Wednesday, December 10, 2008
A reduction in heat tolerance after Sympathectomy
DOPAMINE, AROUSAL, CREATIVE DRIVE AND IDEA GENERATION
Dopamine in the mesolimbic pathway increases general arousal and goal directed behaviors and decreases latent inhibition; all three effects increase the creative drive of idea generation. This has led to a three-factor model of creativity involving the frontal lobes, the temporal lobes, and mesolimbic dopamine.[34]
Behavior disorders
Pharmacological blockade of brain dopamine receptors increases rather than decreases drug-taking behavior. Since blocking dopamine decreases desire, the increase in drug-taking behaviour may be seen as not a chemical desire but as a deeply psychological desire to just 'feel something'.
The effect of reduced DOPAMINE
In humans, however, drugs that reduce dopamine activity (neuroleptics, e.g. some antipsychotics) have been shown to reduce motivation, and to cause anhedonia a.k.a. the inability to experience pleasure.[13] Selective D2/D3 agonists pramipexole and ropinirole, used to treat Restless legs syndrome, have limited anti-anhedonic properties as measured by the Snaith-Hamilton Pleasure Scale.[14] (The Snaith-Hamilton-Pleasure-Scale (SHAPS), introduced in English in 1995, assesses self-reported anhedonia in psychiatric patients.)
Additionally, users of stimulants often have depleted dopamine levels after withdrawal from these sometimes addictive substances.
Sociability is also closely tied to dopamine neurotransmission. Low D2 receptor-binding is found in people with social anxiety. Traits common to negative schizophrenia (social withdrawal, apathy, anhedonia) are thought to be related to a hypodopaminergic state in certain areas of the brain.
Abnormalities in dopaminergic neurotransmission have also been demonstrated in painful clinical conditions, including burning mouth syndrome,[26] fibromyalgia [27] [28] and restless legs syndrome.[29]
Salience
Dopamine may also have a role in the salience ('noticeableness') of perceived objects and events, with potentially important stimuli such as: 1) rewarding things or 2) dangerous or threatening things seeming more noticeable or important.[31] This hypothesis argues that dopamine assists decision-making by influencing the priority, or level of desire, of such stimuli to the person concerned.
Since blocking dopamine decreases desire, the increase in drug-taking behaviour may be seen as not a chemical desire but as a deeply psychological desire to just 'feel something'.
Deficits in dopamine levels are implicated in attention-deficit hyperactivity disorder (ADHD), and stimulant medications used to successfully treat the disorder increase dopamine neurotransmitter levels, leading to decreased symptoms.
Dopamine is reduced by Sympathectomy
Dopamine has many functions in the brain, including important roles in behavior and cognition, motor activity, motivation and reward, inhibition of prolactin production (involved in lactation), sleep, mood, attention, and learning. Dopaminergic neurons (i.e., neurons whose primary neurotransmitter is dopamine) are present chiefly in the ventral tegmental area (VTA) of the midbrain, substantia nigra pars compacta, and arcuate nucleus of the hypothalamus.
In the frontal lobes, dopamine controls the flow of information from other areas of the brain. Dopamine disorders in this region of the brain can cause a decline in neurocognitive functions, especially memory, attention, and problem-solving. Reduced dopamine concentrations in the prefrontal cortex are thought to contribute to attention deficit disorder. It has been found that D1 receptors are responsible for the cognitive-enhancing effects of dopamine.[7]
In the frontal lobes, dopamine controls the flow of information from other areas of the brain. Dopamine disorders in this region of the brain can cause a decline in neurocognitive functions, especially memory, attention, and problem-solving. Reduced dopamine concentrations in the prefrontal cortex are thought to contribute to attention deficit disorder. It has been found that D1 receptors are responsible for the cognitive-enhancing effects of dopamine.[7]
Effect of reduced Dopamine
Enlargement of the Breast—A New Side Effect of Transaxillary Cervical Sympathectomy: Case Report
http://ves.sagepub.com/cgi/content/abstract/20/1/50
Breast enlargement after thoracoscopic sympathectomyhttp://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B7XNJ-4S7S2X0-1&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=3f96573d845688f9c13551c594353d73
Mia: Dopamine is also a neurohormone released by the hypothalamus. Its main function as a hormone is to inhibit the release of prolactin from the anterior lobe of the pituitary.
Prolactin has many effects including regulating lactation, orgasms, and stimulating proliferation of oligodendrocyte precursor cells.
It stimulates the mammary glands to produce milk (lactation): Increased serum concentrations of prolactin during pregnancy cause enlargement of the mammary glands of the breasts.
The present evidence suggests that the tonic discharge of normally functioning sympathetic nerves is capable of facilitating the response to angiotensin and that sympathectomy results in an abolition of this effect.
B. G. Zimmerman Ph.D.1
(Circulation Research. 1962;11:780.)
© 1962 American Heart Association, Inc.
Effect of Acute Sympathectomy on Responses to Angiotensin and Norepinephrine
(Circulation Research. 1962;11:780.)
© 1962 American Heart Association, Inc.
Parallels between post sympathectomy patient's symptoms and Chronic Fatigue Syndrome
Dr. Goldstein's CFS/FM protocol revolves around his understanding of these ailments as neurosomatic disorders. In helping to define such disorders, Dr. Goldstein says patients afflicted "do not feel, think, or function properly because the brain does not handle information properly." According to his research, Dr. Goldstein believes brain circuitry and transmittal of data for proper bodily function and health have become altered in conditions like CFS. Further, Dr. Goldstein comments "how the brain, the immune system, and the hormonal system simultaneously regulate the function of each other…is usually 'out of whack' in various ways in patients with neurosomatic disorders."
Dr. Goldstein believes that neurotransmitters, chemical substances that act as information messengers in the brain, are abnormally low in this condition. Norepinephrine and dopamine are two such neurotransmitters lacking in CFS patients. When these are decreased, the brain has difficulty assessing relevance of the numerous messages it constantly receives. Because of this, mentally challenging situations such as taking a test or sensory stimulating situations such as a shopping at a mall can be overwhelming.
Another cause of this easily distractible state is elevated levels of substance P. Substance P is a chemical that transmits pain messages. Overproduction of substance P results in increased sensations of pain.
Article by John W. Addington on Jay A. Goldstein's book:
Dr. Goldstein believes that neurotransmitters, chemical substances that act as information messengers in the brain, are abnormally low in this condition. Norepinephrine and dopamine are two such neurotransmitters lacking in CFS patients. When these are decreased, the brain has difficulty assessing relevance of the numerous messages it constantly receives. Because of this, mentally challenging situations such as taking a test or sensory stimulating situations such as a shopping at a mall can be overwhelming.
Another cause of this easily distractible state is elevated levels of substance P. Substance P is a chemical that transmits pain messages. Overproduction of substance P results in increased sensations of pain.
Article by John W. Addington on Jay A. Goldstein's book:
Betrayal by the Brain: The Neurologic Basis of Chronic Fatigue Syndrome, Fibromyalgia Syndrome, and Related Neural Network Disorders
Published by Haworth Press, 1996
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