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32 Cards in this Set

  • Front
  • Back
Causes of pediatric epilepsy
Perinatal and neonatal insults
genetic susceptibility
Causes of Adult epilepsy
status epilepticus
Idiopatic
trauma
complex febrile seizures
Causes of elder epilepsy
tumor
idiopatic
neurogenerative disorder
cerebrovascular incidence
Functions of different areas of brain
occipital - vision
parietal - primary somatosensory
temporal - memory, language and emotion
frontal - motor, impulsive behavior, apathy, psychomotor retardation
corpus callosum - separates cerebral hemispheres
What area of the brain is the primary and secondary location of seizures
Temporal and frontal
Types of seizure
generalized (bilateral) and partial (unilateral)
Generalized seizures breakdowns
Absence - occur in childhood, gives blank stares and looks like not paying attention
Myoclonic- muscle jerkiness
Tonic/Clonic- increase tone/stiffness, increase rhythm
Tonic -increase tone
Atonic - jerkiness that leads to crashing on heads
Partial seizures subcategories
1. simple partial seizures - awareness and mentation is not impaired

2. complex partial seizures- awareness and mentation is impaired.
Juvenile Myoclonic Epilepsy
Onset is during puberty and happens in the morning with a muscle twitch and leads to seizures later that day
-preventable with benzodiazepene, keppra, depakote, lamictal
Lennox gastaut syndrome
combination of all seizures, hard to treat, goal is unable become seizure free
characteristics of primary generalized epilepsy
begins in both hemisphere
hereditary link
onset associated with age, mainly children
often an abnormal EEG
generally no structural leison
typically normal IQ and neurological exam
Characteristics of partial seizures
begin focally
no hereditary link, idiopathic
onset has a bimodal distribution (<20 and >60 yrs old)
EEG generally normal inter-ictally
may or may not have structural leison or MRI
major receptors in epilepsy
GABA
Ion Channels
- Na, K and Ca
Amino Acid
-Glutamate
GABA Receptors
Formed within the axon terminal by decarboxylation of glutamate
- inhibitory neurotransmitter
- regulate Cl flux
- multiple binding sites
Levels of GABA
Normal level - increase levels of Cl intracellulary

Low GABA levels - increase levels of Na intracellulary
Ion Channel receptors
Na - voltage controlled gating
Maintains intracellular Na concentration much lower (more neg) than extracelluar, via Na/K ATPase pump
-channels open via membrane depolorization, allowing influx of Na ions
Amino Acid Receptors
Glutamate is an excitatory neurotransmitter
Receptor subtypes
-NMDA: fluxes Na and Ca
-AMPA :fluxes Na
Vigabatrin
Enhances GABA levels by inhibiting GABA transaminase
Tiagabine
Blocks the reuptake of GABA
Barbituates (phenobarbital and primidone)
Benzodiaepines, clobazam, valproate, felbamate, topiramate
Enhances Cl conductance through GABA-A receptors, which enhances GABA
Drugs that block fast sodium channels
Phenytoin, fosphenytoin,carbamazepine,valproate, felbamate,lamotrigine,topriamate, oxcarbazepine, zonisamide, rufinamide
Drugs that enhances sodium channel slow inactivation
lacosamide
Drugs that reduce t-type calcium current in the thalamic cortical pathway.
Ethosuximide, valproate and zonisamide
Drugs that affect calcium channels in an unknown fashion
Felbamate, oxcarbazepine, and lamotrigine
Drugs that reduces l-type calcium current
Topiramate
Drugs that bind to the alpha- 2 delta subunit of the voltage gated calcium channel, modulating the release of glutamate, noradrenaline and substance P Can also be used for pain
Pregabalin
Drugs that bind to alpha 2 delta auxiliary subunit of voltage sensitive calcium channels and reduces excitatory inward L type calcium current
Gabapentin
Ezogabine
opens K channels in the brain
Adverse effects: neurogenic bladder, people can't tell when need to urinate.
Amino Acid Receptor
- Glutamate
Felbamate - blocks NMDA
Topiramate - blocks kainate
Lamotrigine - blocks glutamate release
Pregabalin - enhances glutamic acid decarboxylase activity
- Reduces release of excitatyr neurotransmitter (glutamate, noradrenaline, substance P)
Levetiracetam
binds at the synaptic vesicle protein SV2A,
-site found in the brain
- acts by enhancing SV2A function, inhibits abnormal bursting of epileptic circuits
*lack of SV2A function would cause seizures.
Pregnancy and AED
Metabolic clearance increases during last trimester
- monotherapy is best and
- monitor serum levels
**by end of pregnancy may be using levels double to triple doses as when first started
poor cognitive outcomes from what drugs during pregnancy
Valproate use druing pregnancy and potentially with phenobarbital and phenytoin.