Epilepsy Flashcards
Seizure vs Epilepsy
Abnormal hypersynchronous discharge of neurons
- Can be provoked or unprovoked
Occurrence of than one unprovoked seizure
Seizure semiology
Signs and symptoms of a seizure from onset throughout the course of the seizure
- Can help identify laterization and localization of onset
Eleptiform discharges
Spikes of activity in brain that appear during inerictal period
- Spikes, sharp waves, spikes and waves, polyspikes, polyspikes and wave
Seizure types:
- Focal onset seizures (Focal aware, Focal impaired awareness, focal to bilateral tonic-clonic)
- Generalized onset seizures (Absence, tonic, clonic, atonic, myoclonic)
- Unknown onset seizures
- Originate in specific region in one cerebral hemisphere; Assoc w/ underlying structural abnormality
- Retains awareness but has auras
- Impaired awareness, start in small part of hemisphere before spreading throughout
- Starts focally but spreads to both hemispheres, leading to stiffening and bilateral jerking
— - Both hemispheres simultaneously
- Temporary loss of conscientiousness, blank stare
- Sudden bilateral extension/flex of head, trunk or limbs
- Bilateral rhythmic jerking, upper and lower limbs
- Sudden/brief loss of muscle tone, falling to floor
- Brief, shock-like involuntary jerkingn
— - Inadequate info to classify but can be possible later
Behaviours and auras associate with which lobe in focal onset seizures?
- Motor agitation, Jacksonian march, speech disruption
- Fear, deja-vu/jamais-vu, derealization, auditory/visual hallucinations
- Vertigo, visual hallucinations, somatosensory stmptoms
- Visual hallucinations (colour, shape, light), loss of vision
- Rising epigastric sensations, gustatory sensations
Frontal lobe
Temporal lobe
Parietal lobe
Occipital lobe
Insular cortex
Epilepsy syndromes:
- Onset in neonates and infants
- Onset in childhood
- Onset at a variable age
- Can disappear in childhood (Self-limited epilepsies)
- Developmental and epileptic encephalopathies (DEE; developmental impairment)
- Etiology-specific syndromes (have specific causes)
— - Self-limited
- DEE
- Genetic-generalized epilepsy syndromes (have genetic origin)
— - Focal epilepsy syndromes
- Generalized epilepsy syndromes
- Combined generalized and focal
Epilepsies w/ onset in childhood
- Self-limited (Childhood epilepsy w/ Centrotemporal spikes)
- Genetic generalized (Childhood absence epilepsy)
- 15-25%, 3-13 years old
- Occur during sleep (tonic-clonic) or waking (focal aware)
- Responsive to drug treatment and remits
— - 10-15%~ 4-8 years old
- Frequent absence seizures w/ blank stare
- Impaired attention, language, executive functions, visuospatial skills
- Remits but constantly misdiagnosed as ADHD
Focal epilepsy syndromes:
- Temporal lobe epilepsy
- Right TLE vs Left TLE + Language deficits
- Frontal lobe epilepsy
- Divided into mesial temporal love epilepsy or neocortical/lateral temporal lobe epilespsy
- Hippocampal sclerosis, wide-eyed stare and automatisms, cognitive impairments
- Don’t respond to drug treatments, need surgery
— - Episodic (declarative) memory, ling term memory consolidation, new info retrieval impaired
- Right TLE: Deficits in verbal mem, Left TLE: Deficits in visuospatial mem
— - Naming ability and verbal fluency affected; also impaired auditory comprehension
————
- Onset at dorsolateral prefrontal cortex
- Short, motor activity (Jacksonian march, motor agitation), retain awareness
- Deficits in language and exec function
Lennox-Gastaut syndrome
Ramussen’s syndrome
Landau-Kleffner syndrome
Reflex epilepsy
- Childhood onset from 2-6 years old
- Daily multiple seizures + atonic drop attacks
- Slowed development or behav disorders as result
— - Inflammatory disease affecting single cerebral hemisphere
- Affects children 6-15 years old w/ inflammation lasting 4-8 months
- Frequent/Severe focal seizures, loss of motor, speech, cog function
- Inflammation causes permanent damage to affected hemisphere
— - Rare disorder between 3-7 years old
- Seizures and progressive loss of language after normal devel
— - Seizures triggered by specific sensory stim, activity or cog event (lights, sounds, hot water, card games, etc)
- May be generalized or focal
Epilepsy treatments:
- Anti-epileptic drugs
- Ketogenic diet
- Vagus nerve stimulation (Neuromodulation)
- Deep brain stimulation (Neuromodulation)
- Surgery (Anterior temporal lobectomy, hemispherectomy, corpus callosotomy)
- First line treatment
- Suppress rapid/excessive neuron firing by blocking Na channels or increasing GABA
— - High fat, low protein, low carbs diet that increases ketone bodies and decreases glucose
- Ketones block site of regulation on vesicular glutamate transporters to prevent release into synapse
— - Stimulates left vagus nerve (CN10) with implanted electrode and signal generator under clavicle
- Activates vagal afferents to brainstem to increase release of norepinephrine and serotonin
— - Chronically implanted electrodes create high freq electrical stim to suppress firing of neurons for a second or more
- Open loop - Stim delivered intermittently
- Closed loop - Stim delivered when device detects seizure beginning
— - Removes seizure focus area not assoc w/ primary sensory/motor areas
- Removes 3-8 cm of anterior tip of temporal lobe
- Removes most or all of one hemisphere
- Sever surface of corpus callosum to stop drop attacks
Variables that predict being seizure free after surgery
- Brain pathology: Structural abnormalities increases chance
- Age at surgery: Younger patients (<30) increases chance
- Duration of seizures: Shorter increases chance
Factors implicated in cognitive dysfunction in epilepsy:
- Underlying etiology
- Epileptic seizures
- Anti-epileptic medications (AED)
- Genetic mutations in TSC1 and TSC2 genes cause brain developmental malformations and epilepsy
— - Damages the brain, leading to impairment
- More harmful w/ longer seizure duration
— - Reduces neuronal excitability which can cause negative side effects on cognition
- Memory and executive function impacted w/ more AED
Memory
- Sensory
- Working memory
- Long-term memory
- Declarative vs Nondeclarative
- Brain regions
Process by which mind encodes, stores and retrieves info
- Sensory info is registered consciously, very short
- Temporary storage and manipulation of limited amount of info, 3-4 capacity
- Storage over long period, unlimited capacity
- Declarative (Events/Episodic and facts/semantic), nondeclarative (learned skills)
- Medial temporal lobe structures (hippocampus, parahippocampal gyrus) for declarative memory
Language
- Expressive vs Receptive
- Brain regions affected
Ability to express onself and comprehend linguistic info, involving naming and verbal fluency
- Expressive: Dependent on frontal lobe (Broca’s area, premotor area)
- Receptive: Dependent on temporal lobe (Wernicke’s area, primary auditory cortex)
- Angular gyrus - Processes written language
Cognitive phenotypes (Baxendale & Thompson, 2020)
- Goal
- Laterality
- Onset of seizures
- Dynamic
- Mood
- Good predictor for verbal learning/language function and visual memory?
- Goal: Investigate usefulness in phenotypes (globally low/high, low executive functioning/processing speed, low language/memory function) to predict seizure and neuropsychological outcomes following epilepsy surgery w/ temporal lobe epilepsy (TLE)
— - No effect of laterality of TLE on cog phenotype… but ppl w/ left TLE more likely to have lower language/memory impairment than right TLE
- Widespread cog impairment had earlier onset of seizures than those who had any of the cog phenotypes
- Cognitive phenotypes are dynamic rather than just showing neurodevelopmental factors or progression
- Phenotypes related to mood; Mem/language impairment assoc w/ anxiety, widespread impairment assoc w/ depression
- Cog phenotypes not found to predict surgical outcome or postoperative cognitive decline in verbal learning/language function… But age, side of surgery, and preoperative function were
- But successful predictor w/ visual memory (greater cog phenotype pre causes greater cog decline post)
