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Epilepsy

Uni of Notts, Neurobiology of Disease, year 2, topic 9

TermDefinition
Seizure A transient occurrence of symptoms caused by abnormal excessive or synchronous neuronal activity
Epilepsy Chronic tendency to develop recurrent unprovoked seizures with neurological & psychosocial consequences
Generalised seizures Seizures simultaneously affecting both hemispheres of the brain, often originating in the cortices & thalamus. Includes tonic & clonic
What the first EEG demonstrate in epilepsy research Hans Berger showed abnormal electrical activity during loss of awareness in seizures
Penfield’s contribution to epilepsy research He electrically stimulated cortical regions during surgery to map seizure foci
Absent seizures Brief loss of awareness but not consciousness, staring, automatisms (involuntary movement), & 3 Hz spike-wave EEG activity; may be triggered by hyperventilation. Possible to grow out of
Myoclonic seizures Brief sudden muscle jerks caused by abnormal cortical discharges
Tonic-clonic seizures Tonic phase causes stiffening, followed by clonic rhythmic jerking & loss of consciousness
Atonic seizures Sudden loss of muscle tone causing collapse/drop attacks
Focal seizures Seizures originating in one hemisphere that may spread to other brain regions
How symptoms can indicate region affected by focal seizure Motor behaviours & automatisms may indicate seizure origin/pathway
How focal seizures can *SOMETIMES* be treated with surgery A defined seizure focus can be resected if it doesn’t involve critical brain regions
How epilepsy is studied in animal models Through brain injury models, genetic rodent models, & chemically induced seizures
Acute slice seizure models & limitations Exposing slices of hippocampal tissue to convulsants then measuring with intracellular electrophysiology. They lack whole-brain networks & often use non-physiological seizure triggers
Interictal spikes Abnormal brief EEG discharges occurring regularly at baseline that may indicate seizure susceptibility
Seizure initiation High-frequency oscillations & microseizures merge as excitation overcomes inhibition
Seizure synchronisation Synaptic connectivity, gap junctions, & network recruitment synchronise neuronal firing
Seizure termination GABAergic inhibition, neurotransmitter depletion, ion shifts, & receptor desensitisation
Epileptogenesis Long-term process where a normal brain becomes chronically seizure-prone
Ictogenesis Neuroglial mechanisms that lead to spontaneous or reflex bursts of epileptic activity, which can occur without preexisting epileptogenesis
Kindling model Repeated subthreshold stimulation eventually causes spontaneous seizures despite seizure inhibition improving in early stages
Neurological changes during epileptogenesis Structural rewiring, molecular changes, & functional network alterations increase seizure susceptibility
Genetic & environmental causes of epilepsy Polygenic factors, developmental malformations, trauma, tumours, infections, & lesions
Antiepileptic drugs mode of action Preferentially bind inactivated voltage-gated sodium channels to suppress high-frequency firing
Why Na+ VGCs can exacerbate epilepsy in certain cases In disorders like Dravet syndrome, inhibitory interneuron sodium channel loss means blockers may worsen seizures
Diagnosis Evidence required to rule out symptom overlap with other symptoms. Videos, EEG, & brain imaging diagnose seizure type to try localise the disorder & treat accordingly
Prolonged seizures (status epilepticus) treatment Benzodiazepines enhance GABA-A signalling & barbiturates prolong GABA-A opening by acting as Positive Allosteric Modulators
Non-pharmacological seizure treatments Surgery, Vagus nerve stimulation by pacemaker, & ketogenic diets
Created by: Denny12
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