Parkinson's Disease Tulip


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Old 12-04-2011, 10:41 AM #41
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reverett123 reverett123 is offline
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reverett123 reverett123 is offline
In Remembrance
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Join Date: Aug 2006
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Default For those who have tuned in late...

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:
Originally Posted by Conductor71 View Post
Rick,

As you know, I experience attacks very similar to yours. I am trying to understand how I have weakness, can barely walk, or speak, yet have a spike in blood pressure. I am normally at 109/80 and yesterday at height of a mild attack it was at 153/100 which scared the heck out of me. If my doctor does not address I honestly feel like I will not make it another five years. This feels so taxing on my system and I know must exacerbate, if not accelerate PD.

I am trying to narrow down whether it is my aldosterone levels, simply a side effect of levodopa, or a primary kidney dysfunction. I was hospitalized three years ago during my pregnancy for a pretty intense kidney infection. So I'd say I am having symptoms of renal tubular acidosis and/or diabetes insipidus as well as the renin-angiotensin deal.

Is polyuria a key element of the aldosterone overload? Does this result in too much sodium in our bloodstream and low potassium? Or do we lose both sodium and potassium through large volumes of urine. I can say I am urinating out way more liquid than I take in, feel parched/dehydrated most of the time, yet at the sam time crave salt. I get the blood pressure spike during an attack then normalize within minutes of urinating.

Sorry to be so graphic...TMI for most. Normally, I'd PM you but I suspect there are many more off us going through this, so doing my part to hopefully help others.

Thanks!

Laura
__________________
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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