w4: Seizure Disorders & Epilepsy Flashcards
Definition of Seizure
sudden disruption in the electrical function of brain
D/T: abnormal excessive discharges of corticol neurons
Definition of Epilepsy
2+ unprovoked seizures more than 24+ hours apart
one unprovoked seizure w/ 60% chance of reoccurence after two unprovoked seizures, within 10 years
Dx of epilepsy syndrome
Epilepsy Syndrome Definition
sizure + abnormal ECG & MRI in a recognizible pattern
age, time of day, triggers, and type of seizure taken into account
Convulsions
involuntary violent spasms of large skeletal muscles of face, arms, neck, legs
Are all convulsions seizures?
Yes
Are all seizures convulsions?
No
Drugs used for seizures should be called ___ and not _____
antiseizure, anticonvulsants
Seizures are caused by the dysregulation of what neurotransmitter?
GABAA
Mechanisms that cause a seizure
- stimulation of CNS excitatory pathways
- inhabition of inhibatory pathways with the CNS
- withdrawal of LT CNS depressants
Which meds need to be tapered due to risk of seizures?
antidepressants
Which medications can cause seizures?
antipsychotic
chloropramzine
clozapine
Causes of Recurrent Seizures in YA
alcohol/drug w/d
brain tumor
idiopathic
illicit drug use
P-TBI
Perinatal insults
Causes of Recurrent Seizures in OA
alcohol/drug withdrawal
brain tumor
cerebrovascular disease (stroke, aneurysm)
CNS degenerative diseases (alzhimers, MS)
MDD
Idiopathic
metabolic d/o
P-TBI
3 Phases of Seizure
preictal
ictus
postictal
Preictal Phase of Seizure
Prodoma
Aura
Prodoma
early clinical manifestations
hours to days before
insomnia, headache, irritability, ill-temper, increased agitation and depression
Aura
focal sizure than generalized tonic-clonic sizure or complex partial seizure
abnormal sensations (taste, smell, visual, auditory experiences), dizziness/numbness, funny feeling
ictus
seizure epiosde
tonic-clonic activity (muscle twitches)
incontinence
Postictal
period following cessation of seizure activity
h/a , confusion, aphasia, memory loss, deep sleep, PARALYSIS
priority during ictus
maintain airway
how long does postictal phase last?
1-2 days
4 Consequences of Seizures
- inc cerebral blood flow
- cerebral oxygen consump inc 60%
- glucose depletion
- accmulation of lactate in brain tissue
Irrversible brian damage occurs after how much time?
after 5 minutes there is irreversible hypoxic brain injury
How are seizures classified?
origin of seizure in the brain (focal/generalized onsent)
degree of awareness during seizure (self, environment)
level of body movement (motor, nonmotor)
Focal Seizures
previously called partial seizures
neurons unilaterally (limited to one part of either L/R hemisphere, but can spread)
with OR w/o of loss of conciousness
aura is common
Focal Sizure Motor Terms: stiffening of body muscles with falling/rigidity + loss of conciousness. fall backwards.
tonic
Focal Sizure Motor Terms: sudden brief loss of muscle tone w/ falling. no loss of conciousness. fall forward.
atonic
Focal Sizure Motor Terms: sudden brief shock like jerks/twitches of arms & legs. may drop things. no loss of conciousness.
myoclonic
Focal Sizure Motor Terms: abrupt loss of conciousness, body stiffening then shaking. sudden cry, loss of bladder control, biting of tongue. 2 mins.
tonic-clonic
Focal Sizure Motor Terms: bimanual or bipedal motor activity. kicking, thrashing, and rubbing hands. hugging. autonomic changes w/o awareness.
hyperkinetic
Focal Sizure Nonmotor: sensory
sensorynumbness, tingling, burning, flashing lights, auditory experiences
Focal Sizure Nonmotor: cognitive
aphasia, hallucination, memory, or attention impairment
Focal Sizure Nonmotor: emotional or affective
fear, agitation, anger, crying, laughing, paranoia
Focal Sizure Nonmotor: autonomic
blushing, pallor, in./dec. HR, hyperventilation, hypoventilation, nausea
Focal Seizure: w/o loss of awareness
recall
responsiveness
conciousness intact
What are focal seizures w/ impared awareness called?
complex focal seizure
Traits of complex focal seizure?
loss of conciousness/awareness
vague/ dream like state
Is the onset and awareness known for focal seizures?
no
FS: Focal to Bilateral Tonic-Clonic Seizure
begins in one part of the brain –> spreads to both sides –> tonic-clonic seizure
is there loss of conciousness in a Focal to Bilateral Tonic-Clonic Seizure?
Yes
Generalized Seizure:
neurons bilaterally
seizure orginate in both sides simultaneously
loss of conciousness
Generalized Seizure: Motor responses
tonic-clonic, tonic, atonic, clonic, myoclonic, myoclonic atonic, clonic-tonic-clonic
Generalized Seizure: Non-Motor responses (absence seizures)
typical
atypical myoclonic
eyelid myoclonia (eyelid twitch)
Generalized Seizures: Epileptic Spasms Overview
episode of sudden flexion/extension of neck/trunk/extremeties
increases in intensity and severity overtime (miss developmental milestones & disability)
Generalized Seizures: Epileptic Spasms Onset
1-12 months
can occur after infancy
Generalized Seizures: Epileptic Spasms, frequency
occurs in clusters of 5-150 per day
worse when infant waking/sleeping
EEG abnormalities
Generalized Seizures: Epileptic Spasms Cause
idiopathic
genetic
metabolic disease
CNS insult
Treatment of Epileptic Spasms
ST adrenicorticotrophic hormone- vigabatrin, corticosteriods, prednisone
surgery when pharmacological tx has failed
What is Epilepsy? (detailed)
complex genetic mutations + environmental effects
abnormalities in synaptic transmissions
imbalance in brain’s neurotransmitters
alterations of receptors and iron channels
development of abnormal nerve connections OR loss of nerves after injury
Epileptogenic Focus: How epilepsy works
- group of hyperexcitable neurons
- corticol excitation spreads
Epileptogenic Focus: How epilepsy works- Tonic Phase
excitatory neurons react to corticol stimulation
fire more frequently and with greater amplitude
Epileptogenic Focus: How epilepsy works- Clonic Phase
inhibatory neurons react to corticol stimulation
Seizure discharge interrupted
What can cause epilepsy? (ILAE proposal)
genetic
structural
metabolic
immune
infections
unkown
How are epilepsies classified?
types of seizures
epilepsy syndromes
Epilepsy Seizure Types
Focal
Generalized
Focal + Generalized
Unknown
Epilepsy Syndromes
Childhood Absence Epilepsy Syndrome
Lennox-Gastaut Syndrome
Juvenile myoclonic epilepsy
Unclassified epileptic seizure
Psuedoseizures
Status Epilepticus
abrupt discontinuation of antiseizure drugs
untreated/inadequately treated persons w/ seizure d/o
faliure of mechanisms in place to stop seizures = abnormally long seizures
rapidly recurring seizure before person has fully regained conciousness from previous seizure
Status Epilepticus: How long are seizures?
tonic-clonic for 5+ minutes
OR
Single seizure for 30+ mins
Why is Status Epilepticus a medical emergency?
high risk for aspiration
cerebral hypoxia
What are the LT consequences of Status Epilepticus?
neuronal death
neuronal injury
alternation in neuronal networks
What is your number 1 prioriy for Status Epilepticus?
administer high flow oxygen
What can you do during Status Epilepticus to help?
put pt on their left side (help secretions come out)
do not suction
Childhood Absence Epilepsy Syndrome: Overview
abnormal actvity occuring many times a day: eye moevements, chewing, blank stare, lack of awarness, swimming movements
child may not aware that seizure activity occured
Childhood Absence Epilepsy Syndrome: onset
4-8 yrs
may disappear during adolescence
Childhood Absence Epilepsy Syndrome: duration
10-20 secs
sudden end –> normal activity
Childhood Absence Epilepsy Syndrome: Tx
antiepileptic drug
Lennox-Gastaut Syndrome:
various generalized seizures (tonic-clonic, atonic, akenetic, absenc, and myoclinic)
EEG - slow spike and wave
results in intellectual disablity and delated psychomotor development
Lennox-Gastaut Syndrome: onset
early childhood, 1-5 yrs of age
Lennox-Gastaut Syndrome: Tx
difficult
drugs, ketogenic diet, vagal nerve stimulator
Juvenile Myoclinic Epilepsy:
myoclinic jerks (neck, shoulders, arms) + generalized tonic-clonic seizures- SINGLE OR REPETITIVE
Aggravated by lack of sleep, excessive alcohol intake
onset in adolescence
Juvenile Myoclinic Epilepsy: when do they occur?
early in the morning
Juvenile Myoclinic Epilepsy: tx
drugs 4L
Unclassified Epileptic Seizures
etiology unknown
seizures do not have distinct clinical and EEG features
Psuedoseizures
nonepileptic phenomena but look like epileptic seizures
dx requires video EEG monitoring to capture spells, determine EEG is normal during clinical events
Simple Febrile Seizure: Unique feature
presents as generalized seizure
temperature >38C
no hypoglycemia
no electrolyte d/o
no CNS infection
Simple Febrile Seizure: Onset
Onset: 3mo - 5yrs
Simple Febrile Seizure: Duration
<5 minutes
without reccurance
Simple Fberile Seizure: MOA
systemic infection w/ release of inflammatory cytokines that cross BBB
stimulate neuronal hyperexcitability trigerring seizure
Complex Febrile Seizure: duration
> 15 mins
Complex Febrile Seizure: frequency
1+ 24 hour period
Complex Febrile Seizure: tx
antipyretic and/or antiepileptic drugs
Complex febrile seizure: overview
have focal characteristics
considered risk factor for development of epilepsy
Dx of Epilepsy in children
more than 2 unprovoked seizures more than 24 hours apart
Barbituates tx?
phenobarbital
benzodiapines tx?
diazepam
hydantoins tx?
phenytoin
Phenytoin-like/Carboxylic acid derivatives tx?
valproic acid
succinimides tx?
ethosuximide
Goal of antiseizure drugs?
suppress neuronal activity to prevent abnormal and reptitive firing w/o intolerable side effects or drug resistance
Seizure D/O Drug Therapy Approach
placed on initial low dose
gradually increased until seizure control acheived
if seizure continue- different drug in small dose increments is added while reducing dosage of initial drug
Antiseizure drug withdrawal period?
6-12 weeks
How antiseizure drugs work: MOA
control movement of electrolytes across neuronal membrrades or affect neurotransmitter balance
resting state: neurons surrounded by inc. electrolyte concentration
influx of Na and Cl enhances neuronal activity
influx of Cl surpresses neuronal activity
Antiseizure MOA: 3 general mechanisms
- stimulate influx of Cl ions –> activates GABA
- delay inflex of sodium ions (red. neuronal excitability)
- delay influx of calcium ions (delay neurotransmitter release)
What drugs potentiate GABA?
phenobarbital
diazepam
Which drugs increase GABA production in nerve terminal?
valproic acid
Phenobarbital : MOA
enhances and potentiates action of GABA
Phenobarbital: Indications for Use
mgt of variety of seizures including tonic-clinic and febrile seizures
Phenobarbital: Desired Effects
surpresses abnormal neuronal d/c that can cause epilepsy
Phenobarbital: Adverse Effects
barbie is breathtaking (resp dep, laryngospasm)
barbie makes you sleepy (drowsy, coma, death)
barbie has fanss everyone (dependence, tolerance), your love for her is longlasting
barbie can deplete you (Vit D/B12, folate)
going out with barbie can give you rash (steven-johnson syndrome)
thrombophlembitis from standing to long
barbie goes out at night- take it at night
once you get hooked you cant stop seeing barbie
barbie withdrawal symptoms (nightmares, insomnia, tremors, hallucination, nausea, vomiting)
Diazepam: MOA
binds to GABA receptor-chloride channels intensifies GABA action
Diazepam: Indications for use
ST seizure control
status epilepticus
anxiety
Diazepam: Adverse effects
VALIUM
V- very low BP
A- accelerated HR
L- low and slow respirations (resp dep)
I- increased alcohol and CNS depressant effects (blurred vision, dizzy, constipation)
U-uknown if oral contraceptives work
M- muscle Weakness
Diazepam: Desired Effects
suppression of abnormal neuronal activity
calming w/o sedation
skeletal muscle relaxation
reduce seizure activity
Drugs that suppress sodium influx
phenytoin & valproic acid
Phenytoins: MOA
delays sodium influx into enurons
Phenytoins: Indications for use
most types fo seizures/epilepsy BUT absence
Phenytoins: desired effects
prevent spread of disruptive electical charges in brain that produce seizures
Phenytoins: AE
PHENYTOINS
bradycardia
v-fib
severe hypotension
hypeglycemia
blood dyscrasias
severe skin and connective tissue reactions
HA
confusion
nervousness, twitching insomnia
peripheral neuropathy (LT use)
Valproic Acid: MOA
delays sodium influx into neurons
aslso effects calcium channels and increases GABA
Valproic Acid: Indications for use
wide range of seizures (absence + mixed)
prevention of migrane HA
tx of BPD
Valproic acid: desired effects
prevents spread of disruptive electrical charges that produce seizures
Valproic Acid: AE
sedation, drowsy, GI upset, prolonged bleeding
Drugs that suppress Calcium Influx
ethosuximide
ethosuximide: indications for use
absence (petit mal) seizures
ethosuximide: MOA
depressed acivity of neurons in motor cortex
- delays calcium influx into neurons by blocking
- raises seizure threshold
ethosuximide: DE
reduced likelyhood that action potential will be generated, keeps neurons from firing to quickly
ethosuximide: AE
psychosis or extreme mood swings, depression with suicidal intent
Ketogenic Diet: indications
when seizures are uncontrollable by medication or extreme AE.
primary treatment for epilepsy before drugs
Ketogenic Edit: MOA
increased ketone bodies and metabolic changes enhance GABA and inhibatory neurotransmitters
Ketogenic diet: benefits
alzhiemers, parkinsons, + degenrative diseases
high efficacy rates in controllign seizure w/ rapid improvement
Ketogenic diet: diet composition
high fat, low carb and protein
stringent water and caloric intake control
3-4g of fat - 1g protein
complications of ketogenic diet
hyperlipedemia
hepatotoxicity
LT monitoring
Keotgenic diet: AE
vomiting
fatigue
constipation
diarrhea
hunger
