in this lecture we are going to cover
the pharmacology of antiepileptic drugs so let’s get right into it the primary
use of antiepileptic drugs is to prevent or control epilepsy commonly
known as seizure a seizure is a sudden burst of uncontrolled electrical
activity in the brain that occurs when neurons become excessively active
seizures can be generally classified into two major groups depending on where
they begin in the brain first focal seizures affect initially only a portion
of the brain typically one hemisphere and may occur with or without impairment
of awareness second generalized seizures affect both sides of the brain at the
same time and almost always cause loss of consciousness
now simplistically seizures can be viewed as the result of an imbalance
between inhibitory and excitatory processes in the brain that produces either too little
inhibition or too much excitation in order to gain better understanding of
how this happens we need to take a closer look at how neurons pass signals
to one another so as you probably already know the main form of communication
among neurons occurs through the travelling wave of electrical excitation
known as an action potential an action potential is orchestrated by the
synchronized opening and closing of ion channels now if we look at the simple
excitatory neuron when at rest the inside is slightly more negative than the outside
an action potential starts when voltage-gated sodium channels open
allowing positively charged sodium ions to rush into the cell thus reversing
the polarization of the membrane consequently membrane depolarization
leads to opening of high-voltage-activated calcium channels which then
allow positively charged calcium ions enter the neuron thereby triggering
release of glutamate from the vesicles into the synaptic cleft
next glutamate binds to two types of receptors on the postsynaptic neuron
first the AMPA receptors that upon binding of glutamate open and permit entry of
sodium ions and the second NMDA receptors that open and permit entry of
calcium ions in addition to that calcium may enter
through low-voltage-activated calcium channels also known as t-type calcium
channels which open in response to small depolarizations
at or below resting membrane potential so all this influx of positive ions again
leads to depolarization and propagation of action potential now as you can
imagine if there is too much glutamate around neurons can become hyperexcitable
and a seizure may result but this normally doesn’t happen because
we also have inhibitory neurons around that put brakes on excitatory impulses these
inhibitory neurons release neurotransmitter GABA which binds to
GABA-A receptors on the excitatory neuron causes them to open and allow negatively
charged chloride ions to enter in this causes the membrane potential to be more
negative on the inside relative to the outside thus limiting the neurons
ability to respond to further stimulation finally once GABA
dissociates from the GABA-A receptor it becomes removed from the synaptic cleft
by reuptake through the GABA-transporter-1 GAT-1 for short and then degraded by an
enzyme gamma-aminobutyric acid aminotransferase GABA-T for short so again
as you can see just like with excess of glutamate too little GABA can also allow
neurons to become hyperexcitable which may lead to seizures now that we covered
the basic mechanism underlying seizures let’s move on to discussing pharmacology
of antiepileptic drugs so the main goal of therapeutic interventions is to
simply lower neuronal excitability and or enhance neuronal inhibition one way
antiepileptic drugs may prevent excessive firing of an action potential
in neurons is simply by blocking voltage-gated sodium channels antiepileptics that block sodium channels and thus reduce the amount of sodium that
enters the neuron include Carbamazepine Oxcarbazepine Lamotrigine
Phenytoin Topiramate Valproic acid and Zonisamide
now another way antiepileptics can slow down hyperactive neurons is by blocking
calcium channels this task gets done by drugs that inhibit high-voltage-activated calcium channels such as Lamotrigine and Topiramate and drugs that
inhibit low-voltage-activated t-type calcium channels such as Valproic acid
and Zonisamide as a side note here keep in mind that many of the antiepileptic
drugs act on multiple targets so as you can see Lamotrigine Topiramate Valproic
acid and Zonisamide can inhibit both calcium channels and sodium channels
furthermore Topiramate has been shown to also inhibit excitatory neurotransmission
by blocking AMPA receptors now couple other antiepileptic drugs namely
Gabapentin and Pregabalin also exert their effects by interacting with high-voltage-activated calcium channels however unlike the other agents
Gabapentin and Pregabalin bind to an accessory subunit of the high-voltage-activated calcium channel called alpha-2-delta-1 because the presynaptic channels
that contain this specific subunit appear to modulate the release of
excitatory neurotransmitters such as glutamate inhibition of alpha-2-delta-1
containing calcium channels by Gabapentin and Pregabalin
is speculated to be one of the main reasons for their antiepileptic effect
another high-voltage-activated calcium channel blocker with unique mechanism of
action is Levetiracetam one of the major mechanisms that is speculated to be
responsible for antiseizure activity of Levetiracetam
is its ability to bind to the so called SV2A protein found in the walls of
vesicles that contain glutamate this binding appears to impair the synaptic
release of glutamate and thus decrease neuronal excitability next we have antiepileptic drug called Felbamate that inhibits excitatory neurotransmission
by blocking NMDA receptors and finally we have drugs that act on the GABA
system the two major classes of drugs that target this system are
Benzodiazepines and Barbiturates which work by binding to GABA-A receptor thus
prolonging the opening of the channel and permitting greater influx of
negatively charged chloride ions into the neuron for more detailed
explanation of their mechanism of action check out my recent video about
Benzodiazepines and Barbiturates next we have drug called Tiagabine which is a
selective inhibitor of the GABA transporter in a nutshell Tiagabine
simply blocks GABA reuptake thereby permitting more GABA to be available for
receptor binding on the postsynaptic neurons last but not least we have drug
called Vigabatrin which irreversibly inhibits GABA-aminotransferase the enzyme responsible for catabolism of GABA thereby effectively
increasing the concentrations of GABA in the brain now when it comes to
side-effects sedation and dizziness can occur with all antiepileptic drugs
hyponatremia can occur with the use of Carbamazepine and Oxcarbazepine visual
field loss can occur with the use of Vigabatrin while double vision can
occur with the use of Lamotrigine and Phenytoin
additionally Phenytoin is known for causing gingival hyperplasia and
hirsutism cognitive problems can occur with the use of Topiramate and Zonisamide Topiramate is also known for causing weight loss weight gain on the
other hand can occur most frequently with the use of Valproic acid although
it has also been reported with the use of Gabapentin and Pregabalin which also
happen to cause peripheral edema in addition to that both Valproic acid and
Felbamate can cause liver toxicity in rare cases the use of Felbamate can
also lead to rare but serious condition called aplastic anemia and with that I
wanted to thank you for watching I hope you enjoyed this video and as always
stay tuned for more

98 Replies to “Pharmacology – ANTIEPILEPTIC DRUGS (MADE EASY)”

  1. Sir you're helping for my future God bless you & your family continue sir that's my one & only request ! I hope you'll do sir thanks for your kind job

  2. I rarely comment stuff but man you’re the best. Thank you so much for your work.
    I’m preparing for farmacology exams (I’m a dentist) and it was like hell on the start. I only remember things if I can visualise them and put them into a logical system and this is what you exactly made in your videos. It helps me so much to understand farmacology, and finally what is most important, it’s really interesting to watch and learn this way at the same time. You simply made farmacology interesting.
    Keep up the good work, you’re doing a verry productive informational help for future medics and farmacologists.
    I wish I could have teachers like you.

  3. I have a test on this drug class in 4 days and I was bummed that you didn’t have a video on it. HOW DID YOU KNOW?!? 🙌🙌🙌

  4. I’d decided to wait for a bit before studying Anti-epileptic Drugs because I knew that your new video would be out soon now. I’m so glad that I took that chance because this video saved so much time and made the concepts crystal clear. Thank you so much for the time that you put into these videos. It’s really hard to make such difficult concepts so simple. Thank you! ♥️

  5. This video helped me get a clear concept about anti-epileptic drugs and their mechanism of action! Thank you so much for this great video 🙂

  6. May God bless you, you're making them really simple and easy to remember. Can you please explain the drugs of asthma/COPD please?

  7. I found your channel some 8 years too late… Though I had good grades on pharmacology, you might have SIGNIFICANTLY REDUCED MY STUDY TIME. The new (bio)med/pharma-studying generation is lucky to have you! 😉

    Anyway, I'm revitalizing my knowledge at 2x speed now!
    Thanks for the work!

  8. Thank you very much for your video! You inspired me to start creating my own content, my favourite so far has been your video on Benzodiazepines and Barbiturates, something I previously had a little difficulty understanding! Thank you again

  9. Hi, I work on the management side of a Pharma company and I'm trying to learn Pharmacology basics to better understand our products and their side effects.

    I love the way your videos are detailed yet short. Thank you very much for these amazing videos

  10. Sir,you are absolutely amazing.your lectures are so clear and concise and precise.This is exactly what I need .Thank You very much for your good work.

  11. Wow! fantastic videos. So clearly explained and amazing animations. This is helping me a lot. Thank you very much.

  12. lomotrigin is Na channel blocker i wasnt expecting from yoiu i love your video but after knowing this i need to verify your every lecture

  13. teacher took one week to cover this topic and you taught this in less than 10 min.
    watching hour before exam very helpful

  14. Thank you for this amazing video. I have epilepsy and take oxcarbazepine but ive never found any information about how it acts on my brain to prevent my seizures. I had no idea it was the sodium channels, i thought it was the chlorine channels. So thank for your great explanation about it

  15. Thankyou so much sir…for such a wonderful expaination…please post a video on Alzheimer's disease also…

  16. Tomorrow med chem exam is there .A 10 min video sufficient to understand whole mechanism thanks for making pharmacology Easy and simple. Very helpful for pharmacology & pharmacy student .plz post more videos

  17. You made that so much easier to understand than my professor did! As an epileptic individual, thank you for helping me better understand how my medication works!

  18. Great video. Really helpful.. Esp.. For 1st exposure to the topic. Thank
    you for making these. Kudos!!

  19. Sir you are the best. Pharmacology concepts are so better with you explaining. Thanks a lot👏🏻

  20. hello thank you for your amazing work, its really helping. what is your reference? because I think my references is old, there is details not matching information you mention.

  21. Thank you for this great video. There was no annoying music or overly happy presenter. I hate when people speak emotionally. You delivered all the facts whitout being annoying.

  22. You are really helping health care professionals with your short and effective "Speed Pharmacology" videos. Thank you very much.

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