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
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