"Sympathectomy is a technique about which we have limited knowledge, applied to disorders about which we have little understanding." Associate Professor Robert Boas, Faculty of Pain Medicine of the Australasian College of Anaesthetists and the Royal College of Anaesthetists

http://www.pfizer.no/templates/Page____886.aspx

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


Compensatory hyperhidrosis is excessive sweating of the abdomen, chest, back, thighs, and face,[6,72] usually in response to increased temperature.[46] This is the most common complication following ETS, reported to occur at an average rate of about 60%, with a range of 3% to 98%.[46] Higher rates have been reported from countries with warmer climates, such as in Asia and the Middle East.[46,82] The sweating can be severe for 10% to 40% of patients.[10] Although it has been written that compensatory sweating diminishes with time, several series have documented continued symptoms with longer-term follow-up.[46] In one series of 270 patients followed for a mean of 15 years postsympathectomy, 67% still complained of compensatory sweating, and overall satisfaction fell from an initial level of 96% to 67%.[55] It is possible that patients begin to notice compensatory sweating some time after ETS, as they are initially more aware of the marked reduction of their primary hyperhidrosis.[46]

The mechanism for compensatory sweating is unclear; the most likely explanation is that sweating in the trunk increases to compensate for the lack of sweating from the denervated areas in order to maintain thermoregulation.[82] The occurrence of decreased sweating in other areas not innervated by the ganglia treated by ETS suggests that the response to ETS is more complex. The soles are the most common area with decreased sweating post-ETS, and, along with the axillae and palms, sweating from these areas could be under cortical control, separate from the hypothalamic centers involved in thermoregulation.[72] It has also been proposed that ganglion destruction affects axons of neurons in the interomediolateral spinal cord, which could lead to cell death or re-organization, changing the control of the sympathetic system by the spinal cord and higher, leading to increased sympathetic tone in the other body areas not treated by ETS.[10] 
http://www.sweathelp.org/English/HCP_Treatment_ETS_Surgery_Complications.asp?printfriendly=true

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

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

Sympathectomy - a surgically induced neuropathy

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

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

oedema associated with the interruption of preganglionic sympathetic tract


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

 We showed that the preganglionic sympathetic tract in the spinal cord was often 
disturbed in patients with multiple sclerosis with myelopathy.' Most patients with com- 
plete 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.

The indications for neurolytic or surgical sympathectomy are uncertain

The indications for neurolytic or surgical sympathectomy are uncertain. There is no clear correlation between the degree or duration of pain relief and the actual period of sympathetic blockade and the same patient may show variable responses on different occasionsv (Loh et al 1980). Some patients demonstrate unexpected responses such as contralateral or delayed blocks and some are made worse (Purcell-Jones &Justins 1988, Evans et al 1980, Kleiman 1954)
http://www.springerlink.com/content/7013w45630522h6k/

Sympathectomy causes depigmentation of the skin

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

Sympathectomy? 
Skin Depigmentation: Could it Be a Complication Caused by Thoracic 
 2009;88:42-43 Ann Thorac Surg 
http://ats.ctsnetjournals.org/cgi/reprint/88/4/e42.pdf 

platelet aggregation significantly lower after sympathecomy

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

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

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

Gustatory sweating is a frequent side effect of sympathectomy

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

Post-sympathectomy neuralgia

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

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

Neuroma following Sympathectomy

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

Autonomic Neuropathy Differential Diagnoses

Differentials 
Aromatic L-amino acid decarboxylase deficiency 
Autonomic dysreflexia syndrome in spinal injuries. 
Dopamine beta-hydroxylase deficiency 
Multiple System Atrophy 
Parkinson Disease 
Parkinson-Plus Syndromes 
Progressive Supranuclear Palsy 
Pure Autonomic Failure 
Surgical sympathectomy 
Syphilis (tabes dorsalis) 
Vagotomy 

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

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

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

Patients need to be carefully counselled before committing to sympathectomy

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

CONCLUSION:

Thoracoscopic sympathectomy is effective in the treatment of hyperhydrosis. However compensatory sweating seems unavoidable and infrequently improves with time. Patients need to be carefully counselled before committing to surgery.
http://www.ncbi.nlm.nih.gov/pubmed/21539945

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

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

In conclusion, thoracoscopic sympathectomy can be done as an outpatient procedure safely and efficiently. Debate continues about the correct transection levels, but at this time there is a consensus that division or clipping is equal to resection. Although the procedure has several severe side effects, they are rare. The predominant complication remains compensatory sweating, which may occur regardless of the level transected or the indication. Future clinical trials should compare some of the different techniques to achieve a global consensus of the surgical approach.
http://ats.ctsnetjournals.org/cgi/content/full/85/2/S764

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

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

post-sympathectomy syndrome

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

Sympathectomy altered electroactivity on the heart

The influences on the cardiac autonomic nerve system of the ETS of upper thoracic sympathetic nerve were seen to be of a lesser degree at rest. However, the response to sympathetic stimulation was suppressed after the surgery.
Eur J Cardiothorac Surg 1999;15:194-198
http://ejcts.ctsnetjournals.org/cgi/content/full/15/2/194

These gustatory phenomena were quite different from physiologic gustatory sweating

In a series of 100 bilateral upper dorsal sympathectomies performed for palmar hyperhidrosis, gustatory sweating and other gustatory phenomena were reported by 68 of 93 patients (73%), followed up for an average of 11/2 years. These gustatory phenomena were quite different from physiologic gustatory sweating: a wide range of gustatory stimuli caused a variety of phenomena in varied locations. There was a negative correlation between the incidence of these phenomena and the occurrence of Horner's syndrome after sympathectomy. Analysis of our observations, and of clinical and experimental work of others, leads to the conclusion that gustatory phenomena after upper dorsal sympathectomy are the result of preganglionic sympathetic regeneration or collateral sprouting with aberrant synapses in the superior cervical ganglion.
http://archneur.ama-assn.org/cgi/content/abstract/34/10/619

the PPG signal and the VLF fluctuations of the PPG parameters enable the assessment of the change in sympathetic nervous system activity after sympathectomy

The photoplethysmographic (PPG) signal, which measures cardiac-induced changes in tissue blood volume by light transmission measurements, shows spontaneous fluctuations. In this study, PPG was simultaneously measured in the right and left index fingers of 16 patients undergoing thoracic sympathectomy, and, from each PPG pulse, the amplitude of the pulse (AM) and its maximum (BL) were determined. The parameter AM/BL is proportional to the cardiac-induced blood volume increase, which depends on the arterial wall compliance. AM/BL increased after the thoracic sympathectomy treatment (for male patients, from 2.60±1.49% to 4.81±1.21%), as sympathetic denervation decreases arterial tonus in skin. The very low-frequency (VLF) fluctuations of BL or AM showed high correlation (0.90±0.11 and 0.92±0.07, respectively) between the right and left hands before the thoracic sympathectomy, and a significant decrease in the right-left correlation coefficient (to 0.54±0.22 and 0.76±0.20, respectively) after the operation. The standard deviation of the BL or AM VLF fluctuations also reduced after the treatment, indicating sympathetic mediation of the VLF PPG fluctuations. The study also shows that the analysis of the PPG signal and the VLF fluctuations of the PPG parameters enable the assessment of the change in sympathetic nervous system activity after thoracic sympathectomy.
http://www.springerlink.com/content/w7n21366239753l5/

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

Bone modeling and remodeling are highly regulated processes in the mammalian skeleton. The exact mechanism by which bone can be modeled at a local site with little or no effect at adjacent anatomic sites is unknown. Disruption of the control of modeling within the temporal bone may lead to various bone disease such as otosclerosis, osteogenesis imperfecta, Paget's disease of bone, fibrous dysplasia, or the erosion of bone associated with chronic otitis media. One possible mechanism for such delicate control may be related to the ubiquitous and rich sympathetic innervation of all periosteal surfaces. Previous studies have indicated that regional sympathectomy leads to qualitative alterations in localized bone modeling and remodeling. In this study, unilateral cervical sympathectomy resulted in significant increases in osteoclast surface and osteoclast number within the ipsilateral bulla of experimental animals. The mechanisms by which sympathectomy leads to increased local bone loss is unknown. Potential mechanisms include disinhibition of resorption, secondary to the elimination of periosteal sympathetics, as well as indirect vascular effects.
http://www.ncbi.nlm.nih.gov/pubmed/8723974
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