catecholamine released from sympathetic nerves, acquires the capacity to activate pain pathways after tissue or nerve injury

What Is Reflex Sympathetic Dystrophy Syndrome or RSD?: "According to the National Institute of Neurological Disorders and Stroke (NINDS), RSD is "a chronic pain condition that is believed to be the result of dysfunction in the central or peripheral nervous systems." 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. Another theory suggests that RSD, which follows an injury, is caused by triggering an immune response and symptoms associated with inflammation"

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Transection below T8-T10 is not accompanied by reflex sweating

Reflex sweating in patients with spina... [Arch Phys Med Rehabil. 1977] - PubMed - NCBI: "Sweat glands derive their innervation from the sympathetic nervous system. The spinal sympathetic structures that are located in the intermediolateral areas extend from T1-L2 segments and are under the control of hypothalamic centers. Cord transection abolishes the supraspinal control of sudorimotor function. Since sympathetic innervation does not follow a clear segmental distribution, normal sweating may be preserved at a higher or lower level than skin sensation. Nonthermoregulatory reflex sweating is an indication of unchecked spinal cord facilitation and is precipitated by afferent stimuli from bladder, rectum, and various other sources. It is usually a manifestation of mass reflex or autonomic crisis and occurs particularly in cervical or high thoracic lesions. Transection below T8-T10 is not accompanied by reflex sweating. The phenomenon of thermal relfex sweating is controversial. Although some aspects of nonthermoregulatory reflex sweating are still unclear, proper immediate and continuing preventive management will reduce the incidence of this and other autonomic manifestations. "

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rates and characteristics of the paresthesia following needlescopic VATS are similar to those observed after conventional VATS

Incidence of chest wall paresthesia ... [Eur J Cardiothorac Surg. 2005] - PubMed - NCBI: "Paresthetic discomfort distinguishable from wound pain was described by 17 patients (50.0%). The most common descriptions were of 'bloating' (41.2%), 'pins and needles' (35.3%), or 'numbness' (23.5%) in the chest wall. The paresthesia resolved in less than two months in 12 patients (70.6%), but was still felt for over 12 months in three patients (17.6%). Post-operative paresthesia and pain did not impact on patient satisfaction with the surgery, whereas compensatory hyperhidrosis in 24 patients (70.6%) did (P=0.001). The rates and characteristics of the paresthesia following needlescopic VATS are similar to those observed after conventional VATS."

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Chronic pain can occur after peripheral nerve injury, infection, or inflammation - sympathectomy is a nerve injury

Blocking sympathetic function, whether by surgical sympathectomy, systemic phentol- amine, or systemic guanethidine, relieves partial nerve injury-induced neuropathic pain in laboratory animal models as well as humans (8, 35, 146, 239, 278). Indeed, sympathectomy does not just relieve pathological pain in the body region ipsilateral to the CRPS-initiating event; rather, it also relieves pain arising from anatomically impossible mirror-image sites, that is, the identical body region contralateral to the initiating event (278). Thus sympathetectomy must somehow quiet the contralateral spread of spinal cord hyperexcitability underlying mirror- image pain.

Alterations in sympathetic fibers rapidly follow pe- ripheral nerve injury. This occurs as sprouting of sympa- thetic fibers, creating aberrant communication pathways from the new sympathetic terminals to sensory neurons (35). Sympathetic sprouting has been documented in the region of peripheral terminal fields of sensory neurons (262), at the site of nerve trauma (57), and within the dorsal root ganglia (DRG) containing cell bodies of sen- sory neurons (248, 343). Each of these sites develops spontaneous activity and sensitivity for catecholamines and sympathetic activation (8, 53).

The clearest evidence that immune activation partic- ipates in sympathetic sprouting comes from studies of the DRG. DRG cells receive signals that peripheral nerve injury has occurred via retrograde axonal transport from the trauma site. These retrogradely transported signals trigger sympathetic nerve sprouting into DRG (205, 308). As a result of nerve damage-induced retrogradely trans- ported signals, glial cells within the DRG (called satellite cells) proliferate (248) and become activated (343); mac- rophages are recruited to the DRG as well (63, 176). In turn, the activated satellite glial cells (and, presumably, the macrophages) release proinflammatory cytokines and a variety of growth factors into the extracellular fluid of the DRG (206, 246–248, 258, 277, 308, 358). These sub- stances stimulate and direct the growth of sympathetic fibers, which form basket-like terminals around the satel- lite cells that, in turn, surround neuronal cell bodies (247, 248, 343). For discussion of satellite cell functions, see section IIIA.

LINDA R. WATKINS AND STEVEN F. MAIER

Department of Psychology and the Center for Neuroscience, University of Colorado at Boulder, Boulder, Colorado

Physiol Rev

82: 981–1011, 2002; 10.1152/physrev.00011.2002.

Stellate ganglion block may relieve hot flashes by interrupting the sympathetic nervous system

Stellate ganglion block may relieve hot flash... [Med Hypotheses. 2007] - PubMed - NCBI: "the wide range of conditions that have been reported to respond favorably to stellate ganglion block suggest that its effectiveness may not be solely the result of increased blood flow nor restricted just to its sphere of innervation. We have found that stellate ganglion block is effective in the treatment of hot flashes in postmenopausal women, as well as those with estrogen depletion resulting from breast cancer treatment. Based on evidence that hot flashes may be centrally mediated and that the stellate ganglion has links with the central nervous system nuclei that modulate body temperature, we hypothesize that the stellate ganglion block provides relief of hot flashes by interrupting the central nervous system connections with the sympathetic nervous system, allowing the body's temperature-regulating mechanisms to reset. If this mechanism can be confirmed, this would provide women with intractable hot flashes with an effective, potentially long-lasting means of relieving their symptoms, and potentially widen the range of indications for stellate ganglion block to include other centrally mediated syndromes."

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Sympathectomy results in a substantial interference in regulatory processes of the body

"ESB  (whether as ETS as ETSC or ELS) generally represents a substantial interference in regulatory processes of the body.  Therefore decision for this operation requires that previously conservative treatments were made. An ESB is therefore at the end of a treatment history, and never at the beginning." 

Dr. Christoph H. Schick, ETS surgeon, President of the International Society of Sympathetic Surgery (ISSS)  

text has been  translated by google from German

http://www.dhhz.de/index.php?page=8&subPage=&section=32  

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

reduction in all proline-richproteins (PRP) in the saliva following sympathectomy

The protein constituents in parasympathetically evoked saliva from normal and short-term sympathectomized parotid gland swere compared. There was a reduction in all proline-richproteins (PRP) in the saliva following sympathectomy. The decrease was quantified for acidic PRP by high- performance ion-exchange chromatography, which showed an increase in the ratio of amylase to other proteins. These results suggest that sympathetic impulses influence the synthesis of PRP and amylase in opposite directions. 

Quarterly Journal ofExperimental Physiology (1988) 73, 139-142

"sympathectomy highlighted the disparity between what is known in practice and what appears in the literature"

The March 2004 edition was quite outstanding, with an excellent editorial reminding the reader that only good results are published. The review on thoracoscopic sympathectomy highlighted the disparity between what is known in practice and what appears in the literature. 

‘Know Your Results’, the topic of the ASGBI Annual Scientific Meeting, is of outstanding importance; what is more, the surgeon has to go on knowing his/her results to ensure standards of practice do not slip.

The Journal appreciates comments and criticism and the correspondence column remains a crucial part of the BJS in its interaction between editors and reader. It is also part of the scientific process.

A more robust and incisive criticism of articles known to be flawed would prevent the retractions that have recently been published in the Lancet.

Christopher Russell, Chairman, BJS Society

Association of Surgeons of Great Britain and Ireland, ANNUAL REPORT 2004

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

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/

Sympathetic nerves protect against blood-brain barrier disruption

http://www.ncbi.nlm.nih.gov/pubmed/7064183

Nerve regeneration commonly occurs following both surgical of chemical sympathectomy

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 minimally invasive procedures using thermal or laser interruption. 

Nerve regeneration commonly occurs following both surgical of 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.

Authors' conclusions: The practice of surgical and chemical sympathectomy for neuropathic pain and CRPS is based on very little high quality evidence. Sympathectomy should be used cautiously in clinical practice, in carefully selected patients, and probably only after failure of other treatment options.

Editorial Group: Cochrane Pain, Palliative and Supportive Care Group.

Publication status: New search for studies and content updated (conclusions changed).

Citation: Straube S, Derry S, Moore RA, McQuay HJ. Cervico‐thoracic or lumbar sympathectomy for neuropathic pain and complex regional pain syndrome. Cochrane Database of Systematic Reviews 2010, Issue 7. Art. No.: CD002918. DOI: 10.1002/14651858.CD002918.pub2. Link to Cochrane Library. [PubMed]

Copyright © 2010 The Cochrane Collaboration. Published by John Wiley & Sons, Ltd.

http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0011684/

It is well recognized that preganglionic sympathectomy involves division of cholinergic elements and sensory fibers

It is well recognized that preganglionic sympathectomy involves division of cholinergic elements and sensory fibers. 
Theodore Cooper, Department of Surgery, St Louis University School of Medicine 
Pharmacological Reviews, 1966 Vol. 18, No. 1. Part I

When sympathectomized rats were injected with the same carcinogen, 24 out of 38 developed tumors

"Lesions od the sympathetic nervous system have been shown to increase the incidence, induction, and take and growth, of tumors. In neurally intact rats which were infected with a known carcinogen, only 1 out of 30 developed a tumor. When sympathectomized (intentional sympathetic nerve interference) rats were injected with the same carcinogen, 24 out of 38 developed tumors. These results confirm that sympathetic block enhances tumor implantation."

"Clearly the autonomic nervous system in exquisitely sensitive to information from all parts of the nervous system and may affect many aspects of the immune response."

"Since immune response is initiated by the nervous system, this appears to be a likely place to look for the cause of disease."

Edward E. Cremata, Neural control of immunity, January/February, 1982 The Digest of Chiropractic Economics

1. Couhard, R. and P. Hein, Cancers de types divers provoqucs par lesion du sympathique, CR. Acad. Sci,  2434-2437, 1957.

2. Couhard, R. and F. Heitz, Production de tumeurs malìgncs consecutivas a des lesions des fibres sympaxhiqucs du neri sciatique chez le cobaye. CR. Amd. Scl", 244: 4-09-411, 1957. 

3. Nayar, KK., Arthur, E. and Ballís,  M4, Th: transmission of tumours induced in cockroaches by nerve severance, Experienria, 27: 183, 1971. 

4. Champy, C.. Lesions neum-sympathìques precedam la canccrixation dans Patlaque de Porganìsmc par les substances cancerîgenes, C.R. Acad. Sci, 248: 3665-1666; 1959. 

 www.usapr.org/paperpdfs/75.pdf

The alpha-adrenergic sensitivity of smooth muscle following sympathectomy

The data obtained suggest alteration of pharmacological characteristics of smooth muscle alpha-adrenoceptors after interruption of the sympathetic nerve.

Fiziol Zh SSSR Im I M Sechenova. 1988 Sep;74(9):1287-93.

blockade of sympathetic nerves - Trigeminal Substance P Neurons in Cluster Headache

A comparison is made with the present opinion on activation of parasympathetic and blockade of sympathetic nerves to explain the various symptoms of a cluster attack.

The Involvement of Trigeminal Substance P Neurons in Cluster Headache. An Hypothesis

Jan Erik Hardebo , M.D.

From the Department of Neurology and Department of Histology, University of Lund, Lund, Sweden.

Headache: The Journal of Head and Face Pain

Volume 24 Issue 6, Pages 294 - 304

Published Online: 22 Jun 2005

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

"sympathectomy of one side of the body leads to an increase in the development of tumors on the denervated side"

Coujard R, Heitz F. Cancerologic: Production de tumeurs malignes consecutives a des lesions des fibres sympathiques du nerf sciatique chez le Cobaye. C R Acad Sci 1957; 244: 409­411.


This suggest that interference with the sympathetic nervous system (SNS) can lead to a compromise of the body's immune system [81–82]. Conversely, an immunological response can alter the response pattern of the sympathetic nervous system. [83]
http://www.chiro.org/LINKS/FULL/VERTEBRAL_SUBLUXATION_2.shtml 

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 & Engineering
Queensland University of Technology

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

Sympathectomy exacerbated the inflammation and osteopathic destruction of arthritic joints

http://www.ncbi.nlm.nih.gov/pubmed/8632052

dynamic cerebral autoregulation is altered by ganglion blockade

We measured arterial pressure and cerebral blood flow (CBF) velocity in 12 healthy subjects (aged 29+/-6 years) before and after ganglion blockade with trimethaphan. CBF velocity was measured in the middle cerebral artery using transcranial Doppler. The magnitude of spontaneous changes in mean blood pressure and CBF velocity were quantified by spectral analysis. The transfer function gain, phase, and coherence between these variables were estimated to quantify dynamic cerebral autoregulation. After ganglion blockade, systolic and pulse pressure decreased significantly by 13% and 26%, respectively. CBF velocity decreased by 6% (P <0.05). In the very low frequency range (0.02 to 0.07 Hz), mean blood pressure variability decreased significantly (by 82%), while CBF velocity variability persisted. Thus, transfer function gain increased by 81%. In addition, the phase lead of CBF velocity to arterial pressure diminished. These changes in transfer function gain and phase persisted despite restoration of arterial pressure by infusion of phenylephrine and normalization of mean blood pressure variability by oscillatory lower body negative pressure.
Conclusions-: These data suggest that dynamic cerebral autoregulation is altered by ganglion blockade. We speculate that autonomic neural control of the cerebral circulation is tonically active and likely plays a significant role in the regulation of beat-to-beat CBF in humans.
Circulation. 106(14):1814-1820, October 1, 2002.
http://www.problemsinanes.com/pt/re/dyslipidaemia/abstract.00003017-200210010-00017.htm;jsessionid=PX6phQHYFG5PD1p2DMS1cJLvG1TbtLLLH0bfJT6vKJgLLx1zn0Xf!1816077220!181195629!8091!-1?nav=reference

Effects of cervical sympathectomy, stage of the estrous cycle and estradiol treatment.

C A CA Nagle, D P DP Cardinali and J M JM Rosner Life Sci 13(8):1089-103 (1973) PMID 4357690

Horner syndrome, pneumothorax, hemothorax, asymmetry of results, intercostal neuralgia, causalgia, hypoesthesia, incomplete results, paresthesia in the anterolateral abdominal wall, dyspareunia

The complications and side effects are very significant, such as irreversible compensatory sweating (20% to 50%), low satisfaction with results, Claude-Bernard-Horner syndrome, pneumothorax, hemothorax, asymmetry of results, intercostal neuralgia, causalgia, incomplete results, and anesthetic complications^11-13.

Retroperitoneoscopic lumbar sympathectomy (video-assisted): this technique is effective in the treatment of isolated or persistent plantar hyperhidrosis (compensatory after thoracic sympathectomy). The treatment consists of removing the nerves of the sympathetic chain located in the abdomen, in the anterolateral portion of the lumbar vertebrae. It requires hospitalization and is carried out under general anesthesia. It may lead to complications such as lesions of structures adjacent to the sympathetic chain, light abdominal distension, neuralgia, and causalgia as well as hypoesthesia in the thighs and groin, limitation of leg movement,
paresthesia in the anterolateral abdominal wall, change in libido, dyspareunia, pulmonary thromboembolism, hemorrhages, arrhythmias, and cardiac decompensation, amongst others. It definitively eliminates plantar hyperhidrosis14,15.  
http://www.scielo.br/scielo.php?pid=S1983-51752011000400008&script=sci_arttext&tlng=en#end

Vasodilation; Vasomotor Disturbances

Complex regional pain syndromes (CRPS) are characterized by vascular disturbances primary affecting the microcirculation in the distal part of the involved extremity. In the acute stage inhibited sympathetic vasoconstriction and exaggerated neurogenic inflammation driven by central and peripheral mechanisms, respectively, seem to be the major pathophysiological mechanisms inducing vasodilation. During the chronic course of the disease as well as early in some patients vasoconstriction dominates the clinical picture induced by changes in the microcirculation itself such as endothelial dysfunction or vascular hyperreactivity, whereas sympathetic vasoconstrictor activity returns and neurogenic inflammation is less severe. It can be suggested that the interaction between different mechanisms underlying vasomotor disturbances as well as the severity of each single mechanism in the individual patient have a great impact on the variety of the overall clinical picture in CRPS. Irrespective of the underlying pathophysiology, measurements of skin temperature differences between the affected and the contralateral extremity can serve as a diagnostic tool in CRPS, in particular when sensitivity and specificity is increased by considering dynamic alterations in skin temperature asymmetries.
http://onlinelibrary.wiley.com/doi/10.1111/j.1526-4637.2010.00914.x/abstract

Epidemiology /Etiology

CRPS is found to result:^[1]
- After traumatic injury (65%)

• 1-2% of all fractures result in CRPS
• Largest risk of CRPS for fractures of the wrist

- After surgical intervention (19%)
- Infection (4%)
- Prior inflammation (2%)
- No clear cause (10%)
A review stated that women are predominantly affected, by a factor of 3,5 and a genetic predisposition has also been theorized.
The disease affects all ages, though most cases are between 50 and 70 years old, and it is generally believed to occur mainly in caucasian and Japanese people.^[4]

Characteristics/Clinical Presentation

The following symptoms have been found in literature:^[5]
- Autonomic and trophic disorders:

• Distal Edema in 80% of the patients
• Skin temperature changes at the affected body part in 80% of the patients, initially warmer and in 40% of patients gradually cools down until colder in comparison to the rest of the body as the disease progresses. Another review mentioned that 30% of the patients start off from the primarily cold stage.3
• In 40% of the patients skin at the affected body part starts showing redness, but becomes pale or livid in later stages
• In 55% altered sweating takes place, with hyperhydrosis being more common than hypohydrosis.
• Hair and nail growth possibly increase in early stages
• Atrophy of skin and muscles in later stages, as well as contractures may severely restrict movement

- Sensory disturbances (90%) typically in a glove or stocking-like distribution

• Spontaneous pain occurs in 75%, usually burning dragging or stinging

• 68% felt in deep structures
• 32% felt in skin
• In 77% pain shows fluctuating intensity, lesser proportion shows shooting pain
• Pain can be increased by orthostasis, anxiety, exercise or temperature changes.
• In many cases, pain is more pronounced at night

• Sensory gain (Mechanical hyperalgesia, allodynia, ...) or sensory loss (hypaesthesia, hypalgesia, …) may be present.

- Motor dysfunction

• Motor weakness
• Severe impairment of complex movements
• Impairment of range of motion, initially by concomitant edema, later by contractures and fibroses
• Neglect like symptoms have been found in some patiënts, described as the body part in question feeling foreign.
• Enhanced physiological tremor in around 50%
• Myoclonus or dystonia, especially in type II CRPS

http://www.physio-pedia.com/Complex_Regional_Pain_Syndrome

Sympathectomy involves division of adrenergic, cholinergic and sensory fibers which elaborate adrenergic substances during the process of regulating viscera

http://pharmrev.aspetjournals.org/content/18/1/611.full.pdf+html

sympathectomy affects the heart, sweating, and circulation

heart rate was significantly reduced at rest (14%), at sub-maximal exercise (12.3%), and at peak exercise (5.7%), together with a significant increase in oxygen pulse (11.8, 12.7, and 7.8%, respectively). The rate pressure product (RPP) was also significantly reduced following the surgical procedure at all three study stages, while all other physiological variables measured remained unchanged. It is suggested that thoracic-sympathetic denervation affects the heart, sweating, and circulation of the respective denervated region

Eur J Appl Physiol. 2008 Sep;104(1):79-86. Epub 2008 Jun 10.

T3 sympathectomy leads to subclinical pupillary dysfunction with a tendency for miosis

We found statistically significant differences (P < 0.001) between the preoperative P/I ratio [0.40 mm (standard deviation, SD 0.07 mm)] and the postoperative basal ratio [0.33 (SD 0.05)] at 24 h. The P/I ratio at 24 h increased from 0.33 to 0.36 (SD 0.09), a nonsignificant increase (P = 0.45), after instillation of medicated eye drops. No differences were observed between the preoperative [0.40 (SD 0.07)] and 1-month basal values [0.38 (SD 0.07)], and instillation of apraclonidine no longer induced a hypersensitivity response.

CONCLUSIONS:

T3 sympathectomy leads to subclinical pupillary dysfunction with a tendency for miosis, even though this impairment is not generally evident on standard physical examination or reported by patients. This subclinical dysfunction may be caused by injury to an undefined group of presympathetic nerve cell axons in caudocranial direction that communicate with the cervical sympathetic ganglia and whose function is mydriatic pupillary innervation.
http://www.ncbi.nlm.nih.gov/pubmed/22044979

Sympathectomy increased the pain threshold and made the sympathectomized rats hypesthetic

Normal adult rats were sympathectomized at L2-L3. The threshold for thermal noxious pain by hot-plate analgesia test and changes in neuropeptides in the lumbar dura mater and dorsal root ganglia using light microscopic immunohistochemistry were assessed and compared with control rats.

Results: In the hot-plate analgesia test, sympathectomized rats increased their hot-plate latency time compared with that of sham-operated rats. Density of calcitonin gene-related peptide immunoreactive fibers in sympathectomy side of the lumbar dura mater decreased to 45.5% compared with the contralateral side. The number and size of calcitonin gene-related peptide immunoreactive cells in dorsal root ganglia showed no difference between sympathectomized and contralateral side.

Conclusion: Sympathectomy increased the pain threshold and made the sympathectomized rats hypesthetic. A large numbers of sensory fibers innervated the lumbar dura mater via L2-L3 sympathetic nerve in rats. Sympathectomy reduced the number of these nerve fibers in the lumbar dura mater. Sympathetic nerves may play an important role for low back pain involving the lumbar dura mater.

http://journals.lww.com/spinejournal/Abstract/1996/04150/An_Anatomic_Study_of_Neuropeptide.4.aspx

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

sympathectomy resulted in complete disappearance of histochemically detected adrenergic and a considerable decrease of cholinergic nerve fibers in the pial arterial walls

sympathectomy resulted in complete disappearance of histochemically detected adrenergic and a considerable decrease of cholinergic nerve fibers in the pial arterial walls. The vasodilatation was much less obvious in sympathectomized than in control animals. This was associated with (and probably caused by) a considerable rise in histochemically detected serotonin activity of the pial arteries walls. After recovery of blood supply to the brain the constriction of the pial arterial active segments restricting the excessive cerebral blood flow, was significantly reduced due, probably, to the sympathetic deprivation. Therefore, the sympathetic control plays an important part in pial arterial responses regulating the adequate blood supply of the cerebral cortex.
http://www.ncbi.nlm.nih.gov/pubmed/7173422

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

It is recently become clear that activated immune cells and immune-like glial cells can dramatically alter neuronal function. By increasing neuronal excitability, these non-neuronal cells are now implicated in the creation and maintenance of pathological pain, such as occurs in response to peripheral nerve injury. Such effects are exerted at multiple sites along the pain pathway, including at peripheral nerves, dorsal root ganglia, and spinal cord. In addition, activated glial cells are now recognized as disrupting the pain suppressive effects of opioid drugs and contributing to opioid tolerance and opioid dependence/withdrawal. While this review focuses on regulation of pain and opioid actions, such immune-neuronal interactions are broad in their implications. Such changes in neuronal function would be expected to occur wherever immune-derived substances come in close contact with neurons.
http://www.ncbi.nlm.nih.gov/pubmed/17706291

most surgeons do not have a clear understanding of their short-term outcomes for the majority of procedures they perform

The public would probably be surprised to know that most surgeons do not have a clear understanding of their short-term outcomes for the majority of procedures they perform.

Of even greater concern is the lack of data on long-term outcomes associated with surgical interventions.

Many surgeons argue that they are too busy and do not have the time and resources to conduct this sort of follow-up. This is not entirely without foundation, but it does seem difficult to defend a stance that says “I will continue to work feverishly at the operations I do but not assess how successful my results are”.

Guy Maddern (ASERNIP-s): No excuse for poor surgical outcomes

MJA INSIGHT, 8 August 2011

sympathectomy cannot by direct effect on the muscle vessels either abolish or lessen claudication

http://pmj.bmj.com/content/29/335/459

Sympathectomy useless, even detrimental

A number of surgical procedures have been developed, which, although well-intentioned, are found unfortunately by further study to prove useless, or even detrimental. It is believed at present that lumbar sympathetic ganglionectomy in the treatment of the post-thrombotic type of ulceration of the lower extremity should be placed in this category.
http://archsurg.ama-assn.org/cgi/content/summary/67/1/2

post-sympathectomy neuralgia is frequent

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 & Wilkins, 2009 - 2064 pages

impairment of the CBF autoregulation after unilateral cervical sympathectomy

Although these findings argued against a neurogenic mechanism, James at al. (1969) reported impairment of autoregulation after unilateral cervical sympathectomy in the babbon. Gotoh et al. (1971/1972) observed impairment of autoregulation in patients with the Shy-Drager syndrome.
It was concluded that the autonomic nervous system plays an important role in the mechanism of autoregulation of CBF and that his mechanism is independent of the chemical control of the cerebral vessels. This was confirmed by direct observation of the pial vessels in cats, where separate sites of action in the vascular tree for autoregulation and chemical control were demonstrated; the autoregulatory reaction was located in pial arteries with a diameter larger than 50 μ, and the reaction to carbon dioxide in pial arteries of smaller diameter (Gotoh et al. 1975).
They concluded that the arteries operating in autoregulation were the larger ones with the dense innervation, while the smaller arteries with sparse innervation were involved in chemical control.
Coronna and Plum (1973) demonstrated the absence of CBF autoregulation in a patient with a Shy-Drager syndrome who had a postganglionic denervation.

Gotoh et al (1979) subsequently showed that autoregulation in patients with this syndrome was impaired irrespective of the localization of the damage to the cervical sympathetic nervous system (preganglionic, central, postganglionic) as judged by the eye instillation test.
Handbook of Clinical Neurology,

Vascular Diseases, Part I by P. J. Vinken, G. W. Bruyn, H. L. Klawans, and J. F. Toole

, Volume 53, Part 1

Elsevier Health Sciences, 1988

Effect of Sympathectomy on Bone Repair

In each, there was a more rapid healing on the non-sympathectomized side, averaging 3 weeks sooner.


http://ebm.rsmjournals.com/content/30/2/123.extract

diabetic autonomic neuropathy has already sympathectomized the patient

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/

extreme case of compensatory truncal hyperhidrosis and anhidrosis over the head and neck region which led to a heatstroke

Thoracic sympathectomy is a commonly performed surgical procedure for the treatment of palmar hyperhidrosis. However, one major complication of such a procedure is compensatory truncal hyperhidrosis. We describe an extreme case of compensatory truncal hyperhidrosis and anhidrosis over the head and neck region which led to a heatstroke.

http://icvts.oxfordjournals.org/content/early/2011/12/20/icvts.ivr121.abstract?sid=89a2ce71-1ea3-4573-9e63-17329e7c09cd

Presence of intense dyschromia in the region corresponding to anhidrosis after sympathectomy

http://ats.ctsnetjournals.org/cgi/content/full/88/4/e42

Sympathectomy depresses the function of the adrenal glands, and deprives the experimental animal of its ability to react completely to the stimuli of an emergency situation

Annals of Surgery, June 1951

Joint inflammation is reduced by dorsal rhizotomy and not by sympathectomy

http://www.ncbi.nlm.nih.gov/pubmed/8017984

Effect of local sympathectomy on 24-h changes in mitogenic responses and lymphocyte subset populations

Wistar male rats received a bilateral superior cervical ganglionectomy or sham-operation and 10 days later were injected with Freund’s complete adjuvant or its vehicle. Two days later, rats were killed at six different time intervals throughout a 24-h cycle. The mitogenic effect of lipopolysaccharide (LPS) and concanavalin A (Con A) and the relative size of lymphocyte subset populations were measured in submaxillary lymph nodes. Cells from sympathectomized lymph nodes showed a lower response to Con A. Freund’s adjuvant injection decreased amplitude of daily rhythm in Con A response, an effect prevented by denervation. Generally, ganglionectomy increased Con A response at the early phase of arthritis. Acrophases for Con A and LPS effect occurred at early afternoon and did not change after ganglionectomy. Administration of Freund’s adjuvant caused a 10-h advance in acrophase of LPS mitogenic activity, an effect prevented by ganglionectomy. Significant 24-h rhythms were observed in relative size of lymph node B and T cells. Denervation augmented amplitude of rhythm in B cells in adjuvant’s vehicle-injected rats. As far as T lymphocyte subsets, acrophases occurred at the afternoon (CD4⁺ and CD4⁺–CD8⁺ cell types) or at night (CD8⁺ cell types). Immunization augmented amplitude of 24-h rhythms in CD4⁺–CD8⁺ cells regardless of innervation whereas denervation counteracted the suppression of daily rhythm in CD8⁺ cells seen in arthritis. The results indicate that some of the changes seen in 24-h organization of immune responses in lymph nodes at an early phase of arthritis are modified by severing the local sympathetic nerves.
http://journals1.scholarsportal.info/details.xqy?uri=/00068993/v888i0002/227_eolso2ppofaa.xml

Interactions between the immune and nervous systems play an important role in modulating host susceptibility and resistance to inflammatory disease

During inflammation, cytokines from the periphery activate the central nervous system through multiple routes. This results in stimulation of the hypothalamic-pituitary-adrenal axis which, in turn through the immunosuppressive effects of the glucocorticoids, generally inhibits inflammation. Recent studies indicate that physiological levels of glucocorticoids are immunomodulatory rather than solely immunosuppressive, causing a shift in patterns of cytokine production from a TH1- to a TH2-type pattern. Interruptions of this loop at any level and through multiple mechanisms, whether genetic, or through surgical or pharmacological interventions, can render an inflammatory resistant host susceptible to inflammatory disease. Over-activation of this axis, as occurs during stress, can also affect severity of infectious disease through the immunosuppressive effects of the glucocorticoids. These interactions have been clearly demonstrated in many animal models, across species, strains and diseases, and are also relevant to human inflammatory, autoimmune and allergic illnesses, including rheumatoid arthritis, systemic lupus erythematosus, Sjogren's syndrome, allergic asthma and atopic skin disease.
http://www.ncbi.nlm.nih.gov/pubmed/11375112?dopt=Abstract

Changes in TH mRNA levels after cold stress or sympathectomy were eliminated by denervation of the adrenal gland

http://www.ncbi.nlm.nih.gov/pubmed/2427735