Epelipsy Flashcards
What is epelipsy?
An epileptic seizure is a transient episode of uncontrolled discharge of cerebral neurones causing a variety of symptoms, usually associated with a disturbance of consciousness
Epilepsy is the term used to describe when such seizures recur
Brief change in behaviour caused by disordered, rhythmic and synchronous firing of populations of neurones
Can be preceded by an aura: numbness, tingling or hallucinations
Causes of epilepsy
70% unknown origin
30%:
* Head trauma
* poisoning
* infection
* brain tumor
* cardiovascular
* maternal injury
howare seizures categorised into groups
Seizures are divided into groups depending on:
1. onset - where they start in the brain
2. awareness affected
3. involvment of other symptoms eg, movement
focal vs generalized seizures
Focal onset - focal point of hyperecitability with potential routes of transfer to other parts of the brain.
Generelized onset - high levels of activity simulatenously at both hemispheres
Importance of correct diagnosis
A drug may be very effective for one particular type of epilepsy but may make other forms of epelipsy worse.
Focal seizures
- person is concious
- symptoms: tingling, twitching, flashing light to joy and fear
- dependent on part of brain affected
- Focal impaired awareness seizures affect larger part of one hemisphere
- person may be confused and show strange repetitive movements called: automatisms
- auditory or visual hallucinations
Generelized seizures
- Absence: Blank, unresponsive, briefly unconcious
- Tonic Clonic: unconcious, stiff muscles (tonic), shake/jerk (clonic)
-afterwards person may feel sleepy, tired, headaches - Atonic: muscles relax
- myclonic: muscles twitch whilst concious
- status epilepticus: continuous or repeated seizures longer than 30mins
Status epilepticus
continuous or repeated seizures lasting longer than 30mins
* medical emergency during tonic clonic
Treatment:
1. buccal midazolam
2. rectal diazepam
emeregency medication may cause breathlesness - person must be closley watched.
Pathophysiology of seizures
- Increase in excitatory inputs via Ach or glutamate
- Reduction in inhibitory drive via GABA
- Change in Na channel activity to redcue threshold and/or increase rate of APs
OR
Change in K+ channel activity to increase rate of APs
cause of increased excitability
- Membrane depolarization - alteration in Na or K+ channel function and/or extracellular potassium build up
- Release of excitatory amino acids (EAA) eg, Glutamate
- Reduced Inhibatory transmission eg reduced GABA transmission
Diagnostic testing of epilepsy
Neurolory consultant required due to high rate of misdiagnosis
Detailed history- eyewitness
Physical exam
ECG
Blood tests
Imaging techniques: CT scan or MRI
Neuropsychological assessment
EEG
Action of AEDs
- Decreased excitatory transmission (glutamate, Ach)
- Increase inhibatory (GABA) transmission
- stabalize membranes and prevent depolarization by inhibiting Na, CA channels and/or activating K+ channels
Mechanism of action AEDs
Inhibit Na+ channels
- Sodium Valproate
- Phenytoin
- Carbamazepine
- Lamotrigine
- Topiramate
Inhibit Ca+ channels
- Ethosuxamide
- Sodium Valporate
- Gabapentin
- Pregablin
- Leviteracetam
Activate K+ channels
- Retigabine