9/29 Seizures/Epilepsy - Bhise Flashcards
terminology:
ictal
post-ictal
interictal
ictal: during a seizure
post-ictal: immediately following seizure
interictal: time between seizures
Todd’s paresis
post-ictal contralateral hemiparesis
epileptiform
on EEG, discharge with appearance of being potentially epileptogenic (spike or sharp wave)
seizure
- transiet episode with signs/sx of abnormal excessive synchronous neuronal activity in brain
- physical manifestations vary based on pattern of network involvement in brain
mapping old terminology to current terminology
grand mal
petit mal
grand mal → generalized
petit mal → focal/partial onset/absent
seizure classification
two general types
multiple subtypes
1. general
- tonic-clonic
- tonic: only stiffening
- clonic: only rhythmic jerking
- myoclonic: rapid brief jerks
- atonic/astatic: loss of postural tone
- absence: brief staring spells
2. focal/partial
- simple partial: no altered consciousness
- complex partial: alteration of consciousness
- secondary generalized
generalized tonic-clonic convulsion
bilateral tonic stiffening of extremeties alternating with clonic jerking
- impaired consciousness
- sympathetic sx: tachycardia, mydriasis
- mild cyanosis at mouth, distal extremities
- foaming at mouth
- urinary incontinence
- lateral tongue biting
- post-ictal fatigue, weakness, amnesia
simple partial seizure
type of focal/partial seizure
- manifestation related to brain region involved
- may be an aura
- no alteration of awareness
- may progress into a CPS or GTC seizure
- post-ictal deficit maybe seen
complex partial seizure
typical presentaiton: staring and alteration of awareness
- possible gaze deviation, forced head deviation, or unilateral/asymmetric limb involvement
- possible automatisms
- might progress into GTC seizure
- might see post-ictal deficit
often no recal of most of event
EARLIEST manifestation helps localize the source brain region
secondary generalized seizure
seizure activity beginning in one part of brain that spreads to involve the rest
transition may be slow over minutes OR fast and appear “generalized” at onset
symptomatic causes of seizure: categories
- metabolic-toxic
- structural
- benign
- genetic
- abnormal substrate
- rare causes
symptomatic causes
metabolic toxic seizure
- electrolyte imbalance
- ingestion
- medication-induced
- rapid withdrawal
symptomatic causes
structural
- head trauma
- stroke
- anoxia
- meningitis/encephalitis
- tumor
- brain malformation (AVM, cortical dysplasia)
symptomatic causes
benign
- fever(children)
- post syncopal
- contact
symptomatic causes
abnormal substrate
- autism
- other genetic disorder
symptomatic causes
rare causes
- inflammatory
- degenerative
- inborn error of metabolism
mechanism of seizure
forces involved
concept of seizure threshold - how?
excitation
- ionic currents: Na, Ca INWARDS
- nt: glu, asp
inhibition
- ionic currents: Cl INWARD, K OUTWARD
- nt: GABA
in seizure, excitation >> inhibition
- excitability to the extent that a seizure is produced occurs due to reduced seizure threshold
how?
- hypersynchronization (synaptic connectivity leading to propagation)
- inability to self-terminate (failure of negative feedback or feed-forward loop)
- changes in extracellular environment
- synapse chanel remodeling → permanency!
mechanism of genetic epilepsies
genetic epilepsies code for proteins in ion channels
→ ion flow is affected (overexcitable or low inhibition)
parts of the brain that are particularly prone to seizing activity
cerebral cortex and hippocampus particularly prone to synchronized bursts of activity
- strong recurrent excitatory connections
- intrinsically burst-generating neurons
- ephaptic interactions among closely spaced neurons
- synaptic plasticity
epilepsy
disorder of the brain that results in seizures that are:
- recurrent
- unprovoked
- stereotyped
seizure etiology
(classification)
- idiopathic → genetic
- symptomatic → structural/metabolic
- cryptogenic → unknown
idiopathic seizures
- genetic in nature without brain insult
- probably polygenic inheritance
ex. benign epilepsy with centrotemporal spikes, childhood absence epilepsy
symptomatic seizures
clear/known brain insult causes seizures
ex. metabolic-toxic, fever, head injury, tumor, meningo-enceph, pre/perinatal ischemic/anoxic injury, neuronal migration defect
cryptogenic seizures
no evidence of a known brain insult or documented testing abnormality
- test for: metabolic, radiologic, genetic evals
- usually see degeneration, progression, regression
- ex. infantile spasms
genetics of seizures
most often polygenic and multifactorial
- single gene can cause epilepsy syndrome
- single gene can cause multiple syndromes or non-seizure disorders (ex. movement disorders)
- diff genes (monogenic), may cause a single epilepsy syndrome
typically involve ion channels: Na, Ca, GABA, K
localization of seizures and effects seen
- temporal: medial vs lateral
- frontal: dorsofrontal, SMA, orbitofrontal
- parietal
- occipital
temporal
- medial: staring, automatism, posturing, fear
- lateral: staring, vertigo, hearing
frontal: brief, bizarre, nocturnal
- dorsolateral: contralateral vision
- SMA: fencing posture
- orbitofrontal: elaborate, sounds, smells
parietal: sensory
occipital: formed visual phenomena
EEG
measures electrical activity over scalp generated by the cortex
- captures wakefulness, drowsiness, stage2 sleep
- epileptiform activity commonly activated in stage2 sleep
when would you get an MRI of brain?
patients with evidence of focality in seizures
- looking for underlying structural lesion (encephalomalacia, cortical dysplasia, stroke, tumor, AVM, etc)
absence seizures
- multiple events daily (could be > 100 daily)
- usually 10s or less, triggered by hyperventilation, return to full awareness
- often unnoticed
- might have subtle automatisms during seizure
- can contribute to poor academic performance
EEG: 3 Hz spike and wave
Lennox Gastaut
starts between infancy-14yo
- most common in 2-3yr old
- more in boys
multiple seizure types seen
- axial tonic
- atonic
- atypical absence
cognitive impairment or regression
EEG: slow spike and wave, GPFA seizures
tx: tough to control
infantile spasms
when/who?
symptoms?
EEG
tx?
onset: 3-18months
* children with trisomy 21 or tuberous sclerosis more susceptible
characteristics
flexor, extensor, or combo events in clusters around sleep-wake transition
West syndrome: combo of spasms, hyparrhythmia, devpt regression
EEG shows hypsarrythmia: chaotic, high ampl, multifocal apikes, electrodecrement
idiopathic, symptomatic, or cryptogenic
tx: ACTH, vigabatrin, steroids, ketogenic diet
benign rolandic epilepsy
most common type of childhood epilepsy
ages 4-15, most commonly 7yo
symptoms
- nightime focal onset or rapid secondary generalized seizure
- speech arrest, drooling, gurgling, facial tonic-clonic activity, facial hemisensory
- infrequent seizures
- cognitive problems (often with language)
EEG: bilateral independent centrotemporal spikes
good outcomes! likely to outgrow, so practitioners might choose not to treat
- if do treat, treat following second seizure
Wada test
- injection of anesthetic into R or L internal carotid artery
- test each hemisphere for memory and language
status epilepticus
one continuous seizure > 30 min
OR
recurrent seizures without regaining consciousness between seizures for over 30 min
acute management of status epilepticus
- ABCs
- IV lorazepam or diazepam
- fosphenytoin
- phenobarbital or valproic acid
- versed drip or pentobarbital coma
