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At 67 diagnosed 3 1/2 y ago and taking Sinemet for nearly two years I count myself lucky in having moderately mild symptoms principally stiffness, forward sloping posture shuffling and some bradycardia. All of these are well taken care of by sinemet when it is working well and I then enjoy walking upright and swinging my arms in comparatively normal fashion - yes the joys and miracle of movement taken for granted until you lose it.There is however a fly in the ointment because the effecftiveness of each 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 might guess that I was having a bad go of indigestion!Also more often than not my left leg 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. In the Algorithm the authors discuss the more usual peak dose dyskinesia and the narrowness of the therapeutic window and the causes of which Brian Collins has described graphically in a number of postings.Then follows ' Choreodystonic dyskinesias are also seen in a second distinct pattern, in which these adventitious movements occur just at the beginning and again at the end of the levodopa response cycle. This has been termed "diphasic dyskinesia" or D-I-D response, a shorthand for "dyskinesia-improvement-dyskinesia").[124] This pattern is much less common than peak-dose dyskinesia and is often difficult to diagnose because the pattern may not he obvious, either to the patient or the clinician, The end-of-dose period of dyskinesias is typically more prolonged and troublesome than the initial dyskinetic period of the levodopa cycle. Although this D-I-D pattern can be very difficult to treat, it may respond to simple measures if the dyskinesias are relatively mild. First, more frequent dosing of carbidopa-levodopa may allow a more continuous "on" state without periodically cycling through the dyskinetic phases.'A little later in the paper they describe how agonists can be helpful. It seems strange that although I have been following the list for almost 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 the 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 dyskenesia the only hit being the algorythm paper which I already had read. I think I have tried about everything to deal with the problem -sinemet with and without cardidopa, sinemet CR , halving tablets and taking at shorter intervals, no protein diet,pergolide (good), ropinoprol( not so good seems to make the dyskenesia worse) The only other regular drug for me is Seleginin twice a day and I've even tried knocking that out to see if it makes any difference.And in the end the only thing that works is to take sinemet at more frequent intervals so that the new dose kicks in before the end of dose takes effect.It seems to me somewhat bizarre that I would have to get on to a regular treamil of sinemet to avoid the effects of sinemet.So far I have declined to do this calculating that I would need 1200 mg levadopa daily to keep me free of problems. Fortunately and here is the strange thing my symptoms are not so bad that I can go without medication for a lot of the time particularly if I am doing a sitting down job like typing this drivel, driving a car or drinking a pint at the Parkinsons Arms.So I find that after getting up at 5.00am I can manage well for several hours and then pop a couple of CR 25/1100 mid morning and a couple more early afternoon and these will cover me for the period I need to be physically active.So sometimes I ask myself 'Why in the hell do you take sinemet at all' And I suspose the answer is that with it I can enjoy being physical and not find it a bore, I don't think that continual distortion of posture is good in the long run, and without any sinemet during the day one gets very weary in the evenings.One bonus with sinemet I can at least play my piano during the "on" stangely better I think before I had Parkinsons- Levadopa seems to improve my rhythm. I can hear someone saying "Whats he worrying about - if you play the piano or do cartwheels- still better at the same time - you don't need to be on the list.' All of which brings me to some final points; 1. I can find no explanation of how this end of dose overdosing occurs.What is the mechanism? 2. How does all this tie up with the theory expounded so admirably by Brian Collins that the therapeutic window narrows with progress of the disease. I don't regard myself as far progressed in pd yet as soon as I started on Sinemet I began to experience the overdose effects aslbeit not during the "on" and this indicates to me that problems with sinemet do not always arise just through narrowing of the theraputic window due to progression of the disease. Any input would be gratefully received (Back to Basics has my support) David Langridge