the clinical results of both surgical and neurolityc sympathectomy are uncertain

Blood diverted from muscle to skin after sympathectomy

However, the clinical results of both surgical and neurolityc sympathectomy are uncertain. Indeed these procedures lead to a redistribution of the blood flow in the lower limbs from the muscle to the skin, with a concomitant fall of the regional resistance, mainly in undamaged vessels. The blood flow will be diverted into this part of the vascular tree, so that a "stealing" of the blood flow may occur.

Vito A. Peduto, Giancarlo Boero, Antonio Marchi, Riccardo Tani

Bilateral extensive skin necrosis of the lower limbs following prolonged epidural blockade

Anaesthesia 1976; 31: 1068-75.

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

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

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

Ide K1, Boushel R, Sørensen HM, Fernandes A, Cai Y, Pott F, Secher NH.

Author information

Abstract

A reduced ability to increase cardiac output (CO) during exercise limits blood flow by vasoconstriction even in active skeletal muscle. Such a flow limitation may also take place in the brain as an increase in the transcranial Doppler determined middle cerebral artery blood velocity (MCA V(mean)) is attenuated during cycling with beta-1 adrenergic blockade and in patients with heart insufficiency. We studied whether sympathetic blockade at the level of the neck (0.1% lidocaine; 8 mL; n=8) affects the attenuated exercise - MCA V(mean following cardio-selective beta-1 adrenergic blockade (0.15 mg kg(-1) metoprolol i.v.) during cycling. Cardiac output determined by indocyanine green dye dilution, heart rate (HR), mean arterial pressure (MAP) and MCA V(mean) were obtained during moderate intensity cycling before and after pharmacological intervention. During control cycling the right and left MCA V(mean) increased to the same extent (11.4 +/- 1.9 vs. 11.1 +/- 1.9 cm s(-1)). With the pharmacological intervention the exercise CO (10 +/- 1 vs. 12 +/- 1 L min(-1); n=5), HR (115 +/- 4 vs. 134 +/- 4 beats min(-1)) and delta MCA V(mean) (8.7 +/- 2.2 vs. 11.4 +/- 1.9 cm s(-1) were reduced, and MAP was increased (100 +/- 5 vs. 86 +/- 2 mmHg; P < 0.05). However, sympathetic blockade at the level of the neck eliminated the beta-1 blockade induced attenuation in delta MCA V(mean) (10.2 +/- 2.5 cm s(-1)). These results indicate that a reduced ability to increase CO during exercise limits blood flow to a vital organ like the brain and that this flow limitation is likely to be by way of the sympathetic nervous system.

Compensatory sweating is not a compensatory mechanism

Compensatory sweating was originally thought to be a mechanism of excessive sweating (in an anatomical region with an intact sympathetic nervous system) to maintain a constant rate of total sweat secretion.90 However, this theory was not confirmed by other studies, demonstrating that compensatory sweating represented a reflex action by an altered feedback mechanism at the level of the hypothalamus which is dependent on the level at which sympathetic denervation occurs. Sympathectomy at the level of the T2 ganglion leads to decreased negative feedback to the hypothalamus. When performing a sympathectomy at a lower level, the negative feedback to the hypothalamus is less inhibited, leading to a decrease in compensatory sweating. Chou et al.91 have proposed the term ‘reflex sweating’ to replace compensatory sweating. Other side effects described in a review article by Dumont89 are gustatory sweating, cardiac effects, phantom sweating, lung function changes, dry hands and altered taste. Besides these side effects there are significant risks of complications during and after surgery (arterial or venous vascular injury, pneumothorax, infection, Horner syndrome etc.).

JEADV 2012, 26, 1–8 Journal of the European Academy of Dermatology and Venereology

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

We studied the balance of activity of sympathetic, parasympathetic, and serotoninergic divisions of the autonomic nervous system in the regulation of the heart function in rabbits. High activities of the sympathetic and parasympathetic system are associated with antagonistic interactions between them. Moderation of activity of these systems could be accompanied by activation of the serotoninergic system. Physiological sympathectomy and parasympathectomy lead to hyperfunction of the serotoninergic system and pathology.

Bulletin of Experimental Biology and Medicine, Vol. 140, No. 5, 2005 PHYSIOLOGY

Disturbances in brain serotonergic systems result in a range of phenotypes such as depression, suicide and anxiety disorders.

http://www.biomedcentral.com/1471-2202/10/50

Post-sympathectomy neuralgia is proposed here to be a complex neuropathic and central deafferentation/reafferentation syndrome

Pain. 1996 Jan;64(1):1-9.

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

Kramis RC1, Roberts WJ, Gillette RG.

Author information

Abstract

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.

http://www.ncbi.nlm.nih.gov/pubmed/8867242

Swelling and oedema is often observed in patients after acute interruption of post-ganglionic sympathetic fibres such as a wide-spread sympathectomy

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 of Neurology, Neurosurgery, and Psychiatry 1992;55:232-239

http://jnnp.bmj.com/content/55/3/232.1.full.pdf

peripheral sympathectomy causes a dramatic increase in NGF levels in the denervated organs

Increased Nerve Growth Factor Messenger RNA and Protein

Peripheral NGF mRNA and protein levels following
sympathectomy
It has been shown previously that peripheral sympathectomy
causes a dramatic increase in NGF levels in the denervated
organs (Yap et al., 1984; Kanakis et al., 1985; Korsching and
Thoenen, 1985).
Increased ,&Nerve Growth Factor Messenger RNA and Protein
Levels in Neonatal Rat Hippocampus Following Specific Cholinergic
Lesions
Scott R. Whittemore,” Lena Liirkfors,’ Ted Ebendal,’ Vicky R. Holets, 2,a Anders Ericsson, and HBkan Persson
Departments of Medical Genetics and’ Zoology, Uppsala University, S-751 23 Uppsala, Sweden, and *Department of
Histology, Karolinska Institute, S-104 01 Stockholm, Sweden

Compensatory sweating is not compensatory

Does compensatory sweating only happen to hyperhidrosis patients who underwent ETS?

The exact reason for compensatory sweating is yet to be determined. There are some physiological explanations for that but none are yet completely proven. The reason for this statement is that compensatory sweating happens in a mild, moderate or a higher level of sweating. The fact that not everyone responds in the same way to the hyperhidrosis operation points to the unknown nature of this problem. More than that patients who underwent thoracic sympathectomy for reasons OTHER than hyperhidrosis also develop compensatory sweating in different intensities. This last statement shows that compensatory sweating happens to both hyperhidrosis patients and non-hyperhidrosis patients who have undergone the surgery.

https://archive.today/FKekr#selection-623.0-627.716

Related articles

• Sympathectomy reduces emotional, stress-induced sweating indicating that it affects the stress-response

Sympathectomy reduces emotional, stress-induced sweating indicating that it affects the stress-response

"...for reasons that are not obvious, many patients with facial hyperhidrosis and hyperhidrosis of the feet will benefit from upper thoracic sympathectomy. " 

(The Journal of Pain, Vol 1, No 4 (Winter), 2000: pp 261-264)

"Bilateral upper thoracic sympathicolysis is followed by redistribution of body perspiration, with a clear decrease in the zones regulated by mental or emotional stimuli, and an increase in the areas regulated by environmental stimuli, though we are unable to establish the etiology of this redistribution." 

(Surg Endosc. 2007 Nov;21(11):2030-3. Epub 2007 Mar 13.) 


"Palmar hyperhidrosis of clinical severity is a hallmark physical sign of many anxiety disorders, including generalized anxiety disorder, panic disorder, posttraumatic stress disorder, and especially social phobia.4 These are increasingly well understood and highly treatable neurobiological conditions. They are mod- erately heritable hard-wired fear responses,5 and are linked to amygdalar and locus coeruleus hyper-reactivity during psycho- social stress.6,7 Anxiety disorders are known to be much more common among women. This is consistent with the finding of Krogstad et al. that among controls sweating was reported more often by men, while among the hyperhidrosis group sweating was reported more often among women."

"A surgical treatment for anxiety-triggered palmar hyperhidrosis is not unlike treating tearfulness in major depression by severing the nerves to the lacrimal glands. We have recently made a similar argument advocating a psychopharmacological, rather then a surgi- cal, first-line treatment for blushing.9" 
(Journal Compilation - 2006 British Association of Dermatologists - British Journal of Dermatology 2006, DOI: 10.1111/j.1365-2133.2006.07547.x)

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

Eur J Appl Physiol. 2004 Oct;93(1-2):245-51. Epub 2004 Aug 25.

Infrared thermography for examination of skin temperature in the dorsal hand of office workers.

Gold JE1, Cherniack M, Buchholz B.

Reduced blood flow may contribute to the pathophysiology of upper extremity musculoskeletal disorders (UEMSD), such as tendinitis and carpal tunnel syndrome. The study objective was to characterize potential differences in cutaneous temperature, among three groups of office workers assessed by dynamic thermography following a 9-min typing challenge: those with UEMSD, with ( n=6) or without ( n=10) cold hands exacerbated by keyboard use, and control subjects ( n=12). Temperature images of the metacarpal region of the dorsal hand were obtained 1 min before typing, and during three 2-min sample periods [0-2 min (early), 3-5 min (middle), and 8-10 min (late)] after typing. Mean temperature increased from baseline levels immediately after typing by a similar magnitude, 0.7 (0.3) degrees C in controls and 0.6 (0.2) degrees C in UEMSD cases without cold hands, but only by 0.1 (0.3) degrees C in those with cold hands. Using paired t-tests for within group comparisons of mean dorsal temperature between successive imaging periods, three patterns of temperature change were apparent during 10 min following typing. Controls further increased mean temperature by 0.1 degrees C ( t-test, P=0.001) at 3-5 min post-typing before a late temperature decline of -0.3 degrees C ( t-test, P=0.04), while cases without cold hands showed no change from initial post-typing mean temperature rise during middle or late periods. In contrast, subjects with keyboard-induced cold hands had no change from initial post-typing temperature until a decrease at the late period of -0.3 degrees C ( t-test, P=0.06). Infrared thermography appears to distinguish between the three groups of subjects, with keyboard-induced cold hand symptoms presumably due, at least partially, to reduced blood flow.

http://www.ncbi.nlm.nih.gov/pubmed/15338221

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

cervical sympathectomy induces mast cell hyperplasia and increases histamine and serotonin content in the rat dura mater

A. Bergerot, A.M. Reynier-Rebuffel, J. Callebert, P. Aubineau, 

Long-term superior cervical sympathectomy induces mast cell hyperplasia and increases histamine and serotonin content in the rat dura mater, 

Neuroscience 96 (2000) 205–213. 


Mast cells are critical players in allergic reactions, but they have also been shown to be important in immunity and recently also in inflammatory diseases, especially asthma. Migraines are episodic, typically unilateral, throbbing headaches that occur more frequently in patients with allergy and asthma implying involvement of meningeal and/or brain mast cells. These mast cells are located perivascularly, in close association with neurons especially in the dura, where they can be activated following trigeminal nerve, as well as cervical or sphenopalatine ganglion stimulation. Neuropeptides such as calcitonin gene-related peptide (CGRP), hemokinin A, neurotensin (NT), pituitary adenylate cyclase activating peptide (PACAP), and substance P (SP) activate mast cells leading to secretion of vasoactive, proinflammatory, and neurosensitizing mediators, thereby contributing to migraine pathogenesis. Brain mast cells can also secrete proinflammatory and vasodilatory molecules such as interleukin-6 (IL-6) and vascular endothelial growth factor (VEGF), selectively in response
to corticotropin-releasing hormone (CRH), a mediator of stress which is known to precipitate or exacerbate migraines. A better understanding of brain mast cell activation in migraines would be useful and could lead to several points of prophylactic intervention.

D 2005 Elsevier B.V. All rights reserved.

Brain Research Reviews 49 (2005) 65 – 76
The role of mast cells in migraine pathophysiology
Theoharis C. Theoharides*, Jill Donelan,
Kristiana Kandere-Grzybowska1

, Aphrodite Konstantinidou2

Peripheral, autonomic regulation of locus coeruleus noradrenergic neurons in brain: putative implications for psychiatry and psychopharmacology

the new data seem to allow a better understanding of how autonomic vulnerability or visceral dysfunction may precipitate or aggravate mental symptoms and disorder.

T. H. Svensson¹

(1)	Department of Pharmacology, Karolinska Institute, Box 60 400, S-104 01 Stockholm, Sweden

Received: 20 June 1986 Revised: 25 November 1986
Psychopharmacology

"Locus coeruleus (LC) is located in the ventrallateral side of the fourth ventricle in the pontine, most of which are noradrenergic neurons projecting to the cortex, cingulate cortex, amygdala nucleus, thalamus, hypothalamus, olfactory tubercles, hippocampus, cerebellum, and spinal cord (Swanson and Hartman, 1975). Norepinephrine (NE) released from the nerve terminal of LC neurons contributes to about 70% of the total extracellular NE in primates brain (Svensson, 1987). It plays important roles not only in arousal, attention, emotion control, and stress (reviewed in Aston-Jones and Cohen, 2005; Berridge and Waterhouse, 2003; Bouret and Sara, 2005; Nieuwenhuis et al., 2005; Sara and Devauges, 1989; Valentino and Van Bockstaele, 2008), but also in sensory information processing (Svensson, 1987). LC directly modulates the somatosensory information from the peripheral system. Under the stress condition, LC could completely inhibit the input from painful stimuli through the descending projection to the spinal cord (Stahl and Briley, 2004). Dys-regulations of LC neurotransmission have been suggested to be involved in physical painful symptoms, attention deficit hyperactivity disorder (ADHD), sleep/arousal disorder, post-traumatic stress disorder, depression, schizophrenia, and Parkinson's disease (reviewed in Berridge and Waterhouse, 2003; Grimbergen et al., 2009; Mehler and Purpura, 2009)."
http://journal.frontiersin.org/Journal/10.3389/fnmol.2012.00029/full

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

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

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

"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/

Other neurological pathways (pathways of the nervous system) involving the cerebral cortex (an area of the brain that processes complex information and regulates voluntary movement) and hypothalamus (a hormone-producing gland in the brain) are also thought to play a role in hyperhidrosis

"Sweat is secreted by sweat glands, normally as a thermoregulatory response. No changes to the sweat glands (e.g. increased quantity or size) are observed in individuals with focal hyperhidrosis, so the condition is hypothesised to arise due to overactivity of the sympathetic nervous system (the section of the nervous system that regulates involuntary muscle movements), which sends the signals to the sweat glands to trigger sweating. Other neurological pathways (pathways of the nervous system) involving the cerebral cortex (an area of the brain that processes complex information and regulates voluntary movement) and hypothalamus (a hormone-producing gland in the brain) are also thought to play a role in hyperhidrosis, as is the parasympathetic nervous system."
https://archive.today/xyNQ2
or
http://sydneynorthneurology.com.au/focal-hyperhidrosis/

functional abnormality detected in the small airway of patients who underwent bilateral dorsal sympathectomy to treat primary hyperhidrosis is still present 3 years after surgery

The main observation of our study was that the functional abnormality detected in the small airway of patients who underwent bilateral dorsal sympathectomy to treat primary hyperhidrosis is still present 3 years after surgery, although the patients remain clinically asymptomatic.

Studies to date evaluate alterations in lung function at 1, 3, and 6 months after sympathectomy. Only 1 recent study provides data 1 year after surgery. Ponce González et al¹⁰ studied a group of 37 patients who underwent forced spirometry before surgery, and at 3 months and 1 year after surgery. They observed a decrease in FVC, FEV₁, and FEF_25%-75% at 3 months, although FVC returned to baseline values at 12 months, whereas FEV₁ and FEF_25%-75% remained significantly low (-2.8% and -11.2%, respectively). These findings are consistent with ours, and corroborate the persistence of minimal bronchial obstruction 3 years after surgery. This appears to be associated with the influence of the sympathetic nervous system on bronchomotor tone.

As previously mentioned, the airway is innervated mainly by the parasympathetic nervous system. Sympathetic innervation, although scant, indirectly affects motor tone and could have caused the mild residual obstructive pattern after surgery. Despite the doubtful role of the sympathetic nervous system in the lung, a series of physiologic studies show the effect of sympathetic nervous activity after bilateral dorsal sympathectomy.^11,12 The first was by Noppen and Vincken⁴, who compared the results of lung function studies (spirometry, diffusion, and lung volumes using plethysmography) in 7 patients before dorsal sympathectomy performed using VATS, at 6 weeks, and at 6 months (previous studies had been performed using invasive techniques [thoracotomy]). A statistically significant decrease was observed in FEV₁, FEF_25%-75%, and total lung capacity 6 weeks after surgery. At 6 months, the authors again evaluated the 35 patients and found that total lung capacity had returned to normal values, whereas FEF_25%-75% remained low. They attributed the permanent decrease in FEF_25%-75% to the sympathetic denervation produced by surgery, and stressed that, in patients with primary hyperhidrosis, bronchomotor tone is influenced by the sympathetic nervous system. This contrasts with the common opinion that motor tone in the airway is not affected by this system. Both the study by Ponce González et al,¹⁰ who evaluated their patients at 1 year, and our study, in which we evaluated patients at 3 years, show that persistence of the decrease in FEF_25%-75% over time is related more to sympatholysis of the ganglia than to VATS.

http://www.archbronconeumol.org/en/bilateral-dorsal-sympathectomy-for-the/articulo/13147806/

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, 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"



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Patients with surgical sympathectomies have low plasma levels of DA and NE [49], whereas EPI:NE ratios are increased

Patients with surgical sympathectomies have low plasma levels of DA and NE [49], whereas EPI:NE ratios are increased (unpublished observations), suggesting decreased sympathetically mediated exocytosis and compensatory adrenomedullary activation.   

Catecholamines 101, David S. Goldstein Clin Auton Res (2010) 20:331–352

"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."



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Cervico-thoracic or lumbar sympathectomy | Cochrane Summaries

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."



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the clinical results of both surgical and neurolityc sympathectomy are uncertain

Blood diverted from muscle to skin after sympathectomy

However, the clinical results of both surgical and neurolityc sympathectomy are uncertain. Indeed these procedures lead to a redistribution of the blood flow in the lower limbs from the muscle to the skin, with a concomitant fall of the regional resistance, mainly in undamaged vessels. The blood flow will be diverted into this part of the vascular tree, so that a "stealing" of the blood flow may occur.

Vito A. Peduto, Giancarlo Boero, Antonio Marchi, Riccardo Tani

Bilateral extensive skin necrosis of the lower limbs following prolonged epidural blockade

Anaesthesia 1976; 31: 1068-75.

Stellate ganglion block - a form of chemical sympathectomy - alleviates anxiety, depression

Among veterans with post-traumatic stress disorder, treatment with a single stellate ganglion block could help alleviate anxiety, depression and psychological pain rapidly and for long-term use, according to results presented at the American Society for Anesthesiologists Annual Meeting.

See Also

• Experts propose nerve blocks to treat PTSD
• DSM-5 PTSD screening may miss previously diagnosed ...
• Amygdala activation could predict PTSD susceptibility ...

Researchers performed a single right-sided stellate ganglion block (SGB) using 7 mL of 2% lidocaine and 0.25% bupivacaine under fluoroscopic guidance on 12 veterans with military-related, chronic extreme post-traumatic stress disorder (PTSD) with hyperarousal symptoms. At baseline, 1 week, 1 month, 3 months and 6 months post-block, PTSD symptoms were assessed using the Clinician Administered PTSD Scale (CAPS) score and the Post-traumatic Stress Self Report (PSS-SR) scale. Depressive symptoms were assessed with the Beck Depression Inventory version 2. Anxiety related symptoms with a generalized anxiety scale score and the State-Trait Anxiety Index and psychological pain with the Mee-Bunney scale.

Study results showed the block was greatly effective in 75% of participants, with a positive effects taking effect often within minutes of SGB. At week 1, there was significant reduction of both CAPS and PSS-SR and researchers found CAPS approached normal-to-mild PTSD levels by 1 month. Anxiety, depression and psychological pain scores also were significantly reduced by the block, according to study results. Overall, positive effects remained evident at 3 months, but were generally gone by 6 months.

Reference:

Alkire MT. A1046. Presented at: American Society for Anesthesiologists Annual Meeting;  Oct. 11-15, 2014; New Orleans.

http://www.healio.com/psychiatry/ptsd/news/online/%7B14e0a858-100a-43b1-a0e0-47c6376cb885%7D/stellate-ganglion-block-alleviates-anxiety-depression-for-veterans-with-ptsd

Permanent pain following sympathectomy

The mean inpatient pain scores were significantly higher in the biportal group (1.2±0.6) than that in the uniportal group (0.8±0.5, P=0.025). For the first three weeks after operation, four out of 20 (20%) patients in the uniportal group constantly suffered from mild or moderate residual pain while eight out of 25 (32%) cases in the biportal group (P=0.366). Among them, two cases in the uniportal group and five cases in the biportal group need to take analgesics.
Chinese Medical Journal, 2009, Vol. 122 No. 13 : 1525-1528

CARDIOVASCULAR CHANGES POST SYMPATHECTOMY

Short- and Long-term Effects

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

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

The so called 'compensatory sweating' is NOT compensatory - BMJ Best Practice

"When patients with intense CH are analyzed, we observe that the amount of released sweat seems to be much greater than was that occurring at the primary hyperhidrosis location, not translating a simple compensation or sweating transference from one site to the other. Therefore, this hyperhidrosis seems to be reflex, mediated neurologically in the sweating regulatory center in the hypothalamus.

In order to avoid this neurologically mediated reflex, the sympathetic afferents to the hypothalamus should be restored, allowing negative feedback to block the efferent projection of the sweating regulatory center on the periphery.(14) Therefore, only the reinnervation of the sectioned sympathetic chain could recover this reflex."

http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1806-37132008001100013&lng=en&nrm=iso&tlng=en

https://archive.today/7B795

Jornal Brasileiro de Pneumologia

Print version ISSN 1806-3713

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

Guidelines for the prevention, diagnosis and treatment of compensatory hyperhidrosis^*

http://bestpractice.bmj.com/best-practice/search.html?searchableText=Hyperhidrosis&aliasHandle=guidelines&languageCode=en
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