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Epilepsy
Uni of Notts, Neurobiology of Disease, year 2, topic 9
| Term | Definition |
|---|---|
| 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 |