Hi Stephan,
Thank you for your detailed response to my question.
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.
In your posting you say, " In early PD it (apomorphine) 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." This
is the crux of the matter. Why does it produce the same 'peak-dose' effects.
Dennis.
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Dennis Greene 47/10
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