Epilepsy Flashcards
Seizure
excessive + abnormal activity between cortical neurons
excessive hypersynchronous neuronal cortical discharge
transient (sudden onset) occurrence (usually <2min duration)
leads to loss of consciousness, shaking + uncontrolled movement, loss of muscle control
generalized seizure
whole brain fires at once
communication between networks
focal seizure
one area is firing excessively
can become generalized if seizure activity spreads through thalamus cortical network
appearance of seizure
determined by where it is propagating (not necessarily where it originates)
networks of spreading
classification of seizure types
focal onset
generalized onset
unknown onset
focal onset
awareness - impaired
motor/non-motor onset
focal to bilateral tonic-clonic
division of motor/non-motor onsets
generalized onset
motor → tonic-clonic, other motor
non-motor: absence
further division of motor/non-motor
unknown onset
motor/non-motor
unclassified
motor → tonic-clonic/epileptic spasms
non-motor → behaviour arrest
electrographical definition of seizures
a clear ictal with sudden, repetitive waveform with defined start, middle, and end
ictal: intense electrical activity
epilepsy
enduring predisposition to seizures - risk/frequent occurrence
1. two+ unprovoked or reflex seizures within 24 hours
2. a single unprovoked/reflex seizure + >60% risk of re-occurrence
3. epilepsy syndrome (genetics)
epilepsy classification
focal
generalized
combined generalized and focal
unknown
epilepsy etiology
structural - brain malformation
genetic - predisposition
infectious - ex. HSV
metabolic - low Na+, glucose
immune - auto-immune, encephalitis
unknown - childhood epilepsy is commonly unknown
rates change with age
seizures in children
different mechanisms of epileptogenesis → babies’ brains are very excitatory - working to develop new networks and connection in short time = easy to become over-excited
different propagation of seizures → not yet myelinated
unique EEG patterns
different responses to medications
different clinical manifestations
ictal apnea
stopped breathing
normal EEG, MRI
cEEG showed subtle signs of seizure
treated with antiseizure medications
likely originated in limbic system
genetic syndromes (1p36 deletion, T18, SCN8A)
mesial temporal lesions
maturation related susceptibility → in posterior limbic cortex, temporal lobe, and midbrain respiratory centers
autonomic manifestations of seizures
ex. hypersalivation
nighttime only, stereotypical (same each time) + short, multiple times per night, no recollection
EEG showed differences in activity between hemispheres
focal seizures - ictal hypersalivation
autonomic manifestations → maturation-related susceptibility of the central autonomic network; lower threshold for epileptogenic activation
frontal sleep related hyper-motor epilepsy
frequent nighttime arousals
stereotyped, abrupt onset and offset
brief, highly stereotyped seizure during nREM sleep
classic frontal lobe epilepsy - disorganized, lots of movement
genetic or structural causes (focal cortical dysplasia type IIb)
overlap with parasomnias
parasomnias
pre-school age, childhood
first 1/2 of night
N3 sleep
5-30 min
single event/night
normal EEG
normal daytime behaviour
benzodiazepines
nocturnal seizures
anytime in infancy through adolescence
randomly through night
N1/N2 stages of sleep
brief <5 min
multiple events/night
abnormal or normal EEG
possible daytime seizures
sodium channel blockers
video EEG
valuable tool in assessment of children with suspected seizures
can support diagnosis of epilepsy - determine type, guide management
Neonatal seizures
seizures are more common in neonates - different presentations and causes
1. GABA-A receptors are excitatory
2. developmental imbalance between excitatory and inhibitory mechanisms
3. delayed maturation of GABA-B, adenosine, and 5-HT receptors
4. high density of NMDA receptors in hippocampus and neocortex
neonatal GABA-A receptors
excitatory rather than inhibitory
excitation is more important in neonatal development → abnormal flow in receptor
excessive excitation = more susceptible to seizures
developmental imbalance between excitatory and inhibitory mechanisms
electrochemical dissociation: GABA-A receptors mature in the spinal cord first = become inhibitory sooner than the brain’s receptors → seizure will continue in cortical GABA-A receptors but won’t show in the spinal cord (movement) because of difference in time of maturation
clonic seizures
activity
rhythmic jerks
focal (one side) or multi-focal
most common cause is stroke
subtle seizures
hard to tell without EEG
abnormal eye movements
cause of neonatal seizures
babies likely don’t have epilepsy
symptomatic cause - infection, stroke, some dysfunction in brain
affect homeostasis
EEG in neonates
assessment of cerebral function and maturation
neurological injury
at <28 weeks, occipital area seizes the most - later decreases in frequency
conventional EEG - electrodes on scalp, measures currently (min); good spatial coverage
amplitude integrated EEG - less electrodes → compression of EEG, measures continuous (hours-days) - pattern recognition; easy to interpret but limited spatial coverage
medications can depress the background of aEEG
maturational changes
shown on aEEG
lots of activity and large spikes at 23 weeks
less drastic spikes at 34 weeks
Congenital Heart Disease - seizure
mildly abnormal EEG
coarctation of aorta
unilateral rhythmic clonic movements
KCNQ2 mutation - K+ channel
unique pattern on ictal EEG/aEEG → seizures
antiseizure meds didn’t work but sodium channel medication did
KCNQ2 associated neontal epilepsy
most common of neonatal epilepsy
- self-limited neonatal epilepsy: seizures between 4-6 days of life; clonic seizures, with or without apnea
- developmental epileptic encephalopathy: presentation depends on pathogenic mutation (loss or gain of function); tonic seizures and markedly abnormal EEG
EEG - artifacts
physiological: muscle; movement
ex. sucking artifact, back patting - will show on EEG
non-physiological: electrical; mechanical; impedance
abnormal paroxysmal (sudden) events in neonates
apnea
jitteriness
hyperekplexia
ocular signs
oral-buccal-lingual movements
complex movements
tonic posturing
abrupt change in vital signs
