Seizure disorders Flashcards
define seizure
abnormal/excessive firing of CNS neurons
define epilepsy
chronic condition recurrent seizure which are not provoked by neurologic insults
2unprovoked more than 24hr apart or
1 unprovoked and probability of further seizures
status epilepticus
seizure lastin >30min or 2 without return to normal mental baseline
focal vs generalised
focal is in one small part or whole hemisphere
general is in two hemispheres
5 things in the evaluation of a seizure
history and physical exam lab tests, screen for drugs as well lumbar puncture if CNS infection suspected EEG CT/MRI brain scan
what is electroencaphalography
electrodes placed on scalp
records electrical activity of the brain
inhibitory neurons
GABA
how does inhibitory transmission work
gaba binds to post synaptic receptor to open chloride ion channels and allowing influx making it hyperpolarized
excitatory neurons
glutamate
how does excitatory transmission work
glutamate binds to NMDA receptor
Na/Ca influx, K efflux
targets for antiepileptic drugs
enhanced excitation (glutamate) membrane depol reduced inhibition (GABA)
epilepsy there is an imbalance in
excitatory and inhibitory processes, more excitation is happening
goals of therapy
eliminate seizures
min side effects
optimize quality of life
remission is
complete cessation of seizures for at least one year
refractory is
2 or more AEDs failed to control seizures
how do you initiate an AED
start low and go slow but if needed push to max tolerated dose
indication for an AED
once diagnosed with epilepsy
first line for adult focal seizure
carbamazepine
levetiracetam
first line for adult generalized tonic clonic
carbamazepine
lamotrigine
first line for absence
valproic acid
ethosuximide
SE for all AEDs
CNS- drowsy, dizzy
GI
toxicities additive
side effects are
dose related
reversible on lowering or discontinuing AED
gingival hyperplasia caused by
phenytoin
describe idiosyncratic reactions
more serious and life threatening
not dose related
no lab test identifies risk
some rare idiosyncratic reactions
SJS
toxic epidermal necrosis
DRESS
fever and rash
risk factors for idiosyncratic reactions
history of previous drug reactions
liver/kidney dysfunction
hematopoisesis or metabolic disorders
idosyncratic reactions rare with
gabapentin pregabalin topiramate OXC LEV
highest risk of idiosyncratic reaction occurence
first 2 months of therapy
more common idiosyncratic reactions
agranulocytosis aplastic anemia thrombocytopenia hepatotoxicity pancreatitis connective tissue disorder
AEDs have two fold increased relative risk of what
suicidal behaviour or idealation
what med do we absolutely avoid in pregnancy and in women of childbearing age
VALPROIC ACID
supplement for pregnant women on AEDs
folic acid 1-3 month prior to conception becuase theres an increased risk of neural tube defects
inducers
carbamaxepine phenytoin phenobarb topiramate oxcarbazepine
inhibtors
valproic acid
when should you monitor serum levels
assess non adherence suspected toxicity adjustment of phenytoin dose manage PK interactions status elipticus
what should patients record
seizure frequency
adverse effects
precipitating factors
labs to monitor
CBC
electrolytes
LFT
before starting AED and at regular intervals during the first months of use
managing AE for new AEDs
use test dose at bed time
if SE delay next dose
if they recur reduce dose
increase as tolerated
managing AE due to peak blood levels
administer with food
change dosing interval
give larger dose at bedtime smaller during the day
extended release formulation
monitoring parameters
seizure frequency, CNS effects, AE daily
CBC, LFT, electrolytes baseline then every 6 months
should see improvment in
1-2 weeks
sig benefit in 1 month
when could you consider discontinuing AEDs
eizure free for 2 years
control easily achieved at low dose
no previous unsuccessful attempts
normal neurologic exam
how do you discontinue an AED
one drug at a time
slowly for at least 2-3 months
immediate emergency care required if
seizure lasts >5min
repeated convulsive seizures
first line treatment for status epilepticus
benzo
if doesnt work use and anticonvulsant
what is a keotgenic diet
high fat
low protein
very low carbs
what does the ketogenic diet do
mimics biochemical changes during starvation so body burns fat producing ketones which are structurally similar to GABA
advantage of ketogenic diet
fewer SE and sometimes more effective
disadvantage of ketogenic diet
need dietician
compliance
unhealthy ?
