AED Flashcards
T/F all seizures have convuslsion
False
Refractory Epilepsy
when epilepsy remains uncontrolled following polypharm.
Some risk factors of epilepsy:
No ID'd risk factors Family History Vascular lesions (Stroke) Head Trauama Birth Related Injuries Febrile Convulsions
Treatments of Epilepsy
Pharamcotherapies
Surgery
Ketogenic Diet
Implanted Device- Vagus nerve, or Deep brain stimulator
General Categories of AED
SV40
Ion channel ligands (NaV ~1.2)
Barbiturates
BZD’s
State Dependent Blockers of NAv channels
Lamotrigine
Carbamazepine (also low efficacy 5HT Reuptake inhibitor)
Enhances Sodium Channel Inactivation
Depakote (also low efficacy block of CaV3 channels)
Vimpat- typically an additive
keep NA channels in an inactive state.
Stereoselective SV2A Binders (inhibitor?)
Levetiracetam- does not bind to NAv channels
Brivaracetam
Reduces NT release
VG-CA channel antagonists
Gabapentin- P/Q type CA2+ Channels. Reduces NT release
AMPA Antagonists
AMPA receptors are glutamanergic ion channels
PerAMPAnel- Non competative antagonist at post synaptic recepots
M-Current
Muscarine senstative ACh ligand gated GPCR Channels
KV7/KCNQ Potassium Channel
Voltage gated K+ Channel
Requires PIP2 For activation:
Hydrolysis of PIP2 decreases M-Current , which makes it harder for Kv7 channels to open, so K+ current reduce, Voltage increases. Makes it easier for epileptic seizures to start.
M-Current Activators
Retigabine- increases K+ flux, thus reduces RMP.
PAMs of GABAa
Benzos
Barbiturates
Benzos are used for
Sedatives, hypnotics, anxiolytics, anticonvulsants
Benzo commonly used for seizures
Clonazepam
HM1A toxin can be used for
Dravets syndrome. It selectively enhances NAv1.1 and NAv 1.3 currents
CBD
Blocks NAv Channels
Antagonist at GPR55
Allosteric modulator at opiod receptors
Stiripentol
Increases GABAergic signaling, increasing release of GABA
