Sympathectomy increased the pain threshold and made the sympathectomized rats hypesthetic

Normal adult rats were sympathectomized at L2-L3. The threshold for thermal noxious pain by hot-plate analgesia test and changes in neuropeptides in the lumbar dura mater and dorsal root ganglia using light microscopic immunohistochemistry were assessed and compared with control rats.

Results: In the hot-plate analgesia test, sympathectomized rats increased their hot-plate latency time compared with that of sham-operated rats. Density of calcitonin gene-related peptide immunoreactive fibers in sympathectomy side of the lumbar dura mater decreased to 45.5% compared with the contralateral side. The number and size of calcitonin gene-related peptide immunoreactive cells in dorsal root ganglia showed no difference between sympathectomized and contralateral side.

Conclusion: Sympathectomy increased the pain threshold and made the sympathectomized rats hypesthetic. A large numbers of sensory fibers innervated the lumbar dura mater via L2-L3 sympathetic nerve in rats. Sympathectomy reduced the number of these nerve fibers in the lumbar dura mater. Sympathetic nerves may play an important role for low back pain involving the lumbar dura mater.

http://journals.lww.com/spinejournal/Abstract/1996/04150/An_Anatomic_Study_of_Neuropeptide.4.aspx

Long-term sympathectomy induces sensory and parasympathetic fibres sprouting, and mast cell activation in the rat dura mater

http://discovery.ucl.ac.uk/1330488/

sympathectomy resulted in complete disappearance of histochemically detected adrenergic and a considerable decrease of cholinergic nerve fibers in the pial arterial walls

sympathectomy resulted in complete disappearance of histochemically detected adrenergic and a considerable decrease of cholinergic nerve fibers in the pial arterial walls. The vasodilatation was much less obvious in sympathectomized than in control animals. This was associated with (and probably caused by) a considerable rise in histochemically detected serotonin activity of the pial arteries walls. After recovery of blood supply to the brain the constriction of the pial arterial active segments restricting the excessive cerebral blood flow, was significantly reduced due, probably, to the sympathetic deprivation. Therefore, the sympathetic control plays an important part in pial arterial responses regulating the adequate blood supply of the cerebral cortex.
http://www.ncbi.nlm.nih.gov/pubmed/7173422

Digital infrared thermal image after T2 sympathicotomy or T3 ramicotomy.

(A) Clear cut change of skin temperature after a T2 sympathicotomy. (B) An even distribution of skin temperature after ramicotomy.

Gossot and colleagues [8] analyzed a group of T2, T3, T4 sympathectomy patients in comparison with a group of patients undergoing a T2, T3, T4 ramicotomy and they reported no statistical difference regarding the incidence of CS between the two groups studied (72.2% and 70.9%). However in terms of the severity of CS (embarrassing, disabling) causing inconveniences to daily life, they reported 27% and 13% incidences in these two groups, respectively. These findings suggest that by preserving the sympathetic trunk, it was possible to reduce the severity of CS.

The preganglionic fibers of the sympathetic nerve to the arm originate mostly from the spinal segments T3–T6 and the postganglionic fibers of the sympathetic nerve to the arm originate from T2 and, to a lesser extent, the T3 ganglia [9]. This implies that the division of preganglionic fibers (rami communicantes) reduces the extent of denervation of the sympathetic nerve as compared with the division of postganglionic fibers (sympathetic trunk) in the treatment of palmar hyperhidrosis.
Sympathectomy or sympathicotomy is one of the procedures used to divide the sympathetic trunk. Sympathicotomy distinctively changes sympathetic nerve distribution in comparison with a ramicotomy. Figure 4A illustrates the clear-cut changes of skin temperature after a T2 sympathicotomy. However the overall sympathetic nerve distribution to the body is not markedly changed after a T3 ramicotomy because a T3 ramicotomy is a procedure that is used to divide one of the preganglionic fibers and to preserve the sympathetic trunk. Figure 4B illustrates an even distribution of skin temperature after T3 ramicotomy.

 http://ats.ctsnetjournals.org/cgi/content/full/78/3/1052#FIG4

Drionic effectively "...reduced sweating for up to 6 weeks..."

Clinical Studies

The following comments are from clinical studies which demonstrated the safety and effectiveness of Drionic:

1. Efficacy of the Drionic unit in the treatment of hyperhidrosis. J Am Acad Dermatol 1987;16:828-832. "...the Drionic unit appears to have a definite place in the treatment of hyperhidrosis." Daniel L. Akins, M.D. John L. Meisenheimer, M.D. Richard L. Dobson, M.D., Professor & Chairman, Dept. of Dermatology From the Department of Dermatology, Medical University of South Carolina, Charleston, South Carolina
   
2. A new device in the treatment of hyperhidrosis by iontophoresis. Cutis 1982;29:82-89. Drionic effectively "...reduced sweating for up to 6 weeks..." Further, the study concluded that "Because of its design, it has great potential for home use." CPT John L. Peterson, M.D. MAJ Sandra I. Read, M.D. COL Orlando G. Rodman, M.D. Chief, Dermatology Service From the Dermatology Service, Dept. of Medicine, Walter Reed Army Medical Center, Washington, DC
3. Tap water iontophoresis in the treatment of hyperhidrosis. Int J Dermatol 26;1987:194-197. "Tap water iontophoresis is a recognized method of reducing sweat in various parts of the body. The Drionic device is a battery-operated method of inducing tap water iontophoresis. This simple device may be used at home and is effective in reducing hyperhidrosis for as long as 6 weeks." Mervyn L. Elgart, M.D., Professor & Chairman, Dept. of Dermatology Glenn Fuchs, M.D. From the Department of Dermatology, George Washington Univ. Medical Center, Washington, DC.
4. Efficacy of the Drionic unit in the treatment of hyperhidrosis. JAm Acad Dermatol 16:828-832, Apr. 1987. Elgart ML, Fuchs G: Tap water iontophoresis in the treatment of hyperhidrosis. Int J Dermatol 26: 194-197, Apr. 1987. (old model)

Patients should be shown images to realize just how bad 'compensatory sweating' can be

The consequence of sympathectomy, the 'cure' for sweaty palms is a full body hyperhidrosis. The term 'compensatory sweating' is clearly misleading.
Top arrow shows area where the body lost its ability to sweat (Anhidrosis)
Middle arrow shows are of 'demarcation line' between Anhidrosis and Hyperhidrosis
Bottom arrow shows area below the injury to the sympathetic chain (sympathectomy) which results in pathological autonomic function. Similar condition is seen in people with Diabetic Neuropathy and following spinal cord injury.

Informing the patient of the seriousness of the consequences before this operation is absolutely necessary

http://ats.ctsnetjournals.org/cgi/content/full/80/3/1160-a

while evidence-based medicine is a noble ideal, marketing-based medicine is the current reality

i.bnet.com/.../spielmans-parry-ebm-to-mbm-jbioethicinqu-2010.pdf

pathological pain, such as occurs in response to peripheral nerve injury

It is recently become clear that activated immune cells and immune-like glial cells can dramatically alter neuronal function. By increasing neuronal excitability, these non-neuronal cells are now implicated in the creation and maintenance of pathological pain, such as occurs in response to peripheral nerve injury. Such effects are exerted at multiple sites along the pain pathway, including at peripheral nerves, dorsal root ganglia, and spinal cord. In addition, activated glial cells are now recognized as disrupting the pain suppressive effects of opioid drugs and contributing to opioid tolerance and opioid dependence/withdrawal. While this review focuses on regulation of pain and opioid actions, such immune-neuronal interactions are broad in their implications. Such changes in neuronal function would be expected to occur wherever immune-derived substances come in close contact with neurons.
http://www.ncbi.nlm.nih.gov/pubmed/17706291

Neuropathic pain is caused by damage to, or dysfunction of the nervous system

http://www.mydr.com.au/pain/neuropathic-pain

Disorders of sweating - Iatrogenic causes: Surgical sympathectomy/sympathotomy

(p. 558)

Primer on the Autonomic Nervous System

 edited by David Robertson, Italo Biaggioni, Geoffrey Burnstock, Phillip A. Low, Julian F.R. Paton

Sympathectomy, ganglionopathies and myelopathies produce such pattern

Segmental Anhidrosis

This pattern occurs when a large, contiguous body area of sweat loss with sharply demarcated borders conforming to sympathetic or somatic dermatomes are present.
Sympathectomy, ganglionopathies and myelopathies produces such pattern. When borders are not well defined and anhidrosis not contiguous, a regional pattern is said to exist. Both postganglionic and preganglionic lesions may produce these distributions. (p.557)

Primer on the Autonomic Nervous System

 edited by David Robertson, Italo Biaggioni, Geoffrey Burnstock, Phillip A. Low, Julian F.R. Paton

Perilesional/Compensatory Hyperhidrosis

Central and/or peripheral denervation of large numbers of sweat glands produces increased sweat output in innervated glands, maximal in contiguous dermatomal regions, occurs in PAF, Ross syndrome, SCI and post-surgical sympathectomy. (p.555)

Primer on the Autonomic Nervous System

David Robertson, Italo Biaggioni, Geoffrey Burnstock, Phillip A. Low, Julian F.R. Paton

Academic Press, 01/11/2011 - 730 pages

sympathectomy cannot by direct effect on the muscle vessels either abolish or lessen claudication

http://pmj.bmj.com/content/29/335/459

reductions in heart rate variability are a predictor of sudden cardiac death, even in individuals without a prior history of cardiovascular disease

Research indicates that a highly variable heart rate increases your capacity to respond and adapt to life’s challenges.
In a sense, it makes your cardiovascular system more flexible. If you’re less able to switch to the rest system, you’re more likely to feel stressed because your body is indicating that there’s danger in the environment – even if there isn’t.
Research has shown that reductions in heart rate variability are a predictor of sudden cardiac death, even in individuals without a prior history of cardiovascular disease.

1. Daniel Quintana

   PhD candidate and researcher at University of Sydney
   

2. Andrew Kemp

   NHMRC Career Development Fellow at University of Sydney
   

http://theconversation.edu.au/depression-can-break-your-heart-literally-1102