Effect of local autonomic denervation on in vitro responsiveness of lymphocytes

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

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

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

Diabetologia

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

 

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

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

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

abnormal sympathetic activity may cause pain following sympathectomy

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

Neuroma formation at the ends of the sympathetic chain after Sympathectomy

The authors conclude recomemnding the application of clips and if the syndrome nevertheless appears novocaine infiltration of the upper end of the sympathetic chain. The authors are convinced that the theory of Hermann and Cooley about neuroma formation at the ends of the sympathetic chain after resection of a segment is true.
http://www.revangiol.com/sec/resumen.php?or=web&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 a cholecystectomy). They are often very painful. It is also known as "pseudoneuroma".

postsympathectomy syndrome

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

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

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

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

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

Postsympathectomy pain and changes in sensory neuropeptides

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

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

Segmental myoclonus was associated with thoracic sympathectomy

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

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

relevant to post-sympathectomy pain

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

compensatory disease may not be immediate after sympahectomy

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

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

Management of Hyperhidrosis

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

denervation supersensitivity of alpha receptors after sympathectomy

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

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

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

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

Related articles

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

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

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

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

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

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

Surgical thoracic sympathectomy such as ESD (endoscopic thoracic sympathectic denervation) or heart transplantation can result in an imbalance between the sympathetic and parasympathetic activities and result in functional changes
in the intrathoracic organs.
Therefore, the procedures affecting sympathetic nerve functions, such as epidural anesthesia, ESD, and heart transplantation, may cause an imbalance between sympathetic and parasympathetic activities (1, 6, 16, 17). Recently, it has been reported that ESD results in functional changes of the intrathoracic organs.


In conclusion, our study demonstrated that ESD adversely affected lung function early after surgery and the BHR was affected by an imbalance of autonomic activity created by bilateral ESD in patients with primary focal hyperhidrosis.
Journal of Asthma, 46:276–279, 2009
http://informahealthcare.com/doi/abs/10.1080/02770900802660949

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

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

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

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

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

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

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

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

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

diabetic autonomic neuropathy has already sympathectomized the patient

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

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

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

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

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

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

Retrograde Changes in the Nervous System Following Unilateral Sympathectomy

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

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

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

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

There is a fairly extensive literature on pain after lumbar sympathectomy

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

"Post sympathectomy syndrome is a poorly understood condition"

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

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

Interventional Pain Management

DK. Baheti, Bombay Hospital

Jaypee Brothers Publishers, 2009

Effect of ganglion blockade on cerebrospinal fluid norepinephrine

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

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

sympathectomy results in a pronounced increase of cerebrospinal fluid production

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

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

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

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

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

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

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

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

Bonica's Management of Pain,

Lippincott Williams & Wilkins, 2009 - 2064 pages

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

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

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

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

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

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

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

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


Information for Health Professionals          Hunter Integrated Pain Service         Updated January 2010

Procedural Intervention Guideline

surgical and chemical sympathectomy can both modulate bone cell function

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

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

Norepinephrine activates pain pathways after nerve injury

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

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

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

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

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

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

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

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

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

sympathectomy induced morphological alterations in the masseter muscles

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

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

Post-sympathectomy neuralgia - pain overlying the scapula

Complications of surgical (Thoracic and Lumbar) Sympathectomy:

Post-sympathectomy neuralgia - pain overlying the scapula

Compensatory sweating - involving the lover back or face

Pneumothorax

Bleeding due to azygos vein or intercostal artery injury

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

Mastery of Vascular and Endovascular Surgery

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

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

Post-sympathectomy pain

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

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."

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"

The vasodilating effect of spinal dorsal column stimulation is mediated by sympathetic nerves - Springer

The vasodilating effect of spinal dorsal column stimulation is mediated by sympathetic nerves - Springer: "Immediately after sympathectomy, the contralateral right arm became increasingly cold and cyanotic and the patient complained of chronic painful coldness and severe cold-intolerance in the right arm. Attempts to pharmacologically vasodilate the arm with felodipine did not affect the local vasoconstriction and pain. Dorsal column stimulation (associated with symmetrical paraesthesia in both arms) induced an immediate and marked (ten-fold) increase in skin blood flow in the right arm (and in the leg), whereas skin blood flow in the left arm remained unaffected. The lack of vasomotor response in the left arm was not due to maximal vasodilatation at rest, since skin blood flow in the left arm showed a normal capacity for axon reflex vasodilatation following antidromic activation of sensory afferents. The results suggest that the marked vasodilatation induced by dorsal column stimulation is mediated by sympathetic vasomotor fibres, via modulation of central neuronal circuits involved in the regulation of skin sympathetic discharge."

Brachial plexopathy is another well recognised but not much publicised side-effect of sympathectomy

Brachial plexus dysfunction (brachial plexopathy) is a form of peripheral neuropathy. It occurs when there is damage to the brachial plexus, an area on each side of the neck where nerve roots from the spinal cord split into each arm's nerves.

Damage to the brachial plexus is usually related to direct injury to the nerve, stretching injuries (including birth trauma), pressure from tumors in the area (especially from lung tumors), or damage that results from radiation therapy.

Brachial plexus dysfunction may also be associated with:

• Birth defects that put pressure on the neck area
• Exposure to toxins, chemicals, or drugs
• General anesthesia, used during surgery
• Inflammatory conditions, such as those due to a virus or immune system problem

In some cases, no cause can be identified.

Symptoms

• Numbness of the shoulder, arm, or hand
• Shoulder pain
• Tingling, burning, pain, or abnormal sensations (location depends on the area injured)
• Weakness of the shoulder, arm, hand, or wrist

http://www.nlm.nih.gov/medlineplus/ency/article/001418.htm

Intense pain following sympathectomy, reduced inspiratory capacity

Intrapleural analgesia after endoscopic thoracic sympathectomy.

Patrícia Gomes da Silva, Daniele Cristina Cataneo, Fernanda Leite, Erica Nishida Hasimoto, Guilherme Antonio Moreira de Barros

Postgraduate Program in Anesthesiology, Botucatu School of Medicine, UNESP, Bauru, SP, Brazil.

PURPOSE To compare analgesia traditionally used for thoracic sympathectomy to intrapleural ropivacaine injection in two different doses. METHODS Twenty-four patients were divided into three similar groups, and all of them received intravenous dipyrone. Group A received intravenous tramadol and intrapleural injection of saline solution. Group B received intrapleural injection of 0.33% ropivacaine, and Group C 0.5% ropivacaine. The following aspects were analyzed: inspiratory capacity, respiratory rate and pain. Pain was evaluated in the immediate postoperative period by means of the visual analog scale and over a one-week period. RESULTS In Groups A and B, reduced inspiratory capacity was observed in the postoperative period. In the first postoperative 12 hours, only 12.5% of the patients in Groups B and C showed intense pain as compared to 25% in Group A. In the subsequent week, only one patient in Group A showed mild pain while the remainder reported intense pain. In Group B, half of the patients showed intense pain, and in Group C, only one presented intense pain. CONCLUSION Intrapleural analgesia with ropivacaine resulted in less pain in the late postoperative period with better analgesic outcomes in higher doses, providing a better ventilatory pattern.

http://lib.bioinfo.pl/meid:154350/pmid

Sympathectomy significantly alters vascular responses

Vascular responses to warming were studied in hemiplegic patients and after sympathectomy, using venous occlusion plethysmography of foot and leg. Comparisons were made with corresponding age groups. The pattern of response was essentially unchanged in hemiplegic patients, but was altered substantially where sympathetic pathways had been interrupted.

Vasomotor Responses in the Extremities of Subjects with Various Neurologic Lesions

I. Reflex Responses to Warming

1. WALTER REDISCH, M.D.; 
 
2. FRANCISCO T. TANGCO, M.D.; 
 
3. LOTHAR WERTHEIMER, M.D.;
4. ARTHUR J. LEWIS, M.D.; 
 
5. J. MURRAY STEELE, M.D.; 
 
6. Dorothy Andrews, B.A.,

http://circ.ahajournals.org/content/15/4/518.abstract

sympathectomy leads to fluctuation of vasoconstriction alternated with vasodilation in an unstable fashion (39). 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

Vascular sympathetic denervation can lead to degeneration of the smooth muscle of arteries leading to medial arterial calcification and stiffening of the arteries

Sympathetic denervation of the peripheral arterial system may occur quite early in the evolution of neuropathy and has major effects on blood flow and vascular responses and causes structural changes in the arterial wall (Edmonds 2004). Vascular sympathetic denervation can lead to degeneration of the smooth muscle of arteries leading to medial arterial calcification and stiffening of the arteries. This calcification may assume the histological characteristics of bone.

   Unilateral lumbar sympathectomy in humans, both in diabetics and non-diabetics, has been show to result in medial wall calcification on the ipsilateral side (Goebel and Fuessl 1983). Unilateral sympathectomy in animals leads to excess deposition of cholesterol on the operated side and the occurrence of cholesterol sclerosis in the rabbit's aorta was accelerated by removal of the coeliac ganglion (Harrison 1938). Furthermore, in animal models, denervation of smooth muscle leads to striking pathological changes, including atrophy of muscle fibres with foci of degeneration (Kerper and Collier 1926). Arterial calcification in initiated within senescent atrophic smooth muscle (Morgan 1980).

   Medial arterial calcification in the Pima Indians is significantly associated with an increased prevalence of cardiovascular mortality (Everhart et al 1988). Medial calcification may be important factor in development of peripheral vascular disease, which in diabetes shows a predilection for the distal arteries below the knee and is unexplained. Chantelau reported an association of below knee atherosclerosis to medial arterial calcification (Chantelau et al. 1995).

p. 653

Autonomic Failure: A Textbook of Clinical Disorders of the Autonomic Nervous System[Hardcover]

Christopher J. Mathias (Author), Roger Bannister (Author)

• Publisher: Oxford University Press, USA; 5 edition (July 24, 2013)
• Language: English
• ISBN-10: 0198566344
• ISBN-13: 978-0198566342

Impaired skin vasomotor reflexes have been found in patients with sympathetic dystrophies, dysautomias, post-regional sympathectomy and diabetic neuropathies

Not surprisingly, diminished vasoconstrictor responses, similar to the current findings, have been found
in patients with sympathetic dystrophies [26], dysautomias [27], post-regional sympathectomy [28] and
diabetic neuropathies [11].


Additionally, there have been a few reports of EM patients benefitting from sympathectomy or neurolitic
irreversible blocks of the lumbar sympathetic ganglia [22,23], while others have found the symptoms of EM to be aggravated by such treatment [24,25], possibly as a result of denervation supersensitivity.
Clinical Science (1999) 96, 507ñ512 (Printed in Great Britain)
Roberta C. LITTLEFORD, Faisel KHAN and Jill J. F. BELCH
University Department of Medicine, Section of Vascular Medicine and Biology, Ninewells Hospital and Medical School,
Dundee DD1 9SY, Scotland, U.K.

After sympathectomy in rats there is an increase in osteoclast-mediated bone resorption as well as an increase in the number of osteoclasts on the sympathectomized side

Paper: Osteoclastic Activation In Periapical Lesions After NPY Knockout (IADR/AADR/CADR 87th General Session and Exhibition (April 1-4, 2009)): "After sympathectomy in rats there is an increase in osteoclast-mediated bone resorption as well as an increase in the number of osteoclasts on the sympathectomized side compared to the control. These findings suggest an inhibitory effect of the SNS on bone resorption via osteoclasts. Our objective was to determine if an SNS mediator, neuropeptide Y (NPY), affects osteoclastic activity after pulpal exposure."

RSD due to nerve injury

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 (redness, warmth, swelling). RSD is not thought to have a single cause, but rather multiple causes producing similar symptoms.

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

progressive hemifacial atrophy following sympathectomy for hyperhidrosis

Some authors consider the disease a variant of mor- phea because the histologic changes are identical to deep scleroderma.2 The possible etiologies include sympathetic denervation, trauma, vascular malformations, immunologic abnormality, heredi- tary disease, or infection by a slow virus.3 To our knowledge, this is the first report of a young patient with a possible association between Parry-Romberg syndrome and thoracoscopic sympathectomy.

Theoretically, thoracoscopic sympathectomy may cause 2 of the aforementioned etiologies of Parry- Romberg syndrome: sympathetic denervation and trauma. Thoracoscopic sympathectomy is a surgical technique for the treatment of palmar hyperhidrosis.

The operation ablates the upper thoracic sympa- thetic nerve ganglions responsible for nerve stimu- lation of the sweat glands of the upper limbs. The most significant complication is Horner’s syn- drome, which results from injury to the stellate sympathetic ganglion.7 In a summary of sympa- thectomies in 67 children and adolescents, compli- cations included Horner’s syndrome in 1 patient (1%) and varying degrees of compensatory sweat- ing in 30 patients (45%).8 Despite the evidence from animal studies that sympathectomy can result in facial atrophy, to our knowledge, there were no previous reports of such an association in humans.

Cutis. 2004;73:343-344, 346.

Endoscopic thoracic sympathectomy remains a fairly controversial procedure

"Studies by ETS surgeons have claimed an initial satisfaction rate around 85-95% with at least 2%-19% regretting the surgery and up to 51% of the patients complaining about decreased quality of life. However, at least one study shows a satisfaction rate as low as 28.6.

Most patients report various adverse reactions as a result of the surgery. And, whilst the results of endoscopic thoracic sympathectomy might appear moderately successful in treating hyperhidrosis, there is a high risk of complications.

Along with the normal side effects of surgery, such as pain, bleeding and bruising, the most frequent post surgical complication is ‘compensatory hyperhidrosis’ – where excessive sweating in seen another part of the body as a result, most commonly the lower back or upper thighs.

There is also the potential surgical complication of a pneumothorax, where air becomes trapped between the lung and the internal chest wall, making breathing difficult and painful. Whilst this can be a life-threatening condition, if not too large it generally resolves over time with out further surgical intervention.

Other fairly common complications of endoscopic thoracic sympathectomy include:

         Rhinitis - inflammation of the nose and

         Gustatory sweating - sweating on the face and neck after eating food,

Rarer complications of endoscopic thoracic sympathectomy as a result of nerve damage include:

         Damage to the phrentic nerve. – Phrentic nerve damage can lead to long term shortness of breath, repair of the nerve during the surgery is also possible in some cases..

         Horner’s syndrome, - a condition that causes drooping of the eyelids.

Endoscopic thoracic sympathectomy remains a fairly controversial procedure; with advocates claiming high success rates and minimal complications when performed correctly, whilst opponents report huge variation in post operation satisfaction levels and poor consistency in the surgical procedure as a result of anatomical variations in the sympathetic nerve network between patients and personal preferences between doctors."

http://www.lasertreatmentclinics.co.uk/Hyperhidrosis_Endoscopic_Sympathectomy/

Autonomic neuropathy in the skin following sympathectomy

In diabetics with the anhidrotic syndrome, autonomic nerve fibres were studied in skin biopsies using argentic techniques and light microscopy. The Minor test was used to differentiate normal from anhidrotic skin areas. In the anhidrotic areas, histology of the nerve fibres showed beading, spindle-shaped thickening and fragmentation adjacent to the sweat glands. These changes were similar to those observed in two patients who had previously undergone lumbar sympathectomy. No abnormalities of the sympathetic nerve endings could be found in biopsies taken from normal areas of the forearm of the same patients. We conclude that the diabetic anhidrotic syndrome, a form of diabetic autonomic neuropathy, is due to a lesion of the sympathetic nerve supply to the skin.

I. Faerman¹, E. Faccio³, I. Calb², J. Razumny¹, N. Franco², A. Dominguez² and H. A. Podestá¹

Diabetologia

Volume 22, Number 2 / February, 1982

Neuralgia due to sympathectomy - Pain following sympathectomy has been described as "an all too common complaint."

Depending on the skill of the surgeon and difficulty encountered performing various intraoperative maneuvers, the incidence of complications following sympathectomy should be the same as that following any other extraperitoneal or extrapleural operation. However, a frequent complication following sympathectomy, and one which is apparently unrelated to operative technique, is that of postsympathectomy neuralgia.

This neuralgia is characterized by aching thigh pain after lumbar sympathectomy or aching shoulder and arm pain after cervical sympathectomy. The pain is intense in severity, sudden in onset and disappearance, and not related to any major neurologic manifestations.

Recently we have reviewed the files of the Vascular Surgical Service at the West Roxbury Veteran's Hospital and the literature on this condition. This report is a presentation of our findings.

Incidence  Pain following sympathectomy has been described as "an all too common complaint."8 Reports have varied in incidence from 2.1% to "practically every case."

http://archsurg.jamanetwork.com/article.aspx?articleid=560162

"sympathectomized arteries become more susceptible to lipid accumulation"

Combined effect of cholesterol feeding and sympathectomy on the lipid content in rabbit aortas

Atherosclerosis

Volume 37, Issue 4, December 1980, Pages 521–528

"sympathectomy is a form of sensory neurectomy" (p.1500)

Bonica's Management of Pain

Scott Fishman, Jane Ballantyne, James P. Rathmell

Lippincott Williams & Wilkins, 2010 - Medical - 1661 pages