Neurodegenerative Disease Overview

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[armandohasudungan]

📌 MAKE THIS LECTURE STICK: FREE PRACTICE QUESTIONS HERE! 🎓

[Josi]

I just attended a speech at my university on neurodegeneritive disease and treatment yesterday! it's wonderful to see the pathology more in depth. thanks so much.

[robhunter]

I have just discovered this while in the throes of pathophysiology and pharmacology exam preparations- your illustrated, quick and clear explanations are extremely helpful for any student. Thank you

[martaroseira]

Am I the only one tat watches this videos because they're freaking interesting and not because I need help studying something. I'm literally on the eleventh grade, I don't need to know this and yet, every time one of this videos comes up on my feed I get extremely excited

[Goodnessezinne-jj]

Writing my exams on Monday and this video came just on time.

[KarthikSubramanianKrishnan]

Awesome Armando Your work is unparalleled!!
Everyone might not remember everything but, you make us all fell good that they learnt something!

[cocopopsmmm]

Hey! Thank you so much for these videos, they are so informative and gets straight to the point and things we need to know for exams. I'm in my final year at university doing BSc Biomedical Sciences and they have been invaluable to my revision. The bit at the end where you scroll up through what you have done is great so thanks so much again! Poppy xx

[DestinyYlisse]

2:12 ALS is known as Lou Gehrig's Disease in the USA.

[ceesvanderklugt]

As a third year medical student I'm subscribed to your channel and I love every video you make!

[Cemolino]

Youre very amazing at teaching and drawing and you help many people like me who are in year 11/12 and wants to go into medicine in uni! Keep doing what you're doing :)

[antiignorance]

You made pathology of nervous system so easy. Thanks 😊

[Besmaht]

This is what’s needed for step. Your welcome. This is it

[joeslacker]

Who would be the best type of doctor to see for these types of diseases?

[JamDaaMan]

Great video! hope to see more soon, Amando.

[Exotixa]

finally someone elaborates more on this :)

[amiejadama]

would love to see a video on the female pelvic anatomy. Your channel is so helpful. Thanks for taking the time to do this

[unkanurganci]

at the SMA part (9:46), you said atrophy of ventral horn but isn't it the ventral root that you showed? (ps: i have no idea about neurology, don't be so judgemental if what i said is completely ridiculous)

[merv]

Thanks! I m going to have biochem exam tmr ! This video is great for revision=). Love this

[andsoon]

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?


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.


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.


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.


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.


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.


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.


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?

[aliluck]

what about neurodegenerative spinocerebellar ataxia (genetic vs injury) ???