• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/111

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

111 Cards in this Set

  • Front
  • Back
Definition: seizure
Sudden rhythmic change in cortical activity resulting form synchronous firing of cortical neurons
-may be accompanied by a behavior change or subjective sensation
Post ictal period
period of lethargy or confusion after a seizure
Focal seizure
Seizure beginning in a local area in one hemisphere
aka partial seizure
Eg:
simple partial (no LOC)
Complex partial (change in consciousness)
Secondarily generalized seizure
New naming system is more decriptive
Generalized seizure
starts in both hemispheres simultaneously
eg:
Absence
Tonic-clonic
tonic
clonic
myoclonic
atonic
Generalized epilepsy
Predisposition to generalized seizures
Partial/focal epilepsy
Predisposition to partial seizures
Generalized tonic-clonic seizure
"grand mal"
initial stiffening--> back and forth shaking
Tonic seizure
just stiffening
Clonic seizure
just shaking
Myoclonic seizure
Brief jerking seizure
Atonic seizure
drop attack
brief loss of muscle tone
Absence seizure
Petit mal
abrupt loss of awareness
may have eye fluttering or automatisms
Simple partial seizure
Focal seziure with no change in level of awareness
-may have aura (subjective symptoms)
- may have focal clonic activity
Aura
subjective symptoms/ sensations
Focal motor seizure
focal clonic activity
Complex partial seizure
Focal seizure with a change in the level of awareness
- preceded by aura
- may secondarily generalize
Catgeories of seizure symptoms
1) subjective/aura
2) motor
3) autonomic
4) cognitiion
Seizure semiology
Classification system looking to accurately describe seizure signs
-
Psychogenic/Pseudo-seizures
Not a real seizure
signs it may be psychogenic:
-tremor
-arching back
-drug seeking behavior
- no loss of awareness
Status epilepticus
Continual seizure activity
continual for >30 minutes and/or series without recovery between
Epilepsy
Predisposition to unprovoked seizures
- 2 or more
- spontaneous
- predisposition--> it doesn't go away
Possible seizure provokers
- Head trauma
- acute stroke
- severe metabolic abnormality
- drug/toxin ingestion
- fever
Symptomatic epilepsy
caused by a brain lesion; may be mentally reatarded
Cryptogenic epilepsy
Caused by a lesion that we can't find
Idiopathic epilepsy
seizures without a brain lesion; usually normal intelligence
Exception to the rule that all focal seizures are symptomatic seizures
- Benign rolandic epilepsy
- unilateral focal motor seizures in kids at night
- resolves by puberty
EEG in epilepsy
Spikes or sharp waves
- generalized if general epilepsy
- focal if focal epilepsy
EEG in seizure
Sudden rhtymic change that evolves over time
Subclinical seizure
Electrical EEG changes without alteration in behavior
Electrophysiology of epileptiform spikes on EEG
Product of large group of neurons firing synchronously--> large rapid negative extracellular potential followed by return to baseline
Childhood absence epilepsy
Idiopathic generalized epilepsy
onset: 4-8
Seizure type: absence
provoke: hyperventilation
intellect: normal
EEG: 3 hz spike and wave
Tx: Ethosuxamide; blocks thalamic t-type Ca2+ channels
Resolution: puberty
Juvenile Myoclonic epilepsy
Idiopathic generalized epilepsy
onset: 12-18
type: myoclonic--> GTC or absence
provoking: waking up in AM
intellect: normal
EEG: 4-4.5 hz generalized spike and wave
Tx: Valproate UNLESS woman of child bearing age--> levetiracetam; can be made WORSE by pheyntoin, carbamezepne, ocarbazepine, neurontin
Resolution: no
Lennox-Gastaut syndrome
Symptomatic generalized epilepsy
seizure type: GTC, myoclonic, absence, atonic, focal
EEG: ?
Tx: none
Benign Rolandic Epilepsy
Idiopathic partial epilepsy (the only one)
Onset; 5-9
Seizure type: focal motor
Provoke: night time
Treatment: not necessary
REsolution: by puberty
Mesial Temporal Lobe Epilepsy
Symptomatic focal epilepsy
Seizure type: Focal seizures originating in hippocampus or amygdala
Aura:
Insular cortex--> nausea
eeg: focal temporal spikes
Tx: most can't be controlled medically; surgery may help
Temporal neocortex--> deja vu
Uncu--> olfactory hallucination
amygdala--> sudden emotional feeling
Association cortex--> perceptual distortions
Insular cortex--> autonomic symptoms
Aura associated with insular cortex
Rising epigastric sensation
Aura associated with temporal neocortex
Deja vu
Aura associated with uncus
olfactory hallucination
Aura associated with amygdala
sudden emotional feeling
Aura associated with association cortex
perceptual distortions
Aura associated with insular cortex
autonomic symptoms
Automatism
repetitive quasi-purposeful movemnts like:
lip smacking
swallowing
fumbling
picking at clothes
Neocortical epilepsy
Seizure: focal origin in the temporal neocortex or frontal lobe with rapid spread and generalization
Frontal Lobe epilepsy
Seizures: automatisms, noises, postures
Origin of seizure: frontal lobe
Provoking: nighttime
** these patients may have preserved awareness
Supplementary motor area seizures
** these seizures may look like psuedoseizures
Causess of epilepsy
- hippocampal sclerosis
- neoplasms
- heterotopias
- cortical dysplasia
- vascular malformation
Gelastic seizure
main motor manifestation is laughing; often due to hypothalamic hamartoma
Versive seizure
seizure where eyes, head, and torso move to one side; may be due to lesion in frontal eye field in the frontal lobes
- lateralizing feature
Mechanisms of seizure generation
1) too much excitation--> too much Na+, Ca2+ current or too much Glutamate or Aspartate stimulation
2) too little inhibition--> two little inward Cl-, outward K+; or too little GABA transmission
Targets for anti-convulsant drugs (4)
1) increase GABA
2) Decrease excitatory Glutamate
3) Block inward positive currents: Na+ or Ca2+
4) Increase outward K+ current

Pleotropic: act by multiple mechanisms
Felbate binding site
NMDA receptor glycine binding site
Benzodiazepine action at GABA receptor
Increases frequence of GABA mediated chloride channel openings
Barbiturate action at GABA receptor
Prolongs duration of Cl- channel opening
AEDs that act on NMDA receptor to decrease glutamatergic stimulation
Felbamate
AEDS that act on GABA
Benzos: diazapam, clonazapam
Barbiturates: phenobarbital, primidone
Gabapentine
Tiagaine--> reuptake inhibitor
Vigabatrin-->inhibits catabolism

*** NOT PREGABALIN (lyrica)
AEDs that act on Sodium channels
Phenytoin
Carbamazepine/Oxocarbazepine
Lacosamide
Zonisamide
AEDs that act on Ca2+ channels
Ethosuxamide ONLY blocks t-type Ca2+ channel--> only for absence
AEDs that act on K_ channels
Valproate
Oxcarbazepne
Pleotropic AEDs
Felbamate (NMDA, Na+)
Lamotrigine
Topiramate
Valproate: GABA, Na+, K+, Ca2+
Valproate does it all
- Ca2+ channel blockade
- Na2+ channel blockade
- potentiation of GABA
Limitations of 1st generation AEDs
- incomplete efficacy
- unfavorable kinetics as enzyme inudcers/inhibitors; high protein binding
- narrow therapeutic range
- CNS effects
- drug interaction
1st generation enzyme inducers
- Phenytoin
- Carbamazepine--> induces it's own metabolism!
- Phenobarbital
1st generation enzyme inhibitors
Valproate
mechanism of phenytoin
inhibition of Na+ channels
Limitations of phenytoin
- high protein binding/ enzyme saturation--> non-linear kinetics
- Adverse effects:
CNS sedation--> acts like alcohol
gum hyperplasia
- hirsuitism
Uses of phenytoin
EMERGENCY for Status Epilepticus
Mechanism of Carbamazepine
INihibition of Na+ channels
Adverse effects of Carbamazepine
-Agranulocytosis and aplastic anemia
-hyponatremia
-stimulates metabolism of other drugs and itself! (tolerance)
Mechanism of phenobarbital
Allosteric modulator of GABA receptor--> increases duration of opening
Adverse effects of phenobarbital
CNS depression
stimulation of hepatic metabolism
Mechanism of primidone
allosteric modulator of GABA
Uses of primidone
PARTIAL SEIZURES
USES OF PHENOBARBITAL
PARTIAL SEIZURES
Mechanism of benzos
increased frequency of GABA channel oening
Uses of benzos
rescue medication in status eplepticus
Adverse effects of benzos
CNS sedation, tolerance, dependence, paradoxical hyperexcitability
Mechanism of valproate (multiple
- inhibition of NA+ channel
activation of K+ channel
GABA enhancing
inhibition of Ca2+ channel
adverse effects of valproate
- hepatotoxicity
- birth defects: neural tube defects
uses of valproate
all types of seizures including partial EXCEPT in young women of child bearing age
mechanism of ethosuxamide
inhibition of T type calcium channels
adverse effects of ethosuxamide
not too many
Uses of ethosuxamide
absence seizures ONLY
Mechanism of oxocarbazepine
same as carbamzepine: inhibition of Na+ channels
adverse effects of oxcarbazepine
hyponatremia
Uses of oxcarbazepine
partial seizures
Mechanism of gabapentin
interferes is GABA uptake
Adverse effects of gabapentin
weight gain
Uses of gabapentin
not great for seizures
great for neuropathic pain
mechanism of lamotrigine
inhibition of Na+ channels and glutamate release; may inhibit Ca2+ channels
Adverse effects of lamotrigine
Steven johnson syndrome
Uses of lamotrigine
pregnancy for generalized and focal epilepsies
mood stabilization in bipolar disorder
mechanism of Felbamate
inhibition of NMDA receptor via glycine binding site
Adverse effects of felbamate
aplastic anemia
severe hepatitis
ionsomia, appetite suppression and weight loss
uses of felbamate
refractory partial seizures
levetiracetam
"vitamin K"

mechanism
pluses
minuses
mechanism: inhibition of Ca2+ currents?

Pluses: first dose is tx; no enzyme induciton

minuses: IRRITABILITY
Topiramate
"dopamax"
Mechanism: inhibition of Na+ channels; increase GABA opening; interfereance with flutmate binding

Adverse: memory and cognitive effects

Uses: appetpite suppression, weight loss, migraine prophylaxis
Pregabalin
mechanism:decreased release of neurotransmitters
adverse: makes you gobble (fat)
Vigabatrin
visual field deficit
p450 inducers
phenobarbital
phenytoin
carbamazepine

** requires enzyme synthesis--> takes time to take effect and wear off**
p450 inhibitors
valproate

** no enzyme synthesis--> immediate inhibition**
AEDS and stevens johnson
lamotrigine

watch for abdominal pain, vomiting, jaundice, fever
AEDs and hematologic damage
Felbamate

watch for abnromal bleedig, acute fever, aemia symptoms
Long term effects of phenytoin
- osteomalaxia
anemia
teratogenesis
facial carsening
hirsuitism
gingival hyperplasia
neuropathy
2 drugs that exacerbate epileptic seizures
Tramadol
Venflaxine
AEDs used for neuropathic pain
Gabapeintin
Carbamazepine
Pregabalin
AEDs used for bipolar disorder
Lamotrogine
Valproate
AEDs used for migrain
Valproate
Topiramate
Zonisamide
First line for Idiopathic generalized epilepsy
Valproic acid
Lamotrigine (pregnancy; risk of stevens johnson)
Levetiracetam
Drug specific for childhood absence epilepsy and mechanism
Ethosuximide
inhibition of T type calcium channels
Drugs with limited indications because of side effects
Felbamate (aplastic anemia; hepatitis)
Vigabatrine
Phenobarbitol
Drugs for focal epilepsy
Carbamazepine
Valproic acid
Lamotrigine
Topiramate
Levetericaetam
Oxcarbazepine
Gabapentin
Phenytoin
Phenobarbital