"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

The Journal of Pain, Vol 1, No 4 (Winter), 2000: pp 258-260

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

After severing the cervical sympathetic trunk, the cells of the cervical sympathetic ganglion undergo transneuronic degeneration
After severing the sympathetic trunk, the cells of its origin undergo complete disintegration within a year.

http://onlinelibrary.wiley.com/doi/10.1111/j.1439-0442.1967.tb00255.x/abstract

Sympathectomy limits blood flow to a vital organ like the brain

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.

PMID: 10971220 [PubMed - indexed for MEDLINE]
1. Acta Physiol Scand. 2000 Sep;170(1):33-8.

GAP-43 mRNA and calcitonin gene-related peptide mRNA expression in sensory neurons are increased following sympathectomy

Sympathectomy has been shown to result in an increased density of fibers immunoreactive for sensory peptides in peripheral targets innervated by both sensory and sympathetic neurons, providing evidence for functional interactions between sympathetic and sensory systems. These findings provided the background for examining the hypothesis that axonal outgrowth is induced from sensory neurons following sympathectomy. We examined the expression of GAP-43 mRNA, a specific marker for axonal outgrowth, in cervical (C3, C7, C8) and thoracic (T1, T2) dorsal root ganglia (DRG) of the rat following bilateral removal of the superior cervical ganglion, to assess whether the described increases in peptidergic afferent fibers reflected axonal outgrowth. In situ hybridization was used with 35S labeled riboprobes complementary to GAP-43 mRNA, and to calcitonin gene-related peptide (CGRP) mRNA, a marker for a major subset of thin-fiber sensory neurons. The density of GAP-43 mRNA nearly doubled by 18 h following sympathectomy and reached a threefold increase by 3 days. By 45 days following surgery, the GAP-43 mRNA level was still nearly twice that of normal animals. CGRP immunoreactivity was also examined: the density of fibers in the iris and cornea of sympathectomized animals was considerably greater from two weeks to 45 days following surgery, than in sham-operated controls. Concomitantly, there was a slight but significant increase in CGRP mRNA expression in T1 and C3 DRG 14 days post
http://www.refdoc.fr/Detailnotice?idarticle=15110598

anatomic variations of the T2 nerve root

6 (9.1%) sides showed a single large ganglion formed by the stellate and the second thoracic sympathetic ganglia. The second thoracic sympathetic ganglion was most commonly located (50%) in the second intercostal space. Conclusion: The anatomic variations of the intrathoracic nerve of Kuntz and the second thoracic sympathetic ganglion were characterized in human cadavers.
Journal of thoracic and cardiovascular surgery Y. 2002, vol. 123, No. 3, pages 498-501 [bibl. : 14 ref.
http://www.refdoc.fr/Detailnotice?idarticle=9466218

immune privilege is lost in the absence of a functional sympathetic innervation of the eye

Mounting evidence points to a role for the sympathetic nervous system in suppressing inflammation. This role might be of specific relevance for immune privilege in the eye, where, sporadically, patients with denervated sympathetic fibers develop chronic inflammation. The present study used mice to investigate whether the robust innervation of intraocular structures by the sympathetic system plays a role in maintaining ocular immune privilege. We first performed surgical removal of the superior cervical ganglion, which supplies sympathetic fibers to the eye, and studied the immune response generated against soluble antigens or allogencic tumor cells injected into the ocular anterior chamber under these conditions. Our results show that in the absence of functional sympathetic fibers, the eye loses its ability to prevent either the immune rejection of intraocular allogeneic tumor cells or the suppression of delayed type hypersensitivity responses against soluble antigens injected in the anterior chamber. This loss of immune privilege is accompanied by a decrease in the concentration of transforming growth factor-β in the aqueous humor. These results suggest that immune privilege is lost in the absence of a functional sympathetic innervation of the eye, allowing intraocular immune responses to become exaggerated. We conclude that ocular sympathetic nerves are critical for the generation and maintenance of immune privilege in the eye through the facilitation of local transforming growth factor-β production.
http://cat.inist.fr/?aModele=afficheN&cpsidt=21889071

Results of life-style surgery:

The rate of compensatory sweating in group 2 (72.7%) was significantly lower than in group 1 (95.4%) (P<0.039). The chance of embarrassing and disabling compensatory sweating was lower in group 2 than in group 1; 76.5% (embarrassing in 8 patients, disabling in 9) in group 1, and 36.4% (embarrassing in 7 patients, disabling in 1) in group 2 which was statistically significant (P<0.006).
http://www.ejcts.ch/cgi/content/full/26/2/396

Sympathectomy is used to treat various conditions, including Raynaud's. But is it effective?

"Recurrent and enhanced vasoconstrictor function 3 months following endoscopic sympathetic block has major implications for its use to treat enhanced vasoconstriction."

http://www.ncbi.nlm.nih.gov/pubmed/12796529

bilateral ETS causes the suppression of cardiovascular response to exercise

HR and BP at rest and cardiovascular response to exercise were similar in patients with palmar hyperhidrosis before ETS and in the normal control population. Therefore, we consider that patients with palmar hyperhidrosis have no overactivity of the sympathetic nerve. However, because bilateral ETS causes the suppression of cardiovascular response to exercise, patients that has been treated with ETS need to be observed during high-level exercise.

http://iars.org/abstracts/browsefile/browse.asp?command=N&absnum=45&dir=S190

Undisclosed side-effects of ETS procedure

After a mean of 123 mo 36 patients could be re-evaluated. Eighteen patients (50%) were free from former symptoms, while sequels were still present in 18 patients (50%).

Numbness and paresthesia are rarely reported in the literature but are present in up to 10% of patients 1 year after a thoracoscopic procedure [2,9]. It is known that numbness and dysesthesia may decrease by time, but long-term results are not known.

Early postoperative sequels are frequently found in VATS procedures, but patients with pain even after years have a nearly 50% chance to eliminate their problems. In addition, numbness and dysesthesia seem to disappear almost completely several years after the procedure.

http://www.ejcts.ch/cgi/content/full/32/3/409

Sympathotomy Instead of Sympathectomy for Palmar Hyperhidrosis: Minimizing Postoperative Compensatory Hyperhidrosis

http://www.mayoclinicproceedings.com/content/78/2/167.refs

Mia: An elective surgical procedure enthusiastically declared "almost miraculous" needs modifications to reduce severe side-effects?

CNS activation following peripheral sympathectomy

Many studies have demonstrated that ablation of the sympathetic nervous system (SNS) alters subsequent immune responses. Researchers have presumed that the altered immune responses are predominantly the result of the peripheral phenomenon of denervation. We, however, hypothesized that chemical sympathectomy will signal and activate the central nervous system (CNS).

Dual-antigen labeling demonstrates that

corticotrophin releasing factor (CRF)-containing neurons in the PVN are

activated by chemical sympathectomy; however, neurons containing

neurotransmitters which may modulate CRF neurons, such as vasopressin,

tyrosine hydroxylase, and adrenocorticotropin, do not coexpress Fos. Our

findings suggest an involvement of the CNS insympathectomy-induced

alterations of immunity.


Brain, Behavior, and Immunity

Volume 12, Issue 3, September 1998, Pages 230-241

Cervical sympathectomy affects the lower extremities, providing further evidence that the effects of this procedure is not local or limited

Bilateral cervical sympathectomy reduced mechanical allodynia and cold allodynia in the rat

model of neuropathic pain suggesting that neuropathic pain, although the lesions are localized in low extremities, may be correlated with functional disturbance of sympathetic nerve fibers of supraspinal or brain level and help explain the mechanism of neuropathic pain.

Korean J Anesthesiol. 1999 Feb;36(2):327-334. Korean.


Effect of cervical sympathectomy and circulatory hypoxia on time course of prostaglandin concentration in brain tissues

http://www.springerlink.c...ontent/j705306763158841/


Some workers suggest a possible "transmembrane" role of PG in the nervous system.


If the increase in the PG level during ischemia is regarded as a protective reaction, it must be admitted that no increase took place 1 day after CSE (cervical sympathectomy) and it was considerably weakened 7-40 days after CSE.


The effect of cerebral ischemia was virtually indistinguishable from the action of CSE itself.


It can be tentatively suggested that PGF plays the main role in the regulation of tone of the vascular wall and in the regulation of metabolism under conditions of ischemia when the sympathetic regulation is disturbed.