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Course: Health and medicine > Unit 8
Lesson 10: Parkinson's disease- What is Parkinson's disease?
- What is Parkinson's disease?
- Movement signs and symptoms of Parkinson's disease
- Non-movement symptoms of Parkinson's disease
- The basal ganglia - The direct pathway
- The basal ganglia - Concepts of the indirect pathway
- The basal ganglia - Details of the indirect pathway
- Putting it all together - Pathophysiology of Parkinson's disease
- Genetics and Parkinson's disease
- Diagnosing Parkinson's disease
- Managing Parkinson's disease with medications
- Managing Parkinson's disease with surgery
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Managing Parkinson's disease with medications
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Want to join the conversation?
- Is L-dopa the same as levodopa?(3 votes)
- Yes, levodopa is also known as L-DOPA for short, as it explains at3:01.(5 votes)
- What is the positive purpose of having an MAOB in our brain to break down the dopamine?(3 votes)
- Neurotransmitters are required to be reuptake by the Pre-synaptic neuron or Astrocytes themselves or else suspended neurotransmitters in the synaptic cleft will keep binding to the receptors and initiate Action potential. An analogy can be made with Sink tap; as long as you keep the tap on, water will keep flowing unless you stop it.(3 votes)
- Are there any natural remedies to help deal with Parkinson's disease?(3 votes)
- L-Dopa is a naturally occurring substance substance. It is the intermediate between Tyrosine and dopamine in the body's pathway to make dopamine. Even though the L-Dopa in the drugs is made in a lab, it is chemically identical (at least it should be) to what occurs in the body. The side effects are a manifestation of the disease state, combined with the fact the dosing and distribution of the dopamine is not as optimized as in a healthy person, not because the drug was made in a lab.(3 votes)
- Why does an increased amount of dopamine in the brain affect how much dopamine the neurons from the substansia nigra release? Why does the same amount of stimulation result in an increased result.(2 votes)
- I think what they meant to say is that giving them dopamine means the dopamine-producing neurons don't have to make them. The neurons in the substantia nigra aren't releasing more dopamine, but there is more dopamine in the brain because it comes directly from the medicine being given. The new dopamine replaces the lost dopamine, as it explains at2:05.(2 votes)
- what is a brain fitness test ?(0 votes)
- You can go onto it through this link: https://www.khanacademy.org/brain-fitness(6 votes)
- how many people in the world actually have parkinsons untreated?(1 vote)
- how levodopa/carbidopa works to control symptoms of Parkinson's disease?(1 vote)
- It breaks down into dopamine for use by the cells of the substantia nigra pars compacta. However, levodopa-caused tremors and dyskinesias can and do result.(1 vote)
- Why can't we create a perfect replica of dopamine?(1 vote)
Video transcript
- [Voiceover] So our friend
here has recently been diagnosed with Parkinson's disease,
and we need to figure out what kind of medications we can give him to help manage the symptoms
that he's experiencing. Now you might have noticed
there that I said manage instead of treat, and you
might reasonably be thinking well wouldn't you want
to treat his symptoms, in other words, make
them completely go away and not just manage them? Well that would be
ideal, but unfortunately we don't currently have any medications that can completely
get rid of the symptoms of Parkinson's disease. In other words, we don't
currently have a way to stop or reverse the
disease progression, the loss of dopamine neurons in the brain that is causing his movement symptoms. So instead, we have to
manage his symptoms. We'll have to give him some medications that will minimize how
much these symptoms crop up and interfere with his
daily living, right? So the management of Parkinson's disease may look quite different
for two different people and that's because the
disease affects everyone a little bit differently. So we want to make sure that we figure out which movement and non-movement symptoms are really affecting our patient here. Really interfering with
his day-to-day tasks so that we can address them properly and not give him any
medications that he doesn't need because we don't necessarily
want to put everyone on every medication right away if the symptoms aren't really causing too many problems, right? Because there can actually be short and long-term side effects that we might want to minimize or delay. So let's say that our patient
here is really struggling with his bradykinesia, his
tremor, and his rigidity and he's also finding himself feeling really depressed lately, so we want to manage these symptoms. These are the key
symptoms for our guy here. These are the ones that
are really decreasing his quality of life, so
what kind of medications would help with these
movement problems here? Well let's start off by
thinking about what's going on inside of our patient that's
causing these problems? He's losing dopamine neurons, right? And when you lose dopamine neurons you end up with reduced levels
of dopamine in the brain. So what can we do? What can we do to fix this? Well, we can try giving him dopamine to replace the dopamine
that he's lost, right? So that seems like a reasonable idea, but there's one sort of caveat there. Dopamine doesn't cross
the blood brain barrier. That barrier that keeps unwanted molecules and substances out of our
central nervous system. So if we just give our guy
here straight up dopamine, the blood brain barrier,
it won't let it cross into his brain, so there
won't be any increase in dopamine in his brain,
which is where we really need to replace it to reduce
these movement symptoms. So we need a way around
this little conundrum here. So what we can actually do is
we can give him a medication that is the precursor to dopamine. So in other words, it
will turn into dopamine in the right circumstances. And lucky for us, this
precursor is called L-DOPA. So here it is, here is L-DOPA. It can cross the blood brain barrier so that's great. We're in business here. So we give our patient here L-DOPA. Oh, and we also know L-DOPA as levodopa, so you might hear that said as well. And L-DOPA can cross that
pesky blood brain barrier and get converted into dopamine. So therefore, it increases dopamine levels in our guy's brain. And just an additional
little note about that, it turns out that if we just give L-DOPA, these enzymes that we
have that hang around outside of the central nervous system, they actually just go ahead
and convert our L-DOPA into dopamine before it even has a chance to get into the brain, so
that's kind of a problem, right? That kind of defeats the
purpose of giving L-DOPA in the first place. So what we'll do about that, is we'll give him another medication called a peripheral
decarboxylase inhibitor and we'll do that at the same time as we give L-DOPA and now this drug, the peripheral decarboxylase inhibitor, it will block those enzymes
from turning our L-DOPA into dopamine before
it gets into the brain. So good, now L-DOPA is getting into his central nervous system and it's turning into dopamine and this is helping with
his movement problems. So L-DOPA is generally considered our most effective medication for dealing with the movement problems in someone like our patient here with idiopathic Parkinson's disease, but there are a few
problems that can arise about five to 10 years after
someone starts taking L-DOPA. One thing that can happen is
something called wearing off. And wearing off is when a dose
of L-DOPA it stops lasting as long as it used to,
so the patient's symptoms become really bothersome again before it's even time to
take the next dose of L-DOPA. So what can we do about this wearing off? Well where does that dopamine go? It's degraded, right? It's being broken down by special enzymes that we have in our brain, so we can try to slow
down that degradation of dopamine, that's what we can do. That way it can hang around a bit longer and keep stimulating
our dopamine receptors and that can help get out patient here through to their next dose of L-DOPA without their symptoms
coming back to bother them. So we can do this with a few
different types of medications. We can use something called a
monoamine oxidase B inhibitor, also known as an MAOB inhibitor. So MAOB is an enzyme that
hangs around in our brain and it breaks down dopamine,
so we don't want that. So we can use an MAOB
inhibitor to stop his breakdown and that allows us to keep
higher levels of dopamine in the brain, good, so that's
one thing that we can do to prevent this wearing off, and another type of medication we can use is called catechol-O-methyltransferase
inhibitor. Man, that's a mouthful. But if we break that down,
the name actually makes sense. So catechol here stands for catecholamine and dopamine is a type of molecule in the catecholamine group. So is epinephrine and norepinephrine. You might have heard of those as well. So these are all catecholemines and methyltransferase here means that this is an enzyme. Remember that the ace part
means that it's an enzyme. This enzyme, what it does, is
it transfers a methyl group onto the dopamine and this
inactivates the dopamine. So already we know that we're going to have to do something about this because we want our
dopamine to stick around for a bit longer. So when we give our patient
here a COMT inhibitor, I'll just go ahead and
shorten this to COMT, we stop that breakdown, right? So we have more dopamine floating around to bind to the receptors,
the dopamine receptors, and to reduce movement symptoms. So another problem that we can see with prolonged use of L-DOPA is too much involuntary movement. Now that's a little unexpected, right? That's kind of the opposite
of what we would expect in someone with Parkinson's disease. I mean, Parkinson's
disease it messes around with out basal ganglia pathways, so that we end up with a
reduction in movement, right? So why are we getting
too much movement here? Well we can think of L-DOPA as a pendulum, a pendulum that is trying
to swing our patient from reduced movements to being able to move normally, but over time after being on L-DOPA for several years, the pendulum can kind of over shoot and we end up with too much movement and we call this dyskinesia, so that presents an interesting
little problem here. Essentially, what we need to think about when we're treating Parkison's disease is that well L-DOPA is our
most effective medication, but if we use it for a long time, there's a chance the pendulum
will swing the other way so to speak and dyskinetic
movements will result. So what do we do? Well sometimes we might
delay starting L-DOPA for as long as we reasonably can. So in other words, we'll try to manage our patient's symptoms without resorting to L-DOPA right away or maybe we'll just try to
use a little bit of L-DOPA and use another medication as well, at least until later on in the disease when we really, really need L-DOPA. L-DOPA is kind of like
the ace up our sleeve, that we want to hang onto
until we want to play it and that way we can maybe delay these long-term side
effects from happening. So then the question
becomes, other than dopamine, what else could we give our patient here that would help him with
his movement problems? Well we could give him something that acts like dopamine, right? Something that stimulates
his dopamine receptors the same way that dopamine does. So let's do that and these
are called dopamine agonists. They play the role of dopamine. Kind of like how a substitute teacher plays the role of the regular teacher and helps teach the class while the regular teacher is away. So when we give him
these dopamine agonists, the neurons with dopamine
receptors are stimulated just as though dopamine
was there doing the job. So you might be wondering, okay well if these dopamine
agonists act like dopamine, then why is L-DOPA the
most effective medication? Shouldn't these agonists
be just as effective? Well while these agonists
do act like dopamine, they're not dopamine, right? They're not a perfect
fit for the receptor. Just like how the substitute teacher just isn't as good a fit for the class as the regular teacher is. So these agonists, they
just aren't as effective as the real thing, but
they can be really helpful maybe early on when
symptoms aren't too bad, when the disease hasn't
progressed too far, or maybe when we're using
them together with L-DOPA, so that maybe L-DOPA can
be used a little bit less. So those are the main types of medications that we would normally use to manage the movement symptoms
of Parkinson's disease, but we also need to manage
the other symptoms, right? Like the depression that
our patient is experiencing. So one thing that we might want to do before we try to treat his depression or any other symptom that someone with Parkinson's disease might experience, is that we would want to figure out if the symptom is due
to the disease itself or if it's a side effect of
one of his other medications. If it is the disease itself and the symptom needs medication, then we would just try to find
the most suitable medication that we can for managing it. And if instead it's a side
effect of a medication that he's already on, then
we would try, if we could, to maybe adjust the dose of
that medication if possible so that he experiences
minimal side effects.