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NS5 - Pathophysiology of Excitation + Inhibition: Epilepsy (i) (1 seizure…
NS5 - Pathophysiology of Excitation + Inhibition: Epilepsy (i)
Brain function
proper = balanced network of excitatory + inhibitory neurons + glial cells
brain damage/gene mutations/developmental abnormalities = altered neuronal networks = seizure/epilepsy
NTs
Glutamate
brain's major excitatory NT
2 Rs
ionotropic (Na, Ca influx) -> fast
metabotropic -> slow
when released into synaptic cleft it binds to R on postsynaptic membrane, causing an Na influx
small depol (EXCITATORY POSTSYNAPTIC POTENTIAL, EPSP)
if EPSP summation occurs AP threshold will be reached
Glutamate antagonists stop seizures
Gamma Amino Butyric Acid (GABA)
major inhibitory NT of CNS
2 Rs
GABAa
postsynaptic
specific recognition sites for NT
Ligand binding causes Cl- influx (hyperpol, INHIBITORY POSTSYNAPTIC POTENTIAL IPSP)
reduces excitability, dampens signals
GABAb
presynaptic autoRs
mediated by outward K+ currents
GABA antagonists cause seizures
most anticonvulsants work by promoting GABA function
Aspartate
excitatory
Epilepsy Aetiology
Genetics - channelopathies
diffcicult to treat (v specific + differs in patients)
mutations in genes for ion channels
brain injury
disrupts RMP
seizures after concussion can (but not always) become epileptic up to 30 years after injury
50% of head trauma patients develop epilepsy
most = idiopathic
infants/children: birth trauma, infections (fever)
adults: head trauma, tumour, stroke, drug abuse, infection
Temporal Lobe Epilepsy (TLE)
acquired sclerosis (shrinking) in hippocampus
30% of sufferers are pharmacoresistant
Epilepsy Intro
can affect glia (support cells)
e.g. astrocytes - damages BBB - albumin in brain
most common neurological problem for people of all ages
incidence = 0.5-1%
can begin as childhood febrile seizures (but they don't always develop epilepsy)
Psychogenic/pseudo seizures
but NO ictal activity on EEG
not epileptic
usually manifestation of psychiatric disease
tonic clonic presentation
1 seizure can...
alter gene expression
cause neurogenesis
remodel synapses
cause cell death
cause gliosis (infamm)
cause vasc remodelling of BBB
cause more seizures (Gower's hypothesis)
Seizure Types
Generalised
begins simultaneously in both hemispheres
focal/partial/localised
originates @ a focus (usually med temporal lobe)
can spread (SECONDARY GENERALISATION), surrounding neutrons synchronise
disordered thoughts, deja vu