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Diseases of the Nervous System > Epilepsy > Flashcards

Epilepsy Flashcards

0
Q

What are two types of epileptic seizures?

A

Generalised and partial seizures

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1
Q

How can epileptic seizures be defined?

A

Sudden, transient and excessive bursts of hypersynchronous activity within a neuronal population (usually the cerebral cortex)

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2
Q

What are 5 types of generalised epileptic seizure?

A 
1 - absence/petit-mal
2 - tonic-clonic/grand mal 
3 - tonic
4 - myoclonic 
5 - atonic
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3
Q

What are the four stages of tonic-clonic seizures?

A

aura ➡️ tonic ➡️ clonic ➡️ post-ictal

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4
Q

What are the clinical signs of an absence seizure?

A

An impairment of consciousness with sudden onset and termination, usually lasting 5-20 seconds

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5
Q

What characteristics of absence seizures can be seen on an EEG?

A

A characteristic spike-wave pattern

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6
Q

How are generalised seizures defined?

A

Whole cortex bilateral seizures

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7
Q

How are partial seizures defined?

A

Epileptic activity confined to one area of brain

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8
Q

What is a secondary generalised seizure?

A

Seizure activity starting in one hemisphere of the brain and spreading to the other

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9
Q

What percentage of epilepsy in drug refractory?

A

30%

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10
Q

What is responsible for hypersynchrony in epilepsy?

A

Imbalances in excitatory and inhibitory inputs to neurones (usually pyramidal cells)

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11
Q

What are four theories behind hypersynchrony in epilepsy?

A

1 - ⬆️ T-type calcium channels (It)
2 - ⬇️ HCN channels (Ih)
3 - ⬆️ deafferentation induced axonal sprouting
4 - dormant inhibitory neurone hypothesis

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12
Q

What are T-type calcium channels?

A

Transient, low-voltage activated channels producing low threshold spikes that allow bursts of action potentials to be fired by pyramidal cells during small depolarising events

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13
Q

How are T-type calcium channels altered in epilepsy?

A

⬆️ It channel activity = increases burst firing and lowers action potential threshold

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14
Q

How are HCN channels altered in epilepsy?

A

⬇️ Ih channels = increased summation of excitatory inputs

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15
Q

What is deafferentation induced axonal sprouting?

A

Neuronal connections lost during epileptogenic injury = ⬆️ axonal projections
(may recruit increased excitatory cells)

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16
Q

what are destabilising channels in relation to epilepsy?

A

sodium and calcium channels with neurones

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17
Q

what are stabilising channels with relation to epilepsy?

A

chloride and potassium channels within neurones

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18
Q

what is the result of altered It channel activity in epilepsy?

A

increased burst firing of action potentials with a lower threshold

19
Q

what are HCN channels?

A

hyperpolarisation activated cyclic nucleotide-gated channels - produce Ih currents that activate during hyperpolarising steps to limit summation of excitatory synaptic inputs

20
Q

what is the dormant inhibitory neurone hypothesis of epilepsy?

A

loss of excitatory innervation to inhibitory cell in epilepsy results in insufficient inhibition of pyramid cells and therefore ⬆️ excitation

21
Q

what are seven known causes of epilepsy?

A

trauma at birth, neurological/neurodegenerative causes, autoimmune, congenital abnormalities, genetic causes, disease and metabolic causes

22
Q

epilepsy due to genetic family disorders is common: true or false?

A

false - genetic, familial epilepsy is very rare

23
Q

what is juvenile myoclonic epilepsy?

A

an idiopathic, generalised epilepsy though to be associated with 6 susceptibility loci - e.g. CACNB4, GABRA1, CLCN2, GABRD

24
Q

what are three forms of autoimmune epilepsy?

A

rasmussen’s encephalitis, anti-NMDA encephalitis and limbic encephalitis

25
Q

how is epileptic activity measured?

A

using an electro-encephalogram (EEG) measuring average local field potentials from apical dendrites in cortical grey matter

26
Q

epilepsy is a result of imbalances between _________ and _________

A

excitation and inhibition

27
Q

imbalances in excitation and inhibition in epilepsy can be a result of ________ or ________ within current/voltage-gated ion channels, e.g. ___, ___, ___, ___

A

mutations or altered expression of sodium, potassium, chloride and calcium channels

28
Q

what drugs are used to treat epilepsy?

A

anticonvulsants

29
Q

what drugs are used to increase stabilising currents in epilepsy?

A

drugs that activate potassium channels, e.g. retigabine

30
Q

what drugs are used to block destabilising currents in epilepsy?

A

drugs that block sodium and calcium channels, e.g. phenytoin (Na and Ca), carbamazepine (Na) and ethosuximide (Ca)

31
Q

in epilepsy, how can synaptic activity be inhibited?

A

by inhibiting glutamate release via inhibition of sodium and calcium channels

32
Q

in epilepsy, how can synaptic inhibition be increased?

A
  • by increasing GABA levels (e.g. vigabatrin/sodium valproate to inhibit GABA transaminase or tiagibine to inhibit the GAT1 transporter)
  • by activating GABAa-R chloride channels (benzodiazepines and barbiturates)
33
Q

what is drug refractory epilepsy?

A

failure to get adequate seizure control with more than three anticonvulsants

34
Q

what is an example of drug-refractory epilepsy?

A

medial temporal lobe epilepsy

35
Q

with regards to GABA transmission, why is medial temporal lobe epilepsy refractory to drug treatment?

A

because current AEDs increase GABA activity, and GABAergic neurones found in patients with MTLE are thought to be depolarising rather than inhibitory

36
Q

during normal development, levels of the _______ are initially high but decrease towards late development, whereas levels of the _______ are initially low but increase towards late development

A

NKCC1 chloride importer is expressed early

KCC2 chloride exporter is expressed late

37
Q

the NKCC1 chloride exporter favours _________ GABAa responses

A

depolarising

38
Q

the KCC2 chloride exporter favours ________ GABAa responses

A

hyperpolarising

39
Q

bicuculline is a _____ antagonist

A

GABAa

40
Q

in the subiculum of patients with MTLE, what effect did the application of the GABAa antagonist bicuculline have on the spontaneous epileptic discharges?

A

the GABAa antagonist blocked these discharges - in the hippocampus of patients with MTLE, they GABAa responses are depolarising rather than hyperpolarising

41
Q

what are depolarising GABAa responses in MTLE thought to be a consequence of?

A

hippocampal sclerosis and cell loss in MTLE resulting in epileptogenic plasticity inducing changes in GABAa responses

42
Q

bumetanide is an ______ antagonist

A

NKCC1

43
Q

where does 30-40% seizure activity arise?

A

the temporal lobe (i.e. the hippocampus, the amygdala and the entorhinal cortex)

44
Q

the __________ is particularly susceptible to pathological changes in MTLE

A

hippocampus

Diseases of the Nervous System (6 decks)

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