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Medsci 317 > Lecture 29; Epilepsy > Flashcards

Lecture 29; Epilepsy Flashcards

1
Q

What essentially is epilepsy?

A

An imbalance between excitation and inhibition

Very simplistic overview.

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2
Q

What is the hallmark characteristic of epilepsy?

A

Abnormal, excessive electrical discharge from neurones (hypersynchronized discharge from the brain)

Often associated with Loss of Consciousness

But

Does not always produce Loss of Consciousness

Not all Loss of Consciousness due to epilepsy (people who faint can jerk a bit)

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3
Q

What is epilepsy a symptom of?

A

Epilepsy is a symptom of brain dysfunction

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4
Q

What are the possible causes of epilepsy?

A

Syndrome with many possible causes;
structural
genetic
metabolic / functional

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5
Q

Define why epileptic seizures occur

A

Seizures occur as a result of abnormal synchronous activation of large numbers of hyperexcitableneurons which are connected in networks

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6
Q

What pathways typically are seizure forming?

epiltogenesis

A

Seizures may be propagated via both normal and abnormal pathways

Seizures spread through synaptic and non synaptic pathways
- gap junctions (Bipasses synapses)

Everyone has neuronal circuitry that can generate seizures(ECT, Drugs)

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7
Q

How many people have epilepsy and how does this differ from epilepsy?

A

0.5 –1 % of the population has epilepsy.

1 in 20 people will have a seizure at some time in their life.

Epilepsy is as a tendency to recurrent seizures.

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8
Q

What are the two broad categories of electroclinical seizures?

A

Focal and Generalised

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9
Q

Define focal seizures;

A

Focal

partial part of the brain

manifestations depend on which part of brain involved

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10
Q

Describe generalised seizures;

A

generalised

Networks involving extensive regions of both hemispheres

Manifestations vary greatly

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11
Q

What is the main functional test for seizures?

A

EEG

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12
Q

What is EEG and what does it show?

A

An EEG is a 30 minute recording from 21 electrodes placed in standard positions on the scalp.

A single EEG will show epileptiform activity in 29-70% of patients with proven epilepsy.

Sensitivity improved by recordings during sleep.

Incidental epileptiform abnormalities are found in 0.5% of healthy young adults

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13
Q

What does EEG identify?

A

EEG is important in identifying the seizure type and hence the correct seizure syndrome for an individual patient

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14
Q

Describe what types of conscious focal seizures there are?

A

Consciousness may be preserved (Simple Partial)

Focal motor
Visual
Somatosensory
Auditory
Psychic
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15
Q

What may lead to an impaired consciousness seizure?

A

Consciousness may be impaired

Complex partial - (aka) Dyscognitive

Patient is unresponsive with subsequent amnesia

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16
Q

What sorts of brain lesions can be associated with focal seizures?

A

Cavernous Angionma

Focal Cortical Dysplasia

Hippocampal Sclerosis

Subependymall Hetrotopia

17
Q

What does GABA transmission do and what drugs allosterically bind to it / treat epilepsy?

A

x2 GABA bind - Cl in hyperpolarises

Allosteric binding sites for Benzodiazepines and Barbiturates (antiepileptic drugs)

18
Q

Are ion channels permanent?

A

No, they are all very plastic.

Ion channels demonstrate frequency dependent changes in synaptic efficiency

Excitatory synapses are potentiated when fire repetitively Inhibitory synapses decrease in efficacy when fire repetitively

NMDA LTP may be involved in long term chronic seizures.

19
Q

What does mutations in K channels lead to?

A

Mutations in voltage gated K channels

Benign familial neonatal epilepsy (children grow out of them)

2 different K channel mutations

20
Q

What can mutations in Na channels lead to?

A

Severe Myoclonic Epilepsy of Infancy (Dravet’sSyndrome) SCN1A

Benign familial Neonatal Epilepsy SCN2A

Generalised Epilepsy with Febrile Seizures plusSCN1A SCN1B SCN2A

Early onset absence seizures SCN1B

Genotype doesnt have consistent phenotype.

21
Q

What causes absence epilepsy?

A

Absence seizures and Ca++ channelsAbsence seizures due to abnormal activation of T-type calcium channels in the thalamus

Hyperpolarisation of thalamic relay neurones produces synchronous depolarisation of the cortex via excitatory neurones

GAERS rats –mutations of T-type calcium channel

22
Q

What are the possible mutations in ligand gated ion channels?

A

AutosomalDominant Nocturnal Frontal Lobe Epilepsy Mutation of Nicotinic AChreceptor

Generalised Epilepsy with Febrile Seizures plus Mutation of GABAa receptor

Angelman’s syndrome
- Deletion of part of Chr15 -contains genes for several GABAareceptor subunits

23
Q

What does surgery on epileptics show?

A

Surgically resected temporal lobe specimens show changes in the ratio and function of Na channels

24
Q

What do epileptic animal models show in terms of changes in brain structure?

A

Overexpression of low threshold Ca currents in thalamic neurones in rats produces model of human absence epilepsydensity, distribution, molecular structure and function of ion channels is altered after seizures

25
Q

What can induce seizures?

A

Blocking Gaba a receptors
Activating glutamate receptors
Blocking some K channels

26
Q

What drugs block GABAa receptors?

A

Blockade of GABAa receptors

bicuculline(competitive antagonist)

picrotoxin(non-competitive antagonist),

penicillin –enters open GABA channels and occludes them

27
Q

What activates glutmate receptors? causing siezures

A

kainate, domoicacid unblocking of NMDA receptors by low Mg2+

28
Q

What antiepileptic drugs target Na channels?

A

Na+ channel blockers –presynaptic

Prevent sustained repetitive firing from extended depolarisation

i.e
carbamazepin
ephenytoin
lamotrigin
esodium valproate
29
Q

What drugs enhance GABA transmission?

A 
vigabatrin
tiagabine
sodium valproat
ebenzodiazepines  (diazepam, lorazepam)
barbiturates  (phenobarbitone)
topirimate
30
Q

What drugs act on Ca channels?

A

Ethosuxamide

Sodium valproate

31
Q

What drugs block glutamate?

A

Topirimate
Lamotrigine
Felbamate
Perampanel (AMPA receptors)

32
Q

What are some autoantibody induced epileptic syndromes

?

A

Anti-voltage gated potassium channels (LGI1):

Anti-NMDA receptor

33
Q

What results from Anti-voltage gated potassium channels (LGI1):?

A

Limbic encephalitis, (prominent amnesia)Focal (dyscognitive) seizures –complex partial seizuresFacio-brachial dystonicseizuresHyponatraemi

34
Q

What results from anti-NMDA receptor antibodies?

A

Psychiatric features

DyskinesiasFocal (dyscognitive) seizures –complex partial seizures

35
Q

What are the effects of seizures?

A

Kindling (theory)

Repetitive exposure to (initially) subthreshold electrical stimulation eventually produces spontaneous seizures

Theory that seizures may beget seizures

36
Q

How do seizures affect the neuronal circuits?

A

Anatomic rearrangements of local circuits

Excitatory axons have collateral branches feedback inhibition and / or excitationusually inhibition more powerful

With neuronal death, there is sprouting of unlesioned axons occurs to fill in dendritic regions

37
Q

How do seizures affect the dengate gyrus?

A

Mossy fibres of granule cells in dentate gyrusinnervate pyramidal cells of CA3 region (inappropriate)

When granule cells die, surviving neurons develop collaterals that form new connections

Form recurrent excitatory connections - alter normal balance between feedback inhibition and excitation

38
Q

What did they find in sprouting in epilepsy associated with?

A

Degree of sprouting correlates with number of evoked seizures

Sprouting may occur even in the absence of overt cell death

Medsci 317 (32 decks)

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