ETS is misrepresented to patients: sympathectomy can cause postsympathectomy pain called sympathalgia in up to 44% of patients

Cell body reorganization in the spinal cord after elective surgery to treat sweaty palms

Wednesday, August 3, 2011

sympathectomy can cause postsympathectomy pain called sympathalgia in up to 44% of patients

The sympathalgia secondary to sympathectomy usually starts around the first 2 weeks of the surgical procedure. It is a dull and cramping pain and occasionally can be a sharp pain. Although it is temporary in some patients, in others it can persist for several months or years.

H. Hooshmand, M.D.
Chronic Pain, page 156

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sympathectomy interrupts neural messages to many different organs, glands and muscles

Acquired cardiovascular disease following Sympathectomy

We found statistically significant differences (P < .05) in both time and frequency domains. Parameters that evaluate global cardiac autonomic activity (total power, SD of normal R-R intervals, SD of average normal R-R intervals) and vagal activity (rhythm corresponding to percentage of normal R-R intervals with cycle greater than 50 ms relative to previous interval, square root of mean squared differences of successive normal R-R intervals, high-frequency power, high-frequency power in normalized units) were statistically significantly increased after sympathectomy. Low-frequency power in normalized units, reflecting sympathetic activity, was statistically significantly decreased after sympathectomy. Low-/high-frequency power ratio also showed a significant decrease, indicating relative decrease in sympathetic activity and increase in vagal activity.

The Journal of Thoracic and Cardiovascular Surgery
Volume 137, Issue 3, March 2009, Pages 664-669

decline in external heart work due to sympathectomy both at rest and under exercise

the muscles that are supplied by these nerves shorten and tighten

This now well-established but generally under-appreciated principle of physiology is aptly known as 'Cannon's Law of Denervation Supersensitivity'. It describes the wide ranging effects of the complete loss of nerve inputs to a variety of bodily structures under experimental conditions. One of the many responses to nerves that are sick or dysfunctional (now termed Disuse Supersensitivity) is that the muscles that are supplied by these nerves shorten and tighten (due to the supersensitivity of both the muscle's specialized stretch receptors and motor nerve-muscle junctions), resulting not only in muscle spasm and stiffness which limit flexibility, but a whole sequence of pain compounding reactions. The two earliest are that localized taut bands of muscle fibers begin to compress the small specialized pain sensing (and now extra-sensitive) nerve fibers within the muscle (known as myofascial tender or trigger points) causing type 1 pain, and the compressed muscles do not allow proper blood flow in, or waste products to be removed. This leads to a build up of lactic acid, which further enhances the perception of pain through type 2 pain mechanisms. Continued and prolonged muscle shortening or contracture gradually leads to increased mechanical tension on the muscle's tendonous attachments to bone, causing all of the various tendonitis (types 1 & 2 pain) syndromes throughout the body. The end result is a truly vicious snowballing cycle of pain, with the muscle shortening further increasing pressure on the nerves.

www.northwestims.com/faq-4.html

Cannon's law of denervation tells us that if a post-ganglionic neurone has it's pre-ganglionic input removed, then it will become super-sensitive to the normal neurotransmitters that mediate that pre-ganglionic input. There is a variety of reasons for this, including up-regulation of receptors for the neurotransmitter(s), post-receptor effects, and impaired removal of neurotransmitters from the synapse

www.anaesthetist.com/anaes/patient/ans/

Most authors do not describe clinically significant capsular adhesions as a predominant finding in the chronic phase of this condition. Instead, pathologic data confirm an active process of hyperplastic fibroplasia and excessive type III collagen secretion that lead to soft-tissue contractures of the aforementioned structures (ie, the coracohumeral ligament, soft tissues of rotator interval, the subscapularis muscle, the subacromial bursae). However, these findings were observed in surgical patients who had severe and late-phase disease and cannot be applied to early phases of the disease.

From the chromosomal, cytochemical, and histologic points of view, the soft-tissue contractures are identical to those seen in a Dupuytren contracture of the hand. These contractures result in the classic progressive loss of ROM of the glenohumeral joint, which affects external rotation and abduction, then flexion, adduction, and extension (in descending order of severity). Despite these histopathologic similarities, the favorable and regressive outcome of adhesive capsulitis differs from the unfavorable and progressive outcome of Dupuytren disease.

http://emedicine.medscape.com/article/326828-overview#a0104

cervical sympathectomy is a psychosurgery

decreased conditioning-related activity in insula and amygdala after autonomic denervation

The degree to which perceptual awareness of threat stimuli and bodily states of arousal modulates neural activity associated with fear conditioning is unknown. We used functional magnetic neuroimaging (fMRI) to study healthy subjects and patients with peripheral autonomic denervation to examine how the expression of conditioning-related activity is modulated by stimulus awareness and autonomic arousal. In controls, enhanced amygdala activity was evident during conditioning to both "seen" (unmasked) and "unseen" (backward masked) stimuli, whereas insula activity was modulated by perceptual awareness of a threat stimulus. Absent peripheral autonomic arousal, in patients with autonomic denervation, was associated with decreased conditioning-related activity in insula and amygdala. The findings indicate that the expression of conditioning-related neural activity is modulated by both awareness and representations of bodily states of autonomic arousal.

http://www.ncbi.nlm.nih.gov/pubmed/11856537

All patients except one suffered from compensatory sweating

Complications in patients with palmar hyperhidrosis treated with transthoracic endoscopicsympathectomy.

Neurosurgery. 1997 Jul ;41 (1):110-3; discussion 113-5 9218302

OBJECTIVE: To assess the complications in a group of patients with palmar hyperhidrosis treated with transthoracic endoscopic sympathectomy. The extraordinarily high incidence of postoperative compensatory hyperhidrosis in our series is stressed and explained. METHODS: The retrospective study included chart reviews and outpatient assessments. Seventy-two patients underwent T2 or T2-T3 endoscopic sympathectomy for primary palmar hyperhidrosis. Patients' hyperhidrosis severity, precipitating factors, postoperative complications, surgical results, and satisfaction were assessed. Severity of palmar hyperhidrosis and compensatory hyperhidrosis was classified by two grading scales. RESULTS: The success rate of sympathectomy was 93%. All patients except one suffered from compensatory sweating,which was the main cause of patients' dissatisfaction postoperatively. Seventeen percent of the patients (12 of 72 patients) experienced new symptoms of gustatory sweating (facial sweating associated with eating). Twenty-one patients experienced other complications, including pneumothorax, Horner's syndrome,nasal obstruction, and intercostal neuralgia.

our ignorance of the mechanisms of primary hyperhidrosis and of the effect of sympathetic ablation

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/

RESPONSE TO SYMPATHETIC BLOCKADE DEPENDS ON THE DEGREE OF SYMPATHETIC TONE BEFORE THE BLOCK

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.

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

Effects of upper abdominal sympathectomy on gastric acid, serum gastrin, and catecholamines

Selective upper abdominal sympathectomy increased basal acid output in rats but was without effect on stimulated acid output, serum gastrin concentration, and gastric mucosal histidine decarboxylase activity. The sympathectomy was verified by fluorescence histochemistry and determination of tissue catecholamines. A drastic reduction in tissue noradrenaline, adrenaline, and dopamine levels occurred after sympathectomy, and fluorescence microscopy showed a complete loss of adrenergic nerve fibers. Vagotomy reduced catecholamine levels in the stomach wall by 50% but did not affect the catecholamine content in the pancreas and small bowel. Surprisingly, combined vagotomy and upper abdominal sympathectomy resulted in lower catecholamine levels than sympathectomy alone in extragastric but not in gastric tissues.

http://www.ncbi.nlm.nih.gov/pubmed/6515311

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

Patients who have undergone sympathectomy are not suitable controls. Why?

Hemodynamic changes in vertebral and carotid arteries were observed after sympathicotomy for PH

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

These gustatory phenomena were quite different from physiologic gustatory sweating

In a series of 100 bilateral upper dorsal sympathectomiesperformed for palmar hyperhidrosis, gustatory sweating and othergustatory phenomena were reported by 68 of 93 patients (73%),followed up for an average of 11/2 years. These gustatory phenomenawere quite different from physiologic gustatory sweating: awide range of gustatory stimuli caused a variety of phenomenain varied locations. There was a negative correlation betweenthe incidence of these phenomena and the occurrence of Horner'ssyndrome after sympathectomy. Analysis of our observations,and of clinical and experimental work of others, leads to theconclusion that gustatory phenomena after upper dorsal sympathectomyare the result of preganglionic sympathetic regeneration orcollateral sprouting with aberrant synapses in the superiorcervical ganglion.

http://archneur.ama-assn.org/cgi/content/abstract/34/10/619

cervical sympathectomy is a psychosurgery

the muscles that are supplied by these nerves shorten and tighten

www.northwestims.com/faq-4.html

www.anaesthetist.com/anaes/patient/ans/

http://emedicine.medscape.com/article/326828-overview#a0104

The courts have become the sole policing body for the medical profession

Major lawsuits, with the major judgments that go with them, may not completely keep negligent physicians from practicing, but they are the one way that currently exists to deter these individuals from practicing their inept brand of medicine. "

Over the years, we have given a lot of thought to why the medical profession adheres to this code of silence. What is it about this profession that causes it to protect its own at the expense of the public?"

Harvey F. Wachsman: Lethal Medicine

Publisher: Henry Holt & Co

Cell body reorganization in the spinal cord after elective surgery to treat sweaty palms

Wednesday, August 3, 2011

sympathectomy can cause postsympathectomy pain called sympathalgia in up to 44% of patients

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