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BB CC > Epilepsy > Flashcards

Epilepsy Flashcards

1
Q

Epilepsy

A

Neurological disorder that represents a brains state that supports recurrent, unprovoked seizures
–> neurological, cognitive, psychosocial and social consequences

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2
Q

Seizures

A

Abnormal, paroxysmal changes in electrical activity of brain

–> reflect large scale synchronous discharges of neuronal networks

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3
Q

Epileptogenesis

A

Process by which normal brain function progresses towards generation of abnormal electrical activity

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4
Q

What proportion of patients are resistant to treatment

A

1/3rd

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5
Q

Status epilipticus

A

Form of epilepsy which is a life-threatening medical emergency
Seizure lasts more than 5 minutes or multiple seizures within 5 minutes without regain of consciousness

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6
Q

Tonic-clonic seizures phases

A 
Premonition
Pre-tonic-clonic phase
Tonic phase
Clonic phase
Postictal phase
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7
Q

Premonition phase

A

Vague sense that seizure is imminent

Peculiar smell, sense of doom

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8
Q

Pre-tonic-clonic phase

A

Few myoclonic jerks or brief clonic seizures

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9
Q

Tonic phase

A

Tonic contraction of axial musculature
Upward eye deviation and pupillary dilatation
Tonic contraction of limbs
Cyanosis
Resp. muscle contraction Epileptic cry- tonic contraction of jaw muscles

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10
Q

Clonic phase

A

Jerks of increasing amplitude followed by relaxation

Sphincter opening may occur

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11
Q

Postictal phase

A

Generalised lethargy
Decreased muscle tone
Headache
Muscle soreness

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12
Q

Diagnosis- clinical history

A

Occurrence 2 or more seizures

Witness account

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13
Q

Structural changes in epilepsy

A

Prominent loss of cells in CA2 and CA3 hippocampal areas

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14
Q

Hippocampal analysis

A 
Loss of neurones
Distortion + compression of layers
Gliosis
Different tract organisation
Sclerotic hippocampus
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15
Q

Hippocampus + medial temporal lobe

A

Hippocampal sclerosis
Sprouting of the mossy fibres of granule cell
May lead to reverberant excitatory circuits
Neurogenesis may also occur

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16
Q

Chandelier cells

A

Special population of interneurones which are GABAergic
Control activity of cortical pyramidal cells
Synapse on axon initial segment (AIS) of pyramidal cells

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17
Q

Chandelier cells in epilepsy

A

Loss of inhibitory chandelier cells increases risk of abnormal excitatory activity

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18
Q

Conditions/procedures with high risk of developing epilepsy

A 
Craniotomy
Traumatic brain injury
Stroke
Aneurysm
Brain tumour
Status epilepticus
CNS infection
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19
Q

Cellular mechanisms underlying seizure

A 
Abnormal neuronal excitability (ion channels)
Decreased inhibition (GABA-dependent)
Increased excitation (Glu-dependent)
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20
Q

Paroxysmal depolarising shift

A

Neurones in epileptic focus burst firing potentials

Particular role of NMDA glutamate receptor

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21
Q

Glial cells

A

Abnormalities may be involved
Have important role in glutamate transport + clearance through glutamate transporters e.g. EAAT1 and EAAT2
–> don’t clear glutamate
–> glutamate overexcites post-synaptic cell

22
Q

Dentate gyrus

A

Within hippocampus
Has granule cell layer
Damaged in epilepsy

23
Q

Mossy fibres

A

Axons of dentate cells in hippocampus

24
Q

Mossy fibre sprouting

A

Axons of dentate cells in hippocampus develop collaterals that grow into abnormal locations
–> inner 1/3rd of dentate gyrus molecular layer

25
Q

Epilepsy + Activation of distinct major signalling pathways

A

mTOR or REST pathway
mTOR –> major regulator of growth + homeostasis
REST –> leads to negative regulation of expression of many genes in CNS

26
Q

Mutation in SCN1B

A

Codes for sodium channel
Generalised epilepsy with febrile seizures
More Na+ into cell –> more depolarisation

27
Q

Mutation in KCN Q2 or 3

A

Codes for M type potassium channel subunit
More K+ out of cell–> more depolarisation
Benign familial neonatal convulsions

28
Q

Sodium channel targets

A

AEDs block voltage gated Na+ channels preferentially in their inactive state

  • -> channels become inactive at lower membrane potentials + time taken to return to resting state is delayed
  • -> refractory period increased
  • -> inhibits sustained repetitive firing
29
Q

Phenytoin

A 
Anticonvulsant
Na channels
0 order kinetics
Inducer of hepatic microsomal enzymes
Not used in absence seizures
30
Q

Carbamazepine

A

Anticonvulsant
Na channels
Inducer of hepatic microsomal enzymes
Not used in absence seizures

31
Q

Valproate

A

Na channels

Used in all types of seizures

32
Q

Topiramate

A

Na channels

Augmentation of GABAa and inhibition of glutamate AMPA/kainite signalling

33
Q

Lamotrigine

A

Na channels
Also activity at Ca channels
Presynaptic inhibition of glutamate release

34
Q

Zonisamide

A

Na channels

35
Q

L-type calcium channels drugs

A 
Mainly expressed post-synaptically, allowing post-depolarisation Ca efflux
Phenytoin
Carbamazepine
Valproate
Topiramate
36
Q

N and P/Q type calcium channels drugs

A

Expressed pre-synaptically where they mediate Ca entry necessary for neurotransmitter release
Topiramate
Levetiracetam –> selectively inhibits only N type
Lamotrigine

37
Q

T type calcium channels drugs

A

Require less depolarisation to be activated

Ethosuximide–> used preferentially in treatment of absence seizures

38
Q

All Ca channels drugs

A

AED blocks Alpha 2 Delta subunit on calcium channel
Gabapentin
Pregabalin

39
Q

GABAa receptor

A

Activation leads to early rapid component of inhibitory transmission
Receptors are permeable to Cl- ions
As ECF Cl- conc. higher than intracellular conc., opening leads to hyperpolarisation

40
Q

Benzodiazepines- Clonazepam (sedation)

A

GABAa receptor

Positive allosteric modulators of the receptors + increase frequency of receptor opening

41
Q

Barbiturates

A

GABAa receptor
Positive allosteric modulators of receptor
Cause prolonged opening times + can directly activate channels at high concentrations

42
Q

Phenobarbitone

A

Barbiturate

Leads to microsomal enzyme induction

43
Q

Levetiracetam

A

Binds to synaptic protein SV2A

Modulates neurotransmitter release

44
Q

Tiagabine

A

Increases extracellular levels of GABA by blocking GABA transporter GAT1
Add on therapy in partial seizures

45
Q

Vigabatrin

A

Inhibits GABA metabolism by inhibiting GABA transaminase

–> stops it getting broken down

46
Q

Perampanel

A

Selective non-competitive agonist of AMPA receptors

47
Q

Felbamate

A

Inhibits NMDA receptors + possible GABAa receptors

48
Q

Focal seizure

A

Carbamazepine
Lamotrigine
Valproate

49
Q

Tonic-clonic seizure

A

Carbamazepine
Lamotrigine
Valproate

50
Q

Absence seizure

A

Ethosuximide

Valproate

51
Q

Myoclonic seizure

A

Valproate
Clonazepam
Levetiracetam

52
Q

Other epilepsy treatments

A

Vagal nerve stimulation
DBS
Ketogenic diet (high fat and low carbs)

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