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NS5 - Pathophysiology of Excitation + Inhibition: Epilepsy (ii)…
NS5 - Pathophysiology of Excitation + Inhibition: Epilepsy (ii)
Seizure Presentations
clinical features depend on location + extent of affected neutrons
tonic-clonic seizures (grand mal epilepsy)
generalised
affects motor cortex
tonic: sustained contracting, stiffening, arched back
clonic: shaking/jerking
tonic/clonic on their own
simple = conscious
complex = unconscious
Absent seizures (petit mal epilepsy)
generalised but not to motor cortex
myoclonic: extremely sudden + brief muscle jerks
atonic: loss of muscle tone, drooping eyelids, nodding head, possible jerks
Electroencephalogram (EEG)
most important neurophysiological tool or diagnosis
diagnosis in frequency + amplitude of waves
records electrical activity in brain (currents in extracellular space generated by pyramidal cells in cortex)
EPSPs make extracellular dipoles
recorded from scalp
measures potential between 2 electrodes
ictal phase (during seizure)
interictal phase (between seizures) - NB diagnosis
postictal phases (after seizures)
good temporal resolution (time)
bad spatial resolution (bad for locating focus)
odd numbered electrodes on left, even on right (localises seizure to hemisphere)
in epileptic brain...
sharp waves/spikes
increased amplitude + frequency
@ least 3Hz, lasting >10s
also look @ background activity abnormalities
inconsistent slowing with respect to behavioural state
Epilepsy treatments
antiepileptic drugs
longterm seizure prevention
don't modify condition, just treat symptoms
phenytoin, valproate, carbamazepine, lamotrigine, gabapentin
anticonvulsants
stop acute seizures
flood brain with GABA
Lorazepam (benzodiazepine), barbiturates
if pharmacoresistant...
hippocampectomy
surgical resection of focus
good seizure free success rate
vagus + DBS
ketogenic diet
Status Epilepticus
severe continuous seizure (@ least 5 mins) with no recovery
normal termination mechanisms fail - emergency
treat aggressively with anticonvulsants
significant morbidity (brain damage) + mortality
may cause neuronal cell death by excitotoxicity
prolonged opening of glutamate R channels
swelling/rupture due to Na+ + H2O influx
toxic intracellular Ca2+ buildup
over activated proteases
disrupts function of organelles
apoptosis