ROLE OF ASERNIP-s: monitoring

New surgical procedures should be monitored after their introduction. The
approval process should decide the type of monitoring to be undertaken.
• As a minimum, audits of indications and outcomes should be done.
• Access to reliable surgical data (local and global), organised in such a
way that performance comparisons can be made.
• It is highly desirable to coordinate and standardise any study designs,
e.g. outcomes measured in the same way for case series and audits
across hospital services or as done in previous studies.
If an audit or controlled clinical study is being contemplated, consider
whether this can be done as part of a multi-centre study.
• Develop/amend internal processes for the reporting of any adverse
events from new procedures and consider external processes e.g. as
part of multicentre audits or advising the Therapeutic Goods Authority
or the New Zealand New Technology Committee re problems with
devices.

MSAC & RACS

THE Australian Story - ASERNIP-s ROLE

2.1 PriorEvaluation
Most techniques new to Australia and New Zealand will have been evaluated
or at least implemented elsewhere in the world first. Issues that should be
considered include:
• Has the technique been previously evaluated?
Hospitals/health services should establish whether an assessment has
already been done through international or national systematic review
or Health Technology Assessment (e.g. INAHTA– International
Network of Agencies for health technology assessment, ASERNIP-S –
Australian Safety and Efficacy Register of New Interventional
Procedures - Surgical, Cochrane Collaboration, MSAC – Medical
Services Advisory Committee), clinical studies, industry reports,
laboratory testing or animal studies, reports of case series overseas,
reports of experiences of the techniques in Australian and New
Zealand facilities (see Appendix 1 for a list of relevant organisations
and their web-sites).
• How reliable is the evaluation?
Interpretation of assessments should include the likely robustness of
the evidence e.g. type of study design, were studies large enough to
show reliable results for morbidity and mortality; were there possible
confounding factors, such as the age of patients?

THE Australian Story - MSAC version

The Medicare Benefits Schedule (MBS) has evolved over time in response to changes in medical practice. Medicare benefits are payable in respect of a medical service listed in the MBS where that service is:

• provided by a medical practitioner, and
• a clinically relevant service (generally accepted in the medical profession as being necessary for the appropriate treatment of the patient).

Medicare item 35003 relates to the performance of cervical or upper thoracic sympathectomy by any surgical approach (irrespective of whether it is conducted by open exposure or endoscopically). Sympathectomy has been listed on the MBS for over three decades, and permitted by any surgical approach since 1991.

The Medical Services Advisory Committee (MSAC) was established in 1998 to advise the Minister for Health and Ageing on the strength of evidence pertaining to new and emerging medical technologies and procedures in relation to their safety, effectiveness and cost-effectiveness and under what circumstances public funding should be supported. MSAC has never considered this procedure, as it was listed on the MBS prior to MSAC's formation, and is therefore not a 'new and emerging medical technology'.

The Government relies on the advice of the medical profession in relation to the clinical relevance of procedures already listed on the MBS. If the Royal Australasian College of Surgeons were to formally advise the Government that it no longer regards this procedure as being clinically relevant, the Government would take appropriate action in relation to the MBS.

Mia: Surgeons performing the surgery ARE Fellows of the Royal Australasian College.

Unstable blood pressure after sympathectomy

Risks

Side effects of sympathectomy may include decreased blood pressure while standing, which may cause fainting spells. After sympathectomy in men, semen is sometimes ejaculated into the bladder, which may impair fertility. After a sympathectomy done by inserting an endoscope in the chest cavity, patients may experience chest pain with deep breathing. This problem usually disappears within two weeks. They may also experience pneumothorax (air in the chest cavity).

http://www.healthatoz.com/healthatoz/Atoz/common/standard/transform.jsp?requestURI=/healthatoz/Atoz/ency/sympathectomy.jsp

Sympathectomy suppresses baroreflex control of heart rate

Endoscopic thoracic sympathectomy suppressed the baroreflex control of heart rate during pressor and depressor tests in patients with palmar or axillary hyperhidrosis.

Endoscopic Thoracic Sympathectomy Suppresses Baroreflex Control of Heart Rate in Patients with Essential Hyperhidrosis

Yurie T. Kawamata, MD^*, Tomoyuki Kawamata, MD, Keiichi Omote, MD, Eiji Homma, MD^*, Tatsuo Hanzawa, MD^*, Toshifumi Kaneko, MD, and Akiyoshi Namiki, MD
2004 International Anesthesia Research Society

Australian Story 3!

from: http://ets-sideeffects.net/index.html
TIMBO McCarty, an Australian/New Zealander who has been suffering from the side-effects of ETS for eight years and has been working on this website alongside me as well as helping organise meetings, had enough of the side-effects and committed suicide on October 29 at the age of 45. His Father and Mother asked me to put this on the website and to let everyone know that he had had enough. Timbo was always there for me as a friend to talk when I felt everything was getting to me. Timbo was also was a fighter. He wanted ETS surgery to be stopped and was depressed that the surgery is still being performed routinely. He was aghast that his surgeon, Dr Lin in Taiwan, who performed ESB (clamping of the T2 nerve), removed his clamps at a fee yet still performed reversals routinely even though so many people have come forward with complaints.....
This is the second suicide in two years from people who have had terrible side-effects.

Support groups for people who had sympathectomy and ended up with disabling side-effects

World Against Sympathectomy	http://www.truthaboutets.com/
The Sympathetic Association	http://home.swipnet.se/sympatiska/index3.htm
Patients Against Sympathetic Surgery	http://www.ets-sideeffects.netfirms.com/
Radisson Group	http://www.noetsuk.com/
Family of Compensatory Sweating Sufferers	http://home.pchome.com.tw/family/vivi12175/
ETS Side Effects	http://www.geocities.jp/etscontroversialop/index.html
Hyperhidrosis Forum	http://www.terra.es/personal8/hiperhidrosis/principal.htm

Sympathectomy is prohibited for patients under 20 years in Taiwan. Why?

Endoscopic thoracic sympathectomy is prohibited for patients under 20 years old in Taiwan 10 January 2005
Min-Huei Hsu Department of Neurourgery, Taipei City Hospital, Zhongxiao Branch Send letter to journal: Re: Endoscopic thoracic sympathectomy is prohibited for patients under 20 years old in Taiwan Email Min-Huei Hsu	Endoscopic thoracic sympathectomy (ETS) has come into widespread use for palmar hyperhidrosis. Side sffects after ETS was widely discussed in Taiwan society in the past few months. Lots of people in Taiwan suffer from hyperhidrosis palmaris. ETS is covered by the National Health Insurance, and patient billing for this operation does not exceed US$ 60. This is why this operation is so popular here 1 . Patients with severe compensatory sweating after ETS must change clothes several times a day (some patients complained that they change as often as 10 times a day), resulting in serious impact on work and social interaction. Patients suffering from such serious side effects in Taiwan have formed a support group based on an Internet discussion forum to request the government to take this problem seriously. Starting in October 2004, The Department of Health, Executive Yuan, Taiwan, has prohibited surgeons from performing this operation on patients under 20 years old. To our knowledge, this type of support group also exists in United States, England, Sweden, Spain and Japan (Table 1). ETS is a relatively safe and simple procedure. However the side effects are possibly devastating 2 . All physicians providing this service and all peoples preparing to undergo this treatment should know this well.

calcium accumulation following sympathectomy

Developmental status of sympathetic innervation in relation to calcium accumulation by submandibular gland following reserpine, surgical sympathectomy or cyclocytidine

CA Schneyer and JH Yu
Proceedings of the Society for Experimental Biology and Medicine, Vol 179, 143-146, Copyright © 1985 by Society for Experimental Biology and Medicine

number of hemorrhages in the denervated half of the brain...

Sh. S. Tashaev

Received: 17 March 1980

---

Adaptive function of the sympathetic innervation of the cerebral vessels during rapid changes in systemic arterial pressure


The number of hemorrhages in the denervated half of the brain, which was twice that. in the intact half, is evidence that the sympathetic innervation of the ...
www.springerlink.com/index/T8J46575171L3G34.pdf - Similar pages - Note this
Without Abstract

Key Words adaptation - hemorrhage - hypotension - hypertension - reinfusion

Laboratory of Physiology of the Cerebral Circulation, Professor A. L. Polenov Leningrad Neurosurgical Research Institute. (Presented by Academician of the Academy of Medical Sciences of the USSR V. N. Chernigovskii.) Translated from Byulleten'' Éksperimental''noi Biologii i Meditsiny, Vol. 90, No. 11, pp. 543–546, November, 1980.

sympathetic innervation, adrenergic receptors, and a possible local catecholamine production in the development of patellar tendinopathy (tendinosis)

Studies on the importance of sympathetic innervation, adrenergic receptors, and a possible local catecholamine production in the development of patellar tendinopathy (tendinosis) in man

Patrik Danielson 1 *, Håkan Alfredson 2, Sture Forsgren 1

1Department of Integrative Medical Biology, Section for Anatomy, Umeå University, Umeå, Sweden 2Department of Surgical and Perioperative Science, Sports Medicine, Umeå University, Umeå, Sweden

email: Patrik Danielson (patrik.danielson@anatomy.umu.se)

^*Correspondence to Patrik Danielson, Department of Integrative Medical Biology, Section for Anatomy, Umeå University, SE-901 87 Umeå, Sweden

Funded by:
Faculty of Medicine at Umeå University
The Swedish National Centre for Research in Sports
The County Council of Västerbotten
The Arnerska Research Foundation

Keywords

tyrosine hydroxylase • (alpha)-1 • (alpha)-2A • (beta)-1 • adrenoreceptors • tenocytes

Abstract

Changes in the patterns of production and in the effects of signal substances may be involved in the development of tendinosis, a chronic condition of pain in human tendons. There is no previous information concerning the patterns of sympathetic innervation in the human patellar tendon. In this study, biopsies of normal and tendinosis patellar tendons were investigated with immunohistochemical methods, including the use of antibodies against tyrosine hydroxylase (TH) and neuropeptide Y, and against 1-, 2A-, and 1-adrenoreceptors. It was noticed that most of the sympathetic innervation was detected in the walls of the blood vessels entering the tendon through the paratendinous tissue, and that the tendon tissue proper of the normal and tendinosis tendons was very scarcely innervated. Immunoreactions for adrenergic receptors were noticed in nerve fascicles containing both sensory and sympathetic nerve fibers. High levels of these receptors were also detected in the blood vessel walls; 1-adrenoreceptor immunoreactions being clearly more pronounced in the tendinosis tendons than in the tendons of controls. Interestingly, immunoreactions for adrenergic receptors and TH were noted for the tendon cells (tenocytes), especially in tendinosis tendons. The findings give a morphological correlate for the occurrence of sympathetically mediated effects in the patellar tendon and autocrine/paracrine catecholamine mechanisms for the tenocytes, particularly, in tendinosis. The observation of adrenergic receptors on tenocytes is interesting, as stimulation of these receptors can lead to cell proliferation, degeneration, and apoptosis, events which are all known to occur in tendinosis. Furthermore, the results imply that a possible source of catecholamine production might be the tenocytes themselves. Microsc. Res. Tech., 2007. © 2007 Wiley-Liss, Inc.

---

Received: 4 July 2006; Accepted: 26 October 2006

If you are wondering why did you gain weight since your sympathectomy....

: Am J Physiol Regul Integr Comp Physiol. 2004 Jun;286(6):R1167-75.

Sympathetic innervation of white adipose tissue and its regulation of fat cell number.

Bowers RR, Festuccia WT, Song CK, Shi H, Migliorini RH, Bartness TJ.

Molecular and Cellular Biology and Pathobiology Program, Medical University of South Carolina, Charleston, South Carolina 29425, USA.

White adipose tissue (WAT) is innervated by the sympathetic nervous system (SNS), and the central origins of this innervation have been demonstrated for inguinal and epididymal WAT (iWAT and eWAT, respectively) using a viral transneuronal tract tracer, the pseudorabies virus (PRV). Although the more established role of this sympathetic innervation of WAT is as a major stimulator of lipid mobilization, this innervation also inhibits WAT fat cell number (FCN); thus, local denervation of WAT leads to marked increases in WAT mass and FCN. The purpose of this study was to extend our understanding of the SNS regulation of FCN using neuroanatomical and functional analyses. Therefore, we injected PRV into retroperitoneal WAT (rWAT) to compare the SNS outflow to this pad from what already is known for iWAT and eWAT. In addition, we tested the ability of local unilateral denervation of rWAT or iWAT to promote increases in WAT mass and FCN vs. their contralateral neurally intact counterparts. Although the overall pattern of innervation was more similar than different for rWAT vs. iWAT or eWAT, its SNS outflow appeared to involve more neurons in the suprachiasmatic and solitary tract nuclei. Denervation produced significant increases in WAT mass and FCN for both iWAT and rWAT, but FCN was increased significantly more in iWAT than in rWAT. These data suggest differences in origins of the sympathetic outflow to WAT and functional differences in the WAT SNS innervation that could contribute to the differential propensity for fat cell proliferation across WAT depots in vivo.

The nervous system and adipose tissue

THE NERVOUS SYSTEM AND ADIPOSE TISSUE
Katharine Dalziel, MD, MBBS, MRCP
1989

...whereas sympathectomy abolishes the
vasoconstrictor reaction, indicating that it is mediated by a local sympathetic axon
reflex.

Extraneous agents, such as large doses of alcohol and morphine, cause increased
lipolysis. This action can be blocked by chemical sympathectomy and is believed to be
due to stimulation of the sympathetic system within the central nervous system.9
Thus the control of metabolism in white fat is complex and dependent on many factors,
both within the adipocytes themselves and in the organism as a whole.

Total chemical sympathectomy in experimental
animals results in loss of shivering and nonshivering thermogenesis, and death within a
few hours.9

Since the effects of sympathectomy on the denervated
area are profound with increased blood flow and warmth and decreased sweating, it is
possible that pain relief is secondary to these phenomena without requiring any sort of
aberrant neural conduction.


This has occurred after stellate ganglion
block37 and lumbar sympathectomy.38 McCallurn and Glynn37 propose that increased
activity in the sympathetic nerves as the effects of the anesthetic block lessen cause
pain, particularly in circumstances where there was abnormal sympathetic activity
before the procedure (such as sympathetic dystrophy). This type of pain is often
resistant to opioid analgesics but may respond well to transcutaneous nerve stimulation.

A similar reduction of fat
mobilization from fat depots occurs after VMH lesions, as after local sympathectomy,
suggesting that the sympathetic pathway to the adipose tissue runs through the VMH.71
These hypothalamic control areas are themselves sensitive to feedback mechanisms.

Lactation and sympathectomy

Cannon and Bright (1) concluded that the autonomic nervous system was
essential to lactation, from their work with a sympathectomized dog. They
describe the effect as a belated one which caused the mother to be indifferent
to her young and the gathering of a viscous, creamy material in the glands.

FACTORS INVOLVED IN THE EJECTION OF MILK*
FORDYCE ELY
Kent~wky Agricultural Experiment Station
AND
W. E. PETERSEN
Minnesota Agricultilral Experiment Station

effect on lactation

A BELATED EFFECT OF SYMPATHECTOMY ON LACTATION
Cannon and Bright Am J Physiol.1931; 97: 319-321

Sympathectomy side effects on the Fox News...

http://www.livevideo.com/video/DA86D572A6634B558B52B5B5AF79DE42/ets-fox-news-sympathectomy-sid.aspx

Australian Story2 (rant)

quote from the ets forum:
"I do realise there are sweat tests conducted after a reversal but my point is that doctors do not do these tests on ETS patients. Therefore how can they generalise and say that after ETS CS will be mild or severe?? They do not do follow ups on ETS patients and if a patient complains of heavy CS the doctor may see it as mild and normal CS for statistical purposes."

http://etsandreversals.yuku.com/topic/3016/t/Eastern-Surgical-Australia.html

My question is: did anybody ever made an attempt at quantifying the scale of the 'compensatory sweating" after the surgery? Is there an attempt made to measure the amount of sweating before and after the surgery? Surely not, it would provide the proof that Sympathectomy causes profound sweating. What else could be the reason for not measuring this very significant side-effect? And then, - based on what!!!? - are the surgeons making the sweeping statements about the % of the people and the severity or scale of sweating after the surgery? Or about patient satisfaction rates??? How are these figures made up? Surely nobody bothered to ask any questions from me...

Why are the surgeons not accountable by providing statistical information on the side-effects after the surgery??? Don't they want to know how effective their surgery is? If it is safe ?! Reliable? Does more good then harm???
My surgeon did not schedule a follow up consultation. If I would have not called him (which I almost didn't), he would have never been told about the side-effects I have experienced. Did he file a report on my condition/case? Of course not. It would harm the statistics. (What statistics?!)

Slowly the surgeons admit to more and more side-effects

Go to Dr Reisfeld's web site to read his new comments about ETS: www.sweaty-palms.com/blushing.html

"Another clinical observation which will need more time for verification is the thought that the higher failure rate of sympathectomy when ETS is done only for facial blushing has to do with the fact that when the sympathectomies were done in the past for vascular problems the success rate was very minimal. At this time we know that higher failure rate was due to a clinical situation which we call denervation hypersensitivity. In essense the blood vessels become very sensitive to certain circulating hormones within the blood system. Dr. Reisfeld believes that the same phenomenon happens in this facial blushing presentation. More time and more clinical experience is needed before there can be a more definite conclusion."

Hopefully this may assist court cases but it sounds like Reisfeld is trying to cover his legal liability in his "at the time we thought..." comments.

Also see how the Australian site www.easternsurgical.com.au (click on blushing) have now admitted "some failures" and had to remove their biased comments about 500 consecutive successes.

Unfortunately the more people who have ETS side effects, the more the statistics become 'significant' to such doctors.

Madonna

Australian Story1

ETS studies are not done in the Australian climate and resulting CS means ETS should never have been allowed here without a review. One conducted by Monash University concluded not enough evidence on ETS is available and that existing ETS studies are flawed.These boards are accountable.
.....Madonna Aussie

Norepinephrine Turnover - increase in plasma NE=increase in brain NE

Norepinephrine Turnover Is Increased in Suprabulbar Subcortical Brain Regions and Is Related to Whole-Body Sympathetic Activity in Human Heart Failure

Anuradha Aggarwal, MBBS; Murray D. Esler, MBBS, PhD; Gavin W. Lambert, PhD; Jacqueline Hastings, PhD; Leonie Johnston, RN; David M. Kaye, MBBS, PhD

From the Baker Medical Research Institute, Melbourne, Australia.

© 2002 American Heart Association, Inc.

This study, for the first time, demonstrates elevated suprabulbar subcortical noradrenergic activity in human CHF and identifies a positive correlation between this and the level of whole-body NE spillover. The findings suggest that the activation of noradrenergic neurons projecting rostrally from the brain stem mediates sympathetic nervous stimulation in CHF.

cerebrovascular CO2 reactivity

Acta Physiol Scand. 1977 Sep;101(1):122-5.Links

Effects of intraventricular 6-hydroxydopamine on cerebrovascular CO2 reactivity in anesthetized rats.

Edvinsson L, Hardebo JE, MacKenzie ET.

Regional cerebral blood flow was measured by the 14C-ethanol technique in anesthetized rats before and after intraventricular injection of 6-hydroxydopamine. This treatment reduced the fluorescence of the central noradrenaline and dopamine nerve terminals, as well as of the perivascular nerve terminals in cerebral vessels. The administration of 6-hydroxydopamine had no significant effect on cerebral blood flow at normocapnia. The cerebrovascular reactivity to hypercapnia was significantly increased in the 6-hydroxydopamine treated animals. The results indicate an involvement of central catecholamine pathways in the cerebrovascular reactivity to hypercapnia.

PMID: 906856 [PubMed - indexed for MEDLINE]

catecholamine neuron in cerebral circulation

J Neurosurg. 1986 Sep;65(3):370-5

A role of the central catecholamine neuron in cerebral circulation.

Yokote H, Itakura T, Nakai K, Kamei I, Imai H, Komai N.

The effect of the central catecholaminergic neurons on the cerebral microcirculation was investigated by means of a unilateral intracerebral injection of 6-hydroxydopamine (6-OHDA) which produced the degeneration of catecholamine (CA) nerve terminals. Subsequent observation with CA histofluorescence revealed an absence of CA fibers in the vicinity of the 6-OHDA injection site. A significant increase in regional cerebral blood flow (rCBF), measured by the hydrogen clearance method, was demonstrated in the CA-depleted cortex under normocapnia as compared with rCBF in the control cortex (CA-depleted cortex 47.0 +/- 2.8 ml/100 gm/min; control cortex 38.5 +/- 3.5 ml/100 gm/min; p less than 0.005). The increased rCBF in the cortex treated with 6-OHDA was suppressed by the iontophoretic replacement of noradrenaline (NA) to the CA-depleted cortex. An iontophoretic replacement of 10(-5) M dopamine (DA) mildly suppressed the increased rCBF in the 6-OHDA-treated cortex. The CO2 reactivity in the CA-depleted cortex was significantly lower than that of the control cortex (CA-depleted cortex 2.13% +/- 0.6%/mm Hg; control cortex 3.53% +/- 0.70%/mm Hg). No change was noticeable in the cerebral glucose metabolism in the CA-depleted cortex in an investigation based on tritiated (3H)-deoxyglucose uptake. It is suggested that the 6-OHDA-induced change in cerebral blood flow (CBF) is not secondary to alterations in cerebral metabolic rate, and that the central NA neuron system innervating intraparenchymal blood vessels regulates CBF through a direct vasoconstrictive effect on the cerebral blood vessels. The central DA neuron system may modulate the cerebral circulation as a mild vasoconstrictor.

Why many patients who undergo SYMPATHECTOMY complain about stuffy nose/a cold for life...?!

AJP - Regulatory, Integrative and Comparative Physiology, Vol 253, Issue 3
494-R500, Copyright © 1987 by American Physiological Society

Articles by Haxhiu, M. A.
Articles by Cherniack, N. S.
A role for the ventral surface of the medulla
in regulation of nasal resistance
M. A. Haxhiu, K. P. Strohl, M. P. Norcia, E. van Lunteren,
E. C. Deal Jr and N. S. Cherniack
Nasal resistance is known to be affected by changes in nasal blood volume
and hence to depend on sympathetic discharge to nasal blood vessels.
Structures located superficially near the ventrolateral surface of the medulla
significantly affect respiratory and sympathetic activity and the tone of the
trachea. To assess the importance of these structures on nasal patency, we
measured transnasal pressure at a constant flow and examined the change in
pressure produced by topically applied N-methyl-D-aspartic acid (NMDA).
Experiments were performed in chloralose-anesthetized, paralyzed, and
artificially ventilated cats. NMDA administered on the intermediate area of
the ventral surface of the medulla decreased transnasal pressure and increased phrenic nerve activity. The response to
NMDA could be diminished or abolished by application to the ventral medullary surface of the NMDA antagonist
2-amino-5-phosphonovalerate (2-APV) or the local anesthetic lidocaine. Carotid sinus denervation and
posthypothalamic decerebration did not alter the nasal and phrenic nerve responses to NMDA; however, cervical
sympathetic denervation decreased these responses, both in intact and in bilaterally adrenalectomized animals. Therefore,
activation of NMDA receptors on structures near the ventral surface of the medulla increases tone in the nasal
vasculature and leads to a response pattern that includes changes in not only phrenic nerve activity and blood pressure
but also nasal patency.

Noradrenaline (NA) has been shown to influence astrocytic and vascular functions related to brain homeostasis

Journal of Cerebral Blood Flow & Metabolism (1997) 17, 894–904;
doi:10.1097/00004647-199708000-00008
Astroglial and Vascular Interactions of Noradrenaline Terminals
in the Rat Cerebral Cortex
Noradrenaline (NA) has been shown to influence astrocytic and vascular functions related
to brain homeostasis, metabolism, local blood flow, and blood-brain barrier permeability.
In the current study, we investigate the possible associations that exist between
NA-immunoreactive nerve terminals and astrocytes and intraparenchymal blood vessels
in the rat frontoparietal cortex, both at the light and electron microscopic levels. As a
second step, we sought to determine whether the NA innervation around intracortical
microvessels arises from peripheral or central structures by means of injections of
N-(2-chloroethyl-N-ethyl-2-bromobenzylamine) (DSP-4), a neurotoxin that specifically
destroys NA neurons from the locus ceruleus. At the light microscopic level, 6.8% of all
NA-immunoreactive nerve terminals in the frontoparietal cortex were associated with
vascular walls, and this perivascular noradrenergic input, together with that of the cerebral
cortex, almost completely disappeared after DSP-4 administration. When analyzed at the
ultrastructural level in control rats, NA terminals in the neuropil had a mean surface area
of 0.53 0.03 m2 and were rarely junctional (synaptic incidence close to 7%). Perivascular
terminals (located within a 3-m perimeter from the vessel basal lamina) counted at the
electron microscopic level represented 8.8% of the total NA terminals in the cortical tissue.
They were smaller (0.29 0.01 m2, P < 0.05) than their neuronal counterparts and were
located, on average, 1.34 0.08 m away from intracortical blood vessels, which consisted
mostly of capillaries (65%). None of the perivascular NA terminals engaged in junctional
contacts with surrounding neuronal or vascular elements. The primary targets of both
neuronal and perivascular NA nerve terminals consisted of dendrites, nerve terminals,
astrocytes, and axons, whereas in the immediate vicinity (0.25 m or less) of the
microvessels, astrocytic processes represented the major target. The results of the current
study show that penetrating arteries and intracortical microvessels receive a central NA
input, albeit parasynaptic in its interaction, originating from the locus ceruleus.
Particularly, they point to frequent appositions between both neuronal and perivascular
NA terminals and astroglial cells and their processes. Such NA neuronal-glial and
neuronal-glial-vascular associations could be of significance in the regulation of local
metabolic and vascular functions under normal and pathologic situations.

redistribution of cerebral bloodflow following sympathectomy!

SM Mueller, DD Heistad and ML Marcus

Effect of sympathetic denervation in dogs.
Total and regional cerebral blood flow during hypotension, hypertension, and hypocapnia.

The major new findings in this study are,
first, that hypotension produces a redistribution of CBF which tends to preserve blood flow to brainstem and to
cerebral gray matter...

1977 American Heart Association

the effect of sympathectomy on ventilation

Influence of cervical sympathetic nerves on ventilation and upper
airway resistance in the rat

K.D. O'Halloran*, A.K. Curran**, A. Bradford+

Influence of cervical sympathetic nerves on ventilation and upper airway resistance in the
rat. K.D. O'Halloran, A.K. Curran, A. Bradford. ©ERS Journals Ltd 1998.
ABSTRACT: The cervical sympathetic trunks innervate the carotid bodies, carotid
baroreceptors, thyroid gland and the upper airway mucosa, structures which can
influence breathing and upper airway resistance. (same in humans)
However, their role in the control of ventilation and upper airway patency
is poorly understood.
A constant airflow was applied to the upper airway through a high-cervical trache-
ostomy in anaesthetized rats breathing spontaneously through a low-cervical trache-
ostomy. The peripheral ends of the cut cervical sympathetic trunks were stimulated
electrically and airflow resistance and ventilation were measured. The effects of cervi-
cal sympathetic trunk section on ventilation were also measured in conscious rats.
In conscious rats, cutting the sympathetic trunks caused a decrease in ventilation
during normoxia but only slightly affected ventilatory responses to hypoxia and
hypercapnia. In anaesthetized rats, sympathetic trunk stimulation caused an inhibi-
tion of breathing which was sometimes followed by excitation. These responses were
unaffected by α- or β-adrenoceptor blockade but were abolished by cutting the
carotid sinus nerves. Sympathetic stimulation also caused a fall in upper airway
resistance which was reduced by bypassing the nose, unaffected by propranolol or
carotid sinus nerve section and abolished by phentolamine.
It was concluded that the cervical sympathetic nerves exert important influences
on ventilation and upper airway resistance.
Eur Respir J 1998; 12: 177–184.

75% PNEUMOTHORAX EXPECTED AFTER SYMPATHECTOMY

A small insignificant pneumothorax can be expected after ETS in about 75% of cases [15], which gets spontaneously absorbed, usually within 24 h.

Comparing T2 and T2–T3 ablation in thoracoscopic sympathectomy for palmar hyperhidrosis: a randomized control trial
A. N. Katara, J. P. Domino, W.-K. Cheah, J. B. So, C. Ning, D. Lomanto
Minimally Invasive Surgical Centre, Department of General Surgery, National University Hospital, 5 Lower Kent Ridge Road, Singapore, 119074
Received: 13 October 2006/Accepted: 2 November 2006
http://medicine.nus.edu.sg/medsur/research_publications_2007.html

Permanent side effects included compensatory sweating in 67.4%, gustatory sweating in 50.7% and Horner's trias in 2.5%. However, patient satisfaction declined over time, although only 1.5% recurred. This left only 66.7% satisfied, and a 26.7% partially satisfied. Compensatory and gustatory sweating were the most frequently stated reasons for dissatisfaction. Individuals operated for axillary hyperhidrosis without palmar involvement were significantly less satisfied (33.3% and 46.2%, respectively).
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1234291/

Orthostatic hypotension after surgery, high mortality

A splanchnic nerve lumbar sympathectomy was a surgical gamble used in about
10% of patients with advanced hypertension. Dramatic benefit was occasionally produced
at the cost of 0.5%–8.8% mortality, impotence and unpleasant orthostatic hypotension (3).


A view from the millennium: the
practice of cardiology circa 1950
and thereafter
Mark E. Silverman, MD, FACCa

Division of Cardiology, Department of Medicine,
Emory University School of Medicine and Chief of
Cardiology, Piedmont Hospital, Atlanta, Georgia,
USA
Manuscript received August 28, 1998; revised
manuscript received November 24, 1998, accepted
January 5, 1999.

Mortality in sympathectomised mice was significantly higher

Results: Mortality in sympathectomised mice was significantly
higher than that in sham operated mice following administration
of Jo-2. This result was also supported by apoptosis data in
which sympathectomised livers exhibited a significant elevation
in the number of apoptotic hepatocytes and caspase-3 activity
after Jo-2 treatment compared with sham operated livers.
Moreover, pretreatment with norepinephrine dose dependently
inhibited the hepatic sympathectomy induced increase in
mortality after Jo-2 injection. Antiapoptotic protein levels of
FLICE inhibitory protein, Bcl-xL, and Bcl-2 in the liver were
significantly lower in sympathectomised mice at one and two
hours following Jo-2 treatment than in sham operated animals.
In addition, interleukin 6 supplementation dose dependently
suppressed the hepatic sympathectomy induced increase in
mortality after Jo-2 treatment.
Conclusions: These results suggest that norepinephrine released
from the hepatic sympathetic nerve plays a critical role in
protecting the liver from Fas mediated fulminant hepatitis,
possibly via mechanisms including antiapoptotic proteins and
interleukin 6.

Chida, Y. and Sudo, N. and Takaki, A. and Kubo, C. (2005)
The hepatic sympathetic nerve plays a critical role in preventing
Fas induced liver injury in mice. Gut, 54 (7). pp. 994-1002.
ISSN 00175749

Cerebral ischemia may increase extracellular choline concentration by interfering with its removal by the circulation and by enhancing its net production from phospholipids.

Focal ischemia enhances choline output and decreases acetylcholine output from rat cerebral cortex

OU Scremin and DJ Jenden
Veterans Administration Medical Center, Albuquerque, New Mexico 87108.

Stroke, Vol 20, 92-95, Copyright © 1989 by American Heart Association

Mia: these changes are present in post-sympathectomy patients as well, providing further proof on cerebral ischemia (Brain MRI) that causes the cognitive function changes in many patients who undergo the surgery.

Sympathectomy complications

26.3% or one quarter of patients with compensatory hyperhidro-
sis considered the complication major and disabling. The average time between surgical sympathectomy
and the appearance of compensatory hyperhidrosis was 4 months (range 1-6 months). The inci-
dence of compensatory hyperhidrosis did not seem to be different after open or endoscopic approach.
Irrespective of approach, two or more levels of denervation and removal of the stellate ganglion produced
noticeably higher incidence. Finally, the incidence of this complication seemed to be 3 times higher when
the surgery was performed for primary hyperhidrosis than neuropathic pain.

The weighted mean incidence of gustatory sweating after upper extremity surgical sympathectomy was
32.3% (range 0-79) (information retrieved from 44 papers and 5,142 patients)
The phenomenon appeared on average 5 months
after surgery. The weighted means appeared substantially greater when the open approach was used, two
or more levels were denervated, the chain was electrocoagulated but left in situ and primary hyperhidrosis
was the indication for the intervention.

The weighted mean incidence of phantom sweating was 38.6 %

The weighted mean incidence of neuropathic pain complications was 11.9% .

Several issues regarding sympathectomy remain open, as the objectives of this review were limited and
specific. This review is geared exclusively around late complications and does not address efficacy or
effectiveness of the procedure. While the vast majority of patients were operated for palmar hyperhidrosis,
the procedure is obviously used for other indications, most importantly ischemia and neuropathic pain.
However, questions around satisfaction of patients with the procedure for a given indication or which
approach is the best for the same indication were not asked. Similarly, we are unable to answer questions
regarding completeness or permanency of the sympathetic denervation..

I S I S
SCIENTIFIC NEWSLETTER
Volume 4 Number 2
Summer Issue 2001

ARE WE PAYING A HIGH PRICE FOR SYMPATHECTOMY? 2

Nevertheless, immediate (perioperative and postoperative) complications (primarily for the open but also
the endoscopic approach) include: fever, hematoma, transient Horner’s syndrome, bleeding, pneumotho-
rax, infection, wound pain, lymphatic leak, chylothorax, arterial injury, brachial plexus injury, etc.17. Late
complications include: permanent Horner’s syndrome, neuralgic pains, unsightly wound appearance, com-
pensatory hyperhidrosis, gustatory sweating and phantom sweating, and in the case of bilateral lumbar
sympathectomy erectile dysfunction in the male and lack of clitoral tumescence in the female18.
I S I S
SCIENTIFIC NEWSLETTER
Volume 4 Number 2
Summer Issue 2001

ARE WE PAYING A HIGH PRICE FOR SYMPATHECTOMY?

ARE WE PAYING A HIGH PRICE FOR
SURGICAL SYMPATHECTOMY?
Andrea Furlana,c MD, Angela Mailisa,b MD, MSc, FRCPC (PhysMed) and
Marios Papagapioua MSc


Conclusions: Surgical sympathectomy irrespective of approach is accompanied by several potentially
disabling complications.

Surgical sympathectomy is performed in thousands of patients around the world primarily for the treatment
of bothersome palmar hyperhidrosis.1-7 Much less frequent indications are: neuropathic pain syndromes
(like Reflex Sympathetic Dystrophy and Causalgia)2;8;9 , ischaemic conditions including peripheral vascular
disease and Raynaud’s phenomena2 and rarely facial blushing10, Prinzmetal’s angina11, as well as migraine,
dysmenorrhea and pancreatitis2;12

I S I S
SCIENTIFIC NEWSLETTER
Volume 4 Number 2
Summer Issue 2001

Nerves regenerate after surgery and cause the abnormal sweating - among other symptoms

Regeneration after cervicothoracic sympathectomy producing gustatory responses.

Bloor K.

Angiology. 1966 Mar;17(3):143-7.Links

Treatment for Gustatory Sweating? Avoid food.

9 months later, within one minute of eating a sour apple, the patient developed severe sweating over the left half of the face and the left chest. The reaction was confirmed by infra-red thermography which proved that the skin temperature in the sweating region had fallen to 3 degrees C. The likely cause of localized gustatory sweating is intra-operative damage of the stellate ganglion or its preganglionic nerve connections. Treatment is limited to avoidance of the precipitating gustatory stimulus.
Dtsch Med Wochenschr. 1992 Oct 9;117(41):1556-60.

Plendl H, Paulus W, Witt TN.

Neurologische Klinik, Klinikum Grosshadern, Universität München.

injury=sympathectomy

Blackwell Synergy - Br J Dermatol, Volume 142 Issue 1 Page 194-195 ...

Pathological gustatory sweating and flushing can develop after injury to preganglionic cervicothoracic sympathetic fibres, an unavoidable consequence of ...
www.blackwell-synergy.com/doi/abs/10.1046/j.1365-2133.2000.03278.x -

Symptoms can appear years after the surgery!

Handbook of Clinical Neurology

by P. J. Vinken, G. W. Bruyn - 1968 - Neurology
Weeks, months, or years after cervicothoracic preganglionic sympathectomy,
gustatory sweating and flushing may develop on the denervated side along with impaired thermoregulatory sweating.
Limited preview - books.google.com/books?isbn=0444828133...

GS - Autonomic Disorder

Gustatory sweating is an autonomic disorder that fre-. quently occurs after parotid. gland. surgery.

Anhidrosis = Hyperthermia

	Semin Neurol 2003; 23: 399-406 DOI: 10.1055/s-2004-817724
Disorders of Sweating
William P. Cheshire1, Roy Freeman2
1Department of Neurology, Mayo Clinic, Jacksonville, Florida 2Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts

ABSTRACT

The clinical spectrum of sweating disorders includes sudomotor excess and deficiency. Hyperhidrosis is characterized by sweating beyond that required to maintain a constant internal body temperature. Hypohidrosis and anhidrosis are distinguished by a reduced or absent ability to generate sweat for the purpose of evaporative heat dissipation. Whereas hyperhidrosis is usually benign, anhidrosis may predispose to hyperthermia.

Gustatory Sweating - damage to the autonomic nervous system

Spectrum of gustatory sweating, with especial
reference to its presence in diabetics with
autonomic neuropathy
Michael M. Bronshvag,4



Certain otherwise normal individ-
uals may have an idiosyncratic response to
one or several foods, and the mechanism of
this sensitivity is not known . It may also be
seen after parotid surgery (auriculotemporal
syndrome) (4), cervical sympathectomy
(usually bilateral) (1) and in diabetic neu-
ropathy (2). The common denominator in
these conditions seems to be damage to the
autonomic nervous system.


Less easy to understand is the syndrome
after cervical sympathectomy (usually bilat-
eral) (1). As with the auniculotemporal syn-
drome, the onset occurs weeks to months
after the surgery and apparently does not
correlate with relapse of the surgical condi-
tion. Although anesthetic block or excision
of the stellate ganglion abolishes the gusta-
tory sweating response in “normal” pa-
tients, it does not have a similar effect in
postsympathectomy gustatory sweating.
Sweating is more profuse if there is no
ipsilateral Homer’s syndrome . The distni-
bution of sweating is the face and almost
always the arm, corresponding to the distni-
bution of innervation from the cervical sym-
pathetic ganglia. Although sensitivity to cm-
culating acetylcholine has been postulated
as the mechanism of production of sweating,
injection of cholinergic substances or acetyl-
choline does not reproduce the syndrome,
and ganglionic blocking agents can interrupt
the syndrome, suggesting that the response
is neural rather than humoral. It is now felt
that sprouting of cholinergic fibers into the
area of the surgical lesion is the cause.
Whether the sprouting axons arise from the
thoracic sympathetic ganglia and meander
past the surgical site, or whether they arise
from the vagus nerve is not established.
Diabetic patients with autonomic neurop-
athy may present with a similar syndrome
(2). The similarity of the syndrome in dia-
betes to that occurring in postsurgical pa-
tients makes it most reasonable to assume
that a lesion has occurred in the autonomic
nervous system with subsequent sprouting
between healthy cholinergic axons and dis-
eased ones. A careful study of diabetic
patients manifesting this phenomenon re-
vealed widespread deficits in the sympa-
thetic and parasympathetic nervous systems .


This suggests that
abnormal sprouting and unusual relation-
ships of unmyelinated fibers to Schwann
cells may be the anatomic bases for painful
diabetic neuropathy . In view of this histo-
logical evidence , it seems reasonable to sug-
gest that the mechanism for gustatory sweat-
ing in diabetic patients with autonomic neu-
ropathy is also axonal degeneration with
abnormal sprouting from continguous ax-
ons. Since in gustatory sweating it is pre-
sumed that the stimulus to the sweat glands
originates in the dorsal motor nucleus of
the medulla, and is diverted to sympathetic
cholinergic axons destined for the face and
perhaps the arm, it is likewise plausible that
adrenergic vasomotor impulses from the
cervical sympathetic chain cause the other
less constant parts of these syndromes such
as goose flesh, vasoconstniction, paraesthes-
ias and flushing.



TheAmericanJournalClinicalNutrition31:FEBRUARY 1978, pp. 307-309. Printed in U.S.A.

Disorders of sweating

PDF
GUSTATORY SWEATING AND OTHER RESPONSES AFTER CERVICO-THORACIC SYMPATHECTOMY
BLOOR Brain.1969; 92: 137-146

Sympathectomy = Autonomic peripheral neuropathy

DrRoy Freeman MBChB
^aCenter for Autonomic and Peripheral Nerve Disorders, Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA

Available online 5 April 2005.

Summary

The autonomic neuropathies are a group of disorders in which the small, lightly myelinated and unmyelinated autonomic nerve fibres are selectively targeted. Autonomic features, which involve the cardiovascular, gastrointestinal, urogenital, sudomotor, and pupillomotor systems, occur in varying combination in these disorders. Diabetes is the most common cause of autonomic neuropathy in more developed countries. Autonomic neuropathies can also occur as a result of amyloid deposition, after acute infection, as part of a paraneoplastic syndrome, and after exposure to neurotoxins including therapeutic drugs.

Mia: and it can occur as a result of surgical or chemical sympathectomy.

people have a decreased quality of life after this procedure

Treatment available to patients with primary hyperhidrosis

Treatment of primary excessive sweating is split into non-surgical and surgical options.

Non-surgical include topical antiperspirants, Iontophoresis, systemic medication and medical injections.

The only viable surgical option is liposuction of armpit tissue. Sympathectomy for hyperhidrosis is not considered as a reliable treatment and recent research has shown that many people have a decreased quality of life after this procedure.

http://www.skinrevision.net.au/blog/page/2/

Sympathectomy=Autonomic Neuropathy

Sympathectomy is a surgery that involves damage to the nerves involved in body temperature regulation, sweating, bloodpressure regulation, and the regulation of many bodily functions, in the maintenance of the body's homeostasis.

Autonomic neuropathy is associated with the following:

• Alcoholic neuropathy
• Diabetic neuropathy
• Parkinson's disease
• Disorders involving sclerosis of tissues
• Surgery or injury involving the nerves
• Use of anticholinergic medications

• Swollen abdomen
• Heat intolerance, induced by exercise
• Nausea after eating
• Vomiting of undigested food
• Early satiety (feeling full after only a few bites)
• Unintentional weight loss of more than 5% of body weight
• Male impotence
• Diarrhea
• Constipation
• Dizziness that occurs when standing up
• Blood pressure changes with position
• Urinary incontinence (overflow incontinence)
• Difficulty beginning to urinate
• Feeling of incomplete bladder emptying
• Fainting
• Abnormal sweating

http://medlineplus.nlm.nih.gov/medlineplus/ency/article/000776.htm

Journal of Clinical Endocrinology & Metabolism, Vol 72,
819-823, Copyright © 1991 by Endocrine Society


Sequential cerebrospinal fluid
and plasma sampling in
humans: 24-hour melatonin
measurements in normal
subjects and after peripheral
sympathectomy

J Bruce, L Tamarkin, C Riedel, S Markey and
E Oldfield
After bilateral T1-T2 ganglionectomy, however, melatonin levels were markedly reduced, and the diurnal rhythm was abolished.

Control of intraocular blood flow

Control of intraocular blood flow.
II. Effects of sympathetic tone
John J. Weiter, Ronald A. Schachar, and J. Terry Ernest
(animal study)

March 7, 1973


Cervical sympathectomy increased ocu-
lar blood flow more than 30 per cent
(Table I). The increase in blood flow was
approximately equal in both the uveal sub-
divisions and the retina. Sympathetic
stimulation decreased ocular blood flow.
The blood flow was decreased by 56 per
cent in the ciliary body, 45 per cent in the
choroid, and 41 per cent in the retina. The
results were similar when the control vs.
experimental eye was alternated.

Eliminates the input of central signals to the pineal gland

December 1, 1971 | vol. 68 | no. 12
Melatonin Metabolism: Neural
Regulation of Pineal Serotonin:
Acetyl Coenzyme A
N-acetyltransferase Activity
David C. Klein, Joan L. Weller, and
Robert Y. Moore

These data indicate that superior cervical
sympathectomy abolishes the N-acetyl-transferase
rhythm by elimination of the input of central signals
to the gland. These signals appear to regulate the
N-acetyltransferase rhythm in the normal rat by
regulation of the release of norepinephrine from the
sympathetic terminals within the pineal gland.

hormones

Cervical sympathectomy affects adrenocorticotropic
hormone and thyroid-stimulating hormone in rats.

Hiroshi Iwama1 , Mamoru Adachi1, Choichiro Tase1 and
Yoichi Akama1
(1) Department of Anesthesiology, Fukushima Medical College, 1
Hikarigaoka, 960-12 Fukushima, Japan
Received: 26 June 1995 Accepted: 1 March 1996

sympathectomy-induced bone resorption

A mechanism for sympathectomy-induced bone resorption in
the middle ear.
Author:Sherman, B E : Chole, R A
Citation:Otolaryngol-Head-Neck-Surg. 1995 Nov; 113(5): 569-81

Now I want to look at the correlative psychological modes of the sympathetic and parasympathetic activity. These are general qualities rather than fixed attributes.

Sympathectomy causes parasympathetic dominance. It will 'reset' your modus operandi. It will change you.

Sympathetic - Parasympathetic
Activity - Receptivity
Speed - Slowness
Tension - Relaxation
Focus - Scope
Convergent thinking - Divergent thinking
Extraversion - Introversion
Goal-oriented - Process-oriented
Agency - Presence
Direction - Elaboration

Doctors in Finland, US and Iran also offer sympathectomy to reduce anxiety, fear, stress, phobias, to reduce aggressiveness, reduce depression (sic!), reduce palpitations. The psychological changes following surgery are widely known among medical professionals, but patients are not told about them. They are told that this is a safe, minimally invasive procedure. Maybe the surgical cut they need is minimal, the procedure is certainly not minimally invasive. It will invade and violate the core of your being. It will change your body and your mind. Many people get depressed because they are not able to cope with this, like a friend who killed himself after 8 years of waiting and hoping that his condition will improve. He was 46.

"Lets just stop a minute to become aware of our own autonomic state: tongue, heart rate, peristalsis, skin – temp and moisture – warm & dry; cold&wet; relaxation/tension. Attentiveness – alert to broad awareness.."

seminar ‘The New Anatomy: Exploring the Mind in the Body’ run at Chiron February-March 2001.

It will be all altered. Sympathectomy produces a parasympathetic dominance.

AUTONOMIC NERVOUS SYSTEM

The Autonomic Nervous System:
Barometer of Emotional Intensity and Internal Conflict

A lecture given for Confer, 27th March, 2001
The material for this lecture is part of a six evening seminar ‘The New Anatomy: Exploring the Mind in the Body’ run at Chiron February-March 2001.

In standard physiology the two parts of the ANS have been perceived as functioning reciprocally: the sympathetic governing arousal, the fight or flight reaction and the parasympathetic involving relaxation, recuperation and digestion. The sympathetic nervous system is activated by any stimulus over an individual’s threshold (and the threshold can vary enormously), including feelings, and by noise, light, drugs and chemicals (e.g. caffeine).In response to the stimulus an immediate anticipatory state is generated by the release of adrenaline. This causes the heart to beat more quickly and strongly, increases blood supply to the muscles, raises blood pressure, dilates the bronchii and increases the breathing rate, raises the blood sugar level for increased energy, speeds up mental activity, increases tension in the muscles, dilates pupils and increases sweating. Non-emergency functions, such as digestion are lessened or suspended. (priming phase – short-term) Walter Cannon coined the phrase ‘fight or flight’ to describe the function of the rapid mobilisation of resources.

ANS and emotional intensity

The Autonomic Nervous System:
Barometer of Emotional Intensity and Internal Conflict

A lecture given for Confer, 27th March, 2001
The material for this lecture is part of a six evening seminar ‘The New Anatomy: Exploring the Mind in the Body’ run at Chiron February-March 2001.

The Autonomic Nervous System has two branches, the Sympathetic and the Parasympathetic, which regulate the involuntary processes of the body, the viscera, and sense organs, glands and blood vessels. In evolutionary terms it is older than the CNS and its anatomical circuitry is broadly dispersed, creating a general response, quite unlike the highly specific pathways and response of the CNS. This generalised, widely distributed structure enables it to mediate overall changes in state; it is part of the limbic system which has also been known as the mammalian or emotional brain.

...– we now know that it is dynamically related to many other parts of the brain especially the orbitofrontal cortex. Autonomic also means self-regulating and this is a key principle of all body systems, which depend of constant feedback in order to maintain homeostasis. There are multiple feedback loops in the body which continually send and receive information about what’s going on and the ANS is part of this wider complex.

The FINOHTA REPORT

"Endoscopic thoracic sympathectomy is associated with significant immediate and long-term adverse effects. This is alarming especially since the operation is performed to alleviate a relatively harmless condition. Many patients also suffer from compensatory hyperhidrosis after ETS. Due to wide variation in the reporting of adverse effects, it is
probable that these have been underreported most of the time. "

SYMPATHECTOMY ON THE FOX NEWS

http://www.livevideo.com/video/DA86D572A6634B558B52B5B5AF79DE42/ets-fox-news-sympathectomy-sid.aspx

SAMPLE OF THE SALES PITCH - THIS IS HOW IT'S DONE

Surgical sympathectomy is the gold standard of treatment for this disease, by which all other treatments must be judged. Upper thoracic sympathectomy has been performed for many years as therapy for hyperhydrosis and several other diseases. There are various surgical approaches available. Prior to the advent of endoscopic transthoracic sympathectomy (ETS), these approaches involved either painful back or neck incisions with possible risk of brachial plexus, or phrenic nerve injury, or Horners syndrome. The introduction of ETS for excessive hand and facial sweating has revolutionized the treatment of this disease. The success rate is in excess of 98%, with very few side effects or serious complications.
Endoscopic sympathectomy is a highly-effective treatment for patients with palmar or facial hyperhydrosis. ETS allows simultaneous treatment of both sides with a very low risk of complications. Attention to surgical detail is important to achieve excellent long-term results. We continue to lead the New York metropolitan area in minimally invasive thoracoscopic procedures, and especially ETS.

THE SYMPATHECTOMY FAILURE

1. Sympathectomy is analogous to the act of killing the messenger. The sympathetic nervous system has the critical job of properly controlling and preserving the circulation in different parts of the body, especially in the extremities. By paralyzing the system, the extremity will be more apt to have disturbance of circulation and is left unprotected from fluctuation in circulation.

Sympathectomy is similar to permanently removing the central heat and air-conditioning system and never replacing it because of malfunction.

Sympathectomy permanently damages the temperature regulatory system. The reason sympathectomy does not cause side effects other than ineffective control of pain as well as impotence and orthostatic hypotension is because it is invariably partial and incomplete.H. Hooshmand, M.D.: Chronic Pain

View Larger Image

9780849386671

Chronic Pain: Reflex Sympathetic Dystrophy Prevention and Management

Hooshang Hooshmand

ISBN 10: 0849386675 / 0-8493-8667-5 
ISBN 13: 9780849386671
Publisher: CRC Pr I Llc
Publication Date: 1993
Binding: Hardcover

Melbourne Surgeon's definition of a very safe procedure

"Thoracoscopic cervical sympathectomy is considered a very safe procedure, with very few problems other than the transient pain mentioned above. Nonetheless, you should know that there is a very small risk - not more than 1 chance in 2000 - that you may experience numbness or weakness in the hand from other nerve damage. A droopy eyelid and small pupil can also occur as a result of the procedure affecting the nerve supply to the eyelid (1%). Excessive sweating of the lower body will occur and this is known as compensatory sweating and can be quite marked. A stuffy nose may result and this change can be permanent requiring nasal spray for life. The face will feel dry after thoracoscopic cervical sympathectomy and this may be annoying. Failure to improve your condition or failure to remove the part of the nerve can occur and this is called a therapeutic failure and is therefore also a risk. Risk to life is < 0.01%."

Not being able to sweat and cool of through the head is more than annoying. 40% of the body heat is released through the top of the head. This will be eliminated. The will be no sweating from the head, neck and shoulders.
The the skin's natural cleaning mechanism, sweating will be eliminated. The skin will become dehydrated, clogged up and more prone to acne. Sympathectomy also lowers the denervated skin's immune responses, it will be more prone to infections. Sympathectomy alters the skin's healing process. People undergoing the opearation will have scar tissue after the operation and from future cutaneous trauma.
Sympathetic denervation impairs epidermal healing in cutaneous wounds
LINCOLN R. KIM, BSCaI KEITH WHELPDALE, MSCb; MA TEUSZ ZUROWSKI, MSCb; BRUCE POMERANZ, MD, PhD°, b

INTRAOCULAR PRESSURE AND DENERVATION

Br J Ophthalmol. 1983 May; 67(5): 297-301.

Ocular sympathetic denervation associated with ocular hypertension: a case report.

D J Brazier

The exact function of the sympathetic nervous system in the regulation of intraocular pressure remains unclear. Many observers have noted reduced intraocular pressure in eyes whose sympathetic supply has been interrupted. A case of ocular sympathetic denervation associated with ocular hypertension is reported. Reports on the relationship between intraocular pressure and sympathetic denervation are reviewed and their relevance to this case discussed.

MANY PATIENTS COMPLAIN ABOUT VISUAL DISTURBANCES, BLURRY VISION AFTER THE SURGERY. THERE IS THE CASE OF ORTHOSTATIC HYPOTENSION CAUSED BY THE SURGERY BY DISABLING REGULATION OF THE BLOODPRESSURE, SO THAT BLOOD POOLS INTO THE LEGS WHEN PATIENTS STAND UP. THIS CAN CAUSE BLURRY VISION. THE SYMPATHETIC NERVES ALSO INNERVATE THE SMOOTH MUSCLE THAT IS INVOLVED IN EYEMOVEMENTS. AND NOW THIS ARTICLE TALKING ABOUT THE CONNECTION BETWEEN INNERVATION AND INTRAOCULAR PRESSURE.
IT IS A WELL-DOCUMENTED FACT THAT THE OPERATION CAN CAUSE HORNER SYNDROME, CAUSING A DROOPY EYELID AND AFFECTING THE PUPILS.

b. Cervical sympathectomy causes photoreceptor-specific cell death in the
rat retina
Jena J. Steinle , , Naarah L. Lindsay and Bethany L. Lashbrook


There was a significant reduction (30%) in photoreceptor numbers in the sympathectomized eye. This loss was due to apoptosis, as there was over a doubling in apoptotic cell numbers after sympathectomy. This loss of photoreceptors in the sympathectomized eye resulted in a significantly reduced width of the outer nuclear layer of the retina when compared to the contralateral eye. Increased glial fibrillary acidic protein (GFAP) staining was also noted after sympathectomy in the ganglion cell layer with streaking toward the bipolar cell layer. These results suggest that loss of sympathetic innervation may cause significant changes to the physiology of the choroid.
Journal of Medical Colleges of PLA

AUTOIMMUNE DISEASE AND INNERVATION

Brain Behav Immun. 2007 May 19; : 17517488
Autoimmune disease and innervation.

Rainer H Straub

In the decades before 1987, most of the research devoted to neuronal innervation was carried
out in primary and secondary lymphoid organs at very different locations. This was an important period in order to understand hard-wiring of immune organs in physiology. Between 1988 and 1997, with the appearance of specific antibodies against neuronal markers, innervation was studied in inflamed tissue of patients and of animals with autoimmune diseases. This period clearly revealed that nerve fibers of, both, the sympathetic and sensory nervous system are altered, but only small amounts of tissue have been investigated by qualitative but not quantitative techniques. Between 1998 and 2007, with the understanding that sympathetic and sensory neurotransmitters might play opposite roles in inflammation, nerve fibers of the different nervous systems have been studied in parallel using quantitative techniques. These studies have been carried out in a large number of patients with long-standing autoimmune diseases. It turned out that sympathetic nerve fibers are lost in chronically inflamed tissue, while substance P-positive nerve fibers sprout into the inflamed area. This might be important because high concentrations of sympathetic neurotransmitters are antiinflammatory whereas substance P has a proinflammatory role. The first challenge for future research is the determination of innervation in the early human autoimmune disease. The second challenge is the identification of reasons for the differential loss of sympathetic in relation to sensory nerve fibers. It might well be that nerve repellent factors specific for the sympathetic nerve fiber might play an important role for the observed differential loss. Whether, or not, a therapy can be based on these findings remains to be established.
[Pubmed] [Scholar] [EndNote] [BibTex] [Doi]

THIS IS WHAT THERMOREGULATORY DYSFUNCTION LOOKS LIKE

CONSIDERABLE HYPERTHERMIA THROUGHOUT THE FACE AND NECK, WHICH IS CONSISTENT WITH AUTONOMIC DYSFUNCTION.
A SURGICALLY INDUCED AUTONOMIC DYSFUNCTION, THAT IS CONSISTENT WITH T2 SYMPATHECTOMY.
A SIGNIFICANT PATERN OF HYPOTHERMIA EXTENDING FROM THE RIGHT ARM INTO THE RIGHT AXILLA, THIS ALSO CORRELATES WITH THERMOREGULATORY DYSFUNCTION.

MORE ON BRAIN COOLING

“The efficiency of SBC (Selective Brain Cooling) is increased by evaporation of sweat on the head and by ventilation through the nose.” (Nagasaka et al. 1998)

“A necessary condition for SBC is a high heat loss capacity from the head itself, without such a heat loss SBC is not possible.” (Cabanac 1993)

“Because the human head sweats more than the rest of the body, heat loss from the head skin could amount to 125-175 Watts under conditions of moderate hyperthermia.” (http://www.editthis.info/corposcindosis/Changes_to_Systemic_Function%2C_part_1Cabanac 1993)

SELECTIVE BRAIN COOLING...IF THERE IS NO SWEATING FROM THE FACE...?

Selective Brain Cooling

Besides the general “heat intolerance”, ETS patients have anecdotally reported what they consider to be a “hot brain” syndrome. In particular, Taiwanese ETS patient and robotics engineer “Hpymaker” has made frequent references in the oral history to this hot brain phenomenon. Songboy1234 has also reported a very disturbing sensation like a fever that occurs when exercise is attempted.

Is there any scientific reason to suppose that ETS surgery could interfere with brain cooling, separate from the general thermoregulatory difficulties already shown? This would depend upon whether the normal human has any mechanism to selectively cool the brain; and if so, whether that mechanism is damaged by sympathectomy. The answers are yes we do; and yes it is.

Studies from decades ago began to confirm Selective Brain Cooling. “Cooling of the head skin . . .produces a significant improvement in the performance of heat-stressed humans.” (Kenney, see Williams & Shitzer, 1974).

The ability to selectively cool the brain during hyperthermia (overheating) has long been an accepted fact in many mammals, such as dogs. Dogs have a network of blood vessels in the head called the “carotid rete” which allows heat exchange between warm blood in arteries and cooler blood in veins. The excess heat escapes through the mouth during panting. Humans do not have a carotid rete, so for some time the notion of selective brain cooling in humans was controversial.

However, it has been shown that at 65.8˚ F (18.8˚ C) ambient temperature the deep trunk temperature of a marathon runner may rise to 107.4˚ F (41.9˚ C) with no clinical sign of heat illness (Cabanac et al. 1979; see Maron, Wagner & Horvath, 1977). Michel Cabanac at the Department of Physiology, Laval University, Quebec has been studying Selective Brain Cooling in Humans since the 1970’s, and has evidently discovered the mechanism by which humans accomplish this.

It turns out that certain veins in the face, such as the ophthalmic veins, will actually reverse the direction of blood flow when the body begins to overheat. The blood in these veins is cooled by evaporation of facial sweat, then flows backwards into the sinus and intercranuim area, cooling the carotid artery and the brain.

“The selective influence of facial fanning on human brain temperature can be attributed, therefore, to cool venous blood perfusing the cavernous sinus and possibly cooling the blood of the internal carotid artery.” (Cabanac et al. 1979)

A group of Japanese physiologists at Kanazawa University have been confirming and expanding upon Cabanac’s findings. Their studies subject people to heat stress and exercise, and measure variables such as skin temperature, core temperature, forehead sweating, and blood flow in the ophthalmic vein. They found “that there are elements within the brain that control the mechanisms for switching the direction of venous flow through the emissary veins to keep the brain cool during hyperthermia.” (Hirashita et al. 1992)

Given that this direction-reversing mechanism requires vascular control in the face, we already have strong reason to suspect that ETS would disturb if not destroy selective brain cooling. Is head sweating also important to this process?

“The efficiency of SBC (Selective Brain Cooling) is increased by evaporation of sweat on the head and by ventilation through the nose.” (Nagasaka et al. 1998)
http://www.editthis.info/corposcindosis/Changes_to_Systemic_Function%2C_part_1