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Old 01-24-2012, 10:11 PM
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reverett123 reverett123 is offline
In Remembrance
 
Join Date: Aug 2006
Posts: 3,772
15 yr Member
reverett123 reverett123 is offline
In Remembrance
reverett123's Avatar
 
Join Date: Aug 2006
Posts: 3,772
15 yr Member
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Paula-
I am just using the sinemet CR having given up the requip late last year. Dyskinesia was a problem at first but I quickly cut back and at present have only head and face involvement in the evenings. I'm still trimming there too. I have a couple of OTC confessions, as well. I asm trying to work in ginger for stomach stimulation but it powerfully starts the DK so I have shelved it for the moment. I assume that it is working on some pretty powerful pathways if it is able to set me jumping with a single tablet. A half is much more manageable.

Finally, there is potassium. I had been taking potassium gluconate (the cheap stuff) for some time (four months?). Each tab yields up 90 mg or about 6 mEq, a weird little unit of measurement to "eq"uilize the various forms available. I started out taking four of them (or 24 mEq) each morning. I have since added another four at midday and a third round at dinner. Total of 1080 mg or 72 mEq plus a normal diet. My Doc has advised that so long as I am peeing like the proverbial race horse that I'm not likely to overdo it.

Despite all that, my pottassium remains stuck on the extreme low end of "normal" at 3.5. I'm eating potassium by the handful plus taking beta-blockers and ACE inhibitors (the lit says that caution is advised in both instances) and the levels barely budged over the last 18 months! So, how much credit should go to potassium and how much of that is relevent to PWP in general?

Turns out, maybe a lot. -


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]


So, despite the fact that potassium plays a huge role in muscles and nerves, and despite the fact that the bladder enhancing powers of levodopa can encourage us to pee away potassium and B-vitamins, we really don't know much more than we did 40 years ago.

All I know is that I am almost freezing - free, that I am getting more functional every day, that I am sleeping better, that I am almost free of leg and foot cramps, etc.
_Rick

Quote:
Originally Posted by paula_w View Post
not amantadine? bob i can't see anyone getting thru life with pd without amantadine. lol i only take 25/100s regular every two hours and am rarely off unless i forget or eat too much. if i have obligations to attend to or an exercise class i take extra. [this you could NOT do in the rehab facility ]

Rick it sounds like you are doing similar meds but you don't get dyskinesia? no other meds? - i'll check your list. what has changed to make it better for you to write the post? my worst symptom is my balance. sometimes it's just not there on right side. I was walking and talking on the phone today and i fell- can't multi task when walking. it was my first fall since the fracture but a soft landing. able to go without a walker some of the time but my balance is a pd symptom, not from the fracture. i wonder if it was a benefit for it to happen because now i have a metal reinforcement in my affected hip and can drive and exercise better than before.

when i took CR, or any other dopaminergic drugs, MAO inhibitors, agonists, comtan, selegiline, stalevo - anything at all, i get dyskinetic.i would encourage anyone to ask their doctor about dropping some of the dopamine drugs and concentrate on regulating the other tramsmitters,

which I feel the other drugs are doing. anxiety is bad [xanax - low dose] enhances GABA; nortriptyline - anticholinergic that boosts NOREPENEPHRINE and may help to regulate ACEPTYLCHOLINE. Clonazepam for anxiety, antiseizure, enhances GABA, which took away my rambling speech and helps my mouth to stay more relaxed. It 's a circuitry that includes all the neurotransmitters so our medications need to reflect that.

Today on a conference call we made some analogies. Remember if one light was out on a string of Christmas lights , they might still work but if multiple lights were out the whole string was useless. Or if an appliance blows a fuse it takes out half of the house appliances but not all of them, leaving some usefulness. we don't blow fuses much anymore except in older house . but protein "circuit blow out" is on the rise. No electricity, no power.
__________________
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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