Parkinson's Disease Tulip


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Old 12-29-2009, 12:20 PM #31
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Originally Posted by indigogo View Post
Paula - I think that is one of the biggest problems PD patients face - the doctors, even the neuros, aren't keeping up - there is an education gap.

I know we've talked about this before, but have you thought of consulting another doc - preferably a Movement Disorder Specialist? They might at least know what you are talking about!

You could use a medical partner that wants to dig as deep as you do!
I hope a movement disorder specialist would know! You are right on both counts - a medical partner without dollar signs in the eyes.

thanks,
paula
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Old 12-29-2009, 03:46 PM #32
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Default We need a Visual Model

Paula,

Glad you're experiencing less dystonia. I don't have it often, just in my foot sometimes but when I do....yowsa!

I ran across this abstract that does a great job in summing up the various parts of the brain impacted by PD and also links them to the various symptoms we experience. For example, "...postural-gait disturbances are due to lesions in gait control systems including basal ganglia, pedunculopontine nucleus and frontal lobe." I'm guessing this is why levodopa does not provide much relief here. Maybe I'll reformat this info into a table and make a sticky- I think it would be a useful reference.

http://linkinghub.elsevier.com/retri...53802006001040

Laura
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Old 12-29-2009, 07:31 PM #33
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so a new pathway into the more serious research highways, those having PIgD [don't know spelling yet] postural and gait disturbances are more likely to fall and get dementia. I think dementia for PD is in need of much attention. I do fear it has not been given enough ; these drugs are pretty strong and we try to do as much as we can.....sometimes. lol But we are not normal. I wrote to someone my inner mess keeps leaking out.

if one doesn't factor moody or well..i really wish it would be changed from 'Parkinson Personality" What an insult! I doth protest. But if you don't factor it in, you are taking advantage of us.

Do we need dementia definitions updated ?

I don't know who i am t alking to .....just whoever and nicely
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Old 12-30-2009, 12:45 AM #34
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Default Not just acetylcholine

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Originally Posted by paula_w View Post


NEUROLOGY 2009;73:1670-1676
© 2009 American Academy of Neurology
History of falls in Parkinson disease is associated with reduced cholinergic activity

N. I. Bohnen, MD, PhD, M. L.T.M. Müller, PhD, R. A. Koeppe, PhD, S. A. Studenski, MD, MPH, M. A. Kilbourn, PhD, K. A. Frey, MD, PhD and R. L. Albin, MD

Conclusions: Unlike nigrostriatal dopaminergic denervation, cholinergic hypofunction is associated with fall status in Parkinson disease (PD). Thalamic AChE activity in part represents cholinergic output of the pedunculopontine nucleus (PPN), a key node for gait control. Our results are consistent with other data indicating that PPN degeneration is a major factor leading to impaired postural control and gait dysfunction in PD.

Does that clear it up for anyone? If it does, please explain it to the rest of us.

Abbreviations: AChE = acetylcholinesterase;this is the good guy for pwp and we take anticholinergics to do the same thing. AChE is the bad guy for Alzheimers patients - needs blocked so it can't do it's job ANCOVA = analysis of covariance; MMSE = Mini-Mental State Examination; PD = Parkinson disease; PPN = pedunculopontine nucleus; PSP = progressive supranuclear palsy; UPDRS = Unified Parkinson’s Disease Rating Scale; VOI = volume of interest.

Disclosure: Author disclosures are provided at the end of the article.

Received March 25, 2009. Accepted in final form August 20, 2009.

http://www.neurology.org/cgi/content...act/73/20/1670

The authors and researchers know the difference right? Doctors don't.
There is such a delicate balance between neurotransmitters in a healthy brain; ours really go out of whack, so I can't imagine what happens when we start adding meds to the mix which inhibit, excite, and otherwise raise hell in our heads, especially when it only is supposed to target one thing- common sense dictates that it's going to mess with a host of other things in our brain- and what scares me is what of those things messed with are closet to being 'normal' in the first place. The meds are a slippery slope....

I just ran across this abstract:

Parkinson's disease (PD) is traditionally viewed as a mainly hypodopaminergic syndrome, with symptoms resulting predominantly from loss of dopamine-producing neurons in the substantia nigra. However, while most of the cardinal motor features of PD respond well to dopaminergic therapy, many other features of the disease do not. Balance impairment and the associated risk of falling represent one of the most prominent and potentially disabling features that are typically refractory to dopaminergic treatment. Therefore, it is possible that lesions in nondopaminergic systems contribute to the pathophysiology of postural instability in PD. Such nondopaminergic lesions are well recognized, certainly in advanced stages of PD where postural instability and falls dominate the clinical presentation. However, it remains unclear which of the identified nondopaminergic lesions is specifically responsible for postural instability and balance impairment. In this review, we argue that cell loss in the locus coeruleus and a resultant central norepinephrine deficit are intimately involved in the pathophysiology of postural instability in PD. If proven to be correct, this link between defective noradrenergic neurotransmission and postural instability could have important implications for the future development of new symptomatic treatments aimed to correct postural instability and preventing falls. Studies in the next 5 years could test this hypothesis, using a battery of complementary research techniques, including advanced neuroimaging (structural, functional imaging and nuclear), neurochemical studies of cerebrospinal fluid, post-mortem clinicopathological analyses and detailed clinical balance evaluations supplemented by posturography studies.


Postural instability in Parkinson's disease: the adrenergic hypothesis and the locus coeruleus

Authors: Grimbergen, Yvette AM1; Langston, J William; Roos, Raymund AC; Bloem, Bastiaan R

Source: Expert Review of Neurotherapeutics, Volume 9, Number 2, February 2009 , pp. 279-290(12)

Publisher: Expert Reviews
http://www.ingentaconnect.com/conten...00002/art00013

One researcher I read wondered why it is that only the dopaminergic responsive symptoms of PD are treated when they largely are NOT the ones that ultimately disable when the ones that do like freezing and falling have no targeted treatments? Why?

Take a look at PDOR- the term 'noradrenergic' occurs 6 times! On the plus side, the drug fipamezole is undergoing clinical trials for use in PD. I suspect one reason more drug research isn't going on here has to do with more money being thrown at the familiar dopa therapies- we need to move beyond just seeing dopamine replacement as a panacea.
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Old 12-30-2009, 08:53 AM #35
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Default tip of the iceberg

Going out till later on......great find Laura. Looking at all the transmitters is very important and I'm glad the emaphsis is shifting to the balance [no pun intended] of them all.

Nortriptyline also helps dyskinesia by the way.

paula
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Old 12-30-2009, 09:34 AM #36
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Default Hi Paula,,

Sounds Like you and I are in the same stage, except the panic attacks and depression. Acceptance would account for that on my part. For your shortness of breath, I have found a nebulizer and an inhaler to be helpful. I suspect the bronchial passages are affected by the PD and the nebulizer relaxes the bronchial passages. At first you will feel like putting a paper bag over your head as the oxygen rush will make you dizzy and lightheaded. But give it time and use regularly, and your breathing will begin to supply your body with the oxygen you have been craving so long.

Good Luck and thanks for bringing up such a fascinating thread,
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