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Antiseizure drugs

Terms in this set (48)

What is the electrolyte mechanism behind seizure generation?
Either too much excitation or too little inhibition

-too much Na+ or Ca2+ inward current lead to excessive release of excitatory neurotransmitters like glutamate and aspartate causing excessive action potentials resulting in seizure

-Too little Cl- influx leads to hypo-polarization thus inhibiting GABA, resulting in unopposed excitatory neurotransmitters and increased in action potential rate leading to seizures
What are the main approaches of anti-seizure drugs?
1. Decrease Action potential propagation by blocking Na+ and Ca2+ influx

2. Increase Cl- influx as to hyper polarize the membrane

Thus, Ca2+ channel blocker, Na+ channel Blocker and Cl-channel opener

*Benzodiazepines and Barbiturates affect Cl- concentration thus they posses anti-seizure activity
What are the conventional drugs used as Anti-seizure medication?
1. Benzodiazepines
2. Barbiturates
3. Phenytoin
4. Carbamazepine
5. Valproate (Valproic acid)
6. Ethosuxide
Mention the newer anti-seizure drugs.
1. Gabapentin
2. Vigabatrine
3. Tiagabine
4. Lamotrigine
5. Topiramate
6. Levetiracetam
7. Felbamate
8. Zonisamide
What are the anti-seizure drugs which main action is blockade of the Na+ channels?
1. Carbamazepine
2. Phenytoin
3. Valproate
4. Phenobarbitone (Blocks Na+ and also affects Cl-)

*They target active or inactive Na+ channels and prolong inactivated Na+ channels

*Prevents influx of Na+ channels, thus preventing action potentials
Phenytoin, Carbamazepine, Valproic acid and high doses of Phenobarbitone mechanism of action is:
Block voltage-dependent sodium channels at high firing frequencies
Which are the drugs that open Cl- channels?
Benzodiazepines:
1. Diazepam
2. Clonazepam
3. Lorazepam
4. Nitrazepam

Barbiturates:
1. Phenobarbitol (both Na+ CB and Cl- channel opener)

GABA transaminase inhibitors:
1. Valproate (Valproic acid)
2. Vigabatrin
*GABA neurons in the brain have transaminase enzyme (similar to MAO in adrenergic neurons) , which is an enzyme that metabolizes GABA


*All of these will cause hyperpolarization of the membrane leading to decrease in seizure activity
(Increase in Chloride influx)
How would a high influx of Cl- affect seizure activity?
Will decrease seizure activity because of hyperpolarization of the membrane potential leading to a great difficulty in depolarization of the membrane
What is the difference between high dose and moderate dose Phenobarbital?
High dose - sodium channel effect
Moderate dose- Chloride/GABA effect
**Mention a structural GABA analog.
Gabapentin, Pregbalin


*Bind to presynaptic voltage gated N-type Ca2+ channel and decrease release of excitatory neurotransmitter Glutamate

*Ca2+ is needed in the presynaptic neuron to help the neurotransmitter vesicle fuse with the membrane so the neurotransmitter can be released into the synaptic cleft
**What is the mechanism of action of Valproic acid?
It is a broadspectrum drug- containing all 3 mechanisms:

1. Open Cl- channels (enhancing GABA transmission)
2. Blocks Voltage dependent sodium channels
3. Blocks T-type Ca2+ channels
What are the anti-seizure drugs targeting the Ca2+ channels?
Transient Ca2+ channel blockers:
1. Ethosuxide
2. Valproic Acid

*Block the T-type Ca2+ current (low threshold current)
-T-thallamic neurons
What is the pathophysiological mechanism for Absence seizures (Petit mal)?
-T-type Ca2+ current abnormality (in the thallamic neurons)

"transient Ca2+ channels"
Name the drugs for the best treatment of Petit mal (absence seizure) epilepsies?
1. Valproate
2. Ethosuximide
What is the main difference between the conventional anti-seizure drugs and the newer drugs?
-Older drugs primary effect was on ionic movement (Na+/Ca2+/Cl-)

-Newer drugs primary effect is on excitatory neurotransmitter glutamate
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