‫بسم هللا الرمحن الرحيم‬

‫ كلية الطب‬- ‫جامعة اجلزيرة‬

Epilepsy (2)
By Dr. Mahmoud Hussien
Salih
MBBS- MRCP- clinical MD internal medicine. MD neurology

2020
 Contents:

◼ How do we treat epilepsy?

➢ Mechanism of action of anti Epileptic Drugs.
➢ Specific AEDs
◼ status Epilepticus.
Treatment
 Anti Epileptic Medications
( first line)
Sodium Valproate Carbamazepine
Broad-spectrum Narrow spectrum

Active against generalized and Active against focal seizures

focal seizures

Active against photosensitive More effective in foal seizure than

seizure valproate

Unlikely to be the first line drug May exacerbate generalized

for female approaching child seizures
bearing age
 Mechanism of action:

◼ The main groups include:

➢ Sodium channel blockers.
➢ Calcium current inhibitors.
➢ GABA enhancers.
➢ Glutamate blockers.
 1.Sodium channel blockers
◼ EDs that target the sodium channels prevent the
return of these channels to the active state by
stabilizing them in the inactive state. In doing so,
they prevent repetitive firing of the axons.
◼ Sodium channel blockers are :
➢ Carbamazepine
➢ Phenytoin
➢ Lamotrigine
 2.Calcium channel
blockers
◼ Calcium channels function as the " pacemakers "
of normal rhythmic brain activity. This is particularly
true of the thalamus.
◼ T-calcium channels have been known to play a
role in absence seizures.
◼ AEDs that inhibit these T-calcium channels are:
➢ Ethosuximide.
➢ Valproate.
 3. GABA enhancers
◼ Gamma-aminobutyric acid (GABA) has 2 types of
receptors, A and B.
◼ When GABA binds to a GABA-A receptor, the
passage of chloride, a negatively charged ion, into
the cell is facilitated via chloride channels.
◼ This influx of chloride increases the negativity of
the cell ( a more negative resting membrane
potential).
◼ This causes the cell to have greater difficulty
reaching the action potential.
◼ The GABA system can be enhanced by :
➢ binding directly to GABA-A receptors
➢ blocking presynaptic GABA uptake
➢ inhibiting the metabolism of GABA by GABA
transaminase
➢ increasing the synthesis of GABA.
◼ GABA is produced by decarboxylation of glutamate
mediated by the enzyme glutamic acid
decarboxylase (GAD). Some AEDs may act as
modulators of this enzyme, enhancing the
production of GABA and down-regulating
glutamate .
◼ Some AEDs function by blocking the reuptake of
GABA (tiagabine [TGB]) or by inhibiting its
metabolism by GABA transaminase (vigabatrin
[VGB]), resulting in increased accumulation of
GABA at the postsynaptic receptors.
 4. Glutamate blockers
◼ Glutamate receptors bind glutamate, an excitatory
amino acid neurotransmitter. Upon binding
glutamate, the receptors facilitate the flow of both
sodium and calcium ions into the cell, resulting in
excitation.