Parkinsonism

Doctor-to-be
Medicoblast
Published in
4 min readJan 25, 2019

We all want something to be named after us, right? I mean, how amazing does Jane’s Meteor or Peterausaurus sound? We, as human beings, have this innate desire for immortality; and since that isn’t possible, having your name engraved in the annals of history seems like the next best thing. Right? Well, technically, unless you’re James Parkinson. Which you’re not. So don’t worry about it, go out there and discover as many things as you can.

One of the most well known neurodegenerative (read: neuro=brain) diseases ever, Parkinson’s Disease, also known as Parkinsonism, has been plaguing humanity since the dawn of time (okay, maybe not dawn of time, but still it’s been around pretty long). Egyptian texts and even those from the Bible has described features similar to this disorder. Its not that surprising either; in today’s world, an estimated seven to ten million people live with this condition, which is a crazy amount if you think about it.

So what exactly is Parkinsonism? Well that’s what I’m here to tell you about. Before we start, I want to remind you, gentle reader, that the cardinal feature of this publication is to make bite sized articles about medical stuff that are easy to understand. Think of them as little nuggets of knowledge. Mmm, nuggets. I wonder if I could get some. Oh wait, its 2:38 am. Never mind. Look, the point is, it’s gonna be simple and fun, so don’t worry, alright?

To start things off, we first need to understand how our muscles work. When you want to move, your brain produces an electrical impulse and electrons (e-) “jump” from one end of one neuron (nerve cells) to another.

When they reach the end of the neuron, they arrive at a junction with another neuron. This junction is called a synapse. The electron then causes chemical changes and chemical substances, called neurotransmitters, are released from the nerve ending so that it can cross the gap to the subsequent neuron.

The neurotransmitter then binds to the postsynaptic (post=after, so postsynaptic neuron= neuron after the synapse) and the electrical impulses are carried on, until it reaches your muscle, telling it to contract and you move. Yay.

That’s all well and good, but common sense would tell you you don’t want to move all the time (or at all, if you’re like me). Therefore, there are two kinds of neurotransmitters in your body. Remember those? They’re the chemicals that carries impulses from one nerve ending to another, over the junction known as a synapse. Anyways, we have two kinds: Excitatory and Inhibitory neurotransmitters. As their name indicates, Excitatory neurotransmitters causes excitation (eg muscle contractions) while Inhibitory neurotransmitters causes inhibition (eg muscle relaxation).

Okay, now that we know the basis of how our nerves work, we can move to today’s topic, Parkinson’s Disease. I know we took a while to get here, but once you understand the basics I’ve outlined above, things get very simple to understand.

So we all know that we have a brain, right? Well, there’s a part of your brain called the midbrain. And in there, there’s an area called the Substansia Nigra.

This is what you see if you cut a section out of the midbrain

The Substansia Nigra is black (Nigra means black in Latin) because it contains pigmented, or coloured, neurons. These neurons are special cause they synthesize a very important neurotransmitter: Dopamine. Its very dope

Dopamine is an Inhibitory neurotransmitter (not exactly, but for the purpose of today’s article we’ll consider it as such). In Parkinsonism, the Substansia Nigra degenerates, leading to decreased production of Dopamine. Less Dopamine=less inhibition=more excitation and that’s why we see symptoms like tremors in people suffering from Parkinsonism.

Normal midbrain versus midbrain with Parkinsonism, showing degenerated Substansia Nigra

And that’s it. That’s what Parkinson’s Disease is. Degenerated Substansia Nigra leading to decreased production of Dopamine leading to decreased inhibition or in other words, more excitation. Other features include a mask like face (due to loss of control of muscles of the face), shuffling gait (due to loss of proper control of leg muscles) and as mentioned previously, tremors (due to loss of inhibition).

Since the disease is caused by lack of Dopamine, the treatment is pretty simple: administer more Dopamine. However, as Dopamine is used up all over the body before reaching the brain where we want it, a combination of Levodopa (L Dopa) and Carbidopa (C Dopa) is given instead. They basically ensure the Dopamine reaches the part of your brain that needs it.

There you have it. That’s the basics of Parkinson’s Disease. Sure, this is definitely not enough to pass exams (if you’re in a medical school. Like me. Please send help), but the idea behind me starting these was to give those not in the medical profession a general idea about medically related stuff. I sure wish other professions will do things like this (I really really want to know how to build a computer can someone teach me in an easy to understand way I’m dumb sorry and thanks). Thanks for reading, see you all next time!

--

--