Seizures Flashcards
Generalized tonic-clonic convulsion
bilateral tonic stiffening of extremities alternating
with clonic jerking
impaired consciousness
sympathetic symptoms: tachycardia, mydriasis
mild cyanosis around mouth, distal extremities
foaming at the mouth
urinary incontinence
lateral tongue biting
post-ictal fatigue, weakness, and amnesia
Briefly describe Tonic Clonic Myoclonic Atonic Absence
Tonic: only stiffening
Clonic: only rhythmic jerking
Myoclonic: rapid brief jerks
Atonic: loss of postural tone –
Absence: brief staring spells
Simple partial vs complex partial
Simple partial – without alteration of consciousness (focal aware)
Complex partial – with alteration of consciousness (focal impaired awareness)
Simple partial seizure
may progress into a CPS or GTC seizure
post ictal deficit may be seen
*focused seizure without alteration
Complex partial seizure
focused seizure with alteration of awareness
typically characterized by staring and poor/no responsiveness
may involve gaze deviation, (forced) head deviation, or unilateral/asymmetric limb involvement
-the asymmetry indicates focal lesion
may have automatisms
may progress into a GTC seizure
often post-ictal
often amnestic - no recall of (most of) event
Secondary generalized seizure
*focal to bilateral tonic-clonic
seizure activity began in one spot in the brain
then spread to involve the rest
may spread slowly, starting as a SPS or CPS
or may spread fast, only manifesting as a generalized tonic-clonic convulsion (aka rapidly secondary generalized)
What are important EEG patterns
for focal vs primary generalized
Focal seizure (focal spike and wave)
Primary generalized seizures (general spike and wave activity)
Primary generalized epilepsy
characterized by primary generalized seizures
can be one seizure type or by multiple seizure
types
Examples:
– Childhood absence epilepsy – absence seizures
– Juvenile myoclonic – myoclonic, tonic-clonic
– Doose syndrome – myoclonic, atonic seizures
– Grand mal on awakening - tonic clonic
Childhood absence epilepsy
multiple events daily, can be over a hundred
seizures per day
unusual to last more than 10 seconds
often unnoticed
contribute to poor academic performance
often triggered by hyperventilation
prompt return to full awareness
may have subtle automatisms during spell
EEG: 3 Hz generalized spike-and-wave
How does localization of focal onset seizures manifest in these lobes
Temporal (medial + lateral) Frontal (dorsolateral, SMA, orbitofrontal) Orbitofrontal Parietal Occipital
Temporal
- medial - automatisms, posturing, fear, deja vu
- lateral - vertigo, hearing
Frontal - brief, bizarre (bicycling), nocturnal
- dorsolateral - contralateral horizontal gaze (FEF)
- Supplementary motor area - fencing posture
- Orbitofrontal - elaborate, sounds, smell.
Parietal - sensory
Occipital - formed visual phenomenon
Benign Rolandic epilepsy
- the most common type of child epilepsy
- benign, usually outgrown so physicians don’t usually treat it.
- treat with first line partial seizure drugs like carbemazepine
- EEG shows individual bilateral centrotemporal spikes
drooling, lack of speech, facial tonic clonic, after awakening is fine.
-nighttime focal onset or rapid secondary generalized seizure
Lennox Gasteut syndrome
Most commonly in 2-3 yr old boys.
multiple seizure types: tonic, atonic, absence, experiences cognitive impairment
difficult to treat
*EEG demonstrates slow spike and wave <2.5 Hz
INfantile spasms
onset between 3 and 18 months of life** YOUNG
West syndrome: combination of spasms, hypsarrhythmia, and
developmental regression
flexor, extensor, or flexor-extensor events occurring in clusters
around sleep-wake transition
EEG shows hypsarrhythmia: chaotic, high-amplitude, multifocal
spikes, electrodecrement and everything flattens out for a second
idiopathic, symptomatic, or cryptogenic
certain populations are more vulnerable such as children affected
with trisomy 21 or tuberous sclerosis
treatment: ACTH, vigabatrin, steroids, ketogenic diet
Describe the mechanism of genetic epilepsies
genetic epilepsies code for proteins in ion channels
cerebral cortex and hippocampus are particularly prone to synchronized bursts of activity
– strong recurrent excitatory connections
– intrinsically burst-generating neurons – ephaptic interactions among closely spaced neurons
– synaptic plasticity