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.

Evaluation of a Portable Device Based on Peripheral Arterial Tone for Unattended Home Sleep Studies

 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

MD admits stellate ganglion block impacts on the insular cortex of the brain and alters emotions

Dr. Lipov says, "What really intrigued me about Dr, DeWall's study was he showed Tylenol exerted this emotional effect by acting on the insular cortex of the brain. That's exactly the same area that's affected by a Stellate Ganglion Block.[4]" The specialist is also Director of Chronic Pain Research at Northwest Community Hospital in Arlington Heights.
http://www.medicalnewstoday.com/releases/227298.php

Individual cardiovascular response to different levels of sympathetic blockade varies widely, depending on the degree of sympathetic tone before the block

The cardiovascular responses to epidural anaesthesia are almost entirely due to the fact that the local anaesthetic injected into the epidural space not only blocks somatic, sensory and motor fibres, but also produces preganglionic sympathetic denervation.

Postganglionic sympathetic nerves play an important role in controlling cardiac function and vascular tone. The most important of the cardiovascular effects are related to blockade of vasoconstrictor fibres (below T4) with resulting dilatation of resistance and capacitance vessels and/or cardiac sympathetic fibres with loss of chronotropic and inotropic drive to the myocardium (T1-5) (Figure 1).

The cardiac sympathetic outflow emerges from C5 to T5 levels, with the main supply to the ventricles from T1 to T43. A significant part of the chronotropic and inotropic control of the heart is mediated through the upper four thoracic spinal segments.
Denervation of preganglionic cardiac accelerator fibres leaving the cord at T1-T5 results in minimal vasodilatory consequences. Changes however in heart rate, left ventricular function and myocardial oxygen demand may occur due to high thoracic epidural blockade and are discussed below.

The major determinant of heart rate is the balance between sympathetic and parasympathetic systems with the latter predominating. A high thoracic epidural anaesthesia (TEA) covering the cardiac segments (T1-T4) produces small but significant reductions in heart rate4-8. During cardiac sympathetic denervation, parasympathetic cardiovascular responses, including those involved in baroreflexes, may dominate.


It was suggested that the sympathetic control of heart rate modified the dominating parasympathetic tone, rather than functioning as an active cardiac accelerator. In this study there was no compensation for changes in preload;
therefore cardiopulmonary baroreceptors affected by changes in central volume secondary to peripheral vasodilatation or vasoconstriction might have altered arterial baroreceptor heart rate reflex as well.



High TEA added to general anaesthesia significantly decreased the cardiac acceleration in response to decreasing blood pressure, suggesting that baroreflex-mediated heart rate response to a decrease in arterial blood pressure depends on the integrity of the sympathetic nervous system. However general anaesthesia, in addition to high levels of epidural anaesthesia, may have modified the balance between sympathetic and parasympathetic tone as well.
By applying power spectral analysis, i.e., frequency analysis of electrocardiographic R-R interval, the individual components of the autonomic nervous system can be discerned and can be used as a sensitive indicator of sympathovagal interaction.


Individual cardiovascular response to different levels of sympathetic blockade varies widely, depending on the degree of sympathetic tone before the block.
Anaesth Intensive Care 2000; 28: 620-635
B. T. VEERING*, M. J. COUSINS†
Department of Anesthesiology, Leiden University Medical Center, Leiden, The Netherlands and Department of Anaesthesia and
Pain Management, University of Sydney, Royal North Shore Hospital, Sydney, New South Wales

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

catecholamine-induced activation of vagal afferent pathways in regulation of sympathoadrenal system activity

Endocr Regul 2011 Jan; 45(1):37-41.


Stress-induced activation of the hypothalamic-pituitary-adrenal axis and sympathoadrenal system is precisely regulated by well-documented negative feedback mechanisms. These include direct negative feedback effect of glucocorticoids on brain structures regulating the hypothalamic-pituitary-adrenal axis activity. However, since the blood-brain-barrier is impermeable to circulating catecholamines, the role of circulating epinephrine and norepinephrine in feedback regulation of the sympathoadrenal system activity is unclear. Here we show that vagal innervation of the adrenal medulla combined with the presence of β-adrenergic receptors on vagal sensory neurons, the epinephrine-induced activation of vagal afferents, and increased plasma epinephrine levels following subdiaphragmatic vagotomy indicate that sensory fibers of the vagus nerve participate in the monitoring of plasma and tissue catecholamine concentrations. Furthermore, it shows that signaling transmitted by vagal afferents regulates sympathoadrenal system activity at the level of the brain. Therefore, we propose that vagal sensory fibers, directly activated by epinephrine and norepinephrine, represent the afferent limb of a negative feedback loop that adjusts the activity of the sympathoadrenal system according to actual plasma and tissue catecholamine levels.

http://www.unboundmedicine.com/medline/ebm/record/21314209

sympathectomy will block the chronotropic response

Around 50% of patients have bradycardia in the following minutes of a bilateral surgery with mean and diastolic blood pressure significant reduction. Since the sympathectomy will block the chronotropic response, a significant increase of the ejection volume is observed when the patient moves in the erect position from dorsal decubitus [6]. Two cardiovascular complications were reported in the literature. First, an asystolic cardiac arrest in an 18-year-old woman during the second side (left) of bilateral sympathectomy for severe hyperhidrosis, requiring resuscitation maneuvers, with no chronic sequelae [7]. The second case was reported in a 23-year-old woman in whom a bilateral T₂ sympathectomy was performed for facial hyperhidrosis. Two years later, following electrophysiologic studies confirming unopposed vagotonic stimulation, she underwent permanent pacemaker insertion for symptomatic bradycardia [8].
http://icvts.ctsnetjournals.org/cgi/content/full/8/2/238

HAZARDS ASSOCIATED WITH CERVICO-THORACIC SYMPATHECTOMY

The need for a realistic appraisal of the potentialities for harm in Cervico-Thoracic sympathectomy is apparent on anatomic grounds alone (Orkin et al. ] 950). Fatalities occur from time to time, but only a few reports of such fatalities find their way into the literature (Adriani et al. 1952). Reported complications associated with Ccrvico-Thoracic sympathectomy, which is, in effect a permanent Stellate
Ganglion block (Moore 1954), include pneumothorax, Horner's syndrome, phrenic and recurrent laryngeal nerve damage, infection from oesophageal puncture, cardiac arrhythmias (Tochinai 1974), and very infrequently cardiac arrest (Moore 1954).
The following is a case report of a healthy 18-year-old woman who had bilateral Cervico-Thoracic sympathectomy done in two stages for severe hyperhidrosis in the palms of her hands.
Two episodes of asystolic arrest occurred during the 2nd stage left Cervico-Thoracic sympathectomy.
The
cause of hyperhidrosis apparently originates
from some poorly understood stimulation of the
sympathetic nervous system (Cloward 1969),
and in sensitive patients this may possibly lead
to excessive vagal stimulation to counteract it,
as illustrated by the bradycardia and asystolic
reaction to the sudden removal of the
sympathetic control, and by the high doses of
sympathomimetic drugs necessary to
recommence cardiac activity. Anatomically the
heart is innervated by the cardiac plexus which
consists of the cardiac nerves derived from the
cervical and upper thoracic ganglia of the
sympathetic trunk and branches of the vagus.
The pacemaker of the heart, the sino-atrial
node, is innervated by both the parasympathetic
and sympathetic nerves (King and Coakley
1958). The ventricular muscle of the heart is
supplied solely by the sympathetic nerves, and
the larger branches of the coronary arteries are
also predominantly innervated by sympathetics
(Woollard 1926). These factors may also have a
bearing on the hazard of a bilateral cervico-
thoracic sympathectomy, which leaves the heart
solely under vagal control. Usually, following
denervation, the heart will initiate its own
impulse, without recourse to external agencies,
but there may be a place for transvenous
electrode cardiac pacing, if spontaneous initiation
of impulse is delayed, or bradycardia is severe.
Anaesthesia and Intensive Care, Vol. V, No. 1, February, 1977

R. F. Y. ZEE
Royal Perth Hospital, Perth

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

'Improved sympathectomy' - is it an oxymoron?

"also it seems like the more bad and negative affects were from 10 to 12 years ago when they had just started performing the surgery.. they must have inproved it alot by now.?"

I'd like to echo what some others have said just so you are completely clear on this issue. This procedure has been performed since the 1920's. Yes, the 1920's. In the 1980's they started to do it using "keyhole" surgery which means they don't have to make a big incision. But, the surgery is no different than what they've been doing for the last 70+ years. It's a nerve injury. You can't "improve" they way you inflict a nerve injury. You can't injure the nerve in some "special" way such that the injury suddenly has a different effect on the body.

The functional name for the this surgery is "sympathetic denervation". It's not some super-advanced, modern cure based on recent discoveries in neurophysiology. It's a primitive, destructive procedure. It's a method used on animals for research. It's brute force method...destroy the pathways to the sweat glands over a large region. Unfortunately, it destroys pathways to and from many other organs including the heart and lungs and causes a large number of neuropathological dysfunction. That hasn't changed in the last ten years. It will not and cannot change in the next 1000 years because it will still be a nerve injury 1000 years from now. I'm not making this up. It's a simple fact. Don't let some doctor take advantage of your ignorance
http://etsandreversals.yuku.com/topic/4919/Should-i-have-ETS-surgery#.Tok-TE8YAyk