the arrythmia isnt atrial fibrillation by any chance?
Yep. Does that mean that you had the same?
More specifically my arrythmia showed in 3 (out of 10) ECGs I did in the past several years (and I do notice that once in a while my heartbeat seems a bit too fast). The medical reports say:
In 1995: arterial fibrillation plus several ventricular extrasystoles
In 2002: ventricular extrasystoles
In 2003: ventricular extrasystoles and possibility of arterial fibrillation
I only did another 2 ECGs after the 2003 one and they were normal.
Actually, on the oxygen side, I forgot to mention in my previous post that my IRM showed a couple of small ischemic lesions (ischemic = lack of blood supply causing lack of oxygen) and a sizeable arachnoid cyst (all in areas of the brain not normally linked with PD). My neurologist says these things are not too worrying and not directly linked with PD, but I'm starting to wonder if there might be a link - e.g., that the arachnoid cyst may be putting pressure on brain blood circulation and thus reducing oxygen for L-dopa creation. After all, the ischemic lesions do prove that somehow there was a moment in the past were there wasn't enough blood in certain places of the brain (though lesions can happen apparently just because of a few secs without blood in that specific part of the brain, so maybe "just" a small blood clot, arrythmia situation, without any real consequences for PD as afterall I don't have any lesions in the PD part of the brain).
Cheers,
lfs
More specifically my arrythmia showed in 3 (out of 10) ECGs I did in the past several years (and I do notice that once in a while my heartbeat seems a bit too fast). The medical reports say:
In 1995: arterial fibrillation plus several ventricular extrasystoles
In 2002: ventricular extrasystoles
In 2003: ventricular extrasystoles and possibility of arterial fibrillation
I only did another 2 ECGs after the 2003 one and they were normal.
Actually, on the oxygen side, I forgot to mention in my previous post that my IRM showed a couple of small ischemic lesions (ischemic = lack of blood supply causing lack of oxygen) and a sizeable arachnoid cyst (all in areas of the brain not normally linked with PD). My neurologist says these things are not too worrying and not directly linked with PD, but I'm starting to wonder if there might be a link - e.g., that the arachnoid cyst may be putting pressure on brain blood circulation and thus reducing oxygen for L-dopa creation. After all, the ischemic lesions do prove that somehow there was a moment in the past were there wasn't enough blood in certain places of the brain (though lesions can happen apparently just because of a few secs without blood in that specific part of the brain, so maybe "just" a small blood clot, arrythmia situation, without any real consequences for PD as afterall I don't have any lesions in the PD part of the brain).
Cheers,
lfs
yes - spooooky isnt it? i also get those other things (for years) but never been caught on ecg.
i take beta blockers which seem to help.
now for the crazy bit.
my experience (ie how it feels and the sequence of events, but without any idea why) is that it is related to constipation! if so the causal link is
pd => slow digestion => af
not
af=>pd
doctors give you a funny look when you say this. mind you, its the same funny look when you complain for years about tendonitis that turns out to be pd.
i havent the time or energy to delve into cardiology as well as neurology so i have mentally put all that to one side.
but there was an interesting news release a while ago about pd being related to blood supply to the brain - did you see that. so what, at least for some people, the link is the other way around and irregularities in heart beats damages the cells in the SN, if they are the most sensitive cells to oxygen levels? i was told that AF 'churns' up the blood. all very interesting!!!
i take beta blockers which seem to help.
now for the crazy bit.
my experience (ie how it feels and the sequence of events, but without any idea why) is that it is related to constipation! if so the causal link is
pd => slow digestion => af
not
af=>pd
doctors give you a funny look when you say this. mind you, its the same funny look when you complain for years about tendonitis that turns out to be pd.
i havent the time or energy to delve into cardiology as well as neurology so i have mentally put all that to one side.
but there was an interesting news release a while ago about pd being related to blood supply to the brain - did you see that. so what, at least for some people, the link is the other way around and irregularities in heart beats damages the cells in the SN, if they are the most sensitive cells to oxygen levels? i was told that AF 'churns' up the blood. all very interesting!!!
wow, I never thought of it that way!!!
Your post just made me think that the heart is a muscle, and food moves along the digestive system because muscles push it,... and PD messes up (at least some) muscles... so it doesn't seem that crazy to me to think that PD could also impact the heart and the digestive system.
But I also read somewhere that researchers suspect that PD starts developing only a few years (around 5 years or something like that) before we get diagnosed with it (they apparently presume that from the rate of cell transmission loss). If that's really true, then at least in my case my heart and digestion problems pre-date PD (much longer than 5 years)... but I guess that as PD develops stronger, it doesn't seem all that crazy to think that PD might start impacting heart and digestive system as you say... and if the 5-year story is not true, then your suggestion messes up my hopothesis that gastric problems might be behind some PD stuff... Zut, this PD thing is a mess! (but I'm sure we'll get there).
Warm regards,
lfs
Your post just made me think that the heart is a muscle, and food moves along the digestive system because muscles push it,... and PD messes up (at least some) muscles... so it doesn't seem that crazy to me to think that PD could also impact the heart and the digestive system.
But I also read somewhere that researchers suspect that PD starts developing only a few years (around 5 years or something like that) before we get diagnosed with it (they apparently presume that from the rate of cell transmission loss). If that's really true, then at least in my case my heart and digestion problems pre-date PD (much longer than 5 years)... but I guess that as PD develops stronger, it doesn't seem all that crazy to think that PD might start impacting heart and digestive system as you say... and if the 5-year story is not true, then your suggestion messes up my hopothesis that gastric problems might be behind some PD stuff... Zut, this PD thing is a mess! (but I'm sure we'll get there).
Warm regards,
lfs
forgot to say that I never saw the article you mention. If you remember anything that makes it easier to find it could you pls let me know?
Hi
The discussion above is interesting though i admit to getting lost in the details. Re gut involvement do you know the work of these researchers at Kings?
http://www.whatsdrivingparkinsons.net/index.html
Re the cause of PD as in topic name, i wonder about the role of genetics? My thoughts are that in thefuture we will find a there is a predisposing genetic link in nearly all cases.
Trying to track down the components of the actual degenerative process Is a little beyond me but i enjoy reading your posts.
The discussion above is interesting though i admit to getting lost in the details. Re gut involvement do you know the work of these researchers at Kings?
http://www.whatsdrivingparkinsons.net/index.html
Re the cause of PD as in topic name, i wonder about the role of genetics? My thoughts are that in thefuture we will find a there is a predisposing genetic link in nearly all cases.
Trying to track down the components of the actual degenerative process Is a little beyond me but i enjoy reading your posts.
Hi Margaret
i hadnt looked at that site before. quite a few people have pointed the finger at heliobactor, including (unless I am mistaken) our own dear Chewexpert who has been bravely battling along this line for years.
i think everyone agrees that there are multiple causes involved.
I personally have a liking for infections and immune systems being involved.
as far as i know, no-one has ever explained why pd ALWAYS has much more effect on one side or the other. to me, in my ignorance, this points towards an infection (or at least an external event of some sort) being the trigger- the genetics of each SNigra being the same. (probably a laughably simplistic view!).
The fact that the disease takes so very long points, for me, to a process that is self-replicating in a controlled way such as an immune system would, but not an external agent like rabies or meningitis that grows exponentially. this fault in the response to the trigger would be genetic.
the way i see the problem can be attacked from two end of the causal string.
at one end looking for initial triggers such heliobactor (or pesticides, or stress or any of the dozen other contenders) and working forward to how this could cause cell death.
at the other end looking at the cells and alpha synuclein deposits and working backward- what causes alpha synuclein to not fold properly,what causes that etc until each end of the string is joined and we have (probably a very complex) causal connection from trigger to on-going cell destruction.
perhaps people with parkin mutation don't even need a trigger - the same fault takes place anyway so its sort of a frayed string at the start with each individual case being on one or other thread but a common effect at the other end.
i hope nobody is daft enough to take any of the above as more than the amateur rantings of an obsessed individual, but i like to take my theories out for an airing occassionaly. I shall now put them back in their box for a bit.
i hadnt looked at that site before. quite a few people have pointed the finger at heliobactor, including (unless I am mistaken) our own dear Chewexpert who has been bravely battling along this line for years.
i think everyone agrees that there are multiple causes involved.
I personally have a liking for infections and immune systems being involved.
as far as i know, no-one has ever explained why pd ALWAYS has much more effect on one side or the other. to me, in my ignorance, this points towards an infection (or at least an external event of some sort) being the trigger- the genetics of each SNigra being the same. (probably a laughably simplistic view!).
The fact that the disease takes so very long points, for me, to a process that is self-replicating in a controlled way such as an immune system would, but not an external agent like rabies or meningitis that grows exponentially. this fault in the response to the trigger would be genetic.
the way i see the problem can be attacked from two end of the causal string.
at one end looking for initial triggers such heliobactor (or pesticides, or stress or any of the dozen other contenders) and working forward to how this could cause cell death.
at the other end looking at the cells and alpha synuclein deposits and working backward- what causes alpha synuclein to not fold properly,what causes that etc until each end of the string is joined and we have (probably a very complex) causal connection from trigger to on-going cell destruction.
perhaps people with parkin mutation don't even need a trigger - the same fault takes place anyway so its sort of a frayed string at the start with each individual case being on one or other thread but a common effect at the other end.
i hope nobody is daft enough to take any of the above as more than the amateur rantings of an obsessed individual, but i like to take my theories out for an airing occassionaly. I shall now put them back in their box for a bit.
ps so yes i agree absolutely about there always being a genetic link except for when people take MPTP, then it doesnt matter. So the same might be true of other poisoning cases but they are really a different disease with the same outcome.
My understanding is that once the dopamine producing cells in the SN are destroyed (for whatever reason - be it genetic, enviromnental or the result of some chemical imbalance) they cannot be regenerated The activity of dopamine transporters is directly linked to the amount of dopamine available. ( Hence the advice to not take l-dopa medication with a full meal , since proteins compete to use the same receptors) . So the only way of counteracting the symptoms of lack of dopamine is to intoduce DA's or l-dopa that cross the blood brain barrier.
Also, we are not mice, and as far as I know it is illegal as well as amoral to carry out an autopsy upon a living pwp. Death does tend to change one's brains structure
Also, we are not mice, and as far as I know it is illegal as well as amoral to carry out an autopsy upon a living pwp. Death does tend to change one's brains structure
Hi,
Thanks for the interesting new perspectives and insights, as well as for your (Margaret’s) kind words on enjoying the postings (despite the detail).
A few of comments from my side:
1. Really interesting link, Margaret; thanks for sharing. Not sure I fully understand the logic behind what they say yet (only did a quick read so far), but the notion that infection and/or h. pylori are linked to PD rings very true to me as I have/had both.
2. Your “little beyond me” comment is important to me as I myself hesitated on that one. Medical terminology can be quite daunting; PD is a complex subject; and most/all of us have no medical background (I clearly don’t). But I’m personally encouraged by the fact that (a) google is always there to help with the terminology, (b) nobody knows our own bodies and history as well as ourselves, (c) any complex problem can always be broken down into smaller easier pieces, and (d) more brains working on a problem is better than fewer brains
.
3. In my opinion genetics may, of course, be part of the problem. Genetic “defaults” has been found to be driving PD in some cases and a genetic “predisposition” may contribute in other cases. But as far as I understand there’s little one can do to change one’s own genetics. So, I’m personally leaving those to the end of my “investigation”, so as to focus first on hypotheses that can be acted upon more easily. So, I like Turnip’s hypothesis that it’s unlikely to be just because of genetics
4. In my view, the point that annebernadette makes is an important one (that once dopamine producing cells are destroyed they cannot be regenerated). I know this is a common understanding, but I personally don’t fully understand on what it is based (and because it would mean bad news for us, please forgive me for challenging it). I do take as a fact that dopamine cell activity goes down with PD progression, but couldn’t that just be explained by the fact that the root causes of PD are still there and continue to do their damage? Also, as an example of what I’m thinking: I read that Azilect (which I’m taking) is a irreversible MAO inhibitor but that its “irreversibility” just spans around 2 weeks. In other words, around 2 weeks after you stop taking it the MAO enzymes it was inhibiting somehow starts working normally again. So, do we know that the same cannot apply to dopamine activity? If somehow we were able to fix the root cause of PD, couldn’t our brains regain some of it’s ability to create dopamine?
If anyone has any insight/hypothesis on irreversibility of dopamine activity loss and/or on what are possible causes of the types of infections that may be linked to PD, I'm obviously extremelly interested.
Warm regards to all,
lfs
Thanks for the interesting new perspectives and insights, as well as for your (Margaret’s) kind words on enjoying the postings (despite the detail).
A few of comments from my side:
1. Really interesting link, Margaret; thanks for sharing. Not sure I fully understand the logic behind what they say yet (only did a quick read so far), but the notion that infection and/or h. pylori are linked to PD rings very true to me as I have/had both.
2. Your “little beyond me” comment is important to me as I myself hesitated on that one. Medical terminology can be quite daunting; PD is a complex subject; and most/all of us have no medical background (I clearly don’t). But I’m personally encouraged by the fact that (a) google is always there to help with the terminology, (b) nobody knows our own bodies and history as well as ourselves, (c) any complex problem can always be broken down into smaller easier pieces, and (d) more brains working on a problem is better than fewer brains
.3. In my opinion genetics may, of course, be part of the problem. Genetic “defaults” has been found to be driving PD in some cases and a genetic “predisposition” may contribute in other cases. But as far as I understand there’s little one can do to change one’s own genetics. So, I’m personally leaving those to the end of my “investigation”, so as to focus first on hypotheses that can be acted upon more easily. So, I like Turnip’s hypothesis that it’s unlikely to be just because of genetics
4. In my view, the point that annebernadette makes is an important one (that once dopamine producing cells are destroyed they cannot be regenerated). I know this is a common understanding, but I personally don’t fully understand on what it is based (and because it would mean bad news for us, please forgive me for challenging it). I do take as a fact that dopamine cell activity goes down with PD progression, but couldn’t that just be explained by the fact that the root causes of PD are still there and continue to do their damage? Also, as an example of what I’m thinking: I read that Azilect (which I’m taking) is a irreversible MAO inhibitor but that its “irreversibility” just spans around 2 weeks. In other words, around 2 weeks after you stop taking it the MAO enzymes it was inhibiting somehow starts working normally again. So, do we know that the same cannot apply to dopamine activity? If somehow we were able to fix the root cause of PD, couldn’t our brains regain some of it’s ability to create dopamine?
If anyone has any insight/hypothesis on irreversibility of dopamine activity loss and/or on what are possible causes of the types of infections that may be linked to PD, I'm obviously extremelly interested.
Warm regards to all,
lfs
Some interesting articles
Blood flow
http://www.neurochallenge.org/neu/2011/09/05/blood-vessels-and-parkinson-disease/
Blood vessels and Parkinson Disease?
On September 5, 2011, in Blog, Medicine, by Dr._Sutherland ....Usually, people don’t think of Parkinson Disease as being related to blood flow, or lack of blood flow, to the brain. However, neurologists have known for a very long time that small strokes in the brain can cause walking and balance problems which may mimic PD. This condition is known as Parkinsonism. The blockage of hundreds or thousands of tiny blood vessels builds up slowly over time and causes dysfunction or death of brain cells. These are akin to “silent” strokes; the person afflicted with them is never aware of any particular event. The end result is slow movement, poor balance, shuffling gait, slow thinking, memory loss. Sound familiar?
We also know that any degenerative neurological condition, such as Alzheimer Disease, Parkinson Disease, or Huntington Disease, seems to progress more rapidly if there is also blockage of the small blood vessels as mentioned above. This is partly the basis for encouraging exercise in people at risk for such diseases. We believe, and studies seem to support, that control of cardiovascular risk factors (high blood pressure, high cholesterol, diabetes) delays the onset and severity of neurological disease, especially in the case of Alzheimer Disease.
In an important new study published in the journal Stroke: Journal of the American Heart Association, researchers from Rush University Medical Center in Chicago, showed that, even in people with seemingly normal brain scans (MRI or CT), there may be small blood vessel blockages seen in the brain at the time of autopsy. Furthermore, they correlated the severity of walking problems with the severity of the blockages. Up to 30% of people with normal brain scans had abnormal blood vessels on autopsy. The implication is that slow movements, decreased balance, and walking abnormalities may not be “normal aging.” This is similar to what we see with memory loss in the elderly; dementia used to be considered normal aging, but we now know that anything beyond mild memory loss suggests that there is an abnormal process occurring in the brain, such as Alzheimer Disease or other problems.
The main point is that we all need to take care of our cardiovascular health through proper diet, exercise, and getting treated for any hypertension, diabetes, or cholesterol problems.
Dr. Paul Jannetta
..MRI Study Shows Brain Blood Vessel Abnormality May Be Factor in Parkinson’s Disease
PRWeb – Thu, Sep 8, 2011....EmailNew: Now the email button gives you a quick and easy way to start a conversation.
Share0Print......A new study of brain MRI scans suggests a potentially treatable blood vessel abnormality may be associated with Parkinson's Disease in some patients. The research is published today in the journal Neurology International by a team of physicians and neuroscientists at Allegheny General Hospital in Pittsburgh.
Pittsburgh, PA (PRWEB) September 08, 2011
A potentially treatable blood vessel abnormality in the brain may be the cause of Parkinson’s Disease in some patients, according to a study published today in the journal Neurology International by a team of leading physicians and neuroscientists at Pittsburgh’s Allegheny General Hospital (AGH).
Recognized worldwide as one of the preeminent authorities on diseases associated with vascular compression of cranial nerves, the study’s lead author, Peter Jannetta, MD, is credited with developing the modern surgical technique to treat such conditions. Called microvascular decompression (MVD), the procedure involves repositioning compressive arteries in the brain and placing a protective pad between the artery and the structure it is compromising.
It was in course of treating a patient for the cranial nerve disease trigeminal neuralgia who also suffered from Parkinson’s Disease that Dr. Jannetta first observed the possible role of vascular compression in Parkinson’s. In addition to vascular compression of the left trigeminal nerve, the patient also had notable compression of an area of the brain called the left cerebral penduncle. The cerebral penduncles are two cylinder-like nerve bundles in the brain stem that act as a conduit for signals that help control motor functioning throughout the body.
After performing MVD of the left trigeminal nerve, Dr. Jannetta decompressed the patient’s cerebral penduncle by mobilizing and repositioning the offending artery. The results were stunning. By post-operative day five, the patient’s Parkinson’s symptoms, including severe tremor and rigidity, had disappeared. She remained symptom free for 18 months, after which she suffered a full recurrence. A follow-up MRI scan showed new compression of the non-treated right cerebral penduncle by the opposite posterior cerebral artery.
Based on this case, Dr. Jannetta and his colleagues at AGH conducted a blinded MRI study analyzing the brains of 20 patients with Parkinson’s and 20 healthy control subjects. The study showed that 78 percent of the Parkinson’s Disease patients had visible arterial compression/distortion of one or both cerebral penduncles.
Of the study’s 20 control subjects, just two had low grade compression of the cerebral penduncle and one of those was subsequently diagnosed with Parkinson’s.
“Though we clearly need to continue our research on a larger scale to substantiate this remarkable observation, the very idea that a manageable vascular abnormality in the brain may be a critical factor in disease onset and manifestation for some Parkinson’s patients is an extremely exciting possibility,” Dr. Jannetta said.
Parkinson’s affects more than one million people in the United States and despite significant advancements over the past several decades in uncovering the pathogenesis of the disease, conventional treatments provide symptomatic relief only.
Dr. Jannetta said his team’s data raises compelling questions that will be addressed in follow up studies: Is there a form of parkinsonism related to arterial compression of the cerebral penduncle? Does unilateral cerebral penduncle arterial compression cause unilateral disease only? Can it cause bilateral Parkinson’s Disease in time? Can MVD relieve parkinsonism and if so, will it be as safe and effective as seen in other diseases?
A multi-center clinical trial to further explore the AGH team’s premise has already been organized and is slated to begin later this year.
In addition to Dr. Jannetta, who serves as Emeritus Professor of Neurosurgery at AGH, other members of the study team included AGH neurosurgeons Donald Whiting, MD, Matthew Quigley, MD, and Joseph Hobbs, MD, neurologist Jon Brillman, MD, and neuro-radiologists Melanie Fukui, MD and Robert Williams, MD.
Dr. Jannetta and his colleagues at the AGH Jannetta Cranial Nerve Disorders Center, including neurosurgeon Khaled Aziz, MD, have performed more than 10,000 microvascular decompression surgeries.
Dr. Aziz’s recent addition to the program has enabled Dr. Jannetta to expand his groundbreaking research into the role of vascular compression in a growing number of cranial nerve and brainstem syndromes, including hyptertension and diabetes.
A landmark paper published by Dr. Jannetta in the August 2010 edition of Surgical Neurology International presented the first evidence that vascular compression of a section of the brain called the medulla oblongata is a factor in Type 2 diabetes.
http://news.yahoo.com/mri-study-shows-brain-blood-vessel-abnormality-may-040210137.html
http://neurotalk.psychcentral.com/thread160149.html
On / off cell switch
Parkinson’s disease power switch located
Published On Wed Oct 6 2010Email Print
Rss ArticleComments (1)Joseph Hall
Health Reporter
In a transformative new study, U.S. researchers have uncovered both the key cause and a promising treatment for Parkinson’s disease.
The degenerative movement disorder occurs when the tiny power plants that fuel afflicted brain cells are turned off, the Harvard University-led study has found.
This power outage may well be reversed by medications that throw a master switch gene controlling the energy-producing cell structures back on, the paper suggests.
“It’s all very exciting . . . because I think it is potentially a breakthrough in Parkinson’s disease,” says Dr. Anthony Phillips, head of neurosciences with the Canadian Institutes of Health Research.
“It’s really coming together nicely. I think it is very, very promising and I think it will get a lot of interest.”
Dr. Clemens Scherzer, the senior paper author, likens the key gene he has identified – known as PGC-1alpha — to the main breaker in a basement electrical console.
“This would be the main power switch that turns everything back on,” says Scherzer, a Harvard neurologist.
Importantly, Scherzer says, there are already approved drugs available that are turning the same genetic master switch on in other diseases like diabetes.
If these drugs can hit the switch in brain cells, as Phillips says is likely, it could provide a treatment that would ward off or reverse the ailment’s crippling onslaught in its earliest stages.
Scherzer says that all the genes that control the energy-producing machinery of a cell – churning structures known as mitochondria – are turned off in Parkinson’s disease.
These mitochondria are divided into five power cells, each of which is genetically inactivated in the disease. But all five centres can be reactivated by targeting the master PGC-1alpha gene, Scherzer says.
“You can think of it like a power switch that, if you turn on this master regulator you can turn the activity of this energy-producing machinery back on,” he says.
Dr. Timothy Greenamyre, vice chair of neurology at the University of Pittsburgh, calls the identification of a mitochondrial cause a “sea change” in the understanding of the ailment.
“This study was really a tour-de-force and Scherzer brought together a lot of groups and their data sets to do this,” says Greenamyre, a movement disorder expert.
“I think he really has to be complimented. This is a very, very solid study.”
Parkinson’s, which affects some 100,000 Canadians and more than 6 million globally, is an attack on dopamine cells in the brain stem, which control motor movements.
In the study, Scherzer’s team actually turned tissue samples of these dopamine cells back on by inducing high levels of the master gene into a cultured mix.
“But (the gene) is a very exciting target for medicines because pharmaceutical companies have realized its importance before in diseases that are much more common than Parkinson’s, such as diabetes,” he says.
Indeed, there are approved diabetes drugs, and several promising medications now being screened, that appear able to throw the PGC-1alpha switch.
“Pharmaceutical companies can now go back and see whether these drugs or tested compounds can cross into the brain of Parkinson’s patients,” Scherzer says.
Phillips says the likelihood that some of these drugs would cross into the brain is high.
Adds Greenamyre: “I agree there’s that potential and it’s very exciting.”
The study appears in the first anniversary issue of the journal Science Translational Medicine, which features research making the jump from the laboratory to practical usage.
Scherzer thinks a combination of environmental chemicals, like pesticides and manganese, plus a variety of genetic risk factors for the disease combine to cause the ailment.
Yet the afflicted, dopamine-producing cells appear to be able to ward these risk factors off when their mitochondria are robust.
Greenamyre’s only caution is that the paper does not definitively show that PGC-1alpha has itself gone off in Parkinson’s disease.
“They show that everything that’s controlled by (it) is down, but they don’t show there’s anything wrong with the breaker switch,” he says.
He says it could be imagined the electrical wiring coming out of the main switch is bad, but that the switch itself is working.
.
Blood flow
http://www.neurochallenge.org/neu/2011/09/05/blood-vessels-and-parkinson-disease/
Blood vessels and Parkinson Disease?
On September 5, 2011, in Blog, Medicine, by Dr._Sutherland ....Usually, people don’t think of Parkinson Disease as being related to blood flow, or lack of blood flow, to the brain. However, neurologists have known for a very long time that small strokes in the brain can cause walking and balance problems which may mimic PD. This condition is known as Parkinsonism. The blockage of hundreds or thousands of tiny blood vessels builds up slowly over time and causes dysfunction or death of brain cells. These are akin to “silent” strokes; the person afflicted with them is never aware of any particular event. The end result is slow movement, poor balance, shuffling gait, slow thinking, memory loss. Sound familiar?
We also know that any degenerative neurological condition, such as Alzheimer Disease, Parkinson Disease, or Huntington Disease, seems to progress more rapidly if there is also blockage of the small blood vessels as mentioned above. This is partly the basis for encouraging exercise in people at risk for such diseases. We believe, and studies seem to support, that control of cardiovascular risk factors (high blood pressure, high cholesterol, diabetes) delays the onset and severity of neurological disease, especially in the case of Alzheimer Disease.
In an important new study published in the journal Stroke: Journal of the American Heart Association, researchers from Rush University Medical Center in Chicago, showed that, even in people with seemingly normal brain scans (MRI or CT), there may be small blood vessel blockages seen in the brain at the time of autopsy. Furthermore, they correlated the severity of walking problems with the severity of the blockages. Up to 30% of people with normal brain scans had abnormal blood vessels on autopsy. The implication is that slow movements, decreased balance, and walking abnormalities may not be “normal aging.” This is similar to what we see with memory loss in the elderly; dementia used to be considered normal aging, but we now know that anything beyond mild memory loss suggests that there is an abnormal process occurring in the brain, such as Alzheimer Disease or other problems.
The main point is that we all need to take care of our cardiovascular health through proper diet, exercise, and getting treated for any hypertension, diabetes, or cholesterol problems.
Dr. Paul Jannetta
..MRI Study Shows Brain Blood Vessel Abnormality May Be Factor in Parkinson’s Disease
PRWeb – Thu, Sep 8, 2011....EmailNew: Now the email button gives you a quick and easy way to start a conversation.
Share0Print......A new study of brain MRI scans suggests a potentially treatable blood vessel abnormality may be associated with Parkinson's Disease in some patients. The research is published today in the journal Neurology International by a team of physicians and neuroscientists at Allegheny General Hospital in Pittsburgh.
Pittsburgh, PA (PRWEB) September 08, 2011
A potentially treatable blood vessel abnormality in the brain may be the cause of Parkinson’s Disease in some patients, according to a study published today in the journal Neurology International by a team of leading physicians and neuroscientists at Pittsburgh’s Allegheny General Hospital (AGH).
Recognized worldwide as one of the preeminent authorities on diseases associated with vascular compression of cranial nerves, the study’s lead author, Peter Jannetta, MD, is credited with developing the modern surgical technique to treat such conditions. Called microvascular decompression (MVD), the procedure involves repositioning compressive arteries in the brain and placing a protective pad between the artery and the structure it is compromising.
It was in course of treating a patient for the cranial nerve disease trigeminal neuralgia who also suffered from Parkinson’s Disease that Dr. Jannetta first observed the possible role of vascular compression in Parkinson’s. In addition to vascular compression of the left trigeminal nerve, the patient also had notable compression of an area of the brain called the left cerebral penduncle. The cerebral penduncles are two cylinder-like nerve bundles in the brain stem that act as a conduit for signals that help control motor functioning throughout the body.
After performing MVD of the left trigeminal nerve, Dr. Jannetta decompressed the patient’s cerebral penduncle by mobilizing and repositioning the offending artery. The results were stunning. By post-operative day five, the patient’s Parkinson’s symptoms, including severe tremor and rigidity, had disappeared. She remained symptom free for 18 months, after which she suffered a full recurrence. A follow-up MRI scan showed new compression of the non-treated right cerebral penduncle by the opposite posterior cerebral artery.
Based on this case, Dr. Jannetta and his colleagues at AGH conducted a blinded MRI study analyzing the brains of 20 patients with Parkinson’s and 20 healthy control subjects. The study showed that 78 percent of the Parkinson’s Disease patients had visible arterial compression/distortion of one or both cerebral penduncles.
Of the study’s 20 control subjects, just two had low grade compression of the cerebral penduncle and one of those was subsequently diagnosed with Parkinson’s.
“Though we clearly need to continue our research on a larger scale to substantiate this remarkable observation, the very idea that a manageable vascular abnormality in the brain may be a critical factor in disease onset and manifestation for some Parkinson’s patients is an extremely exciting possibility,” Dr. Jannetta said.
Parkinson’s affects more than one million people in the United States and despite significant advancements over the past several decades in uncovering the pathogenesis of the disease, conventional treatments provide symptomatic relief only.
Dr. Jannetta said his team’s data raises compelling questions that will be addressed in follow up studies: Is there a form of parkinsonism related to arterial compression of the cerebral penduncle? Does unilateral cerebral penduncle arterial compression cause unilateral disease only? Can it cause bilateral Parkinson’s Disease in time? Can MVD relieve parkinsonism and if so, will it be as safe and effective as seen in other diseases?
A multi-center clinical trial to further explore the AGH team’s premise has already been organized and is slated to begin later this year.
In addition to Dr. Jannetta, who serves as Emeritus Professor of Neurosurgery at AGH, other members of the study team included AGH neurosurgeons Donald Whiting, MD, Matthew Quigley, MD, and Joseph Hobbs, MD, neurologist Jon Brillman, MD, and neuro-radiologists Melanie Fukui, MD and Robert Williams, MD.
Dr. Jannetta and his colleagues at the AGH Jannetta Cranial Nerve Disorders Center, including neurosurgeon Khaled Aziz, MD, have performed more than 10,000 microvascular decompression surgeries.
Dr. Aziz’s recent addition to the program has enabled Dr. Jannetta to expand his groundbreaking research into the role of vascular compression in a growing number of cranial nerve and brainstem syndromes, including hyptertension and diabetes.
A landmark paper published by Dr. Jannetta in the August 2010 edition of Surgical Neurology International presented the first evidence that vascular compression of a section of the brain called the medulla oblongata is a factor in Type 2 diabetes.
http://news.yahoo.com/mri-study-shows-brain-blood-vessel-abnormality-may-040210137.html
http://neurotalk.psychcentral.com/thread160149.html
On / off cell switch
Parkinson’s disease power switch located
Published On Wed Oct 6 2010Email Print
Rss ArticleComments (1)Joseph Hall
Health Reporter
In a transformative new study, U.S. researchers have uncovered both the key cause and a promising treatment for Parkinson’s disease.
The degenerative movement disorder occurs when the tiny power plants that fuel afflicted brain cells are turned off, the Harvard University-led study has found.
This power outage may well be reversed by medications that throw a master switch gene controlling the energy-producing cell structures back on, the paper suggests.
“It’s all very exciting . . . because I think it is potentially a breakthrough in Parkinson’s disease,” says Dr. Anthony Phillips, head of neurosciences with the Canadian Institutes of Health Research.
“It’s really coming together nicely. I think it is very, very promising and I think it will get a lot of interest.”
Dr. Clemens Scherzer, the senior paper author, likens the key gene he has identified – known as PGC-1alpha — to the main breaker in a basement electrical console.
“This would be the main power switch that turns everything back on,” says Scherzer, a Harvard neurologist.
Importantly, Scherzer says, there are already approved drugs available that are turning the same genetic master switch on in other diseases like diabetes.
If these drugs can hit the switch in brain cells, as Phillips says is likely, it could provide a treatment that would ward off or reverse the ailment’s crippling onslaught in its earliest stages.
Scherzer says that all the genes that control the energy-producing machinery of a cell – churning structures known as mitochondria – are turned off in Parkinson’s disease.
These mitochondria are divided into five power cells, each of which is genetically inactivated in the disease. But all five centres can be reactivated by targeting the master PGC-1alpha gene, Scherzer says.
“You can think of it like a power switch that, if you turn on this master regulator you can turn the activity of this energy-producing machinery back on,” he says.
Dr. Timothy Greenamyre, vice chair of neurology at the University of Pittsburgh, calls the identification of a mitochondrial cause a “sea change” in the understanding of the ailment.
“This study was really a tour-de-force and Scherzer brought together a lot of groups and their data sets to do this,” says Greenamyre, a movement disorder expert.
“I think he really has to be complimented. This is a very, very solid study.”
Parkinson’s, which affects some 100,000 Canadians and more than 6 million globally, is an attack on dopamine cells in the brain stem, which control motor movements.
In the study, Scherzer’s team actually turned tissue samples of these dopamine cells back on by inducing high levels of the master gene into a cultured mix.
“But (the gene) is a very exciting target for medicines because pharmaceutical companies have realized its importance before in diseases that are much more common than Parkinson’s, such as diabetes,” he says.
Indeed, there are approved diabetes drugs, and several promising medications now being screened, that appear able to throw the PGC-1alpha switch.
“Pharmaceutical companies can now go back and see whether these drugs or tested compounds can cross into the brain of Parkinson’s patients,” Scherzer says.
Phillips says the likelihood that some of these drugs would cross into the brain is high.
Adds Greenamyre: “I agree there’s that potential and it’s very exciting.”
The study appears in the first anniversary issue of the journal Science Translational Medicine, which features research making the jump from the laboratory to practical usage.
Scherzer thinks a combination of environmental chemicals, like pesticides and manganese, plus a variety of genetic risk factors for the disease combine to cause the ailment.
Yet the afflicted, dopamine-producing cells appear to be able to ward these risk factors off when their mitochondria are robust.
Greenamyre’s only caution is that the paper does not definitively show that PGC-1alpha has itself gone off in Parkinson’s disease.
“They show that everything that’s controlled by (it) is down, but they don’t show there’s anything wrong with the breaker switch,” he says.
He says it could be imagined the electrical wiring coming out of the main switch is bad, but that the switch itself is working.
.
thanks,the article about dr janetta was the one i couldn't recall.
i have just read the most interesting (ie reinforces my own prejudices ) article on parkonsons
http://archneur.ama-assn.org/cgi/content/full/65/6/705
its called [u]There Is No Parkinsons Disease.[/u]
I think it relevant to any individual looking for the cause of their instance of PD.
i have just read the most interesting (ie reinforces my own prejudices ) article on parkonsons
http://archneur.ama-assn.org/cgi/content/full/65/6/705
its called [u]There Is No Parkinsons Disease.[/u]
I think it relevant to any individual looking for the cause of their instance of PD.
I totally agree - the 'one size fits all' umbrella diagnosis is counter-productive to finding separate 'tailor made' cures for the different segments that make up the PWP population.
Individual medical histories seem of scant interest to the Neuro once you have been generically labelled as a PWP.
Individual medical histories seem of scant interest to the Neuro once you have been generically labelled as a PWP.
Wow. The article on oxygen opens a whole new set of perspectives for me. Until now, I have been struggling with the point that if lack of oxygen might be killing any of my dopamine-related cells, how come it didn't show up in my IRM. The point that “up to 30% of people with normal brain scans had abnormal blood vessels on autopsy” sort of answers that one. And it goes without saying that the possibilities on the other two articles look very interesting too (the one on vascular compression of cranial nerves in particular rings very close to home for me).
My special thanks to Krugen68 for the article that argues there isn’t a single type of PD. Makes me feel proud of having written “your PD” in the title of this post.
Cheers,
lfs
My special thanks to Krugen68 for the article that argues there isn’t a single type of PD. Makes me feel proud of having written “your PD” in the title of this post
.Cheers,
lfs
Hi,
In my previous postings I have been focusing a lot on possible PD causes that make our brain produce less dopamine than it should (by looking at all the components that get in the dopamine creation "formula"). It may be helpful to also look into more detail at the other "big" possibility: that the cause may be something that is destroying the dopaminic cells. As turnip rightly pointed out after my first post, this may be "the" cause - and at the very least it must be considered a very serious candidate.
I haven't seen any "formula" for this part. So far I only have a "laundry list" of possible candidates, which is as follows:
1. Deficiency in NACH (mainly consists of vit B9/folic acid) deficiency.
This one generates both deficiency in the creation of L-Dopa and in the
oxidation of brain cells. So far I've measured folic acid (and my level is
ok). Not too sure this is the same as measuring NACH (which is made of a few
other things too), but at least in my case I don't seem to be missing the
main ingredient.
2. Low oxygen in the brain. This is a tough one as it's difficult to measure,
difficul to act upon... and I see it as a good candidate for my own case.
3. Genetic problems. This is another tough one. While I presume we can
measure several of these genes that are known to give problems when defective,
I'm not sure normal folks like us can easily act upon them. But, of course,
many smart researchers seem to be trying to figure out ways amazing ways to
correct the problems such "defects" originate which is great.
4. Infection and/or toxic implications of hosting nasty bacteria/viruses. This
is another of my personal top candidates because my lab tests seem to
indicate I have had infection signs for a while now. Only problem is that I
have no clue where the infection comes from. Googling infection produces a
horribly long list of possible candidates. So far the ones that I've
heard that ring a bell for my own specific case are:
a. H. Pylori (but I tested negative a few months ago and still have PD).
b. Other gastro-intestinal related (still doing more tests to try to figure
out if I can find a yes/no to this one).
c. Dental related. Someone just sent me something about
dental "cavitations", which are basically pools of bacteria that remain
in the places where you got teeth extracted (and I had my wistom teeth
extracted a while ago). Apparently other type of dentist work can also
create situations where you get stuck with plenty of bacteria for a long
time.
5. Toxic metal poisoning. A week ago I would have dismissed this one for my own
personal case. But now I think the following are valid suspects for my own
case:
a. Lead (from the small bullet I have in my arm since a kid).
b. Mercury (from my dental fillings).
I have no idea if the quantities of lead and mercury I have are big enough to
be toxic... but I intend on finding out.
If you are aware of other candidates for this list please do let me know. Warm regards to all,
lfs
In my previous postings I have been focusing a lot on possible PD causes that make our brain produce less dopamine than it should (by looking at all the components that get in the dopamine creation "formula"). It may be helpful to also look into more detail at the other "big" possibility: that the cause may be something that is destroying the dopaminic cells. As turnip rightly pointed out after my first post, this may be "the" cause - and at the very least it must be considered a very serious candidate.
I haven't seen any "formula" for this part. So far I only have a "laundry list" of possible candidates, which is as follows:
1. Deficiency in NACH (mainly consists of vit B9/folic acid) deficiency.
This one generates both deficiency in the creation of L-Dopa and in the
oxidation of brain cells. So far I've measured folic acid (and my level is
ok). Not too sure this is the same as measuring NACH (which is made of a few
other things too), but at least in my case I don't seem to be missing the
main ingredient.
2. Low oxygen in the brain. This is a tough one as it's difficult to measure,
difficul to act upon... and I see it as a good candidate for my own case.
3. Genetic problems. This is another tough one. While I presume we can
measure several of these genes that are known to give problems when defective,
I'm not sure normal folks like us can easily act upon them. But, of course,
many smart researchers seem to be trying to figure out ways amazing ways to
correct the problems such "defects" originate which is great.
4. Infection and/or toxic implications of hosting nasty bacteria/viruses. This
is another of my personal top candidates because my lab tests seem to
indicate I have had infection signs for a while now. Only problem is that I
have no clue where the infection comes from. Googling infection produces a
horribly long list of possible candidates. So far the ones that I've
heard that ring a bell for my own specific case are:
a. H. Pylori (but I tested negative a few months ago and still have PD).
b. Other gastro-intestinal related (still doing more tests to try to figure
out if I can find a yes/no to this one).
c. Dental related. Someone just sent me something about
dental "cavitations", which are basically pools of bacteria that remain
in the places where you got teeth extracted (and I had my wistom teeth
extracted a while ago). Apparently other type of dentist work can also
create situations where you get stuck with plenty of bacteria for a long
time.
5. Toxic metal poisoning. A week ago I would have dismissed this one for my own
personal case. But now I think the following are valid suspects for my own
case:
a. Lead (from the small bullet I have in my arm since a kid).
b. Mercury (from my dental fillings).
I have no idea if the quantities of lead and mercury I have are big enough to
be toxic... but I intend on finding out.
If you are aware of other candidates for this list please do let me know. Warm regards to all,
lfs
Don't understand it no where near as much as you do,but like you i keep trying to understand WHY.The person who right the reply" you have got it so why worry" ,i do think is quite right but i find it difficult to.I truly believe mine is drug induced Pd through years of taking anti-depressants.Having said that,i feel worse because it makes me angry and that definitely does not help.I am going to see consultant in April and will mention it to him,but don't think they ever will admit it could be.But when reading causes on different website it clearly states that this is one of the causes.
HI Hopeful
I understand why you want to but it will be a waste of time.
As K says, (apologies if i misinterpret) consultants don't treat individuals they treat populations. From their point of view there is nothing to be gained from investigating individual lines of causation. They are only concerned with the resulting illness presented to them and what interventions to use.
that is why, shouting to the PUK, WHAT WE NEED IS A PERMANENT SCIENTIFIC RESOURCE WE CAN BOUNCE QUESTIONS OF NO MATTER HOW SILLY. Doesnt need to be a professor, a good phd student would do(going rate 1 big mac and a frothy coffee per hour). there are dozens of people desperate to know more about what has happened to them and the nhs is not designed to satisfy that basic need. the regular specialist spots are useful but it is a very different need.
come on puk, this would do a lot of psychological good to a lot of people recently diagnosed and others!
I understand why you want to but it will be a waste of time.
As K says, (apologies if i misinterpret) consultants don't treat individuals they treat populations. From their point of view there is nothing to be gained from investigating individual lines of causation. They are only concerned with the resulting illness presented to them and what interventions to use.
that is why, shouting to the PUK, WHAT WE NEED IS A PERMANENT SCIENTIFIC RESOURCE WE CAN BOUNCE QUESTIONS OF NO MATTER HOW SILLY. Doesnt need to be a professor, a good phd student would do(going rate 1 big mac and a frothy coffee per hour). there are dozens of people desperate to know more about what has happened to them and the nhs is not designed to satisfy that basic need. the regular specialist spots are useful but it is a very different need.
come on puk, this would do a lot of psychological good to a lot of people recently diagnosed and others!
Hi lfs
Without getting too 'tree huggy' after reading John Coleman's book when I was first dx, I reviewed my shampoos, deodorants, toothpaste, talc, hair gel etc etc
When I googled some of the ingredients I was astonished
The same applies to some common household products
Without getting too 'tree huggy' after reading John Coleman's book when I was first dx, I reviewed my shampoos, deodorants, toothpaste, talc, hair gel etc etc
When I googled some of the ingredients I was astonished
The same applies to some common household products
Hi Hopefull,
Thanks for your post and I'm glad you're also trying to understand the why. I personally believe that we may all have slightly different causes for our PDs and thus finding which one is the cause for each one of us (or at least having some good hypotheses about it) will helps us better determine what we can do to manage it better... (or, if we get really lucky, even perhaps reverse some of the damage). Nobody knows for sure, of course, and maybe I'm totally wrong, but I am surely going to try to find out the causes of my PD.
Thanks for mentioning anti-depressants as a possible cause. I confess I hadn't thought of it before and also the that I find the whole link between depression and PD a little intriguing. The reason I hand't thought of before is because I personally never took any anti-depressors, so haven't really looked into it in any detail (sorry for that). The reason I find the subject intriguing is that (a) I also keep reading stuff that suggests that there is a link between lack of dopamine and depression but, while I'm myself obviously running low on dopamine, I don't think I'm feeling depressed (or ever had, actually); and (b) until I read your post, I was under the impression that anti-depressors were actually good for PD. I guess my (possibly very wrong) impression came from the fact that many anti-depressors seem to be MAO-inhibitor... and my PD medication (Azilect) is also a MAO-inhibitor. But I may just have jumpted to conclusions: maybe the anti-depressors you've been taking is not a MAO-inhibitor... or maybe it's a different kind. Actually, I'd be curious to find out. Do you know what kind it is? If not, would you mind sharing the brand? (I could try to find out).
Warm regards,
lfs
P.S. Please don't think I understand much more about this than you or other folks on this forum. You'd be surprised
Thanks for your post and I'm glad you're also trying to understand the why. I personally believe that we may all have slightly different causes for our PDs and thus finding which one is the cause for each one of us (or at least having some good hypotheses about it) will helps us better determine what we can do to manage it better... (or, if we get really lucky, even perhaps reverse some of the damage). Nobody knows for sure, of course, and maybe I'm totally wrong, but I am surely going to try to find out the causes of my PD.
Thanks for mentioning anti-depressants as a possible cause. I confess I hadn't thought of it before and also the that I find the whole link between depression and PD a little intriguing. The reason I hand't thought of before is because I personally never took any anti-depressors, so haven't really looked into it in any detail (sorry for that). The reason I find the subject intriguing is that (a) I also keep reading stuff that suggests that there is a link between lack of dopamine and depression but, while I'm myself obviously running low on dopamine, I don't think I'm feeling depressed (or ever had, actually); and (b) until I read your post, I was under the impression that anti-depressors were actually good for PD. I guess my (possibly very wrong) impression came from the fact that many anti-depressors seem to be MAO-inhibitor... and my PD medication (Azilect) is also a MAO-inhibitor. But I may just have jumpted to conclusions: maybe the anti-depressors you've been taking is not a MAO-inhibitor... or maybe it's a different kind. Actually, I'd be curious to find out. Do you know what kind it is? If not, would you mind sharing the brand? (I could try to find out).
Warm regards,
lfs
P.S. Please don't think I understand much more about this than you or other folks on this forum. You'd be surprised
Hi Turnip
I don't live in the UK and I'm not sure I understand what a "consultant" is (doesn't exist here)... but if my guess is correct, it doesn't sound like someone with a medical degree... and so difficult to imagine they can allow themselves even to comment, much less advise, on anything that deviates from the very well known and proven medical stuff.
From my side, I'd also very much welcome a real scientific resource we could ask questions. I've been trying to do that by scheduling appointments which different doctors, only to find that it takes a huge amount of time to get an appointment, and by the time I get to explain why I'm there, the appointment is over.... and never mind the cost (I'm happy I have a good insurance).
Hi Kruggen68,
You're right that these are good candidates too (despite the fact that it's a bit scary that they are so widespread... makes one not know where to start). Do you have a view on specific ones that may be more likely at stake?
BRs,
lfs
I don't live in the UK and I'm not sure I understand what a "consultant" is (doesn't exist here)... but if my guess is correct, it doesn't sound like someone with a medical degree... and so difficult to imagine they can allow themselves even to comment, much less advise, on anything that deviates from the very well known and proven medical stuff.
From my side, I'd also very much welcome a real scientific resource we could ask questions. I've been trying to do that by scheduling appointments which different doctors, only to find that it takes a huge amount of time to get an appointment, and by the time I get to explain why I'm there, the appointment is over.... and never mind the cost (I'm happy I have a good insurance).
Hi Kruggen68,
You're right that these are good candidates too (despite the fact that it's a bit scary that they are so widespread... makes one not know where to start). Do you have a view on specific ones that may be more likely at stake?
BRs,
lfs