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

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

"Lumbar sympathectomy/Sympathectomy and Hydrocephalus sharing one common finding"

http://en.diagnosispro.com/disease_comparison-for/lumbar-sympathectomy-versus-hydrocephalus/16143-22570.html


DiagnosisPro is a medical expert system.^[1] It provides exhaustive diagnostic possibilities for 11,000 diseases and 30,000 findings.^[2] It is supposed to give the most appropriate differential however this is not always the case.^[3] Between Oct 2008 and Oct 2009 the site averaged 61,000 visits per month. ^[4]
http://en.diagnosispro.com/disease_comparison-for/lumbar-sympathectomy-versus-hydrocephalus/16143-22570.html


Hydrocephalus also known as "water in the brain," is a medical condition in which there is an abnormal accumulation of cerebrospinal fluid (CSF) 

http://en.wikipedia.org/wiki/Hydrocephalus

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/

Ischemic spinal cord injury has been reported after sympathectomy

Toole's Cerebrovascular Disorders

E. Steve Roach, James F. Toole, Kerstin Bettermann, José Biller

0 Reviews

Cambridge University Press, 31/01/2010 - Medical - 408 pages

The practice of sympathectomy for treating neuropathic pain is based on very weak evidence. Furthermore, complications of the procedure may be significant.

Cochrane Summaries^beta

Independent high-quality evidence for health care decision making

http://summaries.cochrane.org/CD002918/cervico-thoracic-or-lumbar-sympathectomy-for-neuropathic-pain

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

There is a fairly extensive literature on pain after lumbar sympathectomy

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

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

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

"Sympathectomy frequently interferes with ejaculation"

Kaplan & Sadock's synopsis of psychiatry:

behavioral sciences/clinical psychiatry

Benjamin J. Sadock, Harold I. Kaplan, Virginia A. Sadock

Lippincott Williams & Wilkins, 2007 - 1470 pages

After peripheral nerve section the amount of GAL produced and present in sensory fibers proximal to the section is dramatically upregulated

Front Neuroendocrinol. 1992 Oct;13(4):319-43.

Galanin in sensory neurons in the spinal cord.

Department of Clinical Physiology, Karolinska Institute, Huddinge University Hospital, Sweden.

The distribution and physiological effects of the neuropeptide galanin (GAL) have been examined in the somatosensory system. GAL is normally present in a few sensory neurons that terminate in the dorsal horn of the spinal cord and it is colocalized with substance P and calcitonin gene-related peptide. After peripheral nerve section, but not dorsal root section, the amount of GAL produced and present in sensory fibers proximal to the section is dramatically upregulated. In parallel functional studies, we could demonstrate that exogenous GAL has a complex effect on the spinal cord reflex excitability, facilitatory at low doses and inhibitory at high doses. Furthermore, GAL inhibits the effect of excitatory neuropeptides physiologically released at the peripheral and central terminals of small diameter afferents that subserve a nociceptive function. After axotomy, the inhibitory effect of GAL is increased. We conclude that GAL may have an important role in the control of nervous impulses that underlie pain states that can occur after peripheral nerve injury.

http://www.ncbi.nlm.nih.gov/pubmed/1281124

Increased expression of galanin in the rat superior cervical ganglion after pre- and postganglionic nerve lesions

http://www.ncbi.nlm.nih.gov/pubmed/7515354

Galanin is a neuropeptide encoded by the GAL gene,^[1] that is widely expressed in the brain, spinal cord, and gut of humans as well as other mammals. Galanin signaling occurs through three G protein-coupled receptors.^[2]
The functional role of galanin remains largely unknown; however, galanin is predominately involved in the modulation and inhibition of action potentials in neurons. Galanin has been implicated in many biologically diverse functions, including: nociception, waking and sleep regulation, cognition, feeding, regulation of mood, regulation of blood pressure, it also has roles in development as well as acting as a trophic factor.^[3] Galanin is linked to a number of diseases including Alzheimer’s disease, epilepsy as well as depression, eating disorders and cancer.^[4][5] Galanin appears to have neuroprotective activity as its biosynthesis is increased 2-10 fold upon axotomy in the peripheral nervous system as well as when seizure activity occurs in the brain. It may also promote neurogenesis.^[2]
http://en.wikipedia.org/wiki/Galanin

Compensatory changes in contralateral sympathetic neurons of the superior cervical ganglion and in their terminals in the pineal gland following unilateral ganglionectomy

The sympathetic noradrenergic neurons of the rat superior cervical ganglia (SCGs) provide the major source of innervation to the pineal gland. The present study sought to determine if this sympathetic innervation can undergo collateral sprouting following partial denervation of the pineal by unilateral removal of the SCG (ganglionectomy), and whether such growth of axon terminals is associated with biochemical changes in the contralateral SCG. In the pineal gland following partial denervation, residual noradrenergic terminals underwent compensatory changes indicative of collateral sprouting, as evidenced by: a rapid reduction in tyrosine hydroxylase (TH) activity and in [3H]norepinephrine (NE) uptake, to about 50% of control by 2 days, which was followed by a gradual but sustained increase to levels of approximately 80% of control by 10 days and a reduction in the intensity and density but not in the distribution of fibers containing NE-induced fluorescence by 2 days, which was followed by a sustained increase. In the contralateral SCG, choline acetyltransferase (CAT) activity, a marker of cholinergic preganglionic terminals, was transiently increased to about 115% of control by 4 days and returned to control levels by 14 days after unilateral ganglionectomy; later, TH activity in noradrenergic cell bodies was gradually increased to about 140% of control by 10 days where it remained for up to 52 days. Unilteral ganglionectomy combined with decentralization of the contralateral SCG by preganglionic nerve cut prevented the compensatory changes in noradrenergic nerve terminals within the pineal.
http://www.ncbi.nlm.nih.gov/pubmed/2861259

Hypertrophy and neuron loss: structural changes in sheep SCG induced by unilateral sympathectomy

Interaction effects between time and ganglionectomy-induced changes were significant for SCG volume and mean perikaryal volume. These findings show that unilateral superior cervical ganglionectomy has profound effects on the contralateral ganglion. For future investigations, it would be interesting to examine the interaction between SCGs and their innervation targets after ganglionectomy. Is the ganglionectomy-induced imbalance between the sizes of innervation territories the milieu in which morphoquantitative changes, particularly changes in perikaryal volume and neuron number, occur? Mechanistically, how would those changes arise? Are there any grounds for believing in a ganglionectomy-triggered SCG cross-innervation and neuroplasticity?
http://www.ncbi.nlm.nih.gov/pubmed/21334426

SYMPATHECTOMY ON THE FATTY DEPOSIT IN CONNECTIVE TISSUE

The effect of unilateral extirpation of the stellate and the superior cervical ganglia on the amount of the pericardial fat and the effect of unilateral extirpation of the lumbar and sacral ganglia on the abdominal and subcutaneous fat on the denervated side make it likely that the effects of the splanchnic nerves on the perirenal fat may be extended to describe the relation between fat storage in and sympathetic innervation of connective tissue in general.
http://ep.physoc.org/content/27/1/1

Patients with sympathectomy are not suitable controls for sleep study. Why?

Exclusions:
Patients with permanent pacemaker, non-sinus cardiac arrhythmias, peripheral vasculopathy or neuropathy, severe lung disease, status postbilateral cervical or thoracic sympathectomy, finger deformity that precludes adequate sensor application, using a-adrenergic receptor blockers, or alcohol or drug abuse during the last 3 years.



The clinic sleep laboratory of the Technion Sleep Medicine Centre, Israel
http://chestjournal.chestpubs.org/content/123/3/695.long
CHEST March 2003 vol. 123 no. 3 695-703


MSAC Application no 1130, Assessment Report

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

ETS considered psychiatric surgery - says Dr Nagy

"ETS (sympathectomy)  can alter many bodily functions, including sweating , heart rate , heart stroke volume , blood pressure , thyroid , baroreflex , lung volume , pupil dilation, skin temperature, goose bumps and other aspects of the autonomic nervous system . It can diminish the body's physical reaction to exercise and/or strong emotion, and thus is considered psychiatric surgery. In rare cases sexual function or digestion may be modified as well. "
http://www.lvhyperhidrosis.com/treatment.html

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/

Sympathectomy decreased CD4+ T-cells in lymph nodes

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

The response to injury in the perihperal nervous system

Persisting neurones switch to a ‘survivor’ phenotype and the expression of hundreds of genes^8,9 is changed to compensate for the loss or diminution of target-derived neurotrophic factors,¹⁰ and in order to regrow their axons across the site of the injury and back into the periphery. Proximal changes, such as synaptic reorganisation in the cortex^11–13 and spinal cord, occur upstream of axotomised first-order motor and sensory neurones, and may influence the functional outcome months or even years later.^14–16 Distal to the injury, a series of molecular and cellular events, some simultaneous, others consecutive, and collectively called Wallerian degeneration, is triggered throughout the distal nerve stump and within a small reactive zone at the tip of the proximal stump (Fig. 2).^17–19

http://web.jbjs.org.uk/cgi/content/full/87-B/10/1309

Distribution of GABA-immunoreactive nerve fibers and cells in the cervical and thoracic paravertebral sympathetic trunk

These data suggest that the GABAergic innervation of paravertebral sympathetic ganglia is more complex than previously suspected. What appears as preganglionic afferents from several spinal segments (C8-Th7) innervate GABAergic neurons in the sympathetic trunk which have ascending axons and focus their inhibitory effects on the cervical sympathetic ganglia, predominantly the SCG. These data suggest that GABAergic small interganglionic neurons form a feed-forward inhibition system, which may be driven by multisegmental spinal input in the paravertebral sympathetic ganglion chain.
http://onlinelibrary.wiley.com/doi/10.1002/cne.903340209/abstract

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 those
seen 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

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

important relationship among cognitive performance, HRV, and prefrontal neural function

These findings in total suggest an important relationship among cognitive performance, HRV, and prefrontal neural function that has important implications for both physical and mental health. Future studies are needed to determine exactly which executive functions are associated with individual differences in HRV in a wider range of situations and populations.
http://www.ncbi.nlm.nih.gov/pubmed/19424767

Low HRV is a risk factor for pathophysiology and psychopathology

The intimate connection between the brain and the heart was enunciated by Claude Bernard over 150 years ago. In our neurovisceral integration model we have tried to build on this pioneering work. In the present paper we further elaborate our model. Specifically we review recent neuroanatomical studies that implicate inhibitory GABAergic pathways from the prefrontal cortex to the amygdala and additional inhibitory pathways between the amygdala and the sympathetic and parasympathetic medullary output neurons that modulate heart rate and thus heart rate variability. We propose that the default response to uncertainty is the threat response and may be related to the well known negativity bias. We next review the evidence on the role of vagally mediated heart rate variability (HRV) in the regulation of physiological, affective, and cognitive processes. Low HRV is a risk factor for pathophysiology and psychopathology. Finally we review recent work on the genetics of HRV and suggest that low HRV may be an endophenotype for a broad range of dysfunctions.
http://www.ncbi.nlm.nih.gov/pubmed/18771686

Fundamentals of psychoneuroimmunology

The long-held concept that the nervous, endocrine and immune systems are separate entities has given way to a new understanding of human biology. Psychoneuroimmunology addresses the realisation that the neural, immune, and endocrine systems are inextricably linked and that the effects of each affect all-the systems work together as a complicated set of triggers and balances, an intertwining of the physiological and emotional states. Beginning with the fundamentals of immune and neuroendocrine function, Fundamentals of Psychoneuroimmunology explores the complexities of behavioural assessment, the basic types of immunity, the importance of immune cell redistribution in the response to challenges such as infection and stress, and the multifaceted roles of nerves, hormones and cytokines.
http://books.google.com/books/about/Fundamentals_of_psychoneuroimmunology.html?id=h0mEge8Oec8C

Sympathectomy should not be considered for such persons because of the risk of permanent worsening of erythromelalgia symptoms

The literature contains reports of remission with sympathectomy, but careful case selection is imperative before this procedure is performed.  Sympathectomy should be considered only for those whose erythromelalgia improves with blocks.  Conversely, if a sympathetic block causes worsening of a person's erythromelalgia, treatment should be discontinued.  Sympathectomy should not be considered for such persons because of the risk of permanent worsening of erythromelalgia symptoms.
Jay S. Cohen MD,
medicationsense.com/articles/2010/erythromelalgia0510.pdf

ganglion block for unbalanced sympathetic nervous system disorders

Stellate ganglion blocks (SGB) are widely used for pain relief in outpatient clinics due to its many therapeutic indications and easy maneuvering. It is used locally over stellate ganglion territory disorders in the craniocervical (head and neck) or upper limbs and systemically for angina pectoris, psychosomatic disorders, hormonal disorders, or unbalanced sympathetic nervous system disorders [1].
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2872892/

sympathectomy can result in spinal cord infarction

Uncommon causes include decompression sickness, which has a predilection for spinal ischemic damage; complications of abdominal surgery, particularly sympathectomy;...

http://www.neurology-asia.com/Spinal_Cord_Infarction.php

For blood pressure control in certain acute hypotensive states (e.g., pheochromocytomectomy, sympathectomy...

Norepinephrine (Levophed ®) -
For blood pressure control in certain acute hypotensive states (e.g., pheochromocytomectomy, sympathectomy, poliomyelitis, spinal anesthesia, myocardial infarction, septicemia, blood transfusion, and drug reactions).
http://www.globalrph.com/norepinephrine_dilution.htm

Unilateral sympathectomy leads to decreases in ventral prostate weight

http://www.biolreprod.org/content/51/1/99

Several autonomic reflexes were dramatically affected after sympathectomy for hyperhidrosis

major effects on local blood flow and temperature are elicited by TES. Complex autonomic reflexes are also affected. The patient should be completely informed before surgery of the side effects elicited by transthoracic endoscopic sympathicotomy (TES). www.ncbi.nlm.nih.gov/pubmed/18540897

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.c...ontent/n823388l26q330m3/

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

After severing the sympathetic trunk, the cells of its origin undergo complete disintegration within a year. After severing the cervical sympathetic trunk, the cells of the cervical sympathetic ganglion undergo transneuronic degeneration. The spinal cord. Changes found in the segment Th1 – Th4 in sheep III and IV closely resembled those seen in the stellate ganglion (Figures 6, 7). Changes in sheep I and II were the same as described in the previous paper (5). The nervus caroticus internus. In all the sheep a myelinated fasciculus was found in this nerve (Figure 8), which proves that the nervus caroticus internus contains a fasciculus of fibres which run from the front to the rear in the anterior sympathetic trunk (5). www.date.hu/acta-agraria/2002-08i/welento.pdf

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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

acute response to surgical denervation and abrupt release of sympathetic tone

Intraoperative predictability of successful outcome depends on monitoring of the acute response to surgical denervation and abrupt release of sympathetic tone.

Information on the long-term physiological sequelae is emerging rapidly. Preoperatively, in addition to abnormal sudomotor control, sympathetic cardiovascular regulation may be affected mildly in severe cases of hyperhidrosis. A blunted reflex bradycardia response to parasympathomimetic maneuvers such as Valsalva maneuver or cold water face immersion, as well as an increased heart rate response
to orthostatic stress, suggests a hyperfunctioning sympathetic discharge that is reversed after ETS.25,69 Because sympathetic cardiac accelerator fibers exit the spinal cord from segments T1 to T4, ETS is believed to simulate a mild physiological !-adrenergic blockade.70 This is because the heart rate at rest and during maximal exercise is lower 6 weeks postoperatively

DIAGNOSIS AND TREATMENT OF HYPERHIDROSIS,  CONCISE REVIEW FOR CLINICIANS
Mayo Clin Proc.     •     May 2005;80(5):657-666 

This injures all the neurons at this level of the spinal cord, some of which may die, and may predispose the patient to spinal cord reorganization and severe compensatory hyperhidrosis

Sympathectomy vs sympathotomy. Sympathectomy, with use of ganglionectomy and by definition, must sever the primary axon from the neuron in the intermediolateral cell column of the spinal cord (red) before primary or collateral synapse in the T2 ganglion. This injures all the neurons at this level of the spinal cord, some of which may die, and may predispose the patient to spinal cord reorganization and severe compensatory hyperhidrosis. Sympathotomy interrupts only axons after potential T2 ganglion synapses, a less injurious effect on the neuron, and is the least destructive procedure possible with successful treatment
of palmar hyperhidrosis.
Mayo Clin Proc 2003;78:167-172.   http://www.mayoclinic.org/medicalprofs/enlargeimage5096.html

Sympathectomy alters bone architecture

These data indicate that guanethidine-induced sympathectomy caused a negative balance of bone metabolism, leading to decreased mass by regulating deposition rather than resorption during modeling and remodeling of bone.
http://www.ncbi.nlm.nih.gov/pubmed/18449939

reduction in hypothalamic dopamine after sympathectomy, which leads to an increase in serum prolactin level

At this point, it is particularly interesting to recall the earlier reports of middle ear bone remodeling in the gerbil after chemical sympathectomy by guanethidine sulfate (86) or hydroxydopamine (85). Although these neurotoxins do eliminate sympathetic activity, there are, in parallel, major central consequences. In particular, both treatments reduce hypothalamic dopamine, which leads to an increase in serum prolactin levels.
http://ajpendo.physiology.org/content/293/5/E1224.full

"Again, patients admitted with any malignancy, cholecystectomy, thyroidectomy, renal disease, cardiac disease, sympathectomy, or vascular graft were eliminated as controls."
This article reviews the evidence that neuroleptics may increase the risk of breast cancer via their effects on prolactin secretion.
Paul M. Schyve; Francine Smithline; Herbert Y. Meltzer
Neuroleptic-induced Prolactin Level Elevation and Breast Cancer: An Emerging Clinical Issue
Arch Gen Psychiatry, Nov 1978; 35: 1291 - 1301.

Body temperature is highly correlated with plasma prolactin in thermally stressed men
(78), suggesting that normal heat defense is associated with decreased central dopamine, and
intraventricular haloperidol produces a coordinated heat-defense response (79). These reports refute a
unique or essential role for central dopamine antagonism in neuroleptic malignant syndrome hyperthermia
and provide additional evidence that state-dependent factors are important mediators of dopamine
antagonist effects.
There is substantial evidence to support the hypothesis that dysregulated sympathetic nervous system hyperactivity is responsible for most, if not all, features of neuroleptic malignant syndrome. A predisposition to more extreme sympathetic nervous system activation and/or dysfunction in response to emotional or psychological stress may constitute a trait vulnerability for neuroleptic malignant syndrome, which, when coupled with state variables such as acute psychic distress or dopamine receptor antagonism, produces the clinical syndrome of neuroleptic malignant syndrome. This hypothesis provides a more comprehensive explanation for existing clinical data than do the current alternatives.

http://ajp.psychiatryonli...i/content/full/156/2/169

dural blood flow decreased significantly in the cervical sympathectomy group

Migraine may affect the autonomic nervous system, but the mechanisms remain unclear. The sympathetic and parasympathetic nervous systems may play different roles in the attack. To explore the effect of blocking the cervical sympathetic nerve on vasodilation of the meningeal vessels, jugular vein calcitonin gene-related peptide (CGRP) and meningeal blood flow changes were measured before and after transection of the cervical sympathetic nerve by electrically stimulating the trigeminal ganglion in Sprague–Dawley (SD) rats. We found that CGRP level and meningeal blood flow increased in both the sham-operated and sympathectomized groups (p<0.05). Compared with the sham-operated group, dural blood flow decreased significantly in the cervical sympathectomy group, but CGRP level was not significantly different between these two groups. The cervical sympathetic nerve may play an important role in the process of neurogenic dural vasodilation in rats; this effect is not entirely dependent on CGRP level.
http://www.autonomicneuroscience.com/article/S1566-0702%2811%2900026-9/abstract

Surgical and chemical sympathectomy can alter cellular proliferation

Surgical denervation and chemical sympathectomy can alter cellular proliferation, B- and T-cell responsiveness and lymphocyte migration in lymphoid organs [17]. In vitro studies have shown that neuropeptides can have numerous effects, either inhibiting or stimulating the proliferation, differentiation
and functions of immune cells [19]*
Development of systemic lupus erythematosus in mice is associated with alteration of neuropeptide concentrations in inflamed kidneys and immunoregulatory organs
Neuroscience Letters 248 (1998) 97– 100

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

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

Spinal myoclonus following a peripheral nerve injury: a case report
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2526081/

Skin denervation in vasculitic neuropathy

Epidermal nerve fiber densities were significantly reduced in the skin of all patients, consistent with concomitant small-fiber neuropathies.
http://www.ncbi.nlm.nih.gov/pubmed/16216940

endoscopic sympathicotomy in carotid and vertebral arteries in the surgical treatment of primary hyperhidrosis

Analyze, in patients with primary hyperhidrosis (PH) who was undergone to videothoracoscopic sympathicotomy, the degree of vascular denervation after surgical transection of the thoracic sympathetic chain by measuring ultrasonografic parameters in carotid and vertebral arteries.

METHODS:

Twenty-four patients with PH underwent forty-eight endoscopic thoracic sympathicotomy and were evaluated by duplex eco-Doppler measuring systolic peak velocity (SPV), diastolic peak velocity (DPV), pulsatility index (PI) and resistivity index (RI) in bilateral common, internal and external carotids, besides bilateral vertebral arteries. The exams were performed before operations and a month later. Wilcoxon test was used to analyse the differences between the variables before and after the sympatholisis.

RESULTS:

T3 sympathicotomy segment was the most frequent transection done (95.83%), as only ablation (25%) or in association with T4 (62.50%) or with T2 (8.33%). It was observed increase in RI and PI of the common carotid artery (p < 0.05). The DPV of internal carotid artery decreased in both sides (p < 0.05). The SPV and the DPV of the right and left vertebral arteries also increased (p < 0.05). Asymmetric findings were observed so that, arteries of the right side were the most frequently affected.

CONCLUSIONS:

Hemodynamic changes in vertebral and carotid arteries were observed after sympathicotomy for PH. SPV was the most often altered parameter, mostly in the right side arteries, meaning significant asymmetric changes in carotid and vertebral vessels. Therefore, the research findings deserve further investigations to observe if they have clinical inferences.

http://www.ncbi.nlm.nih.gov/pubmed/16186983

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

Compensatory hyperhidrosis is excessive sweating of the abdomen, chest, back, thighs, and face,[6,72] usually in response to increased temperature.[46] This is the most common complication following ETS, reported to occur at an average rate of about 60%, with a range of 3% to 98%.[46] Higher rates have been reported from countries with warmer climates, such as in Asia and the Middle East.[46,82] The sweating can be severe for 10% to 40% of patients.[10] Although it has been written that compensatory sweating diminishes with time, several series have documented continued symptoms with longer-term follow-up.[46] In one series of 270 patients followed for a mean of 15 years postsympathectomy, 67% still complained of compensatory sweating, and overall satisfaction fell from an initial level of 96% to 67%.[55] It is possible that patients begin to notice compensatory sweating some time after ETS, as they are initially more aware of the marked reduction of their primary hyperhidrosis.[46] The mechanism for compensatory sweating is unclear; the most likely explanation is that sweating in the trunk increases to compensate for the lack of sweating from the denervated areas in order to maintain thermoregulation.[82] The occurrence of decreased sweating in other areas not innervated by the ganglia treated by ETS suggests that the response to ETS is more complex. The soles are the most common area with decreased sweating post-ETS, and, along with the axillae and palms, sweating from these areas could be under cortical control, separate from the hypothalamic centers involved in thermoregulation.[72] It has also been proposed that ganglion destruction affects axons of neurons in the interomediolateral spinal cord, which could lead to cell death or re-organization, changing the control of the sympathetic system by the spinal cord and higher, leading to increased sympathetic tone in the other body areas not treated by ETS.[10]  http://www.sweathelp.org/English/HCP_Treatment_ETS_Surgery_Complications.asp?printfriendly=true

Sympathectomy - a surgically induced neuropathy

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

http://en.wikipedia.org/wiki/Diabetic_neuropathy

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

oedema associated with the interruption of preganglionic sympathetic tract

Swelling and oedema is often observed in patients with Raynaud's disease or causalgia after acute interruption of post-ganglionic sympathetic fibres such as a wide-spread sympathectomy. Complete sympathetic 

block dilates vein and capillary and increases peripheral pooling, which raises hydrostatic the shins and feet (fig 2), constipation and 

abdominal distention, and dysuria were observed. Oedema was not noted in the 

hands or face. 

 There were no signs or abnormal laboratory data suggesting heart failure, renal failure, liver dysfunction, thyroid dysfunction or local inflammation. Venography of the left leg did not show obstruction in the deep veins. 

 We showed that the preganglionic sympathetic tract in the spinal cord was often 

disturbed in patients with multiple sclerosis with myelopathy.' Most patients with com- 

plete transection of the spinal cord due to injury showed swelling of the lower limbs or 

oedema, but they gradually subsided within several months even without restoration of 

somatic function. Probably some compensatory mechanism improves the hydrostatic 

condition in the chronic stage and explains why oedema is not noted in patients with 

chronic autonomic failure syndrome.

http://www.ncbi.nlm.nih.g...f/jnnpsyc00488-0062b.pdf