sympathectomy affects the immune system: 8/14/11

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

After severing the cervical sympathetic trunk, the cells of the cervical sympathetic ganglion undergo transneuronic degeneration
After severing the sympathetic trunk, the cells of its origin undergo complete disintegration within a year.
http://onlinelibrary.wiley.com/doi/10.1111/j.1439-0442.1967.tb00255.x/abstract

Saturday, August 20, 2011

This injures all the neurons at this level of the spinal cord, some of which may die, and may predispose the patient to spinal cord reorganization and severe compensatory hyperhidrosis

Sympathectomy vs sympathotomy. Sympathectomy, with use of ganglionectomy and by deﬁnition, must sever the primary axon from the neuron in the intermediolateral cell column of the spinal cord (red) before primary or collateral synapse in the T2 ganglion. This injures all the neurons at this level of the spinal cord, some of which may die, and may predispose the patient to spinal cord reorganization and severe compensatory hyperhidrosis. Sympathotomy interrupts only axons after potential T2 ganglion synapses, a less injurious effect on the neuron, and is the least destructive procedure possible with successful treatment
of palmar hyperhidrosis.
Mayo Clin Proc 2003;78:167-172. http://www.mayoclinic.org/medicalprofs/enlargeimage5096.html

Sympathectomy alters bone architecture

These data indicate that guanethidine-induced sympathectomy caused a negative balance of bone metabolism, leading to decreased mass by regulating deposition rather than resorption during modeling and remodeling of bone.
http://www.ncbi.nlm.nih.gov/pubmed/18449939

Friday, August 19, 2011

reduction in hypothalamic dopamine after sympathectomy, which leads to an increase in serum prolactin level

At this point, it is particularly interesting to recall the earlier reports of middle ear bone remodeling in the gerbil after chemical sympathectomy by guanethidine sulfate (86) or hydroxydopamine (85). Although these neurotoxins do eliminate sympathetic activity, there are, in parallel, major central consequences. In particular, both treatments reduce hypothalamic dopamine, which leads to an increase in serum prolactin levels.
http://ajpendo.physiology.org/content/293/5/E1224.full

"Again, patients admitted with any malignancy, cholecystectomy, thyroidectomy, renal disease, cardiac disease, sympathectomy, or vascular graft were eliminated as controls."
This article reviews the evidence that neuroleptics may increase the risk of breast cancer via their effects on prolactin secretion.
Paul M. Schyve; Francine Smithline; Herbert Y. Meltzer
Neuroleptic-induced Prolactin Level Elevation and Breast Cancer: An Emerging Clinical Issue
Arch Gen Psychiatry, Nov 1978; 35: 1291 - 1301.

Body temperature is highly correlated with plasma prolactin in thermally stressed men
(78), suggesting that normal heat defense is associated with decreased central dopamine, and
intraventricular haloperidol produces a coordinated heat-defense response (79). These reports refute a
unique or essential role for central dopamine antagonism in neuroleptic malignant syndrome hyperthermia
and provide additional evidence that state-dependent factors are important mediators of dopamine
antagonist effects.
Thereis substantial evidence to support the hypothesis that dysregulatedsympathetic nervous system hyperactivity is responsible formost, if not all, features of neuroleptic malignant syndrome.A predisposition to more extreme sympathetic nervous systemactivation and/or dysfunction in response to emotional or psychologicalstress may constitute a trait vulnerability for neurolepticmalignant syndrome, which, when coupled with state variablessuch as acute psychic distress or dopamine receptor antagonism,produces the clinical syndrome of neuroleptic malignant syndrome.This hypothesis provides a more comprehensive explanation forexisting clinical data than do the current alternatives.

http://ajp.psychiatryonli...i/content/full/156/2/169

dural blood flow decreased significantly in the cervical sympathectomy group

Migraine may affect the autonomic nervous system, but the mechanisms remain unclear. The sympathetic and parasympathetic nervous systems may play different roles in the attack. To explore the effect of blocking the cervical sympathetic nerve on vasodilation of the meningeal vessels, jugular vein calcitonin gene-related peptide (CGRP) and meningeal blood flow changes were measured before and after transection of the cervical sympathetic nerve by electrically stimulating the trigeminal ganglion in Sprague–Dawley (SD) rats. We found that CGRP level and meningeal blood flow increased in both the sham-operated and sympathectomized groups (p

0.05). Compared with the sham-operated group, dural blood flow decreased significantly in the cervical sympathectomy group, but CGRP level was not significantly different between these two groups. The cervical sympathetic nerve may play an important role in the process of neurogenic dural vasodilation in rats; this effect is not entirely dependent on CGRP level.
http://www.autonomicneuroscience.com/article/S1566-0702%2811%2900026-9/abstract

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

Surgical and chemical sympathectomy can alter cellular proliferation

Surgical denervation and chemical sympathectomy can alter cellular proliferation, B- and T-cell responsiveness and lymphocyte migration in lymphoid organs [17].

In vitro studies have shown that neuropeptides can have numerous effects, either inhibiting or stimulating the proliferation, differentiation and functions of immune cells [19]* Development of systemic lupus erythematosus in mice is associated with alteration of neuropeptide concentrations in inﬂamed kidneys and immunoregulatory organs

Neuroscience Letters 248 (1998) 97– 100

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.

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

cross-inhibitory control of various afferent in the spinal cord

In conclusion, our results suggest that cross-inhibitory control by various afferents in the spinal cord may exist in the feet as well as in the contralateral hand. The release of cross-inhibitory control by T3 sympathicotomy results in vasoconstriction and a decrease of skin temperature on the contralateral hand and the feet.

The basic neuronal network for this reciprocal organization is probably located in the spinal level (15). Therefore, the reduction in the contralateral skin temperature may be explained by cross-inhibitory control of various afferent in the spinal cord.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2722005/

Contralateral temperature changes of the finger surface during video endoscopic sympathectomy for palmar hyperhidrosis
http://www.ncbi.nlm.nih.gov/pubmed/8832515

Receptor hypersensitivity is a common problem

Because of their size and location, injuries to the sympathetic ganglia or chain is rarely indicated or performed. Receptor hypersensitivity is a common problem after significant sympathetic injury, including clammy hands, erythema, and allodynia. When sympathetic nerves regenerate, they may establish aberrant connections to sensory receptors, muscles, or other sympathetics receptors; this may lead to an over-response or abnormal response.
http://wiki.cns.org/wiki/index.php/Injury,_Sympathetic_Nerve

Sympathectomy suppresses cell-mediated (T helper-1) responses

In vivo, chemical sympathectomy suppresses cell-mediated (T helper-1) responses, and may enhance antibody (T helper-2) responses. Noradrenergic innervation of spleen and lymph nodes is diminished progressively during aging, a time when cell-mediated immune function also is suppressed. In animal models of autoimmune disease, sympathetic innervation is reduced prior to onset of disease symptoms, and chemical sympathectomy can exacerbate disease severity.
Annu Rev Pharmacol Toxicol. 1995;35:417-48.

we conclude that the sympathetic nervous system influences the metabolic activity of the aorta

The effect of chemical sympathectomy with 6-hydroxydopamine (6-OH-DA) on collagen formation in the aortic wall was investigated in rabbits and rats. Eight weeks after 6-OH-DA treatment of rabbits, there was a significant increase an collagen content in aortas and histologic changes in the elastic elements within the media. The possibility of a direct effect of 6-OH-DA on connective tissue formation was investigated in a subsequent experiment in rats. The rates of collagen synthesis and prolyl hydroxylase activity (PHA) were determined in aortas and in the fibrotic granuloma around subcutaneously implanted polyvinylalcohol sponges. Rates of collagen synthesis and PHA were significantly increased in the aortas of 6-OH-DA treated rats, but not in fibrotic granuloma, confirming the changes seen in the aorta of rabbits and suggesting that 6-OH-DA does not directly affect collagen synthesis. We conclude that the sympathetic nervous system influences the metabolic activity of the aorta. Our data indicate that when the aortic wall is deprived of adrenergic nervous stimulation, changes occur which resemble those seen in natural aging of the aorta. It is plausible to assume that such a metabolic derangement in the vessel wall will make these vessels more vulnerable to additional stresses.

Experimental and Molecular Pathology
Volume 28, Issue 3, June 1978, Pages 279-289

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/

"sympathectomy leads to an increase in the development of tumors on the denervated side"

Limited sympathectomy does not reduce severity of side-effects

On univariate and multivariate analysis, the extent of denervation was not associated with the occurrence or the severity of compensatory sweating.

Compensatory sweating and temporary relief/recurrence were equally considered to be the main causes of dissatisfaction. CONCLUSION: Compensatory sweating was the most common long-term complication of thoracodorsal sympathectomy for primary hyperhidrosis. Its incidence and severity were not associated with the extent of sympathectomy.

http://www.ncbi.nlm.nih.gov/pubmed/12514588

a reduction of the muscular tone and to a secondary neurovascular disorder after sympathectomy

early lymphocytosis was absent in sympathectomized subjects

Peripheral white and red blood cell changes were studied in response to acute insulin-induced hypoglycaemia in six normal, six splenectomized and five sympathectomized (tetraplegic) subjects. The normal subjects were restudied during beta (propranolol) and beta-selective (metroprolol) adrenergic blockade.

In the normal subjects a lymphocytosis immediately followed the acute hypoglycaemic reaction (R) with a neutrophilia 2 h later. The early lymphocytosis was absent in sympathectomized subjects and reduced under beta blockade in normal subjects, indicating mediation via an adrenergic mechanism.

Haemoglobyn, packed cell volume and total erythrocyte count rose maximally at R in all groups except the sympathectomized subjects in vhom all parameters declined progressively from basal values.

Peripheral blood cell changes in response to acute hypoglycaemia in man

European Journal of Clinical Investigation, Volume 13 Issue 1, Pages 33-39, 1982

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

Surgical and chemical sympathectomy can alter cellular proliferation

Surgical denervation and chemical sympathectomy can alter cellular proliferation, B- and T-cell responsiveness and lymphocyte migration in lymphoid organs [17]. In vitro studies have shown that neuropeptides can have numerous effects, either inhibiting or stimulating the proliferation, differentiation and functions of immune cells [19]*
Development of systemic lupus erythematosus in mice is associated with alteration of neuropeptide concentrations in inﬂamed kidneys and immunoregulatory organs
Neuroscience Letters 248 (1998) 97– 100

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

Autonomic dysequilibrium (local sympathectomy) leading to obesity

A similar reduction of fat mobilization from fat depots occurs after VMH lesions, as after local sympathectomy, suggesting that the sympathetic pathway to the adipose tissue runs through the VMH.
Bray and York hypothesize that the change in energy balance in animals after VMH lesions is a result of autonomic dysequilibrium. The sympathetic outflow is reduced and the parasympathetic outflow increased. This shift in balance results in hyperinsulinemia and altered metabolic pathways leading to obesity. During the digestion and metabolism of a meal, the autonomic nervous system provides important (but not sole) feedback control on satiety.

The Nervous System and Adipose Tissue, By Katharine Dalziel, MD, MBBS, MRCP
Clinics in Dermatology
October-December 1989, Volume 7, Number 4, pages 62-77