> From: Ida & Andre Kamphuis <[log in to unmask]>
> Quite some time ago I wrote to the list that it was my impression that t=
wo
> kinds of dyskinesia existed, one combined by dystonia, the other not. Th=
ere
> was, as far as I remember, no reaction. But months after that I did rea=
d
> in a mail from David Langridge, to my surprise, the text I have quoted
> below. After reading this I followed the instructions about med. schedul=
es.
> The results were unbelievable. The daily time of my wild dyskinesia was
> reduced from 8 hours to 2 hours. To identify a dyskinesia as a wearing o=
ff
> one, one has to attend to the time that passes from the intake of sineme=
t to
> the start of the dyskinesia concerned.
>
> Ida Kamphuis, Holland
>
> Quote from David Langridge:
>
> There is however a fly in the ointment because the effecftiveness of eac=
h
> dose of sinemet is curtailed because mainly at the end of a dose when it=
's
> effect is beginning to wear off I experience an unpleasant drug induced
> state akin to dyskinesia but not in it's wild form- I can best describe=
it
> as a sort of mainly internal writhing with incipient neck movements and
> body swaying all reasonably controllable although an outside observer
> mightguess that I was having a bad go of indigestion!Also more often tha=
n
> not my leftleg goes rigid and I find it harder to walk than if I had not
> taken Sinemet.So here is a drug induced problem which seeems to more or
> less fit the term diphasic dyskinesia which I first came upon in the
> 'Algorithm for Parkinsons Disease' a very worthy paper published in
> Neurology and obtainable from our archives.
>
> diphasic dyskinesia" or D-I-D response, a shorthand for
> "dyskinesia-improvement-dys=ADkinesia").[124] This pattern is much less
> common than peak-dose dyskinesia and is often difficult to diagnose beca=
use
> the pattern may not he obvious, either to the patient or the clinician, =
The
> end-of-dose period of dyskine=ADsias is typically more prolonged and
> troublesome than the initial dyskine=ADtic period of the levodopa cycle.=
> .It seems strange that although I have been following the list for almos=
t
> two years I have seen no mention of this problem except in a
> posting from Ida Kampuis in October and amongst many other interesting
> things she sais <<<<
> An important difference between the two states of hyperkinesia is that t=
he
> end of meds one is combined with high muscle tension end
> the other much less so. This makes the former the most troubling one.
> During the former walking is more impaired or impossible.>>>>. As
> mentioned above I have experienced this end of meds muscle tension.Also =
I
> have searched in the archives and found no mention of diphasic dyskenesi=
a
> the only hit being the algorythm paper which I already had read.
>
>
> --------------------------------------------------------------
> Vriendelijke Groeten / Kind regards,
>
> Ida Kamphuis mailto: [log in to unmask]
>
>
Hi Ida
I included an exert from my alt explantion of PD that correlates with
your diphasic dyskinesia . I maybe wrong but my Zone B is expanding
and I fear will soon swamp zone A . In that case I will be left with
only zone C ( a very limited improvement with L-dopa ) and zone B (
dyskinesia ) . If this is true then the two forms of dyskinesia are
really the same . One can only postulate two forms if they occur
together in the same drug taking . That is there is yet another zone
above zone A that is dyskinesic .
INTERFERING WITH THE SPASM
One of the best ways of interfering with the spasm os to increase the
neurtransmitter dopamine even in cases where the PD is not caused by a
dopamine shortage . Dopamine dampens the spasm a bit like a shock
absorber danpens a badly balanced car wheel . Just like with a car
wheel at certain range of speeds this dampening effect actually makes
things worse ( the wheel and damper are in sync ) so dopamine increase
at certain concentrations makes things worse ( dyskinesia ).
DOPAMINE LEVEL IN BRAIN AFTER TAKING DOPAMINE
BOOSTING DRUG ( L-DOPA )
l
l
l ++++
l + Zone A +++
l ____+_________________+_________
l + Zone B +
l _+____________________________+___________
l + Zone C +
l+________________________________________________+__
Time =AC >
( I apologise for the diagram but could not do much better with my
offline mailreader )
Zone C
In this zone the boost of dopamine is least so the effects are
minimal . All the PD symptoms are there . ( In my case I am dragging
my left leg when I walk )
Zone A
In this zone the boost of dopamine is maximum and the PD symtoms are
lessened or gone I often feel a bit strange .( In my case I walk
normaly without trying )
Zone B
This is the danger zone where the dampening effect of the increase
dopamin eis in sync with the PD spasm and makes the condition worse .
( IN my case my left leg becomes uncontrolable . The only way I can
describe it to a person who has not experienced it . It is like trying
to stand aand young child who is trying to attract your attention is
pulling and pushing at your leg . ) BUT and this is a BIG BUT unlike
driving a car with an unbalanced wheel that vibrates at only certain
fixed speeds the range of zone B is not fixed . With the brain any
strong pattern gets emphasised and expanded . Zone B is an extremely
strong pattern and so the more it occurs, the larger its range . The
expansion of zone B often completely destroys the advantage of taking
dopamine boosting drugs .
I nearly always experience dyskinesia 4 - 6 hours after taking my
last L-dopa pill of the day . I have sometimes experienced it 3/4 hour
after the first pill for a few minutes . I sometimes get it on and off
during the day . I put this down to the dopamine level being about the
zoneA/zoneB boundary .
If one stops going into zone B by not taking dopamine boosting
drugs then zone B range will shrink . Unfortunately this from what I
read this is not very fast . It is therefore important to avoid
dyskinesia not just for temporary discomfort .
peace
Alastair ( [log in to unmask] )
