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12-03-2010, 03:25 PM | #1 | ||
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I have been a bit surprised to hear that many with dyskinesias believe it to be caused by the combined use of l-dopa and an agonist. Does anyone here have dyskinesias and is NOT taking an agonist?
It's very interesting that Rick quit Requip and his dyskinesias went away...has anyone else quit an agonist and had dyskinesia go away? I also noted Paula's comment, today I think, that comtan gave her dyskinesias and that when she quit taking it, they went away, or at least that's what I got from the post. Our neuro is really pushing comtan...I hate to add another drug unless we could quit the mirapex at the same time, that might actually make it worth trying. |
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12-03-2010, 11:49 PM | #2 | ||
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In Remembrance
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i've been adjusting meds since my aricept "experience' which set me on a neurotransmitter journey. So this is a recent med protrocol and it involves quite a few "heavy duty " drugs but except for sinemet, no dopaminergics. I didn't realize this until i got dosages right. Many years ago they were making people on DAs give up their drivers license because of "sleep attack" risk in canada. There may be people there that only take sinemet and i'd love to hear from anyone else who has this blend.
We could make a pwp chemical protocol guide. Recipe Book. adding that above line was a wise crack and really I'd like to know if we actually need tbem both at the same time. People are taking both to avoid dyskinesia but that in itself may cause it; especially in more advanced patients.
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paula "Time is not neutral for those who have pd or for those who will get it." Last edited by paula_w; 12-04-2010 at 12:28 AM. |
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12-04-2010, 10:13 AM | #3 | ||
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In Remembrance
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The D-2 Dopamine Receptor
Although there are five distinct types of dopamine receptors, they fall into two broad categories: excitatory and inhibitory. As the labels suggest, the former activates a process while the latter prevents it or regulates it in some way. The D2 receptor falls into the latter category. [inhibitory] When the dopamine process is interrupted, the result can be any one of a wide range of neuro-psychiatric and movement disorders that can include not only tardive dyskinesia, but Tourette's syndrome, Parkinson's disease and others. http://www.tardivedyskinesia.com/tre...e-agonists.php Exp Neurol. 2010 Aug;224(2):395-402. Epub 2010 May 7. Dyskinetic potential of dopamine agonists is associated with different striatonigral/striatopallidal zif-268 expression. Carta AR, Frau L, Pinna A, Morelli M. Department of Toxicology, University of Cagliari, Cagliari, Italy; Centre of Excellence for Studies on Neurobiology of Addiction, Cagliari, Italy. acarta@unica.it Exp Neurol. 2010 Nov;226(1):11-4. Abstract In the dopamine-depleted striatum, an altered post-synaptic signalling of efferent neurons might underline the onset of variable dyskinetic responses to dopaminergic agonists. We have previously shown that a subchronic treatment with the D1 agonist SKF-38393 and the D2 agonist ropinirole induces a dyskinetic response of high and low intensities respectively, in 6-hydroxydopamine-lesioned rats. Here, zif-268 mRNA expression was evaluated in striatonigral and striatopallidal neurons to assess a neurochemical marker of these different dyskinetic responses upon drug administration. Acute and subchronic SKF-38393 (3mg/kg) increased zif-268 expression per neuron in the striatonigral pathway, albeit the number of neurons displaying high early-gene levels was reduced by the subchronic treatment. Zif-268 mRNA in striatopallidal neurons was not affected by SKF-38393 treatments. In contrast, ropinirole (5mg/kg) did not alter zif-268 mRNA in striatonigral neurons acutely, whereas ropinirole decreased zif-268 mRNA subchronically. Both acute and subchronic ropinirole decreased zif-268 levels in the striatopallidal pathway. The differential expression of zif-268 in striatonigral and striatopallidal neurons might provide a biochemical correlate of the dyskinetic outcome displayed by SKF-38393 and ropinirole treatments, suggesting that evaluation of neuronal responses upon drug administration provides a tool for the preclinical characterization of dyskinetic potential beyond behavioural tests. http://www.ncbi.nlm.nih.gov/pubmed/20452347
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paula "Time is not neutral for those who have pd or for those who will get it." Last edited by paula_w; 12-04-2010 at 11:19 AM. Reason: clarity |
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12-04-2010, 10:48 AM | #4 | |||
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I am going to turn to the research to highlight how very little is known about Levodopa Induced Dyskinesia (LID). This recent study indicates that genetics and our exposure to tobacco influences our likelihood of developing dyskinesia. People who have never smoked and who have an alteration impacting their D2 receptors are more likely to get dyskinesia and to see it appear earlier.
Just as an aside, most research on dyskinesia seems to center on the dopamine receptors and the timing of synaptic stimulation. Note: Dyskinesia is nearly non-existant in Duodopa patients. Dyskinesia is less to do with levodopa, and much more to do with delivery and maintaining consistent therapeutic plasma levels. When there is too much circulating in us at once, we get the wiggles. BTW, it's funny that the focus is on the extra movement, for me, I feel so wiped out by it, I can take half a day to get back on the 'normal' train. Since there is a strong correlation between receptors and LID, and agonists work solely with our receptors, it would seem logical that if taken with levodopa, we might get a little more dyskinetic. I once mistakenly took 2 doses of Sinemet while only using that drug. I had a reaction, but it was not dyskinesia. Further, when neuros try to make the case that levodopa be avoided or delayed, they really have nothing to base it on save a few studies that show you may delay levodopa therapy for a few years. What they don't tell you that is longitudinally, after 5-6 years of diagnosis, patients will have roughly same med needs with Sinemet and experience the same level of dyskinesia and those first years, those patients had to live with inferior symptom control or were undermedicated. I really don't know how someone could even tolerate the side effects of an agonist if you have to go beyond the barely therapeutic dosages. At lower dosages I already had behavior problems. At the levels we would need go to sustain clinical benefit, I could not imagine what might happen. The notion that levodopa therapy should be delayed dates back to 1978! Current recommendation of the AAN is to use what improves quality of life most for patient in balance with long term need for levodopa. I understand why they want to delay dyskinesia, but now genetics may play a role in that too? Yeesh, at this point, I'd be most impressed with a doctor who promoted daily exercise over all else as the most important treatment early on; it costs nothing, and has the best side effect profile. Laura |
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"Thanks for this!" says: | krugen68 (12-05-2010), paula_w (12-04-2010), RLSmi (12-04-2010), sunflower4u (12-04-2010), tulip girl (12-10-2010), VICTORIALOU (12-10-2010) |
12-04-2010, 11:55 AM | #5 | ||
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Junior Member
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I suffer with "wearing off" dyskinesia and take only sinemet - no agonist, no comptan. The dyskinesia started as soon as I started sinemet. It has increased over time and decreased my "on time". Interesting comments from Laura. I have never smoked and did not start sinemet until 4 years after diagnosis. I am tremor dominant and the sinemet does help just does not last as long as it did when I started it. Increasing dosage or decreasing dosage intervals results in more dyskinesia.
Sunflower Last edited by sunflower4u; 12-04-2010 at 11:58 AM. Reason: spelling |
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"Thanks for this!" says: | jeanb (12-04-2010), VICTORIALOU (12-10-2010) |
12-04-2010, 12:17 PM | #6 | |||
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Quote:
Thanks! Laura |
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12-04-2010, 12:23 PM | #7 | ||
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In Remembrance
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sunflower when you first started sinemet , were you on any agonists or comtan together with the sinemet? and now what kind of levodopa/carbidopa are you taking - regular? CR? i can't take CR either - that makes me dyskinetic- i only take regular 25/100s. i guess it's a matter of controlling the medication dosage at all times.
I also get end of dose dyskinesia.
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paula "Time is not neutral for those who have pd or for those who will get it." |
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12-04-2010, 01:00 PM | #8 | ||
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Laura
My weight has varied from 95 - 160 lbs with the same results. I am 5' 5". I have tried diet modifications - gluten free, dairy and egg free but no change. Paula I started on only sinemet 25/100. Tried the CR but dyskinesia got worse. It seemed to build in my system increasing dyskinesia and not giving me any longer "on time". Same with comptan. Mirapex and Requip increased my tremor so tried them for only a short time. Amantadine did nothing but give me scratchy eyes. My MDS is a believer in sinemet. He may be starting a duodopa trial that I hope to participate in. My other option is DBS. I was diagnosed 11 years ago. 6 1/2 years on sinemet. I now take 5 25/100 per day. First dose at 8:30, last dose at 5:00. Remeron and LDN at night and get a good 8 hrs of sleep with no tremor. |
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12-04-2010, 05:54 PM | #9 | |||
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I'm taking stalevo and a very low dose of mirapex (.25) 3 or 4 times a day.
My doctor (MDS-researcher) has assured me that my getting dyskinesias is inevitable. But for now she thinks I don't have dyskinesias yet because I stay undermedicated most of the time, and that is postponing the start of dyskinesias. It's pretty much only on trips that I fully medicate myself. At home I try to take one dose less than prescribed and just deal with the increased OFFs. Jean
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Jean B This isn't the life I wished for, but it is the life I have. So I'm doing my best. |
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12-04-2010, 11:08 PM | #10 | |||
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Knock wood !!!! No dyskinesia yet on only sinemet 4 (25/100) daily and selegeline (not an agonist).
The only time I've experienced dyskinesias so far is when I first started taking sinemet and in trying to find the correct dosage had dyskinesia when I had too high a dosing of sinemet, when I lowered it- they went away. dodged that bullet for the moment Quote:
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