ETS misrepresentations: No compensatory sweating after botulinum toxin... [Br J Dermatol. 2005] - PubMed

Thursday, August 23, 2012

No compensatory sweating after botulinum toxin... [Br J Dermatol. 2005] - PubMed - NCBI

No compensatory sweating after botulinum toxin... [Br J Dermatol. 2005] - PubMed - NCBI:

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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

sympathectomy affects the heart, sweating, and circulation

heart rate was significantly reduced at rest (14%), at sub-maximal exercise (12.3%), and at peak exercise (5.7%), together with a significant increase in oxygen pulse (11.8, 12.7, and 7.8%, respectively). The rate pressure product (RPP) was also significantly reduced following the surgical procedure at all three study stages, while all other physiological variables measured remained unchanged. It is suggested that thoracic-sympathetic denervation affects the heart, sweating, and circulation of the respective denervated region

Eur J Appl Physiol. 2008 Sep;104(1):79-86. Epub 2008 Jun 10.

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

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

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

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/

cervical sympathectomy is a psychosurgery

ATELECTASIS IS A COMMON PULMONARY COMPLICATION FOLLOWING THORACIC AND UPPER ABDOMINAL PROCEDURES

General anesthesia and surgical manipulation lead to atelectasis by causing diaphragmatic dysfunction and diminished surfactant activity. The atelectasis is typically basilar and segmental in distribution. After induction of anesthesia, atelectasis increases from 1 to 11% of total lung volume. End-expiratory lung volume is also found to be decreased.

Postoperative atelectasis is extremely common. Lobar atelectasis is also common. The incidence and prevalence of this disorder are not well documented.

http://emedicine.medscape.com/article/296468-overview#a0104

Atelectasis occurs regularly after induction of general anesthesia, persists postoperatively, and may contribute to significant postoperative morbidity and additional health care costs. Laparoscopic surgery has been reported to be associated with an increased incidence of postoperative atelectasis.

Anesth Analg 2009; 109:1511-1516

the muscles that are supplied by these nerves shorten and tighten (due to the supersensitivity

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

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

Thursday, August 23, 2012

No compensatory sweating after botulinum toxin... [Br J Dermatol. 2005] - PubMed - NCBI

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