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A PA20023 > Epilepsy and Convulsants > Flashcards

Epilepsy and Convulsants Flashcards

1
Q

What is epilepsy

A
  1. Sudden, excessive high frequency neuronal discharge
  2. Not random but highly synchronous- many neurons at once
  3. A disorder of the cerebral cortex
  4. May be loss of consciousness
  5. Behavioural changes related to site of discharge - focus
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2
Q

Define Ictal

A
  1. Ictal (from Latin – a blow or stroke) – the actual seizure or convulsion
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3
Q

Define interictal

A
  1. Interictal – quiescent state between seizures – some abnormal spike activity can be recorded
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4
Q

Define epileptogenesis

A
  1. Epileptogenesis – the underlying process leading to development of epilepsy
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5
Q

What are causes of epilepsy

A
  1. 70% idiopathic/cryptogenic - Unknown causes
  2. genetic - rare familial disorders
  3. congenital - structural abnormalities -dysplasia
  4. birth trauma - ischaemia
  5. neurological/neurodegenerative - elderly
  6. head trauma - penetrating or non-penetrating- rewiring of damaged brain tissue- leads to epilepsy
  7. metabolic - glucose/electrolyte imbalance
  8. disease - meningitis, tumour, abscess
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6
Q

What are two methods to detect epilepsy

A
  1. Electro-EncephaloGraphy (EEG)

2. Magneto-EncepahloGraphy (MEG)

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7
Q

Describe how to carry out Electro-EncephaloGraphy (EEG)

A
  1. Put on surface of head
  2. Can pinpoint activity in brain
  3. Record generalised seizure- every electrode shows it- synchronised
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8
Q

Describe how to carry out Magneto-EncepahloGraphy (MEG)

A
  1. Look at magnetic fields rather than electrical activity
  2. continuous wave not discrete points- better picture of where it is occurring
  3. But more expensive
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9
Q

What is used for imaging epilepsy

A
  1. PET – monitors local metabolism
  2. MRI – structure and volume
  3. fMRI – relates activity to structure
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10
Q

What are invasive approaches to record epilepsy

A
  1. dural electrode arrays
    - Expose surface of brain and put dural electrode array on surface of brain to pinpoint where seizure is
  2. implanted depth electrodes
    - Bands of insulation alternating with exposed bits
    - Record depth of brain
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11
Q

Describe EEG of normal

A
  1. normal- flat line with little synchronisation
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12
Q

Describe EEG of Grand mal seizure

A
  1. Synchronisation
  2. Generalised seizure
  3. High frequency synchronisation-tonic phase
  4. Clonic- bigger amplitude and lower frequency
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13
Q

Describe EEG of Petit mal

A
  1. Spike wave activity- 15 sec

2. Involved with brief period of loss of consciousness but no loss of posture

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14
Q

Describe EEG of partial seizure

A
  1. Only on one side of brain
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15
Q

Describe a Grand-mal seizure

A
  1. tonic phase- output from cortical areas is such a high frequency the limbs can tremor and stiffen but don’t move a lot
  2. Clonic phase- frequency falls and movement of muscles is much more obvious
  3. Post-ictal phase- relative lethargy and tiredness
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16
Q

Where do seizure occur

A
  1. Anywhere
  2. subcortical rare
  3. mostly cortical - frontal, parietal, occipital, temporal
  4. Temporal most prevalent - 30-40%
    a) Hippocampus, entorhinal cortex, amygdala
    b) drug refractory
    c) surgical resection
17
Q

What is a radical temporal lobectomy

A
  1. Removal of temporal lobe including entorhinal cortex and hippocampus- used to
  2. Less radical now
  3. Much more precision- only part that needs to be removed
18
Q

What is resective surgery

A
  1. Resective surgery for chronic epilepsy
  2. EEG identifies where seizure activity is arising
  3. MRI- structural correlation
19
Q

How do seizures arise

A
  1. Cortical activity - dynamic balance between inhibition and excitation
  2. Two levels
  3. Intrinsic - ion channels - Individual cells
  4. Network - synaptic transmission
  5. Disturbed balance - excessive synchrony and epilepsy
    a) increase excitation, normal inhibition
    b) decrease inhibition, normal excitation
    c) decrease inhibition, increase excitation
20
Q

Describe basis of epilepsy discharge

A
  1. At start of seizure a sudden step in depolarisation
  2. Long train in prolonged depolarisation
  3. Paroxysmal shift- big shift at start
21
Q

Describe intrinsic balance - membrane ion channels

A
  1. Destabilising depolarising ion channel current in membrane of every neuron- sodium or calcium flowing into cell
  2. Balanced by stabilising/hyperpolarising currents- potassium leaving or chloride ions entering
  3. If balance lost then cells become hyperexcitable and more likely to coordinate activity abnormally
22
Q

Describe synaptic balance

A
  1. Glutamate is principle source of excitation

2. Balanced by inhibition by GABA

23
Q

Describe Synaptic excitation

A
  1. Synaptic excitation is controlled by synaptic inhibition in neuronal networks
  2. Excitatory glutamate neurons can excite each other
  3. Glutamate neurons also excite inhibitory GABA neurons
  4. GABA neurons control and limit excitation
  5. Loss of inhibition leads to runaway synchrony and epilepsy
24
Q

How can synaptic and intrinsic factors initiate and prolong a seizure

A
  1. In initial phase of epileptic event Ampa receptors are very important
  2. Excess activity causes depolarisation
  3. NMDA receptors- Contribute to excitation in prolonged way when cell is depolarised
  4. If membrane depolarises they become more important and activated
  5. Voltage gated ca2+ channels are opened by depolarisation
  6. Sub-threshold voltage gated Na+ channels are Opened by depolarisation- Not ones in charge of action potential
  7. All lead to continuation of depolarisation
25
Q

How do seizures stop

A
  1. Gluatamate depletion- Less to release
  2. Glutamate receptors desensitisation- Less effective over time
  3. K+ channel activation
  4. Na+ channel inactivation
26
Q

How can you treat epilepsy

A
  1. Block destabilizing currents- Sodium and calcium currents
  2. Increase stabilizing currents- Increases potassium current flow into cell
  3. Reduce synaptic excitation
    a) Block glutamate release
    b) Block glutamate receptors
  4. Increase synaptic inhibition
    a) Increase GABA release
    b) Potentiate GABA receptors
27
Q

How can you block voltage gated Na-channels

A
  1. 3 states
    a) Closed channel
    b) Open channel
    c) Inactivated state
  2. Drugs that block Na-channels- bind to inactivated state so can’t return to closed channel
28
Q

What are some drugs that block Na-channels

A
  1. phenytoin (++)
  2. carbamazepine (++)
  3. lamotrigine (++)
  4. sodium valproate (+)
29
Q

How do you block voltage gated Ca-channels

A
  1. bind directly to stop them opening
30
Q

What are some drugs that block Ca-channels

A
  1. ethosuximide (++) - specifically, useful for absent seizures
  2. gabapentin
  3. phenytoin
31
Q

How can you block glutamate release

A
  1. Anticonvulsant blocks sodium channel activity
  2. Action potential arise by sodium channel opening, causing calcium channel opening, causes glutamate release
  3. Reducing action potential reduces glutamate release can also reduce glutamate release directly
  4. Drugs that reduce glutamate release
  5. Na-channel block
  6. Ca-channel block
  7. Reducing vesicle fusion - Levetiracetam
32
Q

How can drugs act at GABA synapses

A
  1. increase GABA levels in synaptic terminals
  2. GABA transaminase inhibitor- increase GABA present
  3. decrease GABA inactivation
  4. enhance postsynaptic response
33
Q

Which drugs increase GABA levels in synaptic terminals

A
  1. vigabatrin (++)

2. sodium valproate (+

34
Q

What do GABA transaminase inhibitors do

A
  1. blocks GABA breakdown
  2. increases GABA levels
  3. increases GABA release
35
Q

How can you decrease GABA inactivation

A
  1. tiagabine
  2. blocks GABA reuptake
  3. increases GABA in cleft
36
Q

How can you enhance postsynaptic response to GABA

A
  1. benzodiazepines
  2. barbiturates
  3. prolong channel open time
37
Q

What are some Alternative anticonvulsants

A
  1. felbamate - blocks NMDA receptors
  2. topiramate - blocks AMPA/kainate receptors
  3. retigabine - activates K-currents
  4. levetiracetam - modifies vesicle release machinery
  5. losigamone - blocks low threshold Na-currents

A PA20023 (19 decks)

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