Session 11

Question 1

What is epilepsy?

Answer 1

Episodic discharge of abnormal high frequency electrical activity in brain leading to seizure.

Question 2

Describe the symptoms of partial seizures.

Answer 2

Involuntary motor disturbances, behavioural changes or an aura.

Question 3

What are tonic-clonic seizures?

Answer 3

Body becomes rigid and patient commonly falls to the floor, tongue is bitten and incontinence of both urine and faeces. Clonic phase begins with generalised convulsions, frothing at the mouth and rhythmic jerking of muscles.

Question 4

What are absence seizures?

Answer 4

Patient will stare, eyelids may twitch, and a few muscle jerks occur. Normal activity is resumed after an attack.

Question 5

What are the differences between primary and secondary causes of epilepsy?

Answer 5

Primary: inherent tendency of an individual towards seizures, where there is no identifiable cause.
Secondary: consequence of a medical condition affecting the brain, e.g. vascular disease or tumours.

Question 6

Give three other causes of seizures apart from epilepsy.

Answer 6

Brain disease, drugs, pyrexia, hypoglycaemia, infections, cerebrovascular accident, metabolic disturbances, provoked seizures.

Question 7

What are the four causes of epilepsy?

Answer 7

1) increased excitatory activity
2) decreased inhibitory activity
3) loss of homeostatic control
4) spread of neuronal hyperactivity.

Question 8

What are the epileptic targets for the treatment of epilepsy?

Answer 8

• Enhancement of GABA action
• Inhibition of sodium channel function
• Inhibition of calcium channel function
• Inhibition of glutamate release or function

Question 9

How do benzodiazepines and valproate sodium work?

Answer 9

Act on GABA-agonists, hence opening chloride ion channels, increasing the threshold for an AP. Causing an inhibitory effect on neurones, reducing the likelihood of epileptic neuronal hyperactivity.

Question 10

How do phenytoin, carbamezepine and lamotrigene work?

Answer 10

Bind to inactivated sodium channels, acting on the neurones causing the high-frequency discharge that occurs in an epileptic fit. Hence reduce the number of functional channels available to generate action potentials.

Question 11

Describe carbamezepine.

Answer 11

Used to treat generalised tonic-clonic and partial seizures. Can cause dizziness, drowsy, vomiting, bone marrow depression. Strong CYP450 inducer.

Question 12

Describe phenytoin.

Answer 12

CYP450 inducer. Not used to treat absence seizures. Can cause dizziness, ataxia, nystagmus and nervousness.

Question 13

Describe lamotrigene.

Answer 13

Prolongs inactivation state of VGSCs. Used to treat partial and generalised seizures.

Question 14

Describe valproate.

Answer 14

Enhances GABA-mediated inhibition. Used to treat partial, tonic-clonic and absence seizures. Can cause sedation, ataxia, tremor and weight gain.

Question 15

Describe benzodiazepine.

Answer 15

Enhances the binding of GABA to chloride channels, increasing chloride current into the neurone, increasing threshold for an AP.

Question 16

Give two ADRs of benzodiazepines.

Answer 16

Sedation, confusion, aggression, dependence, respiratory and CNS depression.

Question 17

What must be considered when managing epilepsy in a pregnant women?

Answer 17

Increased risk of seizures if treatment is stopped.
Certain AEDs are associated with congenital malformations, especially valproate.
Lamotrigene is the safest.
Give folate supplements to reduce risk of neural tube defects.

Question 18

What is the link between AEDs and contraception?

Answer 18

Failure rate times 4 with carbamezepine and phenytoin.

Question 19

What is status epilepticus?

Answer 19

A single convulsion lasting more than 30 minutes, or convulsions occurring back to back with no recovery time between them.

Question 20

What can uncontrolled convulsions lead to?

Answer 20

Hypoxia, physical injury, sudden death.

Question 21

What is the treatment for status epilepticus?

Answer 21

Protect the airways, deliver oxygen, identify the cause and terminate the seizure. First line treatment is benzodiazepines, e.g. lorazepam IV. Then IV phenytoin. If still failing, ITU referral and paralysis and intubation required.

Question 22

Give three causes of Parkinsonism

Answer 22

Drug induced, vascular, multiple systems atrophy, corticobasal degeneration, progressive supranuclear palsy.

Question 23

What is idiopathic parkinson’s disease?

Answer 23

Neurodegenerative disorder that has a progressive loss of dopaminergic neurones in the substantia nigra.

Question 24

What is the classic triad of parkinsonism?

Answer 24

Tremor, rigidity and bradykinesia.

Question 25

How does loss of dopaminergic neurones result in parkinsonism?

Answer 25

Causes reduced inhibition in the neostriatum, allowing increased production of ACh. Chain of abnormal signalling leads to impaired mobility.

Question 26

What is multiple system atrophy?

Answer 26

Associated with degeneration of nerve cells in specific areas of the brain. Causes problems with movement, balance and autonomic functions.

Question 27

What is Wilson’s disease?

Answer 27

Accumulation of copper in the tissues, resulting in neurological and hepatic disease. Copper-dopamine complexes form, resulting in parkinsonism.

Question 28

What is corticobasal degeneration?

Answer 28

Neurodegenerative disease involving the cerebral cortex and basal ganglia. Marked disorders in movement and cognitive dysfunction.

Question 29

Describe dopamine synthesis.

Answer 29

L-tyrosine > L-DOPA > Dopamine.

Question 30

How is dopamine degraded?

Answer 30

Via monoamine oxidase or catechol-O-methyl transferase enzyme.

Question 31

Describe the function of L-DOPA.

Answer 31

L-dopa crosses the blood brain barrier, taken up by dopaminergic cells in the substantia nigra and converted to dopamine.

Question 32

What is given alongside L-DOPA?

Answer 32

A peripheral DOPA decarboxylase inhibitor, to prevent peripheral breakdown. E.g. carbidopa.

Question 33

Describe the role of dopamine receptor agonists?

Answer 33

Bind to dopamine receptor agonists directly to produce the required response. E.g. Apomorphine.

Question 34

What are impulse control disorders?

Answer 34

Dopamine dysregulation syndrome, including:

• pathological gambling
• hypersexuality
• compulsive shopping
• desire to increase dosage
• punding (collecting and organising things)

Question 35

Describe the role of monoamine oxidase B inhibitors.

Answer 35

Enhances dopamine levels in the brain by preventing degredation. E.g. Rasagaline.

Question 36

Describe the role of COMT inhibitors.

Answer 36

E.g. Entacapine. Reduces peripheral breakdown of L-DOPA.

Question 37

Describe the role of anticholinergics in the management of parkinson’s disease.

Answer 37

Antagonistic effect to dopamine. Able to treat tremors. Have no effect on bradykinesia.

Question 38

What is myasthenia gravis?

Answer 38

Autoimmune condition, causing blockage/degredation of the nAChR at the NMJ by antibodies. Causes a fluctuating fatiguability in skeletal muscles, especially extraocular muscles.

Question 39

How is myasthenia gravis treated?

Answer 39

Acetylcholinesterase inhibitors. However, an excess dose can cause a cholinergic crisis.

Question 40

Give three side-effects of acetylcholinesterase inhibitors.

Answer 40

S- salivation
S- sweating
L- lacrimation
U- urinary incontinence
D- - diarrhoea
G- GI hypermobility
E- Emesis