Epilepsy

Question 1

Describe a partial seizure

Answer 1

Partial seizure involves one hemisphere, can cause motor disturbance, behavioural change, unpleasant smell

• Simple: retain awareness
• Complex: lose awareness, lip smacking

Question 2

Describe generalised seizures and the different types

Answer 2

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

Question 3

Possible causes of epilepsy

Answer 3

Primary - no identifiable cause

Secondary - due to brain injury and hypoxia, tumours, alcohol/drugs

Question 4

Investigations of epilepsy

Answer 4

CT scan to rule out any structural abnormalities

EEG

Question 5

Management of epilepsy

Answer 5

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

Question 6

Mechanism of action of sodium valproate

Answer 6

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

Question 7

ADRs and DDIs of sodium valproate

Answer 7

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

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

Question 8

Mechanism of action of carbamazepine

Answer 8

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

Question 9

ADRs and DDIs of carbamazepine

Answer 9

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.

Question 10

Complications of epilepsy

Answer 10

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

Question 11

What is status epilepticus

Answer 11

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

Question 12

Treatment of status epilepticus

Answer 12

Assess ABCs

Give Benzodiazepines or IV Phenytoin

Question 13

Mechanism of action of benzodiazepines

Answer 13

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.

Question 14

ADRs of benzodiazepines

Answer 14

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

Question 15

Pathophysiology of epilepsy

Answer 15

= 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

Question 16

Epilepsy differential diagnosis

Answer 16

Vasovagal syncope
Hypoglycaemia
Migraine
TIA/stroke
Movement disorders 
Panic attacks