyper - and hypothermia in contrast, the blood flow and skin temperature on the non- sympathectomized side are significantly lower after exposure to a cold environment (39). This phenomenon may explain the reason for spread of CRPS. In the first four weeks after sympathectomy, the Laser Doppler flow study shows an increased of blood flow and hyperthermia in the extremity (40). Then, after four weeks, the skin temperature and vascular perfusion slowly decrease and a high amplitude vasomotor constriction develops reversing any beneficial effect of surgery (39). According to Bonica , "about a dozen patients with reflex sympathetic dystrophy (RSD) in whom I have carried out preoperative diagnostic sympathetic block with complete pain relief, sympathectomy produced either partial or no relief (40)"

Chronic Pain: 

 Reflex Sympathetic Dystrophy : Prevention and Management

Hooshang Hooshmand

CRC PressINC, 1993 - Medical - 202 pages

Postsympathectomy pain of such severity that parenteral narcotics afforded no relief

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

Incidence of chronic pain after minimal-invasive surgery for sponta... - PubMed - NCBI

Incidence of chronic pain after minimal-invasive surgery for sponta... - PubMed - NCBI: "After a median follow up of 59 months (range 35-79) 41 (68.3%) patients were completely free from any complaints. However 19 (31.7%) patients suffered from chronic pain. Two of them (3.3%) required daily oral pain medication. The incidence of chronic complaints was more frequent in patients with pleurectomy (47.1%) as compared to patients with mechanical pleurodesis only (25.6%; P=0.107). On a visual analog pain scale (ranging from 0 to 100) five (8.3%) patients described a pain intensity <10, 12 (20%) patients between 10 and 20 and two (3.3%) patients >50. In the majority of the patients the pain was located in the area of the trocar incisions. Six (10%) patients had a chronic complaints in the ipsilateral shoulder.
CONCLUSIONS:
The incidence of chronic postoperative complaints after minimal-invasive procedures for spontaneous pneumothorax is relatively high. This has to be considered if minimal-invasive procedures are discussed to be an alternative to simple drainage therapy for the first episode of spontaneous pneumothorax."

Eur J Cardiothorac Surg. 2001 Mar;19(3):355-8; discussion 358-9.

Incidence of chronic pain after minimal-invasive surgery for spontaneous pneumothorax.

Despite the simplicity and rapidity of the procedure, some patients experience intense, in some cases persistent, postoperative pain

Jornal Brasileiro de Pneumologia - The incidence of residual pneumothorax after video-assisted sympathectomy with and without pleural drainage and its effect on postoperative pain:

"Anteroposterior chest X-ray in the orthostatic position, while inhaling, was absolutely normal in 18 patients (32.1%), and residual pneumothorax was detected in 17 patients (30.4%). When the patients were separated into two groups (those who had received drainage and those who had not), 25.9% (7 patients) and 34.4% (10 patients), respectively, presented residual pneumothorax, with no difference between the two groups (p = 0.48) (Figure 1).

The additional alterations were laminar atelectasis and emphysema of the subcutaneous cellular tissue.

Chest X-rays in the orthostatic position, while exhaling, revealed residual pneumothorax in 39.3% (22 patients) and was absolutely normal in 25% (14 patients). On the same X-rays, when patients were analyzed separately, residual pneumothorax was seen in 33.3% of the patients who had received drainage (9 patients) and in 44.8% (13 patients) of those who had not, with no difference between the two groups (p = 0.37) (Figure 1).

The low-dose computed tomography scans of the chest detected residual pneumothorax in 76.8% (43 patients). In the patients submitted to postoperative drainage, this rate was 70.3% (19 patients), compared with 82.7% (24 patients) in those without pleural drainage, with no difference between the two groups (p = 0.27) (Figure 1). Therefore, the overall rate of occult pneumothorax (only visible through tomography), revealed on anteroposterior X-rays was 35.7% (20 patients): 48.2% while patients were inhaling and 41.1% while patients were exhaling. The VAS score in the PACU ranged from 0 to 10, with a mean of 2.16 ± 0.35.

Regarding characteristics, 44.6% of the patients reported chest pain upon breathing and 32.1% reported retrosternal pain. The same evaluation performed in the infirmary, during the immediate postoperative period, ranged from 0 to 10, with a mean of 3.75 ± 0.30, being 69.6% of chest pain upon breathing and 78.6% of retrosternal pain. On postoperative day 7, according to VAS, pain ranged from 0 to 10, with a mean of 2.05 ± 0.31; regarding characteristics, it was continuous in 32.1% of the cases, and retrosternal in 26.8%. On postoperative day 28, pain ranged from 0 to 3, with a mean of 0.17 ± 0.08, 7.1% of mechanical rhythm and 5.4% upper posterior."

Jornal Brasileiro de Pneumologia

Print version ISSN 1806-3713

J. bras. pneumol. vol.34 no.3 São Paulo Mar. 2008

http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1806-37132008000300003&lng=en&nrm=iso&tlng=en

Acute pain following needlescope-VATS (nVATS) sympathectomy for palmar hyperhidrosis

"...recently Sihoe et al. [10] have reported that pre-emptive wound infiltration with a local anaesthetic reduces the postoperative wound pain following needlescope-VATS (nVATS) sympathectomy for palmar hyperhidrosis. The concept of pre-emptive analgesia has gained popularity following
experimental work, demonstrating that early control of pain can alter its subsequent evolution as well as the recognition that nociception produces important physiological responses, even in adequately anaesthetised individuals, and the understanding that for many individuals the minimisation of pain can improve clinical outcomes [11].
The pre-emptive analgesia is based on the intuitive idea that if pain is treated before the injury occurs, the nociceptive system will perceive less pain than if analgesia is given after the injury has already occurred. The preoperative administration of analgesic will modify the afferent nociceptive barrage from the site of injury, thus preventing the development of central sensitisation and hyperalgesia [12].
Thus, we have focussed on this argument in the aim of the present study, which is to determine whether pre-emptive local analgesia (PLA) has an effect to reduce acute postoperative pain following standard-VATS (s-VATS) sympathectomy, in view of n-VATS being considered less painful
than the s-VATS procedure [4,5]."

http://ejcts.oxfordjournals.org/content/37/3/588.full.pdf+html
European Journal of Cardio-thoracic Surgery 37 (2010) 588—593
Pre-emptive local analgesia in video-assisted thoracic surgery sympathectomy

Alfonso Fiorelli, Giovanni Vicidomini, Paolo Laperuta, Luigi Busiello,
Anna Perrone, Filomena Napolitano, Gaetana Messina, Mario Santini*
Thoracic Surgery Unit, Second University of Naples, Naples, Italy
Received 28 March 2009; received in revised form 21 July 2009; accepted 31 July 2009; Available online 12 September 2009

"sympathicotomy may cause a temporary impairment of the caudal-to-rostral hierarchy of thermoregulatory control and changes in microcirculation"

Patients with palmar hyperhidrosis have been reported to have a much
more complex dysfunction of autonomic nervous system, involving compensatory high parasympathetic activity as well as sympathetic overactivity (13, 14), suggesting that sympathicotomy initially induces a sympathovagal imbalance with a parasympathetic predominance, and that this is restored on a long-term basis (14). Therefore, thoracic sympathicotomy may cause a temporary impairment of the caudal-to-rostral hierarchy of thermoregulatory control and changes in microcirculation.

The reduction of finger skin temperature on the non-denervated side may be due to either a decrease in the cross-
inhibitory effect or the abnormal control of the inhibitory fibers by the sudomotor center (6).
Vasoconstrictor neurons have been found to be largely under the inhibitory control of various afferent
input systems from the body surface, whereas sudomotor neurons are predominantly under excitatory
control (15). The basic neuronal network for this reciprocal organization is probably located in the spinal level (15). Therefore, the reduction in the contralateral skin temperature may be explained by cross-inhibitory control of various afferent in the spinal cord.
In particular, our study showed that, following bilateral T3 sympathicotomy, the skin temperatures on
the hands increased whereas the skin temperatures on the feet decreased. These findings suggest a
cross-inhibitory control between the upper and lower extremities. However, the pattern of skin
temperature reduction on the feet differed from that on the contralateral hand. The skin temperature on
the feet did not decrease after right T3 sympathicotomy but decreased significantly after bilateral T3
sympathicotomy.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2722005/

sympathectomy, although having varying results, does seem to increase the severity of autoimmune disorders

Allostasis - a state of imbalance responsible for Autoimmune disorders

In general, enhancing the sympathetic tone decreases both T0-cell and NK cell functions but not the proliferation of splenic B cells (Dowdell and Whitacre, 2000). In contrast, chemical sympathectomy, although having varying results, does seem to increase the severity of autoimmune disorders (Dowdell and Whitacre, 2000)
As far as metabolism, catecholamines promote mobilization of fuel stores at time of stress and act synergistically with glucocorticoids to increased glycogenolysis, gluconeogenesis, and lipolysis but exert opposing effects of protein catabolism, as noted earlier. One important aspect is regulation of body temperature (Goldsttein and Eisenhofer, 2000) Epinephrine levels are also positively related to serum levels of HDL cholesterol and negatively related to triglycerines. However, perturbing the balance of activity of various mediators or metabolism and body weight regulation can lead to well-known metabolic disorders such as type 2 diabetes and obesity.

At the same time, increased sympathetic activitation and nerephinephrine release is elevated in hypertensive individuals and also higher levels of insulin, and there are indications that insulin further increases sympathetic activity in a vicious cycle (Arauz-Pacheco et al.,1996)

As a result of either local production, cytokines often enter the the circultion and can be detected in plasma samples. Sleep deprivation and psychological stress, such as public speaking, are reported to elevate inflammatory cytokine level in blood (Altemus et al., 2001) Circulting levels of a number of inflammatory cytokines are elevated in relation to viral and other infections and contirbute to the feeling of being sick, as well as sleepiness, wiht both direct and indirect effects on the central nervous system (Arkins et al., 2000; Obal and Kueger, 2000)

Inflammatory autoimmune diseases, such as multiple sclerosis, rheumatoid arthritis, and type 1 diabetes, reflect an allostatic state that consists of at least three principal causes: genetic risk factors, (...) factors that contribute to the development of tolerance of self-antigens (...) and the hormonal mikieu that regulates adaptive immunes responses (Dowdell and Whitacre, 2000)

Allostasis, homeostasis and the costs of physiological adaptation

By Jay SchulkinCambridge University Press, 2004

Allostasis is the process of achieving stability, or homeostasis, through physiological or behavioral change. This can be carried out by means of alteration in HPA axishormones, the autonomic nervous system, cytokines, or a number of other systems, and is generally adaptive in the short term ^[1]

"Similar low values are observed in patients with sympathectomy and in patients with tetraplegia"

"Patients with progressive autonomic dysfunction (including diabetes) have little or no increase in plasma noradrenaline and this correlates with their orthostatic intolerance (Bannister, Sever and Gross, 1977). In patients with pure autonomic failure, basal levels of noradrenaline are lower than in normal subjects (Polinsky, 1988). Similar low values are observed in patients with sympathectomy and in patients with tetraplegia. (p.51)



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

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




Anhidrosis is the usual effect of destruction of sympathetic supply to the face. However about 35% of patients with sympathetic devervation of the face, acessory fibres (reaching the face through the trigeminal system) become hyperactive and hyperhidrosis occurs, occasionally causing the interesting phenomenon of alternating hyperhidrosis and Horner's Syndrome (Ottomo and Heimburger, 1980). (p.159)



Disorders of the Autonomic Nervous System
By David Robertson, Italo Biaggioni
Edition: illustrated
Published by Informa Health Care, 1995
ISBN 3718651467, 9783718651467"

sympathectomy severs both vasomotor and sensory fibres

CUTANEOUS INNERVATION IN MAN BEFORE AND AFTER LUMBAR SYMPATHECTOMY:EVIDENCE FOR INTERRUPTION OF BOTH SENSORY AND VASOMOTOR NERVE FIBRES. 

ORIGINAL ARTICLES

ANZ Journal of Surgery. 73(1-2):14-18, January 2003.
COVENTRY, BRENDON J. BM BS, PhD, FRACS *; WALSH, JOHN A. MD, FRACS +

Abstract:
Background: Rest pain and severe ischaemia in patients who are unable to be offered (further) surgery to revascularize the lower limb is still problematic. Lumbar sympathectomy has been used for many years but the mechanisms by which this works are not absolutely clear. Both sensory and vasomotor fibres travel in the lumbar sympathetic chain and the effects of lumbar sympathectomy on these nerve types have been investigated in the present paper.

Methods: Immunohistochemical methods were used to detect neuropeptides contained in sensory and vasomotor nerves in the lower limb skin of (i) patients having amputations for peripheral vascular disease (PVD) after previous (chemical or surgical) sympathectomy; (ii) patients having amputations for PVD without previous (chemical or surgical) sympathectomy; and in control normal skin. The three groups are compared and the results are discussed.

Results: Normal and PVD controls had intact sensory and vasomotor nerves around dermal cutaneous blood vessels, but these were completely or virtually completely lost after lumbar sympathectomy, by either chemical or surgical means.

Conclusions: Lumbar sympathectomy severs both vasomotor and sensory fibres, suggesting that relief of rest pain may be explained not only by increased cutaneous and muscle blood flow, but also by nociceptive sensory denervation.

"Sympathectomy is a destructive procedure that interrupts the sympathetic nervous system"

Cervico-thoracic or lumbar sympathectomy for neuropathic pain | Cochrane Summaries: "Sympathectomy is a destructive procedure that interrupts the sympathetic nervous system. Chemical sympathectomies use alcohol or phenol injections to destroy sympathetic nervous tissue (the so-called "sympathetic chain" of nerve ganglia). Surgical ablation can be performed by open removal or electrocoagulation (destruction of tissue with high-frequency electrical current) of the sympathetic chain, or by minimally invasive procedures using thermal or laser interruption. Nerve regeneration commonly occurs following both surgical or chemical ablation, but may take longer with surgical ablation.

This systematic review found only one small study (20 participants) of good methodological quality, which reported no significant difference between surgical and chemical sympathectomy for relieving neuropathic pain. Potentially serious complications of sympathectomy are well documented in the literature, and one (neuralgia) occurred in this study.

The practice of sympathectomy for treating neuropathic pain is based on very weak evidence. Furthermore, complications of the procedure may be significant."



'via Blog this'

Many injuries to the nervous system are followed by incomplete recovery or even increasing disability over time

Many injuries to the nervous system are followed by incomplete recovery or even increasing disability over time. Some of these long term effects are due to the loss of access to growth factors called neurotrophins that provide essential support for adult nerve cells. We recently discovered that immune responses can be triggered by injury leading to inflammation around the damaged nerve cells. Control of inflammation may therefore allow the remaining nerve cells to survive until treatments that enable them to regenerate can be developed.

http://www.neura.edu.au/health/nerve-and-spinal-cord-injury

24-hour melatonin measurements in normal subjects and after peripheral sympathectomy

J Clin Endocrinol Metab. 1991 Apr;72(4):819-23.

Sequential cerebrospinal fluid and plasma sampling in humans: 24-hour melatonin measurements in normal subjects and after peripheral sympathectomy.

Bruce J1, Tamarkin L, Riedel C, Markey S, Oldfield E.

Author information

Abstract

Simultaneous measurements of plasma and cerebrospinal fluid (CSF) melatonin and urinary excretion of 6-hydroxymelatonin were performed in four normal volunteers and one patient before and after upper thoracic sympathectomy for the control of essential hyperhidrosis. For normal individuals, hourly 24-h melatonin concentrations in plasma and CSF exhibited similar profiles, with low levels during the day and high levels at night. Peak plasma levels varied from 122-660 pmol/L, and the peak CSF levels from 94-355 pmol/L. The onset of the nocturnal increase in melatonin did not occur at the same time for each individual. Urinary 6-hydroxymelatonin levels also exhibited a daily rhythm, with peak excretion at night. The individual with the lowest nocturnal levels of circulating melatonin also had the lowest excretion of 6-hydroxymelatonin. In the patient with hyperhidrosis, a prominent melatonin rhythm was observed preoperatively in the CSF and plasma. After bilateral T1-T2 ganglionectomy, however, melatonin levels were markedly reduced, and the diurnal rhythm was abolished. These results provide direct evidence in humans for a diurnal melatonin rhythm in CSF and plasma as well as regulation of this rhythm by sympathetic innervation.

http://www.ncbi.nlm.nih.gov/pubmed/2005207

Effect of local autonomic denervation on in vitro responsiveness of lymphocytes

The results further indicate that an appropriate sympathetic and parasympathetic local environment may be needed for immunomodulation, as well as for cyclosporine activity in lymphoid tissue.
Journal of the Autonomic Nervous System
Volume 62, Issue 3, 17 February 1997, Pages 155-162
http://www.sciencedirect.com/science?_ob=ArticleURL&amp;_udi=B6T05-3PKTG6C-6&amp;_user=10&amp;_rdoc=1&amp;_fmt=&amp;_orig=search&amp;_sort=d&amp;view=c&amp;_acct=C000050221&amp;_version=1&amp;_urlVersion=0&amp;_userid=10&amp;md5=da81efda6c250763623b89537aed8109

diabetic autonomic neuropathy is due to a lesion of the sympathetic nerve supply to the skin

"We conclude that the diabetic anhidrotic syndrome, a form of diabetic autonomic neuropathy, is due to a lesion of the sympathetic nerve supply to the skin."

Diabetologia

Volume 22, Number 2, 96-99, DOI: 10.1007/BF00254836

 

Sympathectomy IS a lesion of the sympathetic nerve supply to the skin (and other structures)

symptoms of Autonomic Neuropathy closely resemble the symptoms described by many who have undergone sympathectomy

the symptoms of Autonomic Neuropathy closely resemble the symptoms described by many who have undergone sympathectomy - a surgery where the surgeon destroys part of the ANS, a surgery that can result in a deranged functioning of the ANS. Surgeons are allowed to market ETS/ESB  as an elective (life-style) procedure, often referred to as a 'cure'. Autonomic neuropathy:
"Cardiovascular symptoms: exercise intolerance, fatigue, sustained heart rate, syncope, dizziness, lightheadedness, balance problems
Gastrointestinal symptoms: dysphagia, bloating, nausea and vomiting, diarrhea, constipation, loss of bowel control
Genitourinary symptoms: loss of bladder control, urinary tract infection, urinary frequency or dribbling, erectile dysfunction, loss of libido, dyspareunia, vaginal dryness, anorgasmia
Sudomotor (sweat glands) symptoms: pruritus, dry skin, limb hair loss, calluses, reddened areas
Endocrine symptoms: hypoglycemic unawareness
Other symptoms: difficulty driving at night, depression, anxiety, sleep disorders, cognitive changes" http://www.aafp.org/afp/2005/0601/p2123.html

abnormal sympathetic activity may cause pain following sympathectomy

Further evidence suggesting that abnormal sympathetic activity may cause pain comes from reports of pain following sympathectomy. This has occurred after stellate ganglion block and lumbar sympathectomy.
The Nervous System and Adipose Tissue, By Katharine Dalziel, MD, MBBS, MRCPClinics in Dermatology 
October-December 1989, Volume 7, Number 4, pages 62-77

Neuroma formation at the ends of the sympathetic chain after 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&amp;i=e&amp;id=227082.
Traumatic neuroma follows different forms of nerve injury (often as a result of surgery). They occur at the end of injured nerve fibres as a form of ineffective, unregulated nerve regeneration; it occurs most commonly near a scar, either superficially (skin, subcutaneous fat) or deep (e.g., after a cholecystectomy). They are often very painful. It is also known as "pseudoneuroma".

postsympathectomy syndrome

In both groups two cases of postsympathectomy syndrome were seen, with one leg being colder and dryer than the other.

Clinical Orthopaedics &amp; Related Research. 360:122-126, March 1999.

Post-sympathectomy neuralgia is a complex neuropathic and central deafferentation/reafferentation syndrome

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

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

Postsympathectomy pain and changes in sensory neuropeptides

Postsympathectomy limb pain, postsympathectomy parotid pain, and Raeder's paratrigeminal syndrome are pain states associated with the loss of sympathetic fibres and in particular with postganglionic sympathetic lesions.

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

Segmental myoclonus was associated with thoracic sympathectomy

Spinal myoclonus was associated with laminectomy, remote effect of cancer, spinal cord injury, post-operative pseudomeningocele, laparotomy, thoracic sympathectomy, poliomyelitis, herpes myelitis, lumbosacral radiculopathy, spinal extradural block, and myelopathy due to demyelination, electrical injury, acquired immunodeficiency syndrome, and cervical spondylosis.
http://www.ncbi.nlm.nih.gov/pubmed/3753263

Spinal myoclonus is typically associated with a localized area of damaged tissue (focal lesion). The injured area may include direct damage of the spinal cord or may cause abnormal changes in the function of the spinal cord.
http://www.wemove.org/myo/myo_pc.html

relevant to post-sympathectomy pain

These data suggest that induction of a prolonged state of mechanical hyperalgesia causes time-dependent alterations in the sympathetic control of peripheral nociceptive mechanisms such that sympathectomy can lead to enhanced hyperalgesic response. These findings may be relevant to post-sympathectomy pain, a clinical entity for which there has been no available animal models.
http://www.sciencedirect.com/science/article/pii/0306452295005307

compensatory disease may not be immediate after sympahectomy

Newer techniques include the use of clips instead of complete transsection of the nerve but reversal is not always possible as nerve destruction can be quick and compensatory disease may not be immediate.

The main complications with sympathectomy include compensatory sweating, phantom sweating, gustatory sweating, Horner syndrome, and neuralgia.

Management of Hyperhidrosis

Aamir Haider, Nowell Solish and Nicholas J. Lowe
www.sweatclinicsofcanada.com/Book.pdf

denervation supersensitivity of alpha receptors after sympathectomy

There is, however, considerable risk of developing a post-sympathectomy pain syndrome that may be the result of a denervation supersensitivity of alpha receptors.

www.mc.vanderbilt.edu/.../Complex%20Regional%20Pain%20Syndrome-1. 
www.thblack.com/links/RSD/ComplexRegionalPainSyndrome48.ppt

 Paradoxically it has been suggested that in some cases there may be abnormal vasoconstriction rather than the expected vasodilatation after sympathectomy.

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

Related articles

• sympathectomy leads to fluctuation of vasoconstriction alternated with vasodilation in an unstable fashion. Following sympathectomy the involved extremity shows regional hyper - and hypothermia
• sympathetic denervation disturbed the patterns of gut immune-associated cell distribution

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

Spinal dorsal column stimulation has been used in the treatment of a patient with a painful vasospastic condition in the right arm following surgical sympathectomy on the left side. After sympathectomy the left arm became constantly dry and warm and consistently lacked skin vasomotor (laser Doppler flowmetry) responses to arousing stimuli, indicating a complete loss of sympathetic vasomotor innervation.
http://www.springerlink.com/content/n823388l26q330m3/

Sympathectomy decreased NE and DA concentrations of muscles to approximately 10% of control values

We studied the effect of unilateral sympathectomy on rat quadriceps and gastrocnemius muscle concentrations of endogenous dihydroxyphenylalanine (DOPA), dopamine (DA), and norepinephrine (NE) and assessed the relationships between these catecholamines in several rat tissues. Catecholamines were measured by reverse-phase high-performance liquid chromatography with electrochemical detection. Sympathectomy decreased NE and DA concentrations of muscles to approximately 10% of control values, whereas the DOPA concentration tended to increase. Relatively high concentrations of DOPA were found in the gastrointestinal tract, kidney, and spleen. No correlations were obtained between the tissue concentration of DOPA and NE. A DA-to-NE ratio approximately 1% was observed in liver, muscle, pancreas, spleen, and heart, whereas we found exponentially increasing DA values with increasing NE concentration in tissues obtained from stomach, small and large intestine, kidney, and lung. In conclusion, endogenous DOPA in muscle tissue is not located in sympathetic nerve terminals but probably in muscle cells. DA concentrations in the gastrointestinal tract and in the kidneys were greater than could be ascribed to its role as a precursor in the biosynthesis of NE.
http://ajpendo.physiology.org/content/256/2/E284.abstract

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

Surgical thoracic sympathectomy such as ESD (endoscopic thoracic sympathectic denervation) 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 parasympathetic 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
http://informahealthcare.com/doi/abs/10.1080/02770900802660949

After severing the cervical sympathetic trunk, the cells of the cervical sympathetic ganglion undergo transneuronic degeneration

In consequence of right-sided smpathectomy at the level of C₅ it was found that in the sheep the cervical sympathetic trunk contains nerve fibres which proceed from cells situated in the first four segments of the thoracic part of the spinal cord and in the stellate ganglion. These fibres are about 85 per cent of all fibres of the sympathetic trunk. The remaining 15 per cent proceed from nerve cells situated nasally of the anterior cervical ganglion.

The spinal cord. Changes found in the segment Th1 – Th4 in sheep III and IV closely resembled thoseseen in the stellate ganglion (Figures 6, 7).

2. After severing the sympathetic trunk, the cells of its origin undergo complete disintegration within
a year.

3. After severing the cervical sympathetic trunk, the cells of the cervical sympathetic ganglion
undergo transneuronic degeneration.
http://onlinelibrary.wiley.com/doi/10.1111/j.1439-0442.1967.tb00255.x/abstract

So numerous are the possible variations that the outcome of a sympathectomy is unpredictable

The sympathetic pathways to the heart are extremely variable in their topography, and the diversity of arrangements encountered accounts for the morphological contradictions in the literature. So numerous are the possible variations that the outcome of a sympathectomy is unpredictable. Where denervation is incomplete, collateral sprouting and regeneration of nerves could even lead to hyperstimulation via the sympathetic pathways.
http://onlinelibrary.wiley.com/doi/10.1002/aja.1001240203/abstract

denervation leads to loss of an important regulatory mechanism in immune system physiology

Alterations in lymphocyte activity does not always correlate with changes in the proportions of T- or B-lymphocyte subsets. Sympathetic denervation leads to loss of an important regulatory mechanism in immune system physiology. This is apparently site specific in that both lymph node and spleen T-cell proliferative responses are reduced.Article by Dr. Brian A. Smith
http://home.earthlink.net/~doctorsmith/hivandchiro.htm

diabetic autonomic neuropathy has already sympathectomized the patient

Although not specific, the symptoms suffered by diabetics from sweating disturbances are fairly typical [5]. Initially there is heat intolerance accompanied by hyperhidrosis of the upper half of the body, particularly affecting the face, neck, axillae and hands. It is of interest that these patients rarely perspire excessively below the umbilicus. This diabetic syndrome has been attributed to a lesion of the sympathetic nerve fibres which control sweat secretion [11] and follow the course of the peripheral nerves [12]. This affects the efferent branch of the reflex arch and is identical to that occurring distal to a surgical sympathectomy [13].

There was no difference found between the histological changes in the nerves of the spontaneous anhidrotic patients
(Fig. 1) and those of the two previously sympathectomized patients.

A number of papers have been published which stressed [22-24] the high failure rate of sympathectomy operations in diabetics. We believe that the failure of the operation is due to the fact that diabetic autonomic neuropathy has already sympathectomized the patient. The results of the present study are compatible with this idea.
http://www.springerlink.com/content/v21h52461037653k/

The amount of compensatory sweating depends the amount of cell body reorganization in the spinal cord after surgery

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

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

Retrograde Changes in the Nervous System Following Unilateral Sympathectomy

In consequence of right-sided smpathectomy at the level of C5 it was found that in the sheep the cervical sympathetic trunk contains nerve fibres which proceed from cells situated in the first four segments of the thoracic part of the spinal cord and in the stellate ganglion. These fibres are about 85 per cent of all fibres of the sympathetic trunk. The remaining 15 per cent proceed from nerve cells situated nasally of the anterior cervical ganglion.
http://onlinelibrary.wiley.com/doi/10.1111/j.1439-0442.1967.tb00255.x/abstract

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

B. Arterial feeders (e.g. thoracic, intercostal, or cervical branch from subclavian or vertebral artery)
1) thromboembolic disease!
2) complications of abdominal surgery (esp. sympathectomy)
3) dural AV fistulas (between radicular arteries and veins outside dura mater) – cause venous
hypertension → characteristic dilated veins that course on spinal cord surface.

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

There is a fairly extensive literature on pain after lumbar sympathectomy

bja.oxfordjournals.org/content/87/1/88.full

"Post sympathectomy syndrome is a poorly understood condition"

Post sympathectomy syndrome is a poorly understood condition, which occurs in up to 50% of patients undergoing sympathectomy. This is proposed to be a complex neuropathic and central deafferentation and reafferentation sydnrome. This can occur anywhere from few days to weeks following chemical or surgical sympathectomy. This is characterized by deep, aching pain with superficial burning and hyperesthesia, which may or may not respond to narcotic analgesics. Tricyclic antidepressants may help to reduce the incidence of postsympathoctomy neuralgia. Phenytoin, Carbamazepine or Gabapentin may be useful to reduce spontaneous pain and allodynia. Mexiletine and I.V. lignocaine may help some patients. Occasionally invasive therapies like sympatheic block or more complete sympathectomy can also help.

Stellate ganglion block is one of the most frequently performed procedures in he practice of chronic pain. It can provide good diagnostic, therapeutic and prognostic value.
It can produce complete sympathectomy to the head and neck structures but only a partial sympathetic block of the upper extremity in some patients with variation in anatomy.

Interventional Pain Management

DK. Baheti, Bombay Hospital

Jaypee Brothers Publishers, 2009

Effect of ganglion blockade on cerebrospinal fluid norepinephrine

Prevention of ganglion blockade-induced hypotension using phenylephrine did not prevent the decrease in CSF NE caused by trimethaphan, and when phenylephrine was discontinued, the resulting hypotension was not associated with increases in CSF NE. The similar decreases in plasma NE and CSF NE during ganglionic blockade, and the abolition of reflexive increases in CSF NE during hypotension in ganglion-blocked subjects, cast doubt on the hypothesis that CSF NE indicates central noradrenergic tone and are consistent instead with at least partial derivation of CSF NE from postganglionic sympathetic nerve endings.

 http://www.mendeley.com/research/effect-of-ganglion-blockade-on-cerebrospinal-fluid-norepinephrine/

sympathectomy results in a pronounced increase of cerebrospinal fluid production

Electrical stimulation of the sympathetic nerves, which originate in the superior cervical ganglia, induces as much as 30% reduction in the net rate of cerebrospinal fluid (CSF) production, while sympathectomy results in a pronounced increase, about 30% above control, in the CSF formation. There is strong reason to believe that the choroid plexus is under the influence of a considerable sympathetic inhibitory tone under steady-state conditions.

http://ukpmc.ac.uk/abstract/MED/6276421

sympathicotomy may cause a temporary impairment of the caudal-to-rostral hierarchy of thermoregulatory control and changes in microcirculation

Patients with palmar hyperhidrosis have been reported to have a much
more complex dysfunction of autonomic nervous system, involving compensatory high parasympathetic
activity as well as sympathetic overactivity (13, 14), suggesting that sympathicotomy initially induces a
sympathovagal imbalance with a parasympathetic predominance, and that this is restored on a
long-term basis (14). Therefore, thoracic sympathicotomy may cause a temporary impairment of the
caudal-to-rostral hierarchy of thermoregulatory control and changes in microcirculation. The reduction
of finger skin temperature on the non-denervated side may be due to either a decrease in the cross-
inhibitory effect or the abnormal control of the inhibitory fibers by the sudomotor center (6).
Vasoconstrictor neurons have been found to be largely under the inhibitory control of various afferent
input systems from the body surface, whereas sudomotor neurons are predominantly under excitatory
control (15). The basic neuronal network for this reciprocal organization is probably located in the spinal
level (15). Therefore, the reduction in the contralateral skin temperature may be explained by cross-
inhibitory control of various afferent in the spinal cord.
In particular, our study showed that, following bilateral T3 sympathicotomy, the skin temperatures on
the hands increased whereas the skin temperatures on the feet decreased. These findings suggest a
cross-inhibitory control between the upper and lower extremities. However, the pattern of skin
temperature reduction on the feet differed from that on the contralateral hand. The skin temperature on
the feet did not decrease after right T3 sympathicotomy but decreased significantly after bilateral T3
sympathicotomy.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2722005/

post-sympathectomy neuralgia is frequent - reported incidence between 15% to 50%

Surgical sympathectomy has a long heritage for the treatment of peripheral vascular disease and various chronic pain problems.

Despite concerns expressed as long ago as 1942 about the efficacy of surgical sympathectomy for the management of non-cancer pain, the procedure was enthusiastically pursued for the management of reflex sympathetic dystrophy or complex regional pain syndrome (CRPS), migraine, dysmenorrhea, epilepsy, chronic pancreatitis, postherpetic neuralgia of the trigeminal nerve, postdiscectomy syndrome, and phantom limb pain. However, systematic reviews have found no tangible evidence supportive of sympathectomy for the management of neuropathic pain. Furthermore, postsympathectomy neuralgia is a common complaint with a reported incidence between 15% to 50%.

As surgery is often mentioned as a cause of CRPS, it is somewhat illogical to consider surgery as an effective treatment. Nonetheless, surgical sympathectomy has a long anecdotal history in the treatment of RSD, and more recently endoscopic and radiofrequency sympathectomy has been tried.

Bonica's Management of Pain,

Lippincott Williams &amp; Wilkins, 2009 - 2064 pages

"pathological pain, such as occurs in response to peripheral nerve injury"

http://www.ncbi.nlm.nih.gov/pubmed/17706291

There are similarities between the delayed onset of the human pain state and the delayed rise in sensory peptides after sympathectomy

The effect of sympathectomy on the calcitonin gene-related peptide (CGRP) level in the rat primary trigeminal sensory neurone was investigated. Six weeks after bilateral removal of the superior cervical ganglion there was a 70% rise in the CGRP content of the iris and the pial arteries, a 34% rise in the concentration in the trigeminal ganglion but no change in the brainstem. The CGRP rise in both end organs suggests that this phenomenon may be common to all peripheral organs receiving combined sensory and sympathetic innervations. The lack of any rise in the brainstem CGRP content raises the possibility that this process spares central terminations. In contrast, the level of neuropeptide Y, a peptide mainly contained in sympathetic terminals, fell to 35% of control values in the iris and pial arteries whilst the trigeminal ganglion and brainstem concentrations remained unchanged. The possible relevance of these observations to the clinical syndrome of postsympathectomy pain (sympathalgia) is discussed. There are similarities between the delayed onset of the human pain state and the delayed rise in sensory peptides after sympathectomy.
http://www.ncbi.nlm.nih.gov/pubmed/3877546

"Post-sympathectomy neuralgia is a severe complication since pain can be permanent, severe, and incapacitating"

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

limited understanding of the role of the sympathetic nervous system in mediating pain

The role of sympathetic blocks in herpes zoster (HZ) and postherpetic neuralgia (PHN) remains controversial due to methodologic shortcomings in published studies and limited understanding of the role of the sympathetic nervous system in
mediating pain.


Information for Health Professionals          Hunter Integrated Pain Service         Updated January 2010

Procedural Intervention Guideline

surgical and chemical sympathectomy can both modulate bone cell function

It is known that surgical and chemical sympathectomy can both modulate bone cell function.  However, the sympathetic
nervous system (SNS) can give rise to both anabolic and catabolic effects [28-31] and its role in regulating bone remodeling is, therefore, controversial. For example, some researches reported that if bone is deprived of its sympathetic innervation, bone
deposition and mineralization is reduced and bone resorption increases [31], while in some other reports a sympathectomy impairs bone resorption [28].
Wei Fan BSc, MSc
Institute of Health and Biomedical Innovation
Faculty of Built Environment &amp; Engineering
Queensland University of Technology

eprints.qut.edu.au/35722/7/35722b.pdf

Norepinephrine activates pain pathways after nerve injury

According to MedicineNet, RSD involves "irritation and abnormal excitation of nervous tissue, leading to abnormal impulses along nerves that affect blood vessels and skin."

Animal studies indicate that norepinephrine, a catecholamine released from sympathetic nerves, acquires the capacity to activate pain pathways after tissue or nerve injury, resulting in RSD.

http://arthritis.about.com/od/rsd/a/rsd.htm

SURGICAL SYMPATHECTOMY ON THE SENSITIVITY TO EPINEPHRINE OF THE BLOOD VESSELS OF MUSCULAR SEGMENTS OF THE LIMBS

Pursuing this study of the effect of epinephrine on muscle blood flow, Duff and Swan (10) reported that during intravenous epinephrine infusions the initial marked dilatation was succeeded by a second phase of moderate dilatation in normal but not in sympathectomized limbs. Because of its absence in chronically sympathectomized limbs this secondary vasodilatation was at that time thought to be an indirect vasomotor effect mediated by the sympathetic nerves. Re-examination of their data in the light of some subsequent critical experiments now reveals that the difference which they found between normal and sympathectomized limbs may be ascribed largely to vascular hypersensitivity in the later.

In the present paper these additional data are reported, and are incorporated with those of Duff and Swan(10); the whole material being interpreted to provide evidence that hypersensitivity of the vessels of skeletal muscle in the upper and lower limbs may result from pre- and postganglionic sympathectomy in man.

EFFECT OF SURGICAL SYMPATHECTOMY ON THE SENSITIVITY TO EPINEPHRINE OF THE BLOOD VESSELS OF MUSCULAR SEGMENTS OF THE LIMBS, ROBERT S. DUFF

J Clin Invest. 1953 September; 32(9): 851–857.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC438413/

sympathectomy induced morphological alterations in the masseter muscles

Sympathectomized animals showed varying degrees of metabolic and morphological alterations, especially 18 months after sympathectomy. The first five groups showed a higher frequency of type I fibres, whilst the oldest group showed a higher frequency of type IIb fibres. In the oldest group, a significant variation in fibre diameter was observed. Many fibres showed small diameter, atrophy, hypertrophy, splitting, and necrosis. Areas with fibrosis were observed. Thus cervical sympathectomy induced morphological alterations in the masseter muscles. These alterations were, in part, similar to both denervation and myopathy. These findings indicate that sympathetic innervation contributes to the maintenance of the morphological and metabolic features of masseter muscle fibres.

http://www.ncbi.nlm.nih.gov/pubmed/11454103

Post-sympathectomy neuralgia - pain overlying the scapula

Complications of surgical (Thoracic and Lumbar) Sympathectomy:

Post-sympathectomy neuralgia - pain overlying the scapula

Compensatory sweating - involving the lover back or face

Pneumothorax

Bleeding due to azygos vein or intercostal artery injury

Winged scapula due to long thoracic nerve injury (p. 517)

Mastery of Vascular and Endovascular Surgery

Gerald B. Zelenock, Thomas S. Huber, Louis M. Messina, Alan B. Lumsden, Gregory L. Moneta

Lippincott Williams &amp; Wilkins, 15/12/2005 - 900 pages

Post-sympathectomy pain

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