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
"Sympathectomy is a technique about which we have limited knowledge, applied to disorders about which we have little understanding." Associate Professor Robert Boas, Faculty of Pain Medicine of the Australasian College of Anaesthetists and the Royal College of Anaesthetists The Journal of Pain, Vol 1, No 4 (Winter), 2000: pp 258-260
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
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
obliteration of the cervical sympathetic peripheral innervation impairs the capability to produce an induced febrile response.
http://www.sciencedirect.com/science/article/pii/S0165572809000575
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.
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.
There is substantial evidence to support the hypothesis that dysregulated sympathetic nervous system hyperactivity is responsible for most, if not all, features of neuroleptic malignant syndrome. A predisposition to more extreme sympathetic nervous system activation and/or dysfunction in response to emotional or psychological stress may constitute a trait vulnerability for neuroleptic malignant syndrome, which, when coupled with state variables such as acute psychic distress or dopamine receptor antagonism, produces the clinical syndrome of neuroleptic malignant syndrome. This hypothesis provides a more comprehensive explanation for existing clinical data than do the current alternatives.
http://ajp.psychiatryonline.org/cgi/content/full/156/2/169
(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.
There is substantial evidence to support the hypothesis that dysregulated sympathetic nervous system hyperactivity is responsible for most, if not all, features of neuroleptic malignant syndrome. A predisposition to more extreme sympathetic nervous system activation and/or dysfunction in response to emotional or psychological stress may constitute a trait vulnerability for neuroleptic malignant syndrome, which, when coupled with state variables such as acute psychic distress or dopamine receptor antagonism, produces the clinical syndrome of neuroleptic malignant syndrome. This hypothesis provides a more comprehensive explanation for existing clinical data than do the current alternatives.
http://ajp.psychiatryonline.org/cgi/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
http://www.autonomicneuroscience.com/article/S1566-0702%2811%2900026-9/abstract
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