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 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

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/

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

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

T-cells, neutrophils and macrophages infiltrate the site of an injury within two days;^40–42 the neutrophil response is very limited in both time and extent. Within hours, endoneurial levels of the early inflammatory cytokines, tumour necrosis factor alpha (TNF-) and interleukin (IL)-1, secreted mostly by Schwann cells, start to increase in the distal nerve stump. Within days, this network has been amplified by cytokines, chemokines and other bioactive molecules released by recruited macrophages, mast cells and activated endothelial cells.^43–51 Some of these molecules influence the behaviour of the Schwann cells (e.g. macrophage derived IL-1 regulates nerve growth factor (NGF) synthesis by Schwann cells)⁵² and others may play a role in the generation and/or maintenance of neuropathic pain.


Pathway selection.
One of the most important determinants of a satisfactory functional outcome is the accuracy of target re-innervation. If axons degenerate without rupture of the basal laminae which surround each Schwann tube, e.g. in an ischaemic or compressive lesion, then the axon sprouts are unlikely to be misrouted upon resolution of the underlying pathology. That is not the case after traumatic injuries in which a nerve is physically disrupted. Whether the resulting proximal and distal nerve stumps are sutured without tension,^143–145 or are bridged by an intervening graft, the axon sprouts which emerge from the proximal stump are bound to encounter unfamiliar Schwann tubes. Most sprouts, once they have negotiated the site of the suture, will remain within the endoneurium of the distal stump or graft. Those nearest to the periphery of the proximal stump may either escape with their Schwann cells into the epineurium through breaches in the damaged perineurium, or they may grow ectopically between the layers of the perineurium. In both situations their behaviour may produce a painful neuroma.
^{http://web.jbjs.org.uk/cgi/content/full/87-B/10/1309}