I take one 50/200 CR plus one half of 25/100 IR every 4 hours. Also, amantadine, 100 mg twice per day. Also, 10 mg methylphenidate once per day. The CR + IR at 2,6,10 am and 2,6,10 pm. I am still in a rehab facility wherein pd meds and meals -served times are almost always in conflict. 7.45 am and 11.45 am are the most effective times for breakfast and lunch. Each time is midway between two times for Sinemet cr + ir. Well timed food servings are rare in the large rehab facility.
Alternative dose patterns would be appreciated.
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I make that 1.5 gms of L-Dopa a day. The half life of CR is higher than 4 hours so it must be adding up during your day (my neuro say one tablet every 12 hours). At that dose CR sounds sensible if it avoids diskinesia but you must be getting a high when the CR starts adding up. It will be distorted by what you eat - maybe try to avoid milk as that competes. Just a thought - if you are on laxatives (standard nursing procedure!) then you may have a quickened transit time in your gut (gastric hurry) which is not good for slow absorption meds. Are they providing physio support for exercise? I have appreciated your posts and wish you the best.
Thank you for the pertinent comments. I seldom experience even mild dyskinesia. My dopamine level is affected by nurses' views about when to deliver my meds, by variability in meal times, by a dietician's menu high in meat and in sugar. Also, in the rehab facility, I have yet to master how much food is needed to adjust levodopa levels. The nurses do not push laxatives on me. Lots of prune juice.
Maybe it would be easier and more productive to work on your food choices? Ask for more vegetables and salads and try to avoid meat and anything loaded with sugar? If that works then tell the doctor responsible for your medication what needs to improve for you and ask him what he can do. Hope you get home soon.
Following on from Kevin's comments on your drug regimen, it's worth doing a levodopa equivalent dose analysis. This takes into account the differing powers of the drugs that you take and produces a single number that approximates your regimen in terms of IR levodopa/carbidopa.
6x200mg controlled release levodopa/carbidopa, scaling factor 0.7, led = 1200*0.7=840mg LED
6x50mg immediate release levodopa/carbidopa, scaling factor 1.0, led = 300*1.0= 300mg LED
2x100mg amantadine, scaling factor 1.0, led = 200*1.0= 200mg LED
Total daily LED = 1340mg
I make no comment about the methylphenidate other than that it is a serious drug.
You will also want to know how the levodopa levels change from minute to minute as the drugs are taken, get absorbed and wear off. I have written an app that does this analysis. You enter the time at which you take a dose, the name of the drug and the size of the dose. It takes into account the pharmacokinetic parameters of the drug to come up with a graph of how plasma levels change with time. You can play "what if" with it.
Thank you for presenting the dosage calculations. Given the aforementioned variables, I have only very occasionally achieved a stable, functional of levodopa-boosted dopamine.
Methylphenidate and amantadine enhance norepinphrine function, amidst whatever else they do.
Thank you so much. This is so helpful. I am so grateful. How many people think to run varying doses before they start? And if the first dose is way off, doing the recalculating is so much harder. Playing with what if on paper is so effective. A legend for the map!
I take one 25/100 IR and one 25/100 ER four times a day at 6,10, 2, and 6. I try to eat 30 minutes to an hour after my doses. If I am in a meeting and cannot eat at 11 or so, my 2 pm does doesn't work well most of the time. I have been diagnosed 3 years.
The nursing home/rehab facility helps many people, but advanced PD using Sinemet CR + IR seems to challenging given variation in food times, med times, food content. To be sure, a few nurses and CNAs are trying to help. Also, the facility is for-profit and is often understaffed. In approximately 11 weeks, I have achieved stable levels of levodopa only rarely, not for long. Lab test results are difficult to see. Not a place for me. I hope to try to return home soon.
Itseems like you havent been on levadopa very long just looking at your previous posts. I take my meds during the day but not overnight unless I wake and find I cant get back to sleep because I have symptoms. I also take an entacopone equivalent to extend the time of the sinamet.
It is difficult to say more without more background. I do know from experience that too much dopamine can give symptoms that mimic too little.
Hope you work it out. As you posted not long ago exercise is also very important for treating pd - maybe John Peppers fast walking to overcome your symptoms.!
I have been oon carbidipa levodopa since early January 2011. Added amantadine in 2013 to diminish sleepiness, on 1st day of amantadine (while still on c/l) my walking improved wonderfully. I have also tried ropinerola and selegiline. I discontinued each of those, but kept using c/l continuously. Sinemet cr + ir has helped me sleep and to move much better when meals and meds are timed properly, and I choose proper foods, thus when my levodopa levels are remaining in an effective range. I am a PIGD parky.
I have been experiencing off time after meals. I probably eat tt much but the blood seems focused toward my upper digestive track. This is kown to occur in some pwp.
Predictors of postprandial hypotension in elderly patients with de novo PD.
The variables with the highest sensitivity and specificity for postprandial hypotension were constipation (89.6 %) and preprandial hypertension at rest or orthostatic hypotension with alternative definition (both 77.1 %), respectively. Our results suggest that these variables predict the presence of postprandial hypotension in elderly patients with Parkinson’s disease, suggesting that postprandial hypotension shares etiologic factors with these potential predictors.
Postprandial hypotension is both common in geriatric patients and an important but under-recognized cause of syncope. Other populations at risk include those with Parkinson disease and autonomic failure. The mechanism is not clearly understood, but appears to be secondary to a blunted sympathetic response to a meal. This review discusses the epidemiology, risk factors, and pathophysiology of postprandial hypotension in the elderly, as well as diagnosis and treatment strategies.
Diagnosis can be made based on ambulatory blood pressure monitoring and patient symptoms. Lifestyle modifications such as increased water intake before eating or substituting 6 smaller meals daily for 3 larger meals may be effective treatment options. However, data from randomized, controlled trials are limited. Increased awareness of this disease may lead to improved quality of life, decreased falls and injuries, and the avoidance of unnecessary testing.
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