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M202 > W19 Epilepsy > Flashcards

W19 Epilepsy Flashcards

1
Q

What is epilepsy?

A
  • Anyone can have an isolated seizure – this is NOT the same as having epilepsy
  • Epileptic seizures occur when ordinary brain activity is disrupted spontaneously and recurrently
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2
Q

What is the definition of a seizure?

A

“A transient paroxysm of uncontrolled discharges, beginning at the epileptic focus, causing an event which is discernible* by the person experiencing the seizure and/or an observer”

*able to be seen or understood

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3
Q

Prognosis of Epilepsy:
(chance of treatment success)

A
  • Good
  • 70-80% of patients become seizure-free
  • About 50% successfully withdraw their medication
  • 20-30% have chronic epilepsy
  • Usually normal function between seizures
  • 5% will not be able to live alone
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4
Q

Mortality in Epilepsy:
Increased by?

A
  • Increased by 2-3 times due to:
  • Accidents
  • Status epilepticus
  • Tumours
  • Cerebrovascular disease
  • Pneumonia
  • Suicide
    (SUDEP – sudden unexpected death in epilepsy)
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5
Q

Causes of Epilepsy? (7)

A

*Cause now identified in ~50% of people globally
*Most common defined causes:
–cerebrovascular disease
–cerebrovascular tumours
–genetic, congenital, or hereditary conditions
–alcohol
–drugs and toxic causes
–head trauma (including neurosurgery)
–post-infective causes (encephalitis/meningitis)

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6
Q

What are the risk factors for Seizures? (9)

A

*Disturbed levels of water/electrolytes
*Disturbed levels of blood glucose
*Altered blood gases
*Raised body temperature
*Altered sleep patterns
*Hormonal disturbance
*Toxicity
*Heredity
*Tumours

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7
Q

How is epilepsy diagnosed?

A
  • Difficult
  • Unpredictable and transient
  • Need a reliable account
  • Use of EEG, MRI and/or CT
    – not conclusive alone
  • Seizures MUST be recurrent and spontaneous
  • EEG records abnormal electrical discharges
  • Has limitations
    – 5% of people without epilepsy have abnormal EEG
    – 40% of people with epilepsy have normal EEG between attacks
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8
Q

Features of Epilepsy:

A
  • Sudden, excessive high frequency neuronal discharge
  • Highly synchronous discharges- Not random
  • A disorder of the cerebral cortex
  • May be loss of consciousness
  • Behavioural changes related to site of discharge (focus)
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9
Q

What is an EEG?
What are some other imaging techniques?

A

Electro-EncephaloGraphy (EEG)
Electroencephalogram - EEG
* Records the activity of populations
(many thousands) of neurones
* reveals synchrony of neuronal activity

  • MEG (Magnetoencephalography)
  • PET (Positron emission tomography)
  • MRI / fMR
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10
Q

Seizure Types
what is it based on?
2 main groups:

A
  • Based on the description of events and EEG
  • Classified according to the international scheme:
    1. Generalised- whole brain
    2. Focal (previously referred to as “partial”)
    -involves small part of brain
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11
Q

What are the different types of generalised seizures? (6)

A

Absence
Tonic-Clonic
Myoclonic
Clonic
Tonic
Atonic

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12
Q

Generalised Seizures
1. Tonic-clonic Convulsions (Grand Mal)
What are the features?

A

*Most common form
*Patient stiffens, falls and convulses
*Laboured breathing, hyper-salivation
*Cyanosis, tongue biting and incontinence
*Lasts a few minutes
*Followed by headache and drowsiness

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13
Q

Generalised Seizures
Tonic and Clonic seizures:
What are the features of tonic?
What are the features of clonic?

A

Tonic seizures
* stiffening of body – head, trunk +/- limbs

Clonic seizures
* rhythmic, motor, jerking movements
* +/- impairment of consciousness
* simultaneous involvement of arms and legs

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14
Q

Generalised Seizures
4. Absence Attacks (Petit Mal)
What are the features?

A
  • Rarer; almost exclusively in childhood and early adolescence
  • Goes blank, stares, eyelids flutter, head flops
  • Last a few seconds
  • Child may not be aware of it
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15
Q

Generalised Seizures (5)
Describe a Myoclonic Seizure? (Abrupt)

A
  • Abrupt, brief, involuntary, shock-like jerks
  • Involve head, limbs or whole body
  • Recovery immediate
  • Not always epilepsy
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16
Q

Generalised Seizures
6. Atonic Seizures

A
  • Sudden loss of muscle tone
  • Quick recovery
  • Very rare
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17
Q

Focal Seizures (also sometimes called Partial Seizures)
1. Simple Focal/Focal Aware Seizures (retains awareness)
What are the Features? (5)
abnormal discharge?

A
  • Abnormal discharge remains localised
  • Consciousness not impaired
  • What happens depends on area of the brain
  • Will vary from person to person
  • Will be the same each time in each person
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18
Q

Focal Seizures
Complex Focal/Focal Altered-awareness Seizures (altered awareness)
Features?

A
  • ‘automatic’ behaviours
  • confusion
  • apparent drunkeness
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19
Q

Focal Seizures:
Secondarily Generalised Seizures

A
  • Simple or complex focal seizures
    – then spread to the whole brain
    – leads to tonic-clonic attack
  • May be a warning ‘aura’
    – symptoms of the partial seizure
20
Q

What is Status epilepticus?

A
  • Serious uncontrolled seizure
  • Convulsive (tonic-clonic) status epilepticus
  • A tonic-clonic seizure lasts for 5 minutes or more, or
  • One tonic-clonic seizure follows another without the person regaining consciousness in between
21
Q

Which areas do seizures arise in the brain?

A
  • Anywhere
  • subcortical rare (thalamus: absence)
  • mostly cortical
    – frontal, parietal, occipital, temporal
  • Temporal most prevalent - 30-40%
    – Hippocampus, entorhinal cortex,
    amygdala
    – Most common seizures that are drug refractory
    – Surgical resection
22
Q

Imaging in epilepsy: Susceptible regions and levels of activity
what do PET,MRI and fMRI scans monitor?

A

MRI- Hippocampus is larger on LHS and smaller on RHS
* PET – monitors local metabolism
* MRI – structure and volume
* fMRI – relates activity to structure

23
Q

How do seizures arise?

A

*Cortical activity - dynamic balance between inhibition and excitation

Two levels of control
*Intrinsic or level of individual cell: determined by ion channels (in neurons)
* At a Network level- controlled by synaptic
transmission

Disturbed balance - excessive synchrony and epilepsy
* INC excitation, normal inhibition
* DEC inhibition, normal excitation
* DEC inhibition, INC excitation

24
Q

WHAT IS THE MAIN CNS…
EXCITATORY NEUROTRANSMITTER?
INHIBITORY NEUROTRANSMITTER?

A

Glutamate
GABA

25
Q

Synaptic and cellular factors can initiate and prolong a seizure:
What are these? (4)

A

Sub-threshold voltage gated Na+ channels
Voltage gated Ca++ channel
NMDA
Glutamate receptors AMPA

26
Q

Synaptic balance:
What are the roles of excitatory and inhibitory neurones?

A
  • Excitatory neurones recurrently excite each other
  • Excitatory recurrently excite inhibitory neurones
  • Inhibitory neurones recurrently control excitation
  • Loss of inhibition can lead to epilepsy
27
Q

How do seizures stop (without intervention)? (4)
[Pharmacology]

A

*Na+ channel inactivation
* K+ channel activation
* Glutamate receptor desensitization
* Glutamate depletion

28
Q

The pharmacological treatment of epilepsy:
Goal of treatment?

A
  • Antiepileptic drugs (AEDs)/anti-seizure medicines (ASMs) decrease the frequency and/or severity of seizures in people with epilepsy
  • Treat the symptoms not the condition
  • Goal: maximise quality of life by minimising seizures and adverse drug effects
29
Q

Mechanism of action of anti-epileptics?

A
  • Antiepileptic drugs inhibit abnormal
    neuronal discharge in epilepsy     but do not resolve the underlying cause (antiepileptic but not antiepileptogenic!)

Epileptogenetic= brain transforms into long lasting state in which recurrent, spontaneous seizures occur.

30
Q

How do we treat epilepsy? (3)
(pharmacological mechanisms)

A
  • Block destabilizing (depolarizing) currents (1)
  • Increase stabilizing currents (hyperpolarizing)
  • Reduce synaptic excitation
  • Block glutamate release (2)
  • Block glutamate receptors
  • Increase synaptic inhibition (3)
  • Increase GABA release
  • Potentiate GABA receptor

Bold: most common approaches

31
Q

Main Mechanisms of AEDs? (summary)
excitatory mechanisms? (3)

A

Decrease excitatory mechanisms
* Inhibition of sodium channel function (1)
* Inhibition of calcium channel function (1)
* Directly inhibit glutamate neurotransmission (2)

Increase inhibitory brain mechanisms
* Enhancement of GABA action (3)

Many AEDs are pleiotropic – multiple modes of action

32
Q

Reducing excitability: Inhibition of
sodium channels

A
  • Many anti-epileptic drugs block voltage-dependent sodium channels to reduce cell membrane excitability
  • Their blocking action is use-dependent
  • This allows the drugs to preferentially block the excitation of cells that are firing repetitively, so can block the high-frequency discharge that occurs in an epileptic fit, without interfering with the low-frequency firing when neurons are in the normal state

3 states: Closed, Open and Inactivated

33
Q

Blocking voltage gated Na-channels:
What are the CNS Drugs that block Na-channels? (4)

A

phenytoin (++)
carbamazepine (++)
lamotrigine (++)
sodium valproate (+)

34
Q

What is meant by drugs that have a
‘Use-dependent blocking action’?

A
  • Depolarisation of a neuron increases the proportion of sodium channels in an inactivated state
  • The drugs bind preferentially to the inactivated state of sodium channels, preventing them from returning to the resting state
  • This reduces the number of sodium channels available to generate action potentials
35
Q

Blocking voltage gated Ca-channels
Drugs that block Ca-channels

A

ethosuximide (++)
gabapentin
phenytoin (?)

36
Q

Blocking glutamate release
What is the rule?
Drugs that reduce glutamate release?

A

Drugs that block Na and Ca channels will
block glutamate release.
* Na-channel block
-phenytoin (++)
-carbamazepine (++)
-lamotrigine (++)
-sodium valproate (+)
* Ca-channel block
-gabapentin
-pregabalin
* Reducing vesicle fusion
-levetiracetam

37
Q

How might we regulate GABA transmission? (3)

A
  • Inhibition of GABA breakdown: increase GABA levels/ increase release
  • Reuptake inhibition: decrease GABA inactivation
  • Activation/regulate the GABA receptor
38
Q

Drugs acting at GABA synapses:
Which drugs:
Increase GABA levels? (2) MoA?
Decrease GABA inactivation? MoA?
Enhance postsynaptic response? MoA?

A

Increase GABA levels
* vigabatrin (++)
* sodium valproate (+)

=GABA transaminase inhibitor blocks GABA breakdown
= increases GABA levels
= increases GABA release

Decrease GABA inactivation
=tiagabine
=Blocks GABA reuptake increases GABA in cleft

Enhance postsynaptic response
=benzodiazepines
=barbiturates
=prolong channel open time

39
Q

Alternative anticonvulsants? (3)

A

1.felbamate
blocks NMDA receptors
2.topiramate
blocks AMPA/kainate receptors
3.retigabine
activates K-currents

40
Q

Carbamazepine must be prescribed by Brand
=Category 1

A
41
Q

Epilepsy
What are the Non-drug Treatments? (4)

A

Surgery
Vagus Nerve Stimulation (VNS)
Deep Brain Stimulation (DBS)
Ketogenic Diets (various types)

42
Q

(Epilepsy- Non-drug Treatments)
What are the different surgeries? (4)

A
  • Resection
    – removes damaged area of brain
  • Multiple subpial transection
    – separates damaged area from rest of brain
  • Corpus callosotomy
    – separates the two hemispheres of the brain
  • Hemispherectcomy
    – removes outer layer of one hemisphere
43
Q

Non-pharmacological treatments –
What is Vagus Nerve Stimulation? (VNS)

A
  • Stimulation with a pacemaker-type device
  • May intercept abnormal brain activity
44
Q

Non-pharmacological treatments –
Deep Brain Stimulation (DBS)

A

stimulates area of brain where seizures originate

45
Q

Non-pharmacological treatments –
Ketogenic Diets (various types)
What is the effect as it allows the brain to do what?

A
  • very high fat diet
  • alters metabolism in the brain
  • brain forced to use ketones for energy rather than
    glucose (and increased presence of decanoic acid
    thought to be a factor)
  • must be medically supervised
46
Q

Epilepsy in Pregnancy

A

Pre-conception
- folic acid supplementation
- specialist advice essential
discontinue therapy?
change drug?
Change to m/r if not already taking?
Establish seizure control with the lowest possible dose of a single drug?

M202 (72 decks)

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