Maybe dyskinesia has different causations. I remember reading a while back that they originally thought that the presentation of involuntary movement after the implants was a result of the transplanted neurons secreting TOO much dopamine. Now this new study indicates it is rogue seretonin and not dopamine related. At least as far as these individual cases are concerned. I don't think they are positing that buspar will alleviate all dyskinesias - they are merely reporting how it affected these particular study participants.
Cal
Quote:
Originally Posted by lindylanka
Forgive me for asking the question, I read the study, and couldn't really get to grips with it, am very tired right now..... Your reply below seems to indicate that there were patients who had transplants years ago, are no longer on ANY pd meds, still have dyskinesias after all that time......... from the rogue overproductive seratonin cells. I am not sure I understand this, surely the reason for having transplants such as these would have been to get rid of dyskinesias anyway, or reduce risk of getting them. So it was experimental........ but the very thing that puts people off taking our gold standard drug, the one that we are told to avoid, and these transplants produce the same things...... the dyskinesias we are told to anticipate and fear, and that we know have given some of the people we know and respect a very hard time.....
It's late here, and I AM tired, but surely there is a difference between the abnormal movement induced by levodopa fluctuation, and those created by these implants.......... they must have different causation, otherwise the whole dyskinesia/l-dopa theory is not what it seems at all.........
perhaps I am just confusing myself....... perhaps someone can come in blazing and put me right  and I promise to behave, I do , I do, I do......
Lindy |