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66 Cards in this Set

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Partial seizures
group of hyperactive neurons with electrical hyperactivity
restricted to one anatomical lesion
2 types fo partial seizures
describe them
elementary partial (focus in motor or sensory cortex, no LOC)
complex partial (focus in temporal lobe, affecting higher brain fxn --> disturbances in psychomotor/psychosensory fxn, altered consciousness)
Generalized seizures
associated with bilateral synchronous and symmetrical EEG discharge
LOC
(can begin as a partial or elementary partial sezizure and eventually progress)
Subtypes of generalized seizures
tonic-clonic (grand mal)
absence
myoclonic
infantile spasms
akinetic/atonic drop attacks
manifestations of elementary partial seizures
motor (frontal cortex tonic and clonic muscle activity)
sensory (hallucinations, from parietal/occipital lobes)
EEG: unilat localized spiking activities, contralateral to seizure presentation)
NO LOC
Jacksonian march
can generalize to tonic clonic
Who is likely to get elementary partial seizures
post-stroke pts
how long do elementary partial seizures last
seconds to minutes
manifestations of complex partial seizures
hallucinations
GI disturbances, dizziness, urination
de ja vu/ jamais vu
fantasy state, memory loss
automatisms
EEG in complex partial
unilateral left side, seen during interictal period or sleep
how long do complex partial seizures last
1-2 mins
what can cause complex partial seizures
birth trauma
stages of tonic clonic seizures
prodromal (autonomic probs, change of mood, can precede by hours)
loss of muscle tone and consciousness
tonic (apnea/cyanotic)
clonic (1-5 mins)
EEG findings in tonic stage of tonic clonic
symmetrical
bilateral
what happens to breathing during tonic-clonic seizures
apnea and cyanosis during tonic
hyperventilation during the clonic
EEG findings in clonic stage of tonic clonic
spike and wave complexes
bilateral and symmetrical
hyperventilation
EEG findings in absence seizures
oscillatory firings in thalamic neurons
mediated by low threshold ca current
3 cps spike/wave complex from thalamus
bilateral and symmetrical
onset of absence seizures
4-8 yo, can convert at puberty
what can elicit absence seizures
hyperventilation
bright light
(these DON'T induce absence variant seizures)
what % of pts with absence seizures --> tonic clonic
50%
absence variant
2-2.5 cps spike and wave
poor prognosis, assoc with dementia
some motor movts
Minor motor seizures
can occur at any age, but usually young
result from perm neuro damage
repetitive, rhythmical, symmetrcal contractions of facial muscles and limbs
EEG of minor motor seizures
polyspike and wave complexes
bilat and symm
Infantile spasms
Prognosis
age specific syndrome (3 mo-2 yr)
90% --> MR
40% --> CP
Manifestations of infantile spasms
flexor spasms or extremities and head for several seconds
EEG of infantile spasms
hypsarrhythmia
cause of infantile spasms
encephalopathy during development
inflammatory therapy can include ACTH/corticosteroids
Akinetic/atonic drop attacks
Prognosis
Manifestations
in kids 2-5 yo
poor prognosis (assoc with MR)
head drooping, falling
EEG of akinetic/atonic drop attacks
polyspike and wave complexes
bilat adn symmetrical
vary in rhythm
MOA Carbamazepine
slows rate of recovery of volatage activated Na channels from inactivation
Pharmacokinetic issues of carbamazepine
autoinduction of p450 --> tolerance
97% metabolic clearance
adverse effects of carbamazapine
diplopia
ataxia
dizziness
nausea
nystagmus
HYPONATREMIA (from SIADH)
aplastic anemia, agranulocytosis (fatal and irreversible)
uses for carbemazepine
partial seizures (first choice)
tonic clonic (first choice)
trigeminal/glossopharyngeal neuralgia
NOT for absecne or minor motor
what can carbemazepine NOT be used for
absence and minor motor seizures
oxcarbemazepine
pro-drug
less autoinduction --> less tolerance
adverse reactions to oxcarbazepine
ataxia
diplopia
SIADH
indications for oxcarbazepine
partial seziures (complex and simple)
tonic-clonic
trigeminal and glossopharyngeal
NOT for absence or minor motor
advantages of oxcarbazepine
less tlerance
fewer hypersensitivity rxns
less severe interactions with polytherapy
phenytoin
NOT CNS depressant
prolongs inactive state of Na channels, prolonging refractory period
pharmacokinetics of phenytoin
LIMITED ACQUEOUS SOLUBILITY
BIOINEQUIVALENCE COMMON
90% met by p450
non-linear relationship btwn dose adn plasma concentrations
benefits of phenytoin
less autoinduction of p450
what drugs can displace phenytoin from albumin
valproate
sulfonamides
--> increased free phenytoin but lower total []
what drugs enhance metabolism of phenytoin
phenobarbital and carbamazepine
adverse effects of phenytoin
ataxia
diplopia
slurred speech
nystagmus
confusion
hypersensitivity rxn (msot common)
gingival hyperplasia
hirsutism
vit K, D, folate deficiency
TERATOGENIC!!!
what are the implications of phenytoin during pregnancy
teratogenic --> cleft lip/palate, heart defect, slowed growth and mental deficiency
indications for phenytoin
= to carb for tonic-clonic and partial seizures
what is used to treat recurrent tonic clonic or focal partial status epi
IV fosphenytoin
phenobarbital
barbiturate with anticonvulsant activity
mechanism of phenobarbital
potentiates GABA effects
pharmacokinetics
MOST POTENT INDUCER OF P450 --> tolerance
increases metabolism of many therapeutic agents
Adverse effects of phenobarbital
sedation
nystagmus and ataxia
w/d
vit d, k, and folate deficiency
paradoxcial hyperkinesia
uses of phenobarbital
partial seizures
tonic-clonic
STATUS EPI
NEONATAL SEIZURES
NOT useful for absence, atonic, infantile
MOA ethosuxamide
slows Ca curretns in thalamic neurons that discharge during ABSENCE seizures
pharmacokinetics of ethosuxamide
doesn't induce p450
adverse effects of ethosuxamide
N/V
drowsiness
urticaria
blood dyscrasias
uses for ethosuxamide
SIMPLE ABSENCE SEIZURES
MOA valproic acid
prolongs recovery of Na channels from inactivation
reduces Ca currents in thalamic neurons
increases GABA
pharmacokinetics valproic acid
doesn't induce p450
use in combo
adverse effects of valproic acid
N/V
fine tremor
weight gain
teratogenic --> spina bifida
thrombocytopenia
hepatotoxicty (fatal hepatic injury)
uses of valproic acidq
FIRST CHOICE FOR ABSENCE SEIZURES
MOST EFFECTIVE FOR MYOCLONIC AND ATONIC
hypsarrhthmia
almost as good as carb for partial and tonic seizures
MOA lamotrigene
delays recovery of Na channels
inhibits Ca channels
adverse rxn of lamotrigene
skin rash (1-2% life-threatening)
toxic epidermal necrolysis
uses of lamotrigene
comp to carbam for partial and tonic clonic
ABSENCE AND MYOCLONIC
good for add-on if used with p450 inducers
pharmacokinetics
no p450 induction
which drugs will increase clearance of OC
carbamazepine
phenobarbital
phenytoin

(these drugs also --> teratogenics)
which drugs --> coagulopathy
carbamazepine
phenobarbital
phenytoin
all promote vit K catabolism


(these drugs --> teratogenicity also)
drugs --> teratogenicty
phenytoin
carbamazepine
valproate
phenobarbital