 |
 |
Thanks for the information!
Nancy Shlaes deGrazia (62/57) of Long Grove IL (formerly of Maplewood, New Jersey a suburb of Hoboken)
"Bernard Barber,Ph.D." wrote:
Hi Phil,Good question .
The Second Brain, by Michael Gershon, M.D.,Chairman Department of Anatomy
and Cell Biology at Columbia University in New York City,( a suburb of
Bayonne, N.J.) Published in 1998 by HarperCollins.We are having a cool 107 to day, in Phoenix, but the humidity is low, then
again an oven is an oven.Bernie
At 12:26 AM 6/17/99 -0500, you wrote:
>I ran across some interesting information that is not particularly
>recent, but it is new to me and probably far less well known than
>it should be. I've written it up in the form of the article below.
>I hope you will find it interesting. Also, I would appreciate any
>further information anyone can offer on this subject.
>
>Phil Tompkins
>Hoboken NJ
>age 61/dx 1990
>
>----------------------------------------------------------------
>
> The Brain in the Gut and Parkinson's Disease
>
>Parkinson's disease (PD) is commonly defined as a degeneration of
>dopamine-producing neurons in the substantia nigra resulting in the
>primary symptoms of resting tremor, stiffness, bradykinesia, and poor
>balance. But there are numerous other symptoms of PD that seem
>remotely, if at all, related to the substantia nigra. These include
>such diverse phenomena as slowed emptying of the stomach contents
>into the small intestine, sexual impotence, sweating, and seborrhea.
>One may well wonder by what mechanism a deficiency of dopamine in the
>substantia nigra results in some of these other symptoms.
>
>Dopamine is produced and used elsewhere in the body besides in the
>substantia nigra. One such site is a vast neural network embedded in
>the gastrointestinal tract known as the enteric nervous system (ENS).
>It is becoming evident that the effects of PD on the involuntary
>functions of the gastrointestinal system are associated with
>degeneration of those dopamine-producing cells located not in the
>substantia nigra but rather in the ENS. The mechanism by which these
>effects are produced is unknown. However, evidence such as Lewy
>bodies in the enteric neurons and loss of dopaminergic neurons in the
>colon points to the involvement of the ENS in PD in a manner
>analogous to the involvement of the brain in PD.
>
>Gastrointestinal effects of PD attributable to the enteric system's
>involvement in the disease include reflux, delayed gastric
>emptying, and decreased motility. Swallowing difficulties and
>constipation, which have aspects falling under both voluntary and
>involuntary control, may be the result of PD in both the brain and
>the ENS.
>
>The ENS is located in the muscle and connective tissues that line
>the digestive organs. It contains some 100 million nerves cells,
>about the same number as are in the spinal chord. Many of its
>structures and chemicals parallel those of the brain, which it
>closely resembles at the cellular level. It has sensory and motor
>neurons, supportive glial cells, information processing circuits
>which transmit and process messages, and immune system cells. It
>has nearly every major substance found in the brain, including all
>the major neurotransmitters. Because of these resemblances, the
>ENS has been called a second brain, or "the brain in the gut."
>
>The ENS performs two major functions. First, it regulates the
>routine activity of the digestive system, by controlling the
>muscles which grind food in the stomach and move it through the
>digestive tract; and it regulates secretions which occur in
>the digestive tract. A particlar example of a control mechanism is>the feedback loop via which detection of fat in the small intestine
>prolongs retention in the stomach of its remaining contents.
>
>In its routine digestive role the ENS can operate quite
>independently of the central nervous system, being only fine-tuned
>by signals from the latter.
>
>The other major ENS function is to assist in preparing the organism
>for facing danger. Upon receipt of a "fight or flight" signal from
>the brain via the vagus nerve, the ENS activates "canned" programs
>to empty the digestive system by vomiting or diarrhea and to
>mobilize an immune mechanism to fight infection.
>
>I take the similarities between the ENS and the brain plus the
>relative independence of the ENS to be further reasons to attribute
>gastrointestinal PD symptoms to direct involvement of the ENS in
>the disease.
>
>The study of Parkinson's disease as it relates to the enteric nervous
>system is relatively new. There is some research in this area, but
>it has not yet yielded information or drugs for managing
>gastrointestinal PD symptoms. Swallowing difficulties and
>constipation in PD are handled in basically the same way as they are
>for people without PD. Sinemet, the principal PD drug, was designed
>to deliver levodopa across the brain-blood barrier to the brain, not
>to the ENS. Effects of PD drugs on the ENS are largely unknown.
>
>Hopefully more research will be done. The NIH has increased
>funding to the new field of neurogastroenterology, and the NPF has
>also provided funds. At least PD can no longer be thought of as a
>disorder eminating from the central nervous system alone.
>
>
> Bibliography
>
>Lewis, Ricki. "Neurogastroenterologists Combine Old And New
>Research Approaches." The Scientist, Vol 10, #10, pp. 13-14. May
>13, 1996. On-line at
>http://www.the-scientist.library.upenn.edu/yr1996/may/
>research_960513.html.
>
>Quigley, Eamonn M.M. "Gastrointestinal Dysfunction in Parkinson's
>Disease." Seminars in Neurology. Vol 16, #3, pp. 245-250.
>September 1996.
>
>"Body's 'Second Brain' May Cause Digestive Disorders." The New
>York Times, Jan. 23, 1996.
>