Neurological Associates
Pain Management Center
Vero Beach, Florida
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H. Hooshmand, M. D. |
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DIPLOMATE AMERICAN BOARD OF PSYCHIATRY AND NEUROLOGY BOARD CERTIFIED IN ELECTROENCEPHOLOGRAPHY BOARD CERTIFIED IN ELECTROMYOGRAPHY BOARD CERTIFIED IN AMERICAN BOARD OF ELECTODIAGNOSTIC MEDICINE INTRACTABLE NEUROLOGY EPILEPSY, PAIN, MS An International Referral Center dedicated to Treatment, Education and Research |
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RSD PUZZLE #66
The Relationship Of RSD With Heart Disease
You have inquired regarding the relationship of RSD with heart disease. Apparently you
have had a pre-existing heart disease that is becoming aggravated by RSD.
RSD causes three independent negative influences on cardiac function.
1. The sympathetic system is responsible for three main functions, i.e., temperature
regulation, vital signs, and regulation of the immune system. The vital signs in the form
of heart beat, blood pressure and respiration are up regulated and accelerated by
stimulation of the sympathetic system. The RSD is not a simple hyperactivity only
stimulation of the sympathetic system. It is the result of dysfunction of the sympathetic
system. This dysfunction shows an instability of the sympathetic system at times causing
fluctuation of blood pressure and at other times causing attacks of fast heart beat.
2. The second reason RSD affects cardiac function is due to the anatomical
innervation of the heart muscles. Of all the visceral organs, the heart has the richest
innervation of the sympathetic system. This is in the form of cardiac plexus which is a
rich plexus of nerves surrounding the heart. In any stressful condition, the natural
response is rapid heart beat and rise of the blood pressure. The RSD being a distressful
type of dysfunction of the sympathetic system, results in repetitive pathological and
exaggerated response of the sympathetic system to stress, chest pain, palpation, and bouts
of high blood pressure.
3. One of the main principles of development of RSD is inflammation. RSD
is a condition with four major features. First, the allodynia and hyperpathia typical with
pains seen with sympathetic dysfunction. Second, motor response to such pain in the form
of vasoconstriction, muscle spasm and tremor. Thirdly, inflammation in the form of skin
rash, swelling of soft tissues of the extremities, and increased circulation in the
visceral structures resulting in osteoporosis, pelvic inflammation, and attacks of
vascular headaches. The same inflammation and increased visceral circulation causes
distress on the heart. Obviously if the patient has already had pre-existing cardiac
disease, the distressful disease of RSD is going to cause further stress on the heart on
the basis of the above mentioned three principles.
H. Hooshmand, M.D.
cc: Eric Phillips
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Copyright © 1997-2006 H. Hooshmand, M.D. No part of this publication may be reproduced, transmitted, stored in a retrieval system other than this specific media, transcribed, or translated into any language without the expressed written permission from the author; H. Hooshmand, M.D. and Eric Phillips and CMNE. This material is for informational and education purposes. It is not meant to take the place of your physician. Before starting, changing, or stopping any treatments or medicines consult your physician.
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The material on the Neurological Associates Pain Management Center Homepage and all it's associated, linked or reference pages is for informational and education purposes. It is not meant to take the place of your physician. Before starting, changing, or stopping any treatments or medicines consult your physician. H. Hooshmand, M.D., Neurological Associates Pain Management Center and Associates will not be held liable for any damage or loss as a result of information provided on this page or associated documentation. Again, this WEB SITE is simply published as an information source and should not be used to treat or make judgments on RSD/CRPS. All associated material on this web site may not be copied, reproduced or quoted without expressed written permission from the owner; Copyright © 1999-2006 H. Hooshmand, M.D.
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This page was last updated on 3/11/2000.