Role of Dopamine in behavior modulation
These findings support the idea that DA signals errors in expectancy and that DA signaling is necessary for certain behavioral responses to unexpected events.
Behavioural Brain Research
Volume 122, Issue 2, 1 October 2001, Pages 193-199
Mitchell F. Roitmana, Gertjan van Dijkb, Todd E. Thielec and Ilene L. Bernstein, ,
Behavioural Brain Research
Volume 122, Issue 2, 1 October 2001, Pages 193-199
Mitchell F. Roitmana, Gertjan van Dijkb, Todd E. Thielec and Ilene L. Bernstein, ,
Sympathectomy eliminates the fight-or flight response and is used as a surgical treatment of anxiety disorders and phobias
What the myriad of anxiety disorders have in common is a state of increased arousal or fear. Anxiety disorders often are conceptualized as an abnormal or exaggerated version of arousal. Much is known about arousal because of decades of study in animals and humans of the so-called fight-or-flight response, which also is referred to as the acute stress response. The acute stress response is critical to understanding the normal response to stressors and has galvanized research, but its limitations for understanding anxiety have come to the forefront in recent years.
Thoracic Sympathectomy In Social Phobia: A Pilot Study
http://www.ispub.com/ostia/index.php?xmlFilePath=journals/ijs/vol7n2/social.xml
Recurrent and enhanced vasoconstrictor function makes Sympathectomy a questionable treatment for vascualr disorders
T2 sympathectomy leads to long-lasting inhibition of palmar sweating, which does not correlate to loss of vasoconstriction. Recurrent and enhanced vasoconstrictor function 3 months following endoscopic sympathetic block has major implications for its use to treat enhanced vasoconstriction.
http://www.neurology.org/cgi/content/abstract/60/11/1770
Neurology 2003;60:1770-1776
© 2003 American Academy of Neurology
http://www.neurology.org/cgi/content/abstract/60/11/1770
Neurology 2003;60:1770-1776
© 2003 American Academy of Neurology
Norepinephrine activates pain pathways after nerve injury
According to MedicineNet, RSD involves "irritation and abnormal excitation of nervous tissue, leading to abnormal impulses along nerves that affect blood vessels and skin."
Animal studies indicate that norepinephrine, a catecholamine released from sympathetic nerves, acquires the capacity to activate pain pathways after tissue or nerve injury, resulting in RSD.
http://arthritis.about.com/od/rsd/a/rsd.htm
Animal studies indicate that norepinephrine, a catecholamine released from sympathetic nerves, acquires the capacity to activate pain pathways after tissue or nerve injury, resulting in RSD.
http://arthritis.about.com/od/rsd/a/rsd.htm
Autonomic Hyperreflexia is caused by noxious stimulation below the level of the lesion in a patient with a sympathectomy at or above T6
...The efferent sympathetic fibers recover from the initial injury but remain unaffected by central inhibitory input from the brain stem and hypothalamus.
The severity and manifestations of autonomic hyperreflexia are affected by the level of the sympathectomy. With mid-thoracic lesions below the level of cardiac accelerator fibers, hypertension is accompanied by reflex bradycardia transmitted via cardiac accelerator fibers and the vagus. In patients whose sympathectomy is above the level of the thoracic cardiac accelerator fibers, tachycardia may occur because cardiac accelerator fibers become part of the efferent sympathetic activity rather than part of the central inhibitory input from the brain stem and hypothalamus. Arrythmias and occasional heart block may accompany changes in heart rate.
Clinical manifestations of autonomic hyperreflexia include vasodilation, decresed sympathetic activity, and increased vagal activity above the level of the lesion such as nasal congestion, flushing, headache, dyspnea, nausea, and visceral muscle contraction. Vasoconstriction and increased sympathetic activity below the level of the lesion cause vasoconstrictive pallor, sweating, piloerection, and somatic muscle fasciculation. Patients also develop hypertension with headache, blurred vision, myocardial infarction, andretinal, subarachnoid and cerebral hemorrhages that may lead to syncope, convulsion and death.
Handbook of Neuroanesthesia
page 343
By Philippa Newfield, James E. Cottrell |
Contributor Philippa Newfield, Stephen Onesti, James E. Cottrell |
Published 2006, Lippincott Williams & Wilkins |
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.
Annu Rev Pharmacol Toxicol. 1995;35:417-48.
Substance P has a proinflammatory role
These studies have been carried out in a large number of patients with long-standing autoimmune diseases. It turned out that sympathetic nerve fibers are lost in chronically inflamed tissue, while substance P-positive nerve fibers sprout into the inflamed area.
- Brain Behav Immun. 2007 Jul;21(5):528-34. Epub 2007 May 22.