What is Parkinson’s disease? | Nervous system diseases | NCLEX-RN | Khan Academy

What is Parkinson’s disease? | Nervous system diseases | NCLEX-RN | Khan Academy

– You may have heard of
Parkinson’s disease before. Maybe when you heard of
someone raising money for the Michael J. Fox Foundation, or maybe you’ve listened to Muhammad Ali speaking about the disease. Both of these guys actually
have Parkinson’s disease, and they’ve done a really good job at raising money for, and
awareness of, the disease. But what exactly is Parkinson’s disease? Parkinson’s disease is a progressive neurodegenerative disease. We call it a progressive disease because it progresses. It worsens over time. We say that it’s a
neurodegenerative disease because during the disease there’s actually a loss, a degeneration, of neurons in the brain. In Parkinson’s disease, we actually see a loss of a particular kind of neuron, and these neurons are
called dopamine neurons. Dopamine neurons make a
little signalling chemical called dopamine, which is really important for allowing us to make normal movements. A lot of these dopamine neurons live in an area of the brain
called the substantia nigra. The substantia nigra we can see here. It sits here in the brain,
above the spinal cord, in the part of the brain
called the midbrain. When these neurons are
lost, there’s a reduction in the amount of dopamine in the brain. Again, that’s because these neurons, they’re used to make a lot of our dopamine and now they’re not here anymore. And this is the really important part, because when there’s this
reduction in dopamine that’s when we start to see the main movement signs
of Parkinson’s disease. Let’s talk about these signs. One of these signs is shakiness, which can often be in
the form of a tremor, maybe in the hand or the finger. A second sign is stiffness. That stiffness is felt when the person bends part of their body. Maybe the arm or the leg or the wrist. When they’re bending that body part, let’s say it’s the arm, the movement just isn’t very smooth. It doesn’t feel very fluid anymore. Instead it actually feels really rigid. A third sign is slowed-down movements. This happens because it
actually takes the person longer to complete a movement. A good way to think about this is to imagine the last
time you were in water. Maybe you went to the pool, or you went to the beach
to go swim in the ocean. You can probably remember trying to do a somersault underwater, or maybe running away from your friends. If you think back, you can remember that it actually took you a lot longer to do these things in water than it would have if you were on land. That’s kind of what it’s like for someone with these
slowed-down movements. They can do them. It just takes a lot longer
for them to do them. The fourth main sign is
problems with balance. Feeling really unsteady,
or really unstable when standing or walking around. Now, not all patients
with Parkinson’s disease will have all of these problems, but most will have them at some point during the course of the disease. Now, this last one that we talked about, the problems with balance, that usually crops up later on, once the person has had the disease for quite a few years. It’s actually these first
three that are normally used to decide whether or not
someone has Parkinson’s disease. All these main movement signs together actually form a symptom complex called Parkinsonism, or Parkinsonian syndrome. That means that Parkinson’s
is actually a disease that causes Parkinsonism. There are a few other
neurodegenerative diseases that can cause Parkinsonism, this symptom complex
that we’re talking about. But Parkinson’s disease
is the most common, so because of this, we
often call Parkinsonism caused by Parkinson’s
disease Primary Parkinsonism, and then we often called Parkinsonism caused by other neurodegenerative diseases Secondary Parkinsonism. Now, Parkinson’s disease
doesn’t just cause Parkinsonism. Remember that this is
a disease of the brain, and when things break down in our brain, our master control center, there’s often more than one kind of symptom. People with Parkinson’s
disease can also experience psychiatric problems such as depression, cognitive problems such as memory loss and trouble with concentration, and lots of other non-movement symptoms. This can include problems
with their sense of smell and problems with their sleeping patterns. The causes of Parkinson’s disease are actually largely not known. For the majority of cases, we actually don’t know
what triggered the disease, so we call these cases ideopathic. “Ideopathic” meaning that
the cause is unknown. While in the vast majority of cases there is no family history of the disease, about 15% of people actually
do have a family history and for these people their Parkinson’s appears to be caused by a mutation in one of a few different genes. Depending on which gene is the culprit, a mutation can either
cause Parkinson’s disease or it can increase a person’s chance of getting Parkinson’s disease. If someone has a problem
with one of the genes that can actually cause the disease they’ll definitely develop
it, but if they have a problem with one of the genes that can increase the chance of getting Parkinson’s disease, they may or may not develop the disease, but they are more likely to than someone who doesn’t
have the mutated gene. Genetics are the culprit once in a while, but again, most of the time, we don’t know what caused
Parkinson’s disease. Despite this, there are some risk factors associated with developing the disease. A risk factor is something that increases your chances of developing a disease. You could say that having
a certain gene mutation is a major risk factor for Parkinson’s, but there are some other
non-genetic risk factors as well. For example, exposure
to certain pesticides and some cleaning chemicals. Older age, so once you
get to about 60 years old your risk of developing
Parkinson’s disease increases and it continues to go up
with each passing year. So as well we have a
history of concussions as a risk factor of Parkinson’s disease, and gender. For some reason, we’re
not entirely sure yet, men are a bit more likely than women to develop the disease. Another risk factor is
regularly breathing in heavy metal particles like copper or manganese or lead. Maybe if you’ve lived
in an industrial area where those might be found in the air. Again, these are risk factors
for Parkinson’s disease, which means that they’re associated with a higher chance of developing the disease. The treatment of Parkinson’s disease will normally involve medication to help deal with the movement symptoms, and to do that, the way that
many of these medications work is by replacing or increasing
dopamine levels in the brain because remember, our
dopamine-producing neurons have degenerated during the disease, and for some patients, the
medication works great. It may be all that they need
to minimize the symptoms. But for most patients, after
they’ve had the disease for several years, their medication just doesn’t really cut it anymore, so when this happens,
they may have surgery to help deal with their symptoms, and the goal of surgery is to inactivate areas in the brain that are causing their movement problems,
like that shakiness or stiffness that we talked about earlier. This brings us to the long-term outlook for someone with Parkinson’s disease. Unfortunately, Parkinson’s
disease is a progressive disease so the disease will continue to develop over the years after diagnosis is made. While none of our current methods are able to stop the disease, medication and surgery
can be really helpful for managing the symptoms, and making sure the person
with Parkinson’s disease has a high quality of life
for as long as possible. I just want to mention
a common misconception that can crop up when we hear
about Parkinson’s disease, which is that Parkinson’s disease only occurs in older people. While it is true that the
average age of diagnosis is around 60 to 65, about five to 10 percent of patients are diagnosed before the age of 50. This is often referred to as young or early onset Parkinson’s disease. For patients with young
Parkinson’s disease, those gene mutations
we talked about earlier seem to be the cause more often than they are for patients diagnosed in the average 60 to 65 year-old range.

100 thoughts on “What is Parkinson’s disease? | Nervous system diseases | NCLEX-RN | Khan Academy

  1. Great video. But I miss one important thing. The differences in Parkinson forms (Tremor-dominant and Akinetic-regidity). So is Tremor-dominant less agressive with more physical problems than cognitive problems. Akinetic-rigidity is very agressive with a lot of cognitive problems.

  2. Hopefuly they'll come out with a good drug that would help. If it is hereditary it will happen. 2025 will be a global research for that. Do they start losing their memory too?

  3. im 20 and my arm and fingers are frequently tremor when holding something like smarthphone,spoon etc
    do i have parkinson disease?

  4. Heavy metals can cause it by blocking zinc and magnesium channel gates in nerve cell membranes. Also glutamate can leak from synapse membranes that are vitamin deficient and mitochondrial membranes also malfunction.

  5. That's it what it feels like walking in water the slow resistance walking against the water. I've had such difficulty in explaining what I feel like. i am a young onset patient and people tend to expect me to be as though I'm in my 40s when my life is really like an 80 year old. Parkinson's is total devastation like the person I used to be died and was replaced by this version that physical and cognitive limitations

  6. Parkinson's is likely caused by free radicals damaging nerve membranes particularly magnesium gates. Also the free radicals attack dopamine producing DNA sections.

  7. Well, I've heard it's rare for people under 50 to get it, but I have very shaky hands. I also get random muscle spasms in my legs. But the only stiffness I get is in my feet, I can barely move it. Has something happened to me these 10 years of life that I don't know of? ;-;

  8. I wonder if I'm developing this I'm 20 but every other day I will lose my balance for no reason and my right arm will stop working and moving and I can't help myself to constantly look up to the right when this happens anyone have any ideas?

  9. thank you. my dad was diagnosed with Parkensons earlier this year, and your videos are helping me understand it better. for some reason i dont get so scared or upset when it explained in a medical/scientific way. xo

  10. Thank you for the video.my mother got diagnosed with Parkinson's yesterday.apart from the tremors and stuff I hadn't a clue about it.very informative.

  11. I'm currently doing a research placement and the scientists there are looking at whether vitamins can prevent the death of those dopamine neurons. So far they are showing brilliant results with vitamins B3 and D3, mainly D3. So if you're a panicker then these vitamins may be a good place to start.

  12. Man I really look forward to getting old and falling apart. A perfect example why there is no "god." Ppl cant just get old and die in peace.. most will develop some insane disease that just makes life miserable. Seriously just fucking kill me if this happens.

  13. I know a person when they pick up something they shake so much and I'm very concerned should I be worried is this Parkinson's disease?

  14. Hi iam frm india..thz disease will affected my father and he died..nd it will affected to my sis in the age of 21 now ..it will affeted to my past family members…nd i afraid to marry ..plz suggest me wht to do

  15. HAVE YOU GUYS SEEN THIS PARKINSON'S CURE VIDEO IN ARGENTINA!!!???!!! https://www.youtube.com/watch?v=KjmCgqjfjwc

  16. Hey my names is Yves , I hope you doing fine . I would like to share with you how we cure Parkinson through oxygene.

    Just check this testimonial from my youtube channel from the link below
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  17. I just want to say THANK YOU from the bottom of my heart for all your videos, I am in nursing school and it's sad to say, but true that your videos teach me much more and engage me much more than any of my professors. THANK YOU X a million! <3

  18. Very helpful information. More educational materials and resources to help those with Parkinson's and their caregivers can be found here: http://akhomehealth.com/home-care-library/parkinsons-disease-challenges-choices/

  19. Why do u feel like i have parkinsons? …… I almost have all 3 of those.. i also have depression,memory loss, and also having a big time troubles in concentration.. and also im 18..

  20. Nasal spray increases the sensitivity of the affected brain structures to dopamine. Improves motility, alive facial expressions, choking out the liquid food and hypertonicity in the extremities.

  21. Can you get Parkinson’s from too much stress , depression, or anxiety? Cause i have all 3 and my hands tremble sometimes but not all the time , or can i have tremors because of something else?

  22. 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?

  23. My dad has this and it's so sad to see him like this.. He sleeps a lot and when he's home he looks around like he don't know where he's at

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