SEIZURES Flashcards
myoclonic seizure
shock like contraction of muscles
isolated jerking
tonic seizure
in children
rigididy as a result of increased tone in extensor muscles
clonic seizure
babies and young children
rapid and repetitive movement
atonic seizure
sudden loss of muscle tone
patients fall if standing
tonic clonic
tonic phase - rigidity followed by clonic rapid motion
seizure definition
paroxysmal disorder of CNS by abnormal cerebral discharges with or without loss of consciousness
convulsion
attack manifested by involuntary muscle movements
epilepsy
repeated seizures due to damage, irritation, chemical imbalance in brain
- sudden electrical discharge
what kind of firing is in seizures
disordered, synchronus, rhythmic
synchronized hyperexcitability
seizure classifications
focal onset
generalized onset
unknown onset
focal onset location
comes from one place in the brain
being in temporal lobe
generalized onset location
all over the brain
focal seizures usually due to
lesion, head trauma, infection
generalized seizures description
loss of consciousness, both brain hemispheres, idiopathic, usually genetic
how do primary generalized seizures propagate
diffuse via interconnections between thalamus and cortex
difference in EEG for focal vs. generalized seizure
focal has different waves
generalized all has the same
aware focal seizures
no loss of consciousness
auras can occur
limited jerking of single part of body
impaired awareness focal seizures
most common
clouding of consciousness
repetitive motor behaviors
POSITICTAL STATE
aura common
generalized absence seizure typical
no convulsions, aura, postictal period, brief loss of consciousness
staring or eye flickering
generalized absence seizure atypical
slower onset than typical
do generalized tonic clonic have aura
no
do focal to bilateral have aura
brief aura
status epileptics definition and goal
seizure lasting > 30 mins
want to bring seizures within 60 minutes
does one seizure make an epilepsy
no
when should we stop drug therapy in seizures
gradually stopped who havent had seizures in 2-5 years
depolarization involves what
activation AMPA and NMDA by glutamate and Ca channels
influx of Ca
hyperpolarization involves what
activation GABA receptors and K+ channels
influx Cl and efflux K+
can we stop epilepsy drugs suddenly
no, higher risk for status epilepticus
drugs that increase risk of seizure
alcohol
bupriopion
theophylline
CNS stimulants
oral contraceptives
depressant withdrawal
clozapine
MOA anticonvulsants
stabilize and reduce neuronal excitability
drugs that decrease sodium influx, prolong inactivation of Na+ channels
carbemazepine
oxcarbazepine
phenytoin
lacosamide
lamotrigine
valproate
drugs that decrease Ca influx
lamotrigine
ethosuximide
valproate
drugs that increase GABA inhibition
barbituates
benzodiazepines
valproate
gabapentin
vigabatrin
tiagabine
excitatory antagonists
felbamate
topiramate
why are there few drugs targeting K channels
hERG target, bad side effects like arrythmias
excitatory pre synaptic targets
Na channels
Ca channels
excitatory post synaptic targets
NMDA
AMPA
inhibitory pre synaptic targets
GABA transporter (GAT-1)
GABA transaminase (GABA-T)
inhibitory post synaptic targets
GABA A and B receptors
phenytoin MOA
binds inactive state Na channel
not isoform selective- other targets
what is fosphenytoin
prodrug phenytoin IV
phenytoin kinetics are
non linear, dose dependent
phenytoin interactions
displaced from plasma proteins (increase blood level conc)
induces P450s (inc. conc of other drugs)
side effects phenytoin
arrythmia
visual
ataxia - loss coordination
GI sx
hirsutism
rash
carbemazepine and oxcarbazepine structure
tricyclic
carbemazepine and oxcarbazepine MOA
binds and stabilizes inactivated state of Na channels
carbemazepine and oxcarbazepine interactions
cyp450, increase its metabolism
carbamazepine side effects
blurry vision, ataxia, GI, sedation, rash (Stevens Johnson sydrome),eosinophillia / DRESS
lacosamide MOA
enhances inactivation of Na+ channels
lacosamide toxicity
dermatological reactions, cardiac risk (PR interval), visual disturbances
barbituates drugs
phenobarbitol
primidone
who is phenobarbital drug of choice in
infants up to 2 months
phenobarbital MOA
binds to allosteric site on GABA a a
increases DURATION Cl- channel opening
phenobarbital toxicities
sedation, dependance (abuse)
benzodiazepine drugs
diazepam
clonazepam
diazepam use
tonic-clonic status epilepticus, rectal gel
diazepine MOA
binds allosteric regulatory site on GABA - A receptor, increases FREQUENCY of Cl- channel opening events
diazepam toxicity
sedation, physcial dependance, not useful for chronic treatment
clonazepam use
acute treatment of epilepsy and absence seizures
gabapentin and pregabalin MOA
increase GABA release, decrease Ca influx, reduce glutamate release
vigabatrin MOA
irreversible inhibitor of GABA-T, which degrades GABA
tigabine MOA
inhibits GAT-1, gaba transporter
felbamate MOA
NMDA receptor antagonist
felbamate toxicity
severe hepatitis
topiramate MOA
AMPA and kainate antagonist
ethosuximide MOA
blocks T type Ca channels in thalmic neurons
lamotrigine MOA
inhibits Na and Ca channels
lamotrigine side effect
skin rash, stevens johnson syndrome
valproate MOA
inhibits Na and Ca chanels
increases GABA
levitiracetam MOA
binds synaptic protein vessel SV2A, interferes with synaptic vessel release and neurotransmission
also interferes with Ca entry
encephalopathy < 3 mo tx
phenytoin
encephalopathy > 3 mo tx
levitracetam
