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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
what are three forms of autoimmune epilepsy?
rasmussen's encephalitis, anti-NMDA encephalitis and limbic encephalitis
25
how is epileptic activity measured?
using an electro-encephalogram (EEG) measuring average local field potentials from apical dendrites in cortical grey matter
26
epilepsy is a result of imbalances between _________ and _________
excitation and inhibition
27
imbalances in excitation and inhibition in epilepsy can be a result of ________ or ________ within current/voltage-gated ion channels, e.g. ___, ___, ___, ___
mutations or altered expression of sodium, potassium, chloride and calcium channels
28
what drugs are used to treat epilepsy?
anticonvulsants
29
what drugs are used to increase stabilising currents in epilepsy?
drugs that activate potassium channels, e.g. retigabine
30
what drugs are used to block destabilising currents in epilepsy?
drugs that block sodium and calcium channels, e.g. phenytoin (Na and Ca), carbamazepine (Na) and ethosuximide (Ca)
31
in epilepsy, how can synaptic activity be inhibited?
by inhibiting glutamate release via inhibition of sodium and calcium channels
32
in epilepsy, how can synaptic inhibition be increased?
- 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
what is drug refractory epilepsy?
failure to get adequate seizure control with more than three anticonvulsants
34
what is an example of drug-refractory epilepsy?
medial temporal lobe epilepsy
35
with regards to GABA transmission, why is medial temporal lobe epilepsy refractory to drug treatment?
because current AEDs increase GABA activity, and GABAergic neurones found in patients with MTLE are thought to be depolarising rather than inhibitory
36
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
NKCC1 chloride importer is expressed early | KCC2 chloride exporter is expressed late
37
the NKCC1 chloride exporter favours _________ GABAa responses
depolarising
38
the KCC2 chloride exporter favours ________ GABAa responses
hyperpolarising
39
bicuculline is a _____ antagonist
GABAa
40
in the subiculum of patients with MTLE, what effect did the application of the GABAa antagonist bicuculline have on the spontaneous epileptic discharges?
the GABAa antagonist blocked these discharges - in the hippocampus of patients with MTLE, they GABAa responses are depolarising rather than hyperpolarising
41
what are depolarising GABAa responses in MTLE thought to be a consequence of?
hippocampal sclerosis and cell loss in MTLE resulting in epileptogenic plasticity inducing changes in GABAa responses
42
bumetanide is an ______ antagonist
NKCC1
43
where does 30-40% seizure activity arise?
the temporal lobe (i.e. the hippocampus, the amygdala and the entorhinal cortex)
44
the __________ is particularly susceptible to pathological changes in MTLE
hippocampus

Diseases of the Nervous System (6 decks)

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