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I will add some comments to the 'morning start-up' discussion hinted by Alan and inquired about by Peter & Camilla Flintermann. The process of optimizing one's medication is perhaps more important than most realize. The several doctors I have consulted spent very little time discussing this with me ... and frankly this seems near universal experience in the small Ridgecrest support group I and my wife are now 'leading'. (My information gathering activity was a priority task upon my diagnosis of PD in 1984; then, there was a lull with only NPF quarterly and occasional articles until November of '93 when a local social psychology practitioner volunteered and coordinated the start-up of monthly meetings that established the group. I have read all that I could find since then. I had known for some years that the best learning is preparing to teach and used this opportunity to motivate my self to get 'into' learning what is known about Parkinsonism.) The variation in prescribing is wide (as can be noted in list postings) as is the response of patients. An uncle with PD does not choose to interact much with me, but I was made aware that he uses the method of arising, taking medication, then returning to bed for an hour or so. This is Peter's regimen also (although meds differ I suspect). I have found that my usual morning is nearly equivalent in that I have taken a first dose of meds and usually small partial breakfast relatively soon while resting in a recliner until feeling ready to do something. For some months, the complication of 'focal dystonia' (my personal diagnosis) became pronounced in my right foot only, originally, has become more bothersome and is currently more painful in the left 'foot'. In more detail, the right foot seems primarily the great toe curling up (which is not typical .. and I conjecture this may relate to a hay scythe accident injury in the top front of the ankle when I was a youth). The left foot curls down and inward to the right with the toes individually pulling both up and down .. involving more and larger muscles. Again, I conjecture that foot scalding injury of that foot when 2 or 3 years old may have 'taught my growng neural networks some trauma response (refer to Claudia's psychophysiology comments) that may have included some permanent effects on how my motor neuronal network functions. Most curious to me is the fact that these muscle spasms in the morning do not occur at all if I take half an l-dopa/carbidopa 25/250 during the night. I tried half a Sinemet CR 50/200 before going to bed and found it put my mind into high gear about 3 or 4 hours later. I now use half of one of these if I arise to urinate before 3 AM and half a regular 25/250 if I awake at 4 or later. I would welcome any medical professional or researcher in dystonia to respond about whether this is the pathology (?) of what is termed secondary dystonia, or X-linked dystonia in Parkinsonism as referenced in the several essays, et cetera I have found on the alt.support.dystonia newsgroup. My dystonia seems directly due to insufficient dopamine. (I tried adjusting the second l-deprenyl tablet that I take at noon to late afternoon with no effect.) Peter, I would suggest that using regular Sinemet (or generic) before arising, as I am now doing to counter my dystonia, might shorten your recovery time in the morning. I also am curious about what effect deleting the Sinemet CR before retiring might do in your instance. It would seem to me that it is more likely to inhibit sleep by tending to enhance dreaming, but be dissipated by the time you arise .. thereby doing harm and no good. I use as little medication as I can as a goal. The side effects have worsened, but the inconvenient dosing before arising seems to work .. and allows me to delay adding another drug. Perhaps this method will prevent the painful prolonged muscle spasms for me .. and I will not need another drug? I consider my left side to be more affected with bradykinesia than before .. and this seems logically likely to force me to use more l-dopa in the future .. or use entacapone, tolcapone, other COMT inhibitor or something. I will also be pleased if an expert can tell us more about the muscle relaxant treatment of dystonia. Unless the muscle relaxant functions to make all muscles flaccid, it would seem necessary for it to function somewhat as the dopamine does in the top end of the central motor system ... or perhaps the nerves feeding pain indications in the muscles and tearing(?) ligaments are not getting their message to the motor controllers that are directing the muscle to contract even though already contracted to extreme stress/strain and twisting in spasm. The use of botulinum toxin weakens the response of single muscles when injected. Sagawa's dystonia is apparently the classification or label for l-dopa responsive dystonia ... which reportedly affects children who exhbit the Parkinsonian symptoms. Is YO-PD perhaps another manifestation of the same basic phenomenon? I will subject the readers to little more this time. I do cheer the expanders of internet Parkinsonism information exchange. There is the consideration of whether better to establish multiple e-mail lists or try to be all united with this first world-wide site. I personally believe that eventually virtual libraries on all subjects that are the central repository for the earth .. available to all .. is the optimum method of having all knowledge available to all learners seeking to know all there is to know about any subject worthy of study... Digital version of libraries at Alexandria, Vatican, Library of Congress, et cetera. Ron <[log in to unmask]> Ronald F. Vetter