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CM Clinical Symposia > Epilepsy (15) > Flashcards

Epilepsy (15) Flashcards

1
Q

Seizures

A

Abnormally excessive and hyper synchronous activity of neurones located predominantly in cerebral cortex

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2
Q

Twitches/convulsions

A

Cortical discharges transmitted to muscles

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3
Q

Classification of seizures

A
  1. Generalised
  2. Partial
  3. Secondary generalised
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4
Q

Generalised

A

Initial activation of neurones throughout both hemispheres (tonic clonic/clonic/atonic)

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5
Q

Partial

A

Initial activation of a limited number of neurones in a part of 1 hemisphere (absence/myoclonic/simple/complex)

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6
Q

Secondary generalised

A

Partial seizure that later spread to involve majority of 2 cerebral hemispheres

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7
Q

Manifestation of partial seizure in parietal lobe

A

Tingling/jerking in leg, arm, face

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8
Q

Manifestation of partial seizure in occipital lobe

A

Flashing lights/spots, vomiting

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9
Q

Manifestation of partial seizure in temporal lobe

A

Strange smell or taste, altered behaviour, deja vu, lip smacking/chewing movements

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10
Q

Manifestation of partial seizure in frontal lobe

A
  • Adversive seizures (Eyes/head both turn to one side)

- Jacksonian seizure (tingling feeling in hand/arm)

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11
Q

EEG

A

Electroencephalogram

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12
Q

EEG uses

A

Scalp electrodes to record electrical activity along scalp - firing of neurones within brain, series of electrical impulses originating in brain are amplified and summed into waves (Spike-wave discharges)

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13
Q

Status epliepticus

A

State of persistent seizure, more than 30 mins/2+ without full recovery

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14
Q

Why is SE a medical emergency?

A

The longer a seizure lasts, less likely it will stop on its own and more likely to reoccur in future

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15
Q

Treatment for SE

A

GABAa receptor agonist e.g. diazepam

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16
Q

Epilepsy

A

2 or more unprovoked seizures

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17
Q

Mechanisms underlying seziures

A

Excitation or inhibition > too much neuronal activity > seizure

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18
Q

Excitation (too much)

A

Ionic - Na+, Ca2+ influx, neurotransmitter - glutamate, aspartate release

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19
Q

Inhibition (too little)

A

Ionic - Cl-influx, K+ efflux

neurotransmitter GABA release

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20
Q

Inhibitory interneurones

A

Allow activity to spread in one direction but not sideways, release inhibitor neurotransmitter GABA

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21
Q

GABA

A

Major inhibitory neurotransmitter, found at 30% of synapses, acts via GABAa or GABAb

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22
Q

GABAa

A

Ligand-gated chloride channel receptor

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23
Q

GABAb

A

G protein-coupled receptor

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24
Q

What determines intrinsic properties of each channel

A

GABAR subunit

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25
Q

Types of epilepsies caused by mutation in GABAa receptor subunits

A
  • Childhood absence epilepsy (CAE)
  • FS (pure febrile seizures)
  • GEFS+ (generalised epilepsy with febrile seizures plus)
  • JME (juvenile myoclonic epilepsy)
  • DS (Dravet syndrome - SMEI severe myoclonic epilepsy in infancy)
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26
Q

Dravet syndrome associated with which mutation

A

GABRG2(Q390X) > loss of 78 C-terminal aa (changes it from transmembrane protein to a globular cytosolic protein)

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27
Q

Febrile seizures

A

Associated with fever

28
Q

Tonic-clonic/grand mal

A

Generalised

29
Q

Myoclonic seizure

A

Involuntary twitching of a muscle/group of muscles

30
Q

Absence seizure

A

Lapses of awareness, staring, last only a few seconds, common in children

31
Q

Complex partial seizure

A

Feeling deja vu, fear, euphoria/depersonalization

32
Q

Tonic seizure

A

Tone is greatly increased, arms/legs sudden stiff movements, during sleep usually involved most/all of brain

33
Q

Post-status epileptics animal models single episode of status epileptics is used to incite

A

Epilpetogenesis (via pilocarpine)

34
Q

Pilocarpine is a

A

Pro-convulsant drug, non-selective muscarinic receptor agonist

35
Q

Purpose of anti epileptic drugs

A

Decreases frequency and/or severity of seizures in people with epilepsy, treats symptom of seizures not underlying epileptic condition

36
Q

Modes of action of anti-epileptic drugs

A
  1. Suppress action potential
  2. Enhance GABA transmission
  3. Suppression of excitatory transmission
37
Q

Suppress action potential using

A

Sodium channel blocker/modulator, potassium channel opener

38
Q

Enhance GABA transmission

A

GABA uptake inhibitor, GABA mimetics

39
Q

Suppression of excitatory transmission

A

Glutamate receptor antagonist

40
Q

Main mechanisms of action

A
  1. Enhancement of GABAergic transmission
  2. Inhibition of Na+ channels
  3. Mixed actions
41
Q

Anti epileptics for partial simple and complex seizures

A

Carbamazepine, phenytoin, valproic acid

42
Q

Anti epileptics for Generalised tonic clonic

A

Carbamazepine, phenytoin, valproic acid

43
Q

Anti epileptics for Absence seizures

A

Ethosuximide, valproic acid

44
Q

Anti epileptics for Atypical absence, atonic, myoclonic seizures

A

Valproic acid

45
Q

Anti epileptics for Febrile seizures

A

Diazepam, rectal

46
Q

Enhancing GABAergic transmission

A
  • Enhance action of GABAa receptors with barbiturates (phenobarbital)/benzodiazepines (clonazepam)
  • Inhibit GABA transaminase (vigabatrin)
  • Inhibit GABA uptake (tiagabine)
47
Q

Benzodiazepines

A
  • Clonazepam
  • Clorazepate
  • Diazepam (valium) and Iorazepam
48
Q

Clonazepam effective against

A

Generalised tonic-clonic, absence and partial seizures

49
Q

Clorazepate effective against

A

Partial seizures (used with other drugs)

50
Q

Diazepam (valium) and lorazepam effective against

A

Status epilepticus when give IV

51
Q

Mechanism of action of benzodiazepines

A

Increase affinity of GABA for its receptor (increases Cl- current, supresses seizure focus by raising action potential threshold, strengthens surround inhibition - prevents spread)

52
Q

Problems with benzodiazepines

A

Sedation, tolerance and dependence, respiratory depression (iv)

53
Q

Inhibition of Na channels

A

Phenytoin, Carbamazepine and oxcarbamazepine, Lamotrigine

54
Q

Phenytoin

A
  • During an action potential voltage-dependent Na channel (closed, open, inactivated)
  • Na channels don’t recover from inactivated state until membrane has repolarised
  • Binds to inactivated state and slows down its recovery
55
Q

Mixed actions

A

Gabapentin, Valproate, Levetiracetam

56
Q

Valproate effective for?

A

Tonic-clonic and absence (bipolar)

57
Q

How is valproate taken?

A

Orally, well absorbed

58
Q

Mechanism of action of valproate

A
  • Inhibits Na channels
  • Decreased GABA turnover (inhibition of succinic semialdehyde dehydrogenase - inhibit GABA transaminase, increased synaptic GABA)
  • Blocks neurotransmitter release by blocking Ca2+ channels
59
Q

Antiepileptics and pregnancy

A

Monotherapy, folic acid recommended, Phenytoin and Valporate not allowed, oxcarbamazepine

60
Q

Foetal hydantoin syndrome caused by

A

Taking phenytoin (sometimes carbamazepine)

61
Q

Foetal hydantoin syndrome symptoms

A

Intrauterine growth restriction with microcephaly, dysmorphic craniofacial features and limb defect (hypoplastic nails and distal phalanges), growth problems and developmental delay, heart defects and cleft lip

62
Q

Foetal valproate syndrome (FVS)

A

6-9% risk of congenital defects

63
Q

Optogenic stimulation used for

A

Partial seizures, use of halorhodopsin similar to GABAa hyperpolarise the neurone in reaction to yellow light

64
Q

Epilespia partialis continua

A

Rare, recurrent motor epileptic seizures that are focal (hands and face)

65
Q

Epilespia partialis continua caused by

A

Large, acute brain lesions from strokes

66
Q

Treatment for Epilespia partialis continua

A

Medication and therapy-resistant, stop secondary generalisation

CM Clinical Symposia (24 decks)

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