Good Morning Gil:
You asked about APOMORPHINE.
Apomorphine is considered to be a drug that works nearly
as well as levodopa. It is described as a dopamine receptor
agonist that stimulates both the D1 and D2 receptors (more
so the D2) in nearly the same way that dopamine does.
It is prescribed for the relief of "off" periods in late stage PD.
In early PD it is used to predict the patient response to
levodopa therapy. Consequently, it would appear to be likely
to produce the same "peak-dose" effects as levodopa.
Since it is usually injected intermittently by the patient
using a single use peninjector perhaps the intervals need to
be increased. There is also a portable pump system which
continuously infuses the patient throughout the day.
Because of the severe side effects (nausea and
decreased blood pressure) domperidone is given to block
these side effects.
Clinical trials are underway for nasal inhalers,
under-the-tongue tablets and suppositories.
What follows is a list posting from Dennis Greene re: his
meds:
From: Dennis Greene <[log in to unmask]>
Date: 6/3/97 11:02am
Subject: apomorphine and dyskinesia
>>> In the six months prior to my recent pallidotomy, I used
apomorphine as a means of releaving the severe 'off' periods I
was then experiencing as an alternative to the equally severe
dyskinesia brought on by even a small increase in sinemet.
(Incidentaly I was taking apomorphine as an under the
tongue lozenge). I found it to be an extremely difficult tool to
use. My response time was much longer than the usual 5
-10 mins (I usually took 20 - 30 mins) and the duration of the
dose was so short (again 20 - 30 mins) that I eventually
reserved its use for those occasions when a severe 'off'
period coincided with a real need to be active.<<<
>>>In addition, I found that using apomorphine before
reaching the 'severe' level of 'off', resulted in the most violent
and painfull dyskinesia I had ever experienced. At the time I
attributed this dyskinesia to the action of the apomorphine
enhancing the action of the levadopa/dopamine already
present in the brain. In other words the dyskinesia was
caused by the levadopa/dopamine as usual and the
apomorphine contributed by making the use of the
levadopa/dopamine more effective. In this respect the action
of apomorphine is not unlike that of other agonists such as
permax.<<<
>>>However, during my pallidotomy, apomorphine alone was
used to turn me 'on' and induce dyskinesia. My last dose of
levadopa had been taken nearly 15 hours before.<<<
>>>In Brian Collins' carefully thought out model, dyskinesia
is the result of dopamine 'overflow' reacting with parts of the
brain which should not be stimulated at that time. My
question is, if that is correct, why does dyskinesia occur
when apomorphine alone is used?<<<
>>> Is it because the apomorphine is enhancing what
by now
must be an extremely low residue of
levadopa/dopamine
(in which case Brian's overflow model remains intact),
or
is there a new mechanism at work (in which case
Brian's
model requires modification).
My own, extremely subjective, feeling is that Brian's model is
very close to what is actually happening, but that it does not
tell the whole story.<<<
I hope this is some benefit to your friend.
Shalom.
Stephan 53/7
