> 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] )