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Charlie Meyer inquires: >People's reactions do different medications differ widely. There had >been anecdotal medical reports that Ambien was helpful for PD. This is >not a double blind study and has no greater validity than the reports of >benefits to PWP from melatonin. I am aware of some reports of adverse >effects from melatonin. What happened to you with Ambien? Whether your >reaction was idiosyncratic or predictable list member should know about >it since Ambien is being prescribed more widely. If your reaction was >an unusual one your neurologist (or you) should report it to the FDA. >What is your source for the statement that "at worst the most highly >addictive sleep aid yet developed"? I will do my best to recreate my study, as I did not save the documents that my statements are based on, except the archives printout on Ambien. From the list archives on Ambien I quote the following excerpts..."Zolpidem (Ambien) is only recommended for use in the short-term treatment of insomnia...If therapy is continued for more than 2 weeks the possibility of a withdrawal syndrome should be considered and abrupt discontinuation of therapy avoided......Zolpidem should be used cautiously in patients with major depression, these patients may become more susceptible to suicidal ideation....Elderly and/or debilitated patients may be more sensitive to the effects of zolpidem". >From the Searle HealthNet page: "Use in the elderly and/or debilitated patients: Impaired motor and/or cognitive performance after repeated exposure or unusual sensitivity to sedative/hypnotic drugs is a concern in the treatment of elderly and/or debilitated patients. " The following from a medline search on melatonin and Parkinsons: Life Sci 60 (2): PL23-PL29 (1997) Melatonin is protective against MPTP-induced striatal and hippocampal lesions. Acuna-Castroviejo D, Coto-Montes A, Gaia Monti M, Ortiz GG, Reiter RJ Instituto de Biotecnologia, Universidad de Granada, Spain. The in vivo effect of melatonin on MPTP-induced neurotoxicity in mouse brain was studied. Melatonin (10 mg/kg) or saline was administered intraperitoneally (i.p.) to mice 30 min prior to a s.c. injection of MPTP (20 mg/kg). After MPTP treatment, the animals received melatonin or saline injections every hour for three hours. Mice were killed 4 hours after the MPTP injection. Regionally-specific increases in lipid peroxidation were observed in corpus striatum and hippocampus (71% and 58%, respectively), but not in cerebral cortex, cerebellum or midbrain. Treatment with melatonin completely reversed the rises in lipid peroxidation products. MPTP-treated mice showed a significant decrease in the striatal tyrosine hydroxylase immunoreactive nerve terminals, an effect that was also prevented by melatonin. These data show that melatonin is neuroprotective in this MPTP model of Parkinson's disease and suggest that melatonin, an endogenous antioxidant and nontoxic compound, may have potential beneficial effects for this neurodegenerative disorder. Also, this hypothesis about the Parkinsonian reduced blink rate interested me: Int J Neurosci 51 (1-2): 99-103 (Mar 1990) The significance of eye blink rate in parkinsonism: a hypothesis. Sandyk R Department of Psychiatry, College of Physicians & Surgeons, Columbia University, NY. Alterations in blink rate have been reported in several neuropsychiatric disorders presumed to result from abnormal central dopaminergic functions. Increased blink rate in schizophrenia, Tardive dyskinesia, Tourette's syndrome and Meige's disease are associated with enhanced dopaminergic functions. Parkinson's disease is associated with reduced dopaminergic functions and decreased blink rate. Thus, blink rate may reflect striatal and mesolimbic dopaminergic activity. Since acute light exposure suppresses melatonin production and darkness stimulates melatonin secretion, blinking may serve to regulate light-dark exposure to the pineal gland and thus to 'fine tune' melatonin production. As there is evidence to suggest that melatonin inhibits the release of dopamine in the striatum and limbic system, increased blink rate may serve to reduce light exposure, increase melatonin secretion and attenuate dopaminergic functions. Conversely, decreased blinking (as is observed in patients with Parkinson's disease) could reflect a compensatory mechanism to increase light exposure, reduce melatonin production and ultimately increase dopamine functions. This model is novel in that for the first time it suggests a functional link among blink rate, melatonin secretion and striatal dopaminergic functions in movement disorders. There is an enormous amount of data regarding the beneficial effect of melatonin on the reduced electro-magnetic field of the PWP, but I'm not too up to date on this school of thought. To address your questions about my adverse reaction to Ambien; I think they fell right into the warnings noted. Ambien allowed me 6 hours of sleep, no more or less. That's its window. I had been accustomed to 7-8 hours sleep most nights taking 1 mg of regular melatonin and 2 mgs of time release melatonin, so fatigue started to creep up on me quickly. When I saw this happening, I tried to switch off with melatonin, but found that the melatonin no longer worked for me. The worst thing was that soon I was caught in a depression that I hadn't seen coming, and I normally don't have trouble with depression. By the end of the 2 or so weeks that I used Ambien, the depression had consumed me and I spent the last 3 days in bed, unable to initiate any activity, overwhelmed by life. When my husband and I finally connected this whole mess to the advent of Ambien, I immediately stopped its use, and rode out the 2 or 3 days it took to start to stabilize sleep again. As bad as I felt at the very end with such sleep deprivation, I noticed the depression start to lift and that encouraged me to hang in there. I can only guess how someone with a history of depression might respond to this drug. I have learned my lesson...the best intentions of the best doctors still can't replace having an intelligent approach to my treatment. I understand that the Parkinsonian sleep disorder is chronic, and Ambien will be a life-long drug for some, but I would caution anyone using it to be alert for signs of depression. Kathie Tollifson [log in to unmask] 46/8