Epilepsy Flashcards
History
First mentioned in 1500 BC
Jackson 1870: the convulsion is only a symptom, and there is disorderly discharge of nerve tissue on muscles.
First EEG in 1931 found heightened AP firing.
Definitions
Seizure: signs or symptoms of abnormal excessive/synchronous neuronal activity
Epilepsy: enduring tendency to have recurrent seizures.
Absent (Generalised)
Mainly childhood onset.
Frequent but brief (<30s)
sudden loss and return of consciousness.
no post-octal state
may be some involuntary movements.
Myoclonic (generalised) symptoms
sudden brief shock-like contractions
bilateral arm jerks most common.
often worse in mornings.
precipitated by sleep deprivation and alc
Tonic-Clonic (generalised)
sudden onset - Gasp then fall
Tonic phase (stiffening) with cyanosis (bluish skin from lack of oxygen)
Clonic phase (jerking)
then has post-octal phase - disorientation
Tongue biting and incontinence common.
headache and muscle pain afterwards.
Atonic (generalised)
lose all muscle tone during the seizure.
become limp
Focal seizures
they originate within networks limited to one hemisphere (unlike generalised)
the seizure can propagate to other regions.
can be with/without awareness.
Temporal lobe seizures (focal) symptoms
Warning (aura) phase before seizure: epigastric (upper abdomen) rising sensation, olfactory/gustatory hallucinations, deja vu.
loss of awareness: blank stare, lip smacking, automatisms (unconscious actions)
how Hippocampal slices study epilepsy
IC recording electrode and glutamate pipettes used.
Downside is its a model of acute, as opposed to recurrent seizures. also non-physiological triggers needed.
To trigger seizure bath medium with low Mg and Ca used (can induce seizures) as well as K+ blocker, or GABA antagonist.
Initiation of seizure
High frequency oscillations and bursting of excitatory neurones initiate. Inhibition is overcome.
Microseizures come together and join to make the main event.
Synchronisation phase of seizure
The network of epileptic neurones synchronise for the main seizure. locally and long range. not only synaptically: gap junctions, field effects, and the microenvironment [K+] all complement the spread of the seizure.
Endogenous mechanism for termination of seizure.
The waves of depolarisation are blocked, synaptic depletion and IC acidification occur.
K+ channels hyper polarise the cells.
Adenosine, endocannabinoids, and opioid peptides aid in the termination.
In vivo epilepsy models.
Induce seizures in mice using drugs (e.g., PTZ), or electrical stimulus. can test drugs for their capability to prevent seizures.
Propagation of generalised seizures.
Sensorimotor cortex propagates to the portico-thalamic networks. the waves of depolarisation here lead to the down regulation of conscious mechanisms.
Epileptogenesis (what can cause epilepsy for individuals) and neurological changes
An injury (e.g., trauma, drug induced, electric shock) then can lead to spontaneous and recurring seizures, following a latent period.
Pilocarpine and kainate are epileptics
Structural changes: loss of inhibitory interneurones, axonal sprouting, neurogenesis, reactions of glia, neuroinflammation, BBB breakdown.
Defects in neuronal channels, receptors, transporters and neuromodulators may occur.
