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Neurobiology of Disease > Epilepsy (NBIO) > Flashcards

Epilepsy (NBIO) Flashcards

1
Q

What is a Seizure?

A

A transient occurrence of signs and/or symptoms due to abnormal excessive or synchronus neuronal activity in the brain

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2
Q

What is epilepsy?

A
  • A pathological and enduring tendency to have recurrent seizures
  • AND
  • By the neuro-biologic, cognitive, psychological and social consequences of this condition
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3
Q

What is a seizure? (2)
And
What do all seizures share?

A

Abnormal neuronal firing in particular brain network
* Seizure is a symptom which:
1. May be experienced
2. May alter consciousness
3. May have external signs
4. Often have EEG signature

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4
Q

What is a seizure? (3)
And
How do seizures differ?

A
  • Brain network involved
  • Signs and symptoms
  • Causes
  • Drug therapy
  • Prognosis
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5
Q

What are the 2 main types of seizures?

A
  1. Generalised seizures
    * Starts simultaneously in both hemispheres
  2. Focal seizures
    * Seizure starts in a focus and then spreads
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6
Q

What are Generalised seizures?

A
  • Originating at some point within and rapidly engaging, bilaterally distributed networks
  1. Typical Absence
  2. Myoclonic
  3. Tonic-clonic
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7
Q

What is an Absence seizure?

A
  • Mainly childhood in onset
  • Freq brief attacks (1-30s)
  • Sudden loss and return of consciousness
  • No aura and no post-ictal state
  • Some invol movts
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8
Q

What are Myoclonus seizures?

A
  • Sudden, brief, shock-like muscle contractions
  • Usally bilateral are jerks
  • Precipitated by sleep deprivation and alcohol
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9
Q

What are Tonic-clonic seizures?

A
  • Sudden onset, gasp, fall
  • Tonic phase with cyanosis
  • Clonic phase
  • Post-ictal phase
  • Tongue bitten and incontinence
  • Noisy breathing
  • Headache and muscle pain after
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10
Q

What are Atonic seizures?

A
  • A rare type, affects more people with neurologic handicaps
  • Complete collapse for a few seconds
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11
Q

What are Focal seizures?

A
  • Originating within networks limited to one hemisphere
  • They propagate–> symp evolve

Old Vs New terminology

  • Simple partial = Focal with awareness
  • Complex partial = Focal without awareness
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12
Q

What are temporal seizures?

A

Warning (Aura)
* Epigastric rising sensation
* Olfactory and gustatory
* Deja vu

Loss of awareness
* Arrest reaction and blank stare
* Oral automatisms (lip-smacking)
* Manual automatisms

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13
Q

How do we study seizures experimentally?

A
  • Hippocampul slices exposed to stimuli provoking acute seizures
  • Animals with CNS injury causing seizures
  • Rodent genetic models
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14
Q

What are the Pros/cons to hippocampul slices?

A
  1. Pros
    * Realistic epileptic discharges creeated
    * V.Det neurophysiology and Neuropahrma
    * More humane

2.Cons
* Reduced model, not all connections present
* Model of acute seizures not recurrent
* Typically non-physiological triggers needed

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15
Q

What have acute slice models taught us?

A
  1. Mechanism dependant on model used
    * Yound rodents
    * GABA function
    * etc
  2. Epiletiform discharges due to combo of effects:
    * Neuronal busting
    * Synaptic
    * Glia
    * Non-synaptic
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16
Q

Epileptic neuron vs Epileptic network?

A
  • Both bursting neurons and tightly connected neurons in a network are needed to cause a seizure
17
Q

What are the stages of a seizure?

A
  1. Initiation
  2. Synchronisation
  3. Termination
18
Q

Explain the Initiation phase of a seizure

A
  • A micro seizure occurs, which is a small area of excessive activity surrounded by an area of inhibition
  • When this inhibition breaks down, the micro-seizures coalesce to form the seizure itslef
  • An imbalance of excitation vs inhibition
19
Q

Explain the Synchronisation phase of a seizure

A
  • The middle phase of a seizure
  • This phase synchronises effects of other axons to other brain regionsto become epileptic
  • How a seizure propagates
20
Q

Explain the Termination phase of a seizure

A
  • Synaptic inhibiton occurs
  • A depolarisation block
  • SYnaptic depletion
  • IC acidification
  • Hyperpolarisation due to K channels
21
Q

What are in vivo models for acute seizures?

A
  • Standard method of drug discovery
  • Give drugs to rodents to see if it prev a seizure when induced
  • Issue is dont test on epileptic brain, test on brain they induce seizure on
22
Q

What is Epileptogenesis?

A

The process following an injury that leads to the first of a series of spontaneous and recurring seizures whether clinically obvious or not

  • Injury –> Latent period –> Recurring seizures
23
Q

What is ‘Kindling’?

A
  • Giving tiny electrical stimulus to hippocampus, repeat every day
  • Causes seizures in rats and then will continue to have them without electrical shock
24
Q

What changes occur during kindling?

A
  • Early on (before seizures) inhibition is increased
  • ‘Over-Kindling’ leads to cell loss and abnormal neuronal sprouting anf spontaneous seizures
  • Memory and spatial deficits can occur
25
Q

What are the 3 major changes in epileptogenesis models?

A
  1. Structural:
    E.g. Neurogenesis, axonal sprouting)
  2. Molecular:
    E.g. Neuronal channels and receptors
  3. Functional:
    E.g. Gap junctions
26
Q

What are the causes of epilepsy?

A

Genetically based (mono+poly genic)

Structural: e.g. malformations of dev

Acquired
* Trauma
* Stroke
* Infection
* Tumour

27
Q

How is epilepsy treated?

A
  • Correct diagnosis
  • Matching drug treatment to syndrome
  • Genral lefe dvice
  • Identifying any surgical candidates
28
Q

What do anti-epileptic drugs target?

A

Key regulators of neuronal excitability

  • Ion channels
  • Neuro-Transmitter receptors
29
Q

Why are Na channels a target?

A
  • Sodium channels are a target – drugs bind better during the activated channel state
  • Prolong the inactivated state of the channel – block increases with repetitive use
  • Reduces burst firing – the onset of the block is slow, allowing some bursts to occur
  • The main action may be to stop the spread of seizure
30
Q

What are non-pharma treatments?

A
  • Resection of epileptic focus
  • Vagal nerve stimulation
  • Ketogenic diet

Neurobiology of Disease (22 decks)

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