Controversies in the Use of Medications, Herbs, and Early DBS for Parkinson's April 2024: youtu.be/RhaUZFczGmc?si=R0N...
Movement Disorders Foundation of Arizona: Movement disorders neurologists Dr. Paarth Shah and Dr. Virgilio Gerald Evidente will be discussing in a panel discussion type of seminar the controversial issues regarding managing Parkinson’s at different stages.
The duo will discuss among others the following: (1) Should levodopa be started early or late in PD?; (2) Should elderly patients be put on dopamine agonists?; (3) How strong is the evidence for efficacy of supplements for PD?; (4) Are natural sources of levodopa better than synthetic levodopa pills?; (5) Can cannabis help PD symptoms and is it safe for PD?; (6) Should deep brain stimulation (DBS) be offered earlier in PD rather than later? If so, how early?
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Bolt_Upright
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Engaging conversation! Perhaps the most remarkable finding was that in brain research, there was a PD misdiagnosis by the neurologists of their department, including these "2 smart guys", in 42% (!) of the cases within the first 5 years. Considering many of the personal experiences reported here, as well as the studies with so-called "significant improvements", it is reasonable to question them to some extent...
I’d take what these guys say with a grain of salt.
Their explanation on how the long life levodopa products work doesn’t seem to tie in with our experience. They put down the side effects like hallucinations agitation and confusion to be dementia. When they caused these effects for my husband the “dementia” quickly disappeared once he stopped the drug. I think it is too much levodopa that causes these effects. They say you need double or triple the dose of the slow release. Again this didn’t seem right. My husband took the 100mg slow release to replace the 50 mg IR madopar as his neurologist said the same thing. It was fine for a week as the levels took a while to build to equilibrium but then I think the levels in his blood reached a too high level causing the agitation, confusion, need to pace and in the end spasming of his muscles and throat to the point he couldn’t breathe properly at which point he stopped taking it and went back to IR at previous levels and quickly recovered.
I'll tell you my personal opinion below and I don't really agree with the two of them, but it's just my poor opinion:
Here we must to know the fundamentals of Parkinson’s disease and yet we just need to read at the entry dopamine on wikipedia and have followed a couple of PwPs for a couple of years to figure it out.
“The dopamine synthesized in the cytoplasm is captured and concentrated within the synaptic vesicles. Storage inside the vesicles is intended to protect the molecule from degradation by monoamine oxidase, and is indispensable for the process of releasing the neurotransmitter into the synaptic space by the nerve impulse.”
I repeat:
“The dopamine synthesized in the cytoplasm is captured and concentrated inside the synaptic vesicles. “
As the cellular structure of the cerebral dopaminergic system is gradually destroyed ,the concentrated dopamine and captured by the synaptic vesicles is no longer sufficient and the parkinson’s patient depends exclusively on the concentration of levodopa in the blood that “fluctuates” that is, it goes up and down according to how much C/L takes, with all the consequences and balancing difficulties of the case that can be read here according to the stages of the PD.
So age has nothing to do with it, but rather does the PwP have the so-called "fluctuations" and to what extent?
Every good neurologist knows this fundamental important fact and is very careful about fluctuations trying to solve the problem on a case-by-case basis with levodopa, dopamine agonists, MAO inhibitors,
I prefer to be simple with only levodopa in the various forms instant, regular, retarded release morning, day, night and HDT for 9 years without any adverse effects experienced by me.
(HDT = Hight Dose Thiamine or vitamin B1 ⭐️⭐️⭐️⭐️⭐️, as mentioned in the video at minute 00:56:00).
Finally, this research clearly demonstrates that dyskynesia is caused by the by disease duration and levodopa dose, but not by the duration of levodopa therapy, but they don't know it.
Quote:
”Delaying the initiation of levodopa has been proposed to reduce the risk of motor complications in Parkinson’s disease. In a 4-year multicentre study in Ghana, Cilia et al. find that motor fluctuations and dyskinesias are predicted by disease duration and levodopa dose, but not by the duration of levodopa therapy.”
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