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Old 09-04-2011, 08:41 AM
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reverett123 reverett123 is offline
In Remembrance
 
Join Date: Aug 2006
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10 yr Member
reverett123 reverett123 is offline
In Remembrance
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Join Date: Aug 2006
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10 yr Member
Default Perhaps a clue

I have mentioned from time to time here a problem that I have that I have assumed to be separate from PD. It involves shifts in potassium and alarming spikes in blood pressure and seems tied to what is called the "renin-angiotensin-aldosterone axis". It is what led me to my current experiments with perindopril, which blocks a crucial part of the cascade involved. Renin is produced by the kidneys and aldosterone and angiotensin by the adrenals as part of our stress response.

One of the most portentous statements in science is, "That's odd...." and there are, indeed, some oddities here. For one thing, I am pretty sure that in addition to myself, that Laura and Tom Isaacs contend with it. Three of us in such a small sample begins to push at the label "coincidence."

The defining feature is a period of extreme weakness lasting a few hours before resolving itself. During these "attacks" muscle tone is near zero and just the opposite of the high tone rigidity we associate with PD. It is during this phase that my blood pressure climbs to over 250/200. This triggers a relief mechanism somewhat like the pop-off valve on a hot water heater. The bladder kicks in and volume reduction lowers the blood pressure.

Those spikes in BP play hell with the BBB.

If there is something to this, you may be experiencing something similar. But it may be something that comes at a particular stage, too.

It may explain why some of us wake up in the same position as we were in when we fell asleep. Or why polyuria is part of PD.

One paper that I found-
From British Medical Journal; 17 February 1973 (Pg 373)
"...comprises rapid transient deteriora-
tion of the Parkinsonian motor deficit, which develops over minutes and usually persist for 1-6 hours These episodes then clear spontaneously. Hypokinesia, tremor, and rigidity may be exacerbated over the period of deterioration. Hypotonia is common and has also been reported. These oscillations in performance are commonest in patients who have been on levodopa for over a year. They usually occur in the afternoon, and they may be repeated in cycles. Their mechanism is not understood....."

They weren't looking for blood pressure spikes punching holes in the BBB. They were taking one of the very first looks at what we call the "On-Off Phenomenon" in the first years of the new wonder drug levodopa.

"...patients who have been on levodopa for over a year."

A lot to think about.

1. J Renin Angiotensin Aldosterone Syst. 2010 Mar;11(1):49-56. Epub 2009 Oct 27.

The role of the central renin-angiotensin system in Parkinson's disease.

Mertens B, Vanderheyden P, Michotte Y, Sarre S.

Department of Pharmaceutical Chemistry and Drug Analysis, Research Group
Experimental Neuropharmacology, Vrije Universiteit Brussel, Laarbeeklaan 103,
1090 Brussels, Belgium.

Since the discovery of a renin-angiotensin system (RAS) in the brain, several
studies have linked this central RAS to neurological disorders such as ischaemia,
Alzheimer's disease and depression. In the last decade, evidence has accumulated
that the central RAS might also play a role in Parkinson's disease.

PMID: 19861346

--------------------------------

Blockade of brain angiotensin II AT1 receptors ameliorates stress, anxiety, brain inflammation and ischemia: Therapeutic implications.

Saavedra JM, Sánchez-Lemus E, Benicky J.

Psychoneuroendocrinology. 2011 Jan;36(1):1-18. Epub 2010 Oct 29. Review.

PMID:
21035950
[PubMed - indexed for MEDLINE]

-----------------------------------------


1. Exp Neurol. 1984 Jun;84(3):666-70.

Reversibility of blood-brain barrier dysfunction in acute hypertension induced by
angiotensin.

Oztaş B, Sandalci U.

The reversibility of blood-brain barrier (BBB) dysfunction was examined in rats
after acute experimental hypertension. A short-lasting (less than or equal to 4
min) acute hypertension was produced by intravenous injection of 20 micrograms/kg
angiotensin. Evans blue, the barrier tracer, was administered intravenously
either prior to or at intervals of 3, 10, 20, 30, and 60 min after the
angiotensin injection. It was observed that the BBB dysfunction showed a peak 30
min after the angiotensin injection. Three of six animals that received Evans
blue 60 min after angiotensin administration showed extravasation of the tracer
on gross inspection. We concluded that BBB dysfunction may remain even 60 min
after an acute hypertensive episode of short duration.


PMID: 6723887 [PubMed - indexed for MEDLINE]

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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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