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BB2 > Epilepsy > Flashcards

Epilepsy Flashcards

1
Q

Define epilepsy.

A

A neurological disorder that represents a brain state that supports recurrent, unprovoked seizures – it has neurobiological, cognitive, psychological and social consequences.

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2
Q

Define seizures.

A

Abnormal, paroxysmal changes in the electrical activity of the brain; they reflect large scale synchronous discharges of neuronal networks.

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3
Q

Define epileptogenesis.

A

The process by which normal brain function progresses towards generation of abnormal electrical activity.

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4
Q

What is the prevalence (%) of epilepsy in the UK?

A

1%

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5
Q

How many people worldwide have epilepsy?

A

65 million

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6
Q

How many patients are resistant to treatment?

A

A third

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7
Q

What is status epilepticus?

A

A form of epilepsy which is a life-threatening medical emergency. Seizures which last more than 5 minutes (or more than a seizure in 5 min, without regain
of consciousness).

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8
Q

What two broad categories are seizures divided into?

A

Generalised and focal

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9
Q

What is a generalised seizure?

A

Arising within and rapidly engaging bilaterally distributed networks

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10
Q

What is a focal seizure?

A

Originating within networks limited to one hemisphere.

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11
Q

What types of generalised seizures are there? (6)

A 
Absence (typical and atypical)
Tonic
Clonic
Tonic-clonic
Atonic
Myoclonic (myoclonic, myoclonic-atonic, myoclonic-tonic)
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12
Q

What are focal seizures characterised according to?

A

Aura, motor, autonomic, awareness/responsiveness (altered or retained).

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13
Q

What might focal seizures evolve to?

A

Bilateral convulsive seizures

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14
Q

What are the general features/phases of a tonic-clonic seizure? (5)

A
  1. Premonition
  2. Pre-tonic-clonic phase
  3. Tonic phase
  4. Clonic phase
  5. Post-ictal period
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15
Q

What is the pre-tonic-clonic phase?

A

A few myoclonic jerks or brief clonic seizures

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16
Q

What happens in the tonic phase of a seizure?

A

Tonic contraction of the axial musculature, limbs and jaw muscles
Respiratory muscle contraction causing the “epileptic cry” and possibly cyanosis
Upward eye deviation and pupillary dilatation

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17
Q

What happens in the clonic phase of a seizure?

A

Jerks of increasing amplitude followed by relaxation (sphincter opening may occur).

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18
Q

What happens in the postictal phase of a seizure?

A

Generalized lethargy, decreased muscle tone, headaches, and muscle soreness.

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19
Q

How is epilepsy diagnosed?

A 
Clinical history (occurrence of 2 or more seizures)
Investigations - EEG, MRI, fMRI, PET, ECG
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20
Q

In temporal lobe epilepsy there is reorganisation of the tissue. In what areas of the hippocampus are there loss of cells?

A

CA2 and CA3 hippocampal areas

21
Q

Why are chandelier cells relevant to epilepsy?

A

In epilepsy, there is loss of chandelier cells. This increases the risk of abnormal excitatory activity.

22
Q

What are chandelier cells? Where do they synapse?

A

GABAergic interneurons that control the activity of cortical pyramidal cells – they synapse on the axon initial segment of pyramidal cells.

23
Q

Secondary epilepsy might be caused by… (7)

A 
Craniotomy
Trauma
Stroke
Aneurysm
Brain tumour
Status epilepticus
CNS infection
24
Q

What cellular mechanisms are linked to the development of epilepsy?

A 
Abnormal neuronal excitability (ion channels)
Decreased inhibition (GABA-dependent)
Increased excitation (Glu-dependent)
25
Q

Glial abnormalities may also be involved in epilepsy. What do glial cells have an important role in?

A

Glutamate transport and clearance through glutamate transporters (such as EAAT1 and EAAT2).

26
Q

What is the paroxysmal depolarising shift phenomenon? What receptors are involved?

A

The resting membrane potential is depolarised by 30-40 mV, causing a sustained burst of action potentials.
NMDA glutamate receptors

27
Q

What are the possible mechanisms linking primary insult to epilepsy?

A

Primary insult causes gliosis, neuron death, and mossy fibre sprouting.
Gliosis and neuron death cause cytokine and growth factor release, which causes changes in receptor and ion channel expression and mossy fibre sprouting.
Mossy fibre sprouting and changes in receptor and ion channel expression cause epilepsy.

28
Q

How is epilepsy linked to the mTOR and the REST pathways?

A

Epilepsy may involve activation of these signalling pathways.

29
Q

What does the mTOR pathway regulate?

A

Growth and homeostasis

30
Q

What does the REST pathway lead to?

A

Negative regulation of the expression of many genes in the CNS

31
Q

Why is epilepsy considered a channelopathy?

A

Genetic analysis confirms the important role of ion channels in many epilepsy syndromes

32
Q

What do anti-epileptic drugs work on?

A

Sodium and calcium channels, as well as the GABA system and glutamate receptors.

33
Q

What AEDs work on sodium channels? (7)

A

Phenytoin (causes liver enzyme induction)
Carbamazepine (causes liver enzyme induction)
Sodium valproate
Lamotrigine (also has activity at calcium channels)
Topiramate (also has activity at glutamate receptors)
Lacosamide
Zonisamide

34
Q

What AEDs work on GABA A receptors? (2)

A

Benzodiazepines e.g. clonazepam

Barbiturates

35
Q

What is the method of action of barbiturates, such as phenobarbitone?

A

They work on GABA A receptors.

Phenobarbitone leads to microsomal enzyme induction.

36
Q

What AEDs work on calcium channels? (2) What sub-unit?

A

Ethosuximide - USED IN ABSENCE SEIZURES

Gabapentin/pregabalin (α2δ subunit)

37
Q

What AED affects neurotransmitter release?

A

Levetiracetam (affects protein SV2A)

38
Q

What AED affects neurotransmitter uptake?

A

Tiagabine (GAT-1 transporter)

39
Q

What AED affects neurotransmitter synthesis?

A

Vigabatrin (inhibition of GABA transaminase)

40
Q

What AEDs affect neurotransmitter receptors? (2)

A

Perampanel (selective non-competitive antagonist of AMPA glutamate receptors)
Felbamate (NMDA receptors)

41
Q

What is Stiripentol?

A

New drug with some similarities of action to barbiturates

42
Q

Which three drugs are used to treat both focal seizures AND tonic-clonic seizures?

A

Carbamazepine
Lamotrigine
Sodium valproate - they all work on sodium channels

43
Q

What two drugs are used to treat absence seizures?

A

Ethosuximide - works on calcium channels

Sodium valproate - works on sodium channels

44
Q

What three drugs are used to treat myoclonic seizures?

A

Sodium valproate - sodium channels
Clonazepam - benzodiazepine (GABA A receptor)
Levetiracetam - affects neurotransmitter release

45
Q

What are the non-pharmacological treatments for epilepsy? (6)

A 
Lobe resection
Corpus callosotomy
Functional hemispherectomy
Vagal nerve stimulation 
Deep brain stimulation
Ketogenic diet
46
Q

How is status epilepticus treated?

A

IV diazepam

47
Q

Which AED has zero order kinetics?

A

Phenytoin

48
Q

Describe three possible cellular mechanisms which are implicated in the generation of seizures.

A 
Abnormal neuronal excitability (ion channels)
Decreased inhibition (GABA-dependent)
Increased excitation (Glu-dependent)

BB2 (32 decks)

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