truly great presentation. cannot praise it more.

So helpful. Thank you for clear explanation and dispelling the myths.

Thank you for this very informative video. I was diagnosed with PD about a year ago. The more I learn about it the more I think I've had this for several years before I was diagnosed with it.

A truly super presentation. so Clear and decisive too Thanks so much!

GREAT INFORMATION AND VIDEO THANKS EVERYONE. I have Parkinson's and type two diabetic Battling for 9 year's. Trimmers, BODY hurts, and feet swell. Balance and walking more. ENJOY YOUR DAY EVERYONE

Thank you so much for this helpful information. So well explained.

Thank you Dr. Chou for all your work with Parkinson's Disease!!!

Thank you so very much.. My friend has just been diagnosed with Parkinsons. Very healpful!!!!

Thanks for this video. I was diagnosed at 57 and am 66 now.

Just started working as a Long Term Care case manager. I found this very informative.

Very informative and easy to understand. THANK YOU sooooo much:)

PD is for a great part mental. It is a brain disease, and the brain controls our movements as well as our thinking and feeling. This man only enumerates physical symptoms. However, it is AS IMPORTANT to talk about the changes in thinking, especially also the difficulty to initiate actions, to DO something. PD patients have great difficulty taking initiative, to just do things. It looks like they don't know or don't want to do something, but they just can't get started. So, many things remain undone, or happen only after the patient is pushed (by herself or other). For this same reason, it seems they do not care anymore about their environment and people. But when pushed a little, their empathy is still there. Etc. -- Somehow this is a tabu area, doctors talk about tremor as if that is all.

Thank-you so much for the important information!! Valuable!!

Thank you for this very informative presentation

My younger brother has this and it’s taking its toll.

Thank you SO MUCh for this information.My husband has just been diagnosed and this helpful talk will help me to know what to expect and how to help my hunband. I am going to go to Movementneurologist.Heard on radio as well that someone specialising movement therapies is most helpful.

My dad was diagnosed with Parkinson’s in the young age of 42. He’s in stage 2 now and I see how it’s slowly affecting him. And he has the shakes pretty bad.

Here goes, Posting this here because I know some of you do research and think I may have stumbled upon a very important insight concerning the etiologies of various neurodegenerative disorders and maybe degenerative disorders in general. I’ll cut to the chase and ask the question and then explain how I got to the hypothesis. It is: Is it possible that distinct neurodegenerative and musculoskeletal degenerative disorders are in fact be specific symptom complexes that correspond to dysfunction of specific substructures of the cervical ganglia which subsequently alter certain functionalities of the choroid plexus and have downstream effects on the basal ganglia and spine? A recent medical situation in my life prompted me to conduct some personal research to better understand my condition. As a result, I became familiarized with the dynamics of a specific system of structures in the body that, if better understood and regarded as a unified whole, could potentially shed a brighter light in the etiologies of degenerative disorders. Essentially, my research led to make connections between three structures in the neck and head: the cervical ganglia, the choroid plexus, and the basal ganglia. A few observations became key in developing this idea about cervical ganglia involvement in degenerative disease. The first had to do with the basal ganglia. Basal ganglia dysfunction can cause a dearth of dopamine in the brain and subsequent cluster headaches and Parkinsonism/movement disorder symptomatology. This structure controls voluntary movement in the body and so in the case of movement disorders, it is usually the culprit. The question then becomes what is the fundamental cause of this dysfunction? jamanetwork.com/journals/jamaneurology/fullarticle/784785 Thinking about a specific syndrome called Eagle’s Syndrome which often presents with symptomatology similar if not identical to that of neurodegenerative/movement disorder. Eagle’s Syndrome is an abnormal ossification and elongation of the styloid process at the base of the skull that interferes with the cervical ganglia and carotid arteries in the neck and creates symptoms. actascientific.com/ASDS/pdf/ASDS-02-0202.pdf I wondered if superior cervical ganglia dysfunction could have downstream effects on the basal ganglia and cause disorder. So I began to attempt to understand the dynamic relationship between the cervical and basal ganglia. I began to look more closely at the cervical ganglia, in particular the superior cervical ganglia. This structure innervates the eye, parts of the face, the throat and sinuses, stimulates mucous production, has a part in regulating heartbeat (an aside: the disruption of the cervical ganglia when an Eagle’s Syndrome sufferer turns their head can result in panic symptoms: palpitations, dry mouth, gagging, so this could be a tool when thinking about mental heath physiopathologies as well), and also found that it is the only peripheral structure that sympathetically innervates areas of the head and brain. In particular, it innervates a structure in the brain called the choroid plexus. This was the next bridge on my way to the basal ganglia. en.wikipedia.org/wiki/Superior_cervical_ganglion The choroid plexus and found that it has a few very important functions: 1. To release transferrin that promotes iron homeostasis in the brain 2. Send agents to bind with antibodies to be flushed out of the system when infections are resolved and 3. Stimulate production of cerebrospinal fluid. That all struck me as fairly promising. en.wikipedia.org/wiki/Choroid_plexus I started with antibodies and found articles about post-infection movement disorders (specifically PANDAS, about which there is now literature about non-pediatric cases) where it is shown that sufferers have anti basal ganglia antibodies. www.ncbi.nlm.nih.gov/books/NBK333433/ It struck me that if a substructure of the cervical ganglia that innervates parts of the choroid plexus that promote production of antibody binding agents is dysfunctional, an infection could very well trigger an indefinite autoimmune response, attacking the basal ganglia and other systems. Some neurodegenerative and degenerative disorders like MS are thought to be autoimmune, and disruption of the cervical ganglia and subsequent introduction of infection could precipitate an indefinite autoimmune response. Symptom progression might depend on the nature of the ganglia dysfunction (if it is ongoing, say, due to injury and resulting occlusion, or intermittent, say, due to Eagle’s Syndrome, in which turning the head causes ganglia disruption), theoretically accounting for the different subtypes of MS. www.nationalmssociety.org/What-is-MS/Definition-of-MS/Immune-mediated-disease I also had the thought that if iron deregulation in the brain could be caused by dysfunction of a specific substructure of the cervical ganglia and subsequently the choroid plexus, maybe iron irregularities in the basal ganglia would be observed in sufferers of movement disorders, and sure enough, it’s observed in most, if not all of them. At this point I felt like I was really onto something. www.ncbi.nlm.nih.gov/m/pubmed/22266337/ And then a thought occurred to me: what if the first domino to fall in the etiologic chain of ALL of these degenerative disorders begins in the cervical ganglia? This could be why there are peripheral nervous system symptoms that manifest early in diseases like MS (the cervical ganglia innervates the eye and throat and heart, so vision dysfunction, dysphasia, heart rhythm problems etc would be some of the first symptoms you’d expect to see in this etiologic formulation). I’d seen papers talk about a corticothalamic basal ganglia circuit, but not much of anything about the cervical ganglia or choroid plexus, and I thought, “maybe the cervical ganglia is part of that circuit, affecting it indirectly but very profoundly.” Not everyone who suffers from degenerative diseases would have Eagle’s Syndrome of course, but maybe there would be occlusion/tortuosity of the ECA or cervical ganglia, or maybe a trauma shifted their positions leaving the cervical ganglia susceptible to injury, or maybe genetic degenerative disorders’ gene expressions simply omit instructions for certain substructures of the cervical ganglia to form and subsequently instruct the choroid plexus. So the idea is, if there are three main tasks of the choroid plexus, then there are seven combinations of those tasks (1; 2; 3; 1+2; 2+3; 1+3; and 1+2+3), and there are two ways for each of those tasks to dysfunction (over-firing or under-firing, although I’m not exactly sure about this detail), then each combination of simultaneous or sole dysfunction of cervical ganglia substructures which correspond to areas of the choroid plexus that are involved with completion of one of these three tasks would represent a distinct symptomatology-i.e., a distinct degenerative disorder. Important to note is that for antibody binding dysfunction due to lack of transferrin to become part of a neurodegenerative symptom complex, it may require an initial infection of a certain type to kick-start an autoimmune response strong enough to manifest in this way. In my reading about PANDAS I came across mention of “molecular mimicry,” and I thought maybe it was possible in the case of infections that feature such molecules, and in patients that have cervical ganglia dysfunction, that since the infection that the immune system (now totally unchecked by transferrin-aided antibody binding) is targeting resembles healthy structures in the body that all of these factors compounded could lead to ongoing destruction of healthy body tissue. It may be the case that I’m off base, or there are ways to easily prove false all that I’ve said, but I don’t know that. That’s why I’m posting, because in the unlikely event that this is not totally crazy, and might actually be plausible, it will be in the hands of people who can do something with it. A theory is judged by its explanatory power, and to me, this one seems to explain a lot. Could it be the skeleton key that unlocks understanding of these diseases and leads to new treatments and potentially cures? Is it simply that the cervical ganglia needs to be attended to more intensively when these disorders manifest? According to the literature, somewhere between 80-95% of Eagle’s Syndrome patients who undergo styloidectomies have complete cessation of symptoms. If I am right about the cervical ganglia’s role in degenerative disorders, and some of these patients’ styloid process was in contact with their ECAs and cervical ganglia, the neurological symptomatologies that presented may well have progressed into full-blown neurodegenerative disorder if left unaddressed. It could very well be the case that these successful surgeries represent instances of the curing of previously thought to be incurable neurodegenerative conditions. But again, Eagle’s syndrome merely represents one mechanism of action that could cause cervical ganglia dysfunction. I’d appreciate any response, even if it’s to tell me why I’m off base. I hope you’ve read with an open mind, and were willing to ask yourself “what if?” So, the question is: is it possible that superior ganglia dysfunction is the primary etiological feature of a host of neurodegenerative disorders? That this could be a unifying theory?

Thank you so much for this nice exposure. It is very helpful.

I love my new INBRIJA inhaler. Anytime I feel an off period I just use my inhaler and I’m back on within minutes of using it.

My symptoms started slowly in my early to mid 40's slowly with off n on tremors in mostly left hand. In my early 50's my legs in my thighs would have this unbelievable strong ache and my hips stiffened. I am walking slower at 57 and the fatigue is very heavy. I just got started on senemet

Thank you for your presentation. I am now convinced that I need to see a neurologist.

very very helpful; even for my researchs. Thanks 😀

Mucuna does not produce dyskinesia. A different study, this time in monkeys (with unilateral parkinsonism induced experimentally), produced very interesting results on the possibility of dyskinesias. One group was treated with Sinemet (levodopa and carbidopa), another with Mucuna plus carbidopa, and the third only with Mucuna. All the animals experienced an improvement in their symptoms. Dyskinesia was then assessed by the study of spontaneous activity in the substantia nigra. Larger dyskinesia appeared in the Sinemet group. In those treated with the combination of Mucuna and carbidopa, dyskinesia seemed more moderate. Interestingly, in those who had only taken Mucuna, no dyskinesia was found

Thank you!!

I have parasomnias, that's how I started looking for the other symptoms. Creepy disease that we don't know so much still. 🤦‍♂️🤷‍♂️

Thank you i ve learn so much today

good videos!

hello. what does it mean a controlled release of a cinema on 27:37

you said guess work how about clinical diagnosis procedures

Words ain't enough to express how grateful I am to Dr Madida for his assistant in resolving and treating my aunt's Parkinson Disease.

It is a pity you donot explain in terms of a block -bleed effects to the older listners

I am computer illiterate and I don't know what to do I can't get a srait answer if you can help me I have some questions about strange things happening to me I tried I can't find out what the semtons are I have tremers and strange things happening to me I don't know who to talk to

This tutorial video has been really beneficial!! parkinson can be chronic if not treated well. Every ailment depends on the lifestyle of a person and everyone should follow a healthy lifestyle along with correct ,medication . You can prefer planet Ayurveda's parkinson's pack for treatment in natural ways and manufacturing products with no side effects.

Isn’t exercise a no-brainer? For anyone?

Yayyy and I'm only 22

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Does anybody know why tremors occurred at rest during the day but does not occur during the night although it is also during a very deep rest!

Great video thanks for your help. Speaking of help it would be helpful if you didn't use the word uh.

Fake and evil

you contracted yourself multiple times. its obvious you care, but i would not personally grant you a masters. Stop talking like me, a PhD in this. It's embarassing.

Parkinson disease 🦠 is a very terrible illness, my Dad suffered from it for 19 years until we finally got a help and a medicine that truly works that helped treat, cure and reversed all his symptoms..My Dad is well again.