Epilepsy Flashcards Preview

OSCE Conditions > Epilepsy > Flashcards

Flashcards in Epilepsy Deck (16):

Describe a partial seizure

Partial seizure involves one hemisphere, can cause motor disturbance, behavioural change, unpleasant smell
- Simple: retain awareness
- Complex: lose awareness, lip smacking


Describe generalised seizures and the different types

A generalised seizure involves both hemispheres
- Tonic Clonic (grand mal): loss of consciousness, stiffness, limb-jerking, loss of bladder control, followed by postictal period
- Atonic: sudden loss of tone
- Myoclonic: muscle jerking
- Absence seizure: unresponsive, 'day dreaming', jerking of body, rapid blinking


Possible causes of epilepsy

Primary - no identifiable cause
Secondary - due to brain injury and hypoxia, tumours, alcohol/drugs


Investigations of epilepsy

CT scan to rule out any structural abnormalities


Management of epilepsy

Can give:
VG-sodium channel blockers eg. Carbamazepine/Phenytoin/Lamotrigine
GABA enhancers eg. Sodium valproate

Sodium valproate = first line for primary generalised seizures
Carbamazepine = first line for partial seizures
Lamotrigine = used in women of child bearing age


Mechanism of action of sodium valproate

Acts to increase the amount of GABA by stimulating synthesising enzymes and inhibiting inactivation enzymes.

Increased GABA leads to increased Cl ion channels opening -> hyperpolarisation, increases threshold for AP generation


ADRs and DDIs of sodium valproate

ADRs: CNS effects eg ataxia, tremor, sedation, teratogensis

DDIs: action inhibited by antidepressants/antagonised by antipsychotics.
Highly protein bound, so displaced by aspirin etc


Mechanism of action of carbamazepine

Blocks Voltage gated sodium channels. Binds to internal side, and blocks when channels are in inactivated state (voltage dependent).
Prolong the inactivation state and set the firing rate back to normal, then detach from binding site


ADRs and DDIs of carbamazepine

ADRs: drowsiness, dizziness, ataxia, motor disturbances, GI disturbance, BP variation, hyponatraemia, teratogenesis

DDIs: acts as a CYP450 inducer, so reduces levels of phenytoin, warfarin,corticosteroids, oral contraceptives
Anti depressants interfere with action.


Complications of epilepsy

Physical injury (falls)
Sudden death
Brain injury
Cognitive impairment
Psychiatric disease


What is status epilepticus

Prolonged seizures (>30mins), without a recovery period of consciousness.
High mortality rate, high risk of brain damage, so medical emergency


Treatment of status epilepticus

Assess ABCs
Give Benzodiazepines or IV Phenytoin


Mechanism of action of benzodiazepines

Act to enhance GABA mediated inhibition by binding at a distinct receptor site on the GABA receptor ion channel and enhancing the binding of GABA.


ADRs of benzodiazepines

Sedation, confusion, impaired coordination, aggression, resp and CNS depression.
Build tolerance with chronic use, can get dependence


Pathophysiology of epilepsy

= Excessive neuronal activity in the brain
Episodic discharge of abnormal, high frequency electrical activity leading to recurrent seizures

Hypersynchronisation of neurones leads to loss of homeostatic control


Epilepsy differential diagnosis

Vasovagal syncope
Movement disorders
Panic attacks