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12-04-2011, 10:41 AM | #41 | |||
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In Remembrance
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Laura and I are dealing with a variant which may or may not be relatively rare and I would like to take a moment to ask a question or two.
1) When you are "off" are you better described as "weak" (unable to summon the energy to move) or "rigid" (unable to overcome muscular resistance)? 2) Is peeing a lot (polyuria) a regular part of your daily cycle? If so, at what point? (i.e. meds coming on or going off; during the night; etc) 3) Are there predictable times of your day when you know that if you slip into an "off" state that it is going to be a real struggle to get back "on"? If so, how do they relate to mealtimes? Your input will be much appreciated. Laura- The pressure rise seems to result from sodium sensitivity. BP climbs rapidly until a "manual" safety valve opens and the peeing begins. That spike is very scary. The one time that I managed to track it I hit 250/200. Scared the wee-wee out of me. So to speak. The bright side is that those of us who deal with that have a certain amount of "stretch" in the blood vessels that mere mortals do not possess. When we flush out the sodium we lose potassium with it. Hypokalemia results. That makes the following interesting- " 1. Acta Med Scand. 1977;201(4):291-97. Kaliuretic effect of L-dopa treatment in parkinsonian patients. Granérus AK, Jagenburg R, Svanborg A. Hypokalemia, sometimes severe, was observed in some L-dopa-treated parkinsonian patients. The influence of L-dopa on the renal excretion of potassium was studied in 3 patients with hypokalemia and in 5 normokalemic patients by determination of renal plasma flow, glomerular filtration rate, plasma concentration of potassium and sodium as well as urinary excretion of potassium, sodium and aldosterone. L-Dopa intake was found to cause an increased excretion of potassium, and sometimes also of sodium, in the hypokalemic but not in the normokalemic patients. This effect on the renal function could be prohibited by the administration of a peripheral dopa decarbodylase inhibitor. It is not known why this effect occurred in some individuals but not in others, but our results indicate a correlation between aldosterone production and this renal effect of L-dopa. PMID: 851038 [PubMed - indexed for MEDLINE]" Aldosterone is a stress hormone. While I am still beating my head against it, it becomes more and more clear that it, along with angiotensin, adrenaline, and cortisol, have a very big role in PD. Quote:
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Born in 1953, 1st symptoms and misdiagnosed as essential tremor in 1992. Dx with PD in 2000. Currently (2011) taking 200/50 Sinemet CR 8 times a day + 10/100 Sinemet 3 times a day. Functional 90% of waking day but fragile. Failure at exercise but still trying. Constantly experimenting. Beta blocker and ACE inhibitor at present. Currently (01/2013) taking ldopa/carbadopa 200/50 CR six times a day + 10/100 form 3 times daily. Functional 90% of day. Update 04/2013: L/C 200/50 8x; Beta Blocker; ACE Inhib; Ginger; Turmeric; Creatine; Magnesium; Potassium. Doing well. |
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"Thanks for this!" says: | Conductor71 (12-04-2011) |
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