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. >