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33 Cards in this Set

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Mechanism of seizure
finite episodes of brain dysfunction resulting from abnormal discharge of cerebral neurons. -A small number of neurons misfire then recruit more neurons to misfire.
Abnormal firiing is due to
-neurotransmitter imbalances
-abnormal chemistries
-poor oxygenation
-hormone imbalances
Excitatory neurtotransmitter imbalances
histmaine, aspartate, glutamate, ach, and norepi
Inhibitory neurtotransmitters imbalances
GABA and dopamine
Partial seizure:
Simple Partial seizures
without impairment of consciousness
-motor symptoms (convulsive jerking)
-autonomic symptoms
-psychic symptoms (altered sensory perception, illusions, hallucinations, affect changes)
-special sensory or somatosensory symptoms (paresthesias)
Partial seizure:
Complex Partial seizures
progressing to or impaired consciousness
-w/ no other features
-w/ other features as in simple partial seizures
-w/ automatisms
Partial seizure:
secondarily generalized
raises treshold and seizure comes into entire brain. pt. don't know what's happening. encompasses both side of brain.
Generalized Seizures (convulsive or nonconvulsive)
-Myoclonic (single or multiple myoclonic muscle jerks)
-Absence seizures (impaired consciousness-often abrupt onset and breif), sometimes with automatisms, loss of postural tone, or enuresis; begin in childhood (formerly, petit mal) and usu cease by age 20 yrs.
-Atonic (astatic or akinetic)
-Infantile spasms
-tonic clonic (tonic phase-less than 1 min) involves abrupt loss of consciousness, muscle rigidity, and respiratory arrest; clonic phase (2-3 min) involves jerking of the body muscles, with lip or tongue biting, and fecal and urinary incontinence; formerly called grand mal
other seizures:
-juvenile myoclonic epilepsy
-lennox-gastaut syndrome
-various childhood syndromes with epilepsy
Treatment goals of epilepsy
-good QOL
-Empower pts. to manage their conditions
-zero seizures
-zero a.e.
-Required maintenance tx
-structural lesion on brain imaging
-neurologic deficit
-definite EEG abnormalities
-further risk of seizure is unacceptable
-->if treatment started=cont. for atleast 2 years before stopping.
Disadvantages of w/drawing
flurry of seizures (risk of status epilepticus and dying)
factors favoring AED withdrawal in well controlled pts.
-seizure free 2-5 yrs.
-single type of seizure disorder
-seizure onset after 2 but before 35 years old.
-EEG normalized with treatment
-normal IQ and neurological exam
how to disc. AED
-choose a 4 month period that is the least stressful
-taper takes 2-6 months (dec. by 25% q 2-4 weeks)
-restart drug if withdrawal seizures occur then restart taper but slower
-assess any increase in anxiety or depression
-reevaluate after 5 years
Provide pt. education and involve patient in decisions
-report any new symptoms (hypersensitivity, flu like, rash)
-stress that lack compliance=inc. seizures
-pt. self-assessment of drug efficacy and ADR
-support groups and cont. learning
-treatment of S.E. (do not put anything in mouth, lay them on their side)
-est. treatment goals with the pt.
Nonpharmacological treatments
Decrease precipitants: stress, sleep deprivation, hyperventilation, sensory stimuli, ETOH, hormonal changes
-surgery
-vagus nerve stimulation
-ketogenic diet (seen in children- high fat, low carbohydrate and protein diet, causing ketosis)
Antiepileptic drug:
Sodium channel blocker
stabilizes neuronal membrane. by blocking voltage gated sodium channgels (PHENYTOIN, CBZ, and LTG)decreases neurotransmitter release, focal firing, action potential propagation, and sz spread)-->results from prolongattion of the inactivated state of the Na channel and the refractory period of the neuron. PB and PHT may exert similar effects at high doses.
vpa, ocbz, ltg, tpm, zns, pht, cbz, fbm
Antiepileptic drug:
Calcium Channel Blocker
Dec. neurotransmitter release, slow depolarization, and spike wave discharges
enzyme inducers
phenytoin, carbamazepine, phenobarbital
enzyme inh.
valproic acid. felbamate, topiramate, and oxcarbamazepine mostly inhibit CYP2C19
competitive inh.
phenobarbital and phenytoin at high conc.
neither inducer or inhibitor
ethosuximide, gabapentin, lamatrogine, tiagabine, levetiracetam, pregablin
when adding phenobarb to pheny
pheny inc., dec., or unchanged
when adding vpa to pht
total pht level dec., free pht conc. inc
when adding pht to cbz
cbz total dec., epoxide inc.
when adding vpa to cbz
cbz total dec. or unchanged, and epoxide inc.
when adding pht to pb
pb inc. dec. or unchanged
when adding vpa to lamotragine
lamatrogine inc. 100%
when adding vpa to tgb
tgb free inc. 40%
GABA receptor allosteric modulator
in the presence of substrates, the frequency of the chloride ion channel opening is inc., thus facilitate the inh, effects of GABA (benzos= inc. frequency of opening, others (PB and other barbiturates)- interact at diff. receptor site on chloride ion channels-->result in inc. duration)==>inc. membrance hyperpolarization and seizure treshold. dec. focal firing)
inhibition of GABA metabolism and reuptake
GABA transaminase is an important enzyme in the termination of action of GABA. the enzyme is irreversibly inactivated by vigabatrin at tx plasma levels and can also be inh. by VPA at very high conc. tiagabine inh. gaba transporters in neurons and ganglia.
NMDA receptor antagonist
dec. slow excitatory neurtotransmission and excitatory a.a. neurotox. aggravates spike-wave discharges. felbamate blocks glutamte NMDA receptors
AMPA/kainite receptor
Dec. fast excitatory neurotransmission and focal firing. PB, TPM