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Parkinson's, Parlodel, Pituitary I'm posting this long message for two reasons: (1) I'd like to hear from medical professionals any explanation of the apparent riddles or contradictions. (2) Other listmembers might be interested in followup with their own physicians. During the introduction to my new primary care doctor, he casually offered to start me on Parlodel (bromocriptine). Like a smart aleck, I quickly replied no thanks, I know the reputation for bad side effects and would just as soon continue with Sinemet and Eldepryl only. But to my astonishment he was talking NOT about Parkinson's Disease but hyperprolactinemia, for which bromocriptine is also the established therapy (and to which I'll refer hence as HPRL). Huh? Driven by twin demons of ignorance and insatiable curiosity, I consulted my little personal library and soon was beset with questions. The answers may be important to others with Parkinson's as well as to me, so I'd like to hear specially from doctors or other authorities who are Parkinsn listmembers. To avoid the clutter of individual footnotes to every statement, I'll just list my references here: 1. Physician's Desk Reference, 1995:2178-2180 2. The Merck Manual, XVI ed: 1059,1066,1067,1799 3. L. Rolak MD, Neurology Secrets: 249 Pituitary All the cells and organs of the body must communicate with one another, commonly by means of hormones or by nerve connections. Each organ responds with its various outputs to specific input signals, often in chains of several links, of which we perceive only the external origin or the end effect. For example, when it's hot we sweat; but a lot happens in between that simple cause and effect. The pituitary, sometimes called the hypophysis, is a bean- size endocrine (ductless) gland just below the center of the brain, attached to the base of the thalamus by a short bundle of dopamin- ergic neurons called the "tubero-infundibular process" (doctorese for "stalk"). It resides in a depression, called the sella turcica for its fancied resemblance to a Turkish saddle, in the bone that forms the base of the cranial cavity. The pituitary secretes several important hormones, for example one whose malfunction produces dwarfism or gigantism. Another is prolactin, which enables newly delivered mothers to nurse. Sometimes the secretion of prolactin is excessive, usually in women but occasionally in men. The condition is called hyperprolactinemia (HPRL), and of itself has no serious effect, but since tumors of the pituitary also secrete prolactin, it always calls for a scan (CAT or MRI) to check for possible tumor. Some tumors are big enough to see and treat by surgery, but some occur as multiple small bodies that don't show in the scan. HPRL also may result indirectly from, say, tumor in the hypothalamus or, I suppose, failure of the dopaminergic neurons in the pituitary connecting stalk. Interestingly, prolactin secretion is inhibited by dopamine or a dopamine receptor agonist. Women with HPRL, or the level normal after a stillbirth or abortion, or who just don't wish to nurse a baby, can be relieved by dopamine agonist therapy. Although others such as cabergoline have been shown effective, bromocriptine is the standard dopamine agonist prescribed in such cases. Even more interesting, dopaminergic therapy is claimed to shrink pituitary tumors! It's also claimed that bromocriptine in dosage adequate to relieve HPRL doesn't affect the output of other pituitary hormones. Parlodel The ergot derivative Parlodel (bromocriptine mesylate) is a potent dopamine agonist that works by stimulating post-synaptic dopamine receptors, rather than by actually replacing dopamine. As PD users of the drug well know, its most common adverse effects are nausea, hallucinations, and mental confusion. Some reported effects such as dyskinesia, I surmise, may result indirectly from failure to balance the agonist action by reducing levodopa dosage. Pituitary secretion of prolactin, as mentioned above, is thought to be inhibited by dopamine which comes, not from the substantia nigra as in PD, but from the stalk connecting the pituitary with the brain. Hence the action of bromocriptine or another dopamine receptor agonist against HPRL should be analogous to the action in PD. Parkinson's Disease It's well established that PD features a lack of dopamine, due to degeneration of the substantia nigra. HPRL may not always be due to lack of dopamine, but at least responds to dopaminergic therapy in the same way. The two sites where PD and HPRL originate are rather close together, suggesting the notion of a link between the two conditions. In my own case, doctors found a deficiency in one pituitary hormone and an excess in another (prolactin) at the same time, nearly 10 years before diagnosis of PD. The CAT and MRI scans of the pituitary showed no tumor, but the organ was atrophied as in the "empty sella syndrome" that ordinarily affects growth in childhood. Therapy was (is) continued replacement of the deficient hormone, and nothing for the prolactin. Since diagnosis of PD about 3 years ago, I've been getting dopamine replacement via Sinemet. Questions 1. How many other Parkinsn listmembers have had the blood test to check for HPRL? Of those, how many tested positive? 2. Is it possible there could be a link between HPRL and PD? 3. If HPRL responds as claimed to a dopamine agonist such as bromocriptine, which only mimics dopamine, why has it not responded, in my case, to the real thing (dopamine replacement)? 4. Is there something special about bromocriptine in its ability to shrink pituitary tumors, as compared to other dopamine agonists which do inhibit prolactin? I hope some of you will find these questions of interest. Cheers, Joe J. R. Bruman (818) 789-3694 3527 Cody Road Sherman Oaks, CA 91403-5013