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03-29-2010, 03:46 PM | #1 | |||
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In Remembrance
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"A transient hypertensive opening of the blood-brain barrier can lead to brain damage " http://www.springerlink.com/content/w5q7574041446w51/
Ron- See if this is a new wrinkle for you. Temporary, acute rises in BP lasting only minutes or less can defeat the BBB and cause damage. So what could produce this spike? More or less chronologically- A constipated child straining at stool. A boy in terror of Hitler or his drunken father. Repressed emotion - especially anger or fear. A constipated adult straining (hereinafter deemed "the Elvis effect"). A PWP whose autonomic controls can cause normal BP to rise rapidly when supine. A PWP struggling to....(you name it) What might prevent this? How about exercise? Or caloric restriction? Nothing exists in isolation, so there is some interaction. The question is how much and when.
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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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03-29-2010, 04:05 PM | #2 | |||
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In Remembrance
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1. Acta Neuropathol Suppl. 1983;8:81-8.
Disturbances of the blood-brain barrier in cerebrovascular disorders. Klatzo I. The disturbances of the BBB in cerebrovascular disorders may affect adversely an underlying basic pathological condition. Breakdown of the barrier associated with extravasation of serum proteins leads to development of vasogenic edema in the brain tissue. An abnormal passage of pharmacologically active substances, such as biogenic amines, may significantly affect cerebral blood flow and metabolism and activate neurons equipped with receptors for these substances. Also, a barrier dysfunction related to faulty out-transport of metabolites may contribute to edema and tissue damage. In cerebral ischemia, following release of arterial occlusion there can be two separate openings of the barrier: the first - occurring promptly after recirculation and related to ensuing reactive hyperemia, the second - after some delay and related to pathological changes in the brain tissue. In some circumstances, such as epileptic seizures, both "hemodynamic" and "tissue" factors may be operative at the same time. The selective features of BBB changes are related to multiplicity of barrier systems residing in cerebral endothelium. <So, are the "barrier systems" in the SN particularly vulnerable?> These selective features are demonstrable during development and during reversibility of postichemic barrier disturbances. Intermittent openings of the barrier observed in chronic hypertension may lead to accumulation of extravasated serum proteins and be responsible for frequently observed edematous changes in this condition. PMID: 6575567 [PubMed - indexed for MEDLINE] My mother was preclampsic and had very high BP while carrying me. I was also born with rickets so D was a factor too.
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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: | girija (03-30-2010) |
03-30-2010, 01:00 AM | #3 | |||
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In Remembrance
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Hi Rick,
There does seem to be a connection between hypertension and PD. There is a lot of data now on the beneficial effects on PD of anti hypertension drugs, like isradipine. It stands to reason that a high blood pressure will force a path through the BBB, more than a lower pressure. I believe that PWP's have a continuous higher BBB permeabilty than a healthy person. Things like a stressful situation can cause a temporary further widening of the BBB, and we freeze. Possibly events like trying to lift a very heavy weight may have a similar effect. Could this cause a spike in blood pressure? The report says, " Intermittent openings of the barrier observed in chronic hypertension may lead to accumulation of extravasated serum proteins" So is this how we get accumulated alpha-synuclein? Ron
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Diagnosed Nov 1991. Born 1936 |
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"Thanks for this!" says: | girija (03-30-2010) |
03-30-2010, 07:18 AM | #4 | ||
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Senior Member
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I have often wondered why the prisoners of concentration camps didn't all have PD, those that lived, that is...not that there were very many of them. Talk about daily chronic stress of the worst kind, surely that would open the BBB like a floodgate? So why weren't the allies, when they liberated the camps, greeted by a crowd of PWP?
The only thing I can think of is that those poor prisoners were starved, many to death, in reality, so perhaps the caloric restriction staved off the PD? I don't know, but I have often wondered about this, yet cannot find any stats for how many concentration camp survivors either had PD when liberated or later got dx'd with it (and if they got it later, how long after liberation). |
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03-30-2010, 07:47 AM | #5 | |||
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In Remembrance
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Ron- I can report firsthand that there is an acute rise in my BP when I am off and even more so when I struggle to physically overcome it.
It should not be surprising, since BP is increased when the muscle tone in the walls of the arteries increases, as I presume it would when all the other muscles are clenched. I suspect that a different set of rules apply for veins. So, if this picture is true, then at some point PD would become self-perpetuating and progression accelerate as the rigor of the muscles indirectly compromised the BBB. <How'd I do, Boss? > PS- Just found that dyskinesia correlates with a drop to near normal BP.
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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. Last edited by reverett123; 03-30-2010 at 08:16 AM. |
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03-30-2010, 08:09 AM | #6 | |||
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Lurking-
A good point that applies across an even wider field. Both acute and chronic populations abound. Yet they are not the same as PWP. In fact, no group fits the bill. How to explain it? The assumption that has sucked up so much time and money over the years is that we just need to look harder. "Further grants are required...." There is another explanation, what I call the "Blue Plate Special." A menu with a column of a few entrees and another with a dozen sides. Maybe a hundred possible combinations. Choose two from the first column and you have something other than the BPS. Choose exclusively from the second and you have a vegetable plate. But choose a "meat and three" and you have PD.
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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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03-30-2010, 08:29 AM | #7 | |||
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In Remembrance
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The title comes from a sci-fi work by Harlan Ellison and is prompted by my meditations upon my hypertension.
Just how much does repressed emotion play in PD? And it may be gender specific. I have learned over the years that, beneath my James Bond-like cool exterior, resides a monkey house that I have to struggle to access at all. Rigid self-control has been my way since childhood and PD seems a reflection of that. Is it in one of the menu columns?
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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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03-30-2010, 09:08 AM | #8 | ||
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In Remembrance
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Oddly tho, look who did get Parkinson's:
Hitler http://news.bbc.co.uk/2/hi/health/406713.stm Mao Zedong [Tse Tung] http://www.notablebiographies.com/Lo-Ma/Mao-Zedong.html and Harry Truman http://www.whitehouse.gov/about/presidents/HarrySTruman http://www.nndb.com/lists/789/000064597/ Quote:
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paula "Time is not neutral for those who have pd or for those who will get it." |
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03-30-2010, 10:27 AM | #9 | |||
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In Remembrance
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Hi Paula,
Just considering politicians, you can add * Pierre Trudeau * Yasser Arafat, * General Franco. * George Wallace * General Patten etc Then you can find similar lists for actors, sportsmen, musicians, and so on. In "Who's Who", there is a far higher % of PD sufferers than in the population. The only common denominator is being famous, but how does that cause PD? I don't think there is evidence that stress causes PD, but it certainly exacerbates it. I would think a prisoner on death row for years as some are, would be subject to at least as much stress as a concentration camp inmate. I don't know of a single case where a long term death row inmate has developed PD. Lurking, It is difficult enough to get a PD diagnosis even today, let alone 1945. These people were sick from every illness going, rickets, malnutrition, dysentry, etc. The older inmates died more readily, and statistically are the class who more readily get PD. The knowledge of PD was poor, these were pre Sinemet days.
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Diagnosed Nov 1991. Born 1936 |
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03-30-2010, 10:38 AM | #10 | |||
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Hi Rick,
I am not sure of your statement, "the rigor of the muscles indirectly compromised the BBB." Which muscles? How can your muscles affect the BBB? Have you any evidence to support the statement? Sorry, I will have to award myself "nul points" for not understanding!!! Ron
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Diagnosed Nov 1991. Born 1936 |
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