cell body reorganization in the spinal cord after sympathectomy

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

Tuesday, December 30, 2014

Peripheral, autonomic regulation of locus coeruleus noradrenergic neurons in brain: putative implications for psychiatry and psychopharmacology

the new data seem to allow a better understanding of how autonomic vulnerability or visceral dysfunction may precipitate or aggravate mental symptoms and disorder.

T. H. Svensson1
(1)Department of Pharmacology, Karolinska Institute, Box 60 400, S-104 01 Stockholm, Sweden
Received: 20 June 1986 Revised: 25 November 1986
Psychopharmacology

"Locus coeruleus (LC) is located in the ventrallateral side of the fourth ventricle in the pontine, most of which are noradrenergic neurons projecting to the cortex, cingulate cortex, amygdala nucleus, thalamus, hypothalamus, olfactory tubercles, hippocampus, cerebellum, and spinal cord (Swanson and Hartman, 1975). Norepinephrine (NE) released from the nerve terminal of LC neurons contributes to about 70% of the total extracellular NE in primates brain (Svensson, 1987). It plays important roles not only in arousal, attention, emotion control, and stress (reviewed in Aston-Jones and Cohen, 2005Berridge and Waterhouse, 2003Bouret and Sara, 2005Nieuwenhuis et al., 2005Sara and Devauges, 1989Valentino and Van Bockstaele, 2008), but also in sensory information processing (Svensson, 1987). LC directly modulates the somatosensory information from the peripheral system. Under the stress condition, LC could completely inhibit the input from painful stimuli through the descending projection to the spinal cord (Stahl and Briley, 2004). Dys-regulations of LC neurotransmission have been suggested to be involved in physical painful symptoms, attention deficit hyperactivity disorder (ADHD), sleep/arousal disorder, post-traumatic stress disorder, depression, schizophrenia, and Parkinson's disease (reviewed in Berridge and Waterhouse, 2003Grimbergen et al., 2009Mehler and Purpura, 2009)."
http://journal.frontiersin.org/Journal/10.3389/fnmol.2012.00029/full

Wednesday, December 24, 2014

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. 
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

Sunday, December 7, 2014

The stellate ganglion has shown to have second and third order neurons that connect with hypothalamus, amygdala, infralimbic, insular and ventromedial temporal cortical regions

"In the course of mapping the sympathetic nervous system to the related regions of the cerebral cortex, Westerhaus and Loewy used pseudorabies virus injections to identify connections of the stellate ganglion. Pseudorabies virus allows identification of neural pathway connections that are 2–3 synapses from the point of injection of the virus. In this manner, the use of pseudorabies virus injection is used to identify cortical areas connected to the stellate ganglion.

The stellate ganglion has shown to have second and third order neurons that connect with hypothalamus, amygdala, infralimbic, insular and ventromedial temporal cortical regions.

These data provides objective, anatomical support for the stellate ganglion interaction with several key structures known to modulate core body temperature, CRPS and PTSD."

http://flipper.diff.org/app/items/info/7052