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Module 202 Theme 1 > Seizure and epilepsy > Flashcards

Seizure and epilepsy Flashcards

1
Q

What is epilepsy?

A

epilepsy is defined as recurring, unprovoked (spontaneous) seizures

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2
Q

What are acute symptomatic seizures provoked by?

A

acute symptomatic seizures are provoked by acute insults such as stroke, alcohol withdrawal, metabolic disturbance

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3
Q

What are the causes of epilepsy?

A

Many causes - idiopathic, mostly caused by genetics

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4
Q

What is generalised onset?

A

electrical discharges appear to start over the whole brain at the same time on EEG

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5
Q

What is partial/focal onset?

A

electrical discharge appears to start in one cortical region and then may remain localized or spread over the whole brain - secondary generalized

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6
Q

Describe idiopathic generalized seizures

A

onset in childhood or adolescence
usually no focal symptoms/signs
often a number of seizure types cluster
a polygenic cause is presumed with no identifiable structural lesion on imaging
generalized (all leads) spike and wave discharges on EEG, photosensitivity may be present

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7
Q

Describe juvenile myoclonic epilepsy

A 
commonest form of primary generalized epilepsy 		
3-12% all epilepsy
juvenile onset, probably lifelong
early morning myoclonic jerks (ask)
photosensitive, sleep deprivation triggers
\+/- absences 
generalized tonic clonic seizures –
occur without warning
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8
Q

Describe a tonic clonic seizure

A

occurs without warning –risk of injury

tonic phase - continuous muscle spasm, fall, cyanosis, tongue biting, incontinence

clonic phase - rhythmic jerking slows and gets larger in amplitude as attack ends

post-ictal (post-seizure) phase - coma, drowsiness, confusion, headache, muscle aching

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9
Q

Describe absences

A

abrupt
short, 5-20 seconds
multiple times/day, can lead to learning difficulties
unresponsive, amnesia for the gap, rapid recovery
tone preserved (or mildly reduced)
eyelid flickering
absences only, tend to remit in adulthood (childhood absence epilepsy)

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10
Q

What are partial seizures

A

Focal onset seizures

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11
Q

What is a simple partial seizure?

A

Patient aware - aura

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12
Q

What is a complex partial seizure?

A

aura/warning with a level of reduced awareness

patients may call these “absences”, “blanks” – this is medically inaccurate terminology

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13
Q

What is secondary generalized?

A

patient may experience a prior warning, either SPS, CPS, or both, before the tonic clonic seizure

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14
Q

Describe a secondary generalized tonic seizure ?

A

warning/aura –eg epigastric rising sensation, altered smell, déjà vu, fear
cannot abort attack
onset sudden
duration 1-3 minutes
then falls , loses consciousness as seizure generalizes
rigidity/ convulsive jerks/ excess salivation
incontinence/tongue bite common
red/blue, wakes in ambulance/A&E

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15
Q

Which lobe is most affected?

A

Temporal lobe

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16
Q

List physical symptoms of temporal lobe epilepsy

A

hallucination of taste, speech and /or smell, visual distortion
epigastric rising sensation (over humpback bridge)
pallor / flushing / heart rate changes (can mimic panic/hyperventilation attacks)
automatisms- semi-purposeful movements
oral- lip smacking, chewing movements
dystonic posturing (limb rises)

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17
Q

List cognitive symptoms of temporal lobe epilepsy

A 
déjà vu / jamais vu
speech arrest (dominant hemisphere)
formed words during the seizure implies non-dominant hemisphere focus
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18
Q

List the affective symptoms of temporal lobe epilepsy

A

fear, elation, depression, anger

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19
Q

Describe a frontal lobe seizure

A

brief 10-30 seconds
rapid recovery, frequent
predominantly nocturnal
forced head /eye deviation to contralateral side
motor activity often bizarre, thrashing
often misdiagnosed as non-epileptic
ictal EEG (during the seizure) is often normal
Jacksonian spread with Todd’s paresis
automatisms, dystonic posturing (overlap TLE)

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20
Q

Describe the symptoms of parietal lobe epilepsy

A

positive sensory symptoms (unlike TIA/stroke)
tingling, pain
distortion of body shape/image
Jacksonian march of positive sensory symptoms

21
Q

Describe the occipital lobe epilepsy

A

typically simple visual hallucinations -balls of coloured or flashing lights
amaurosis (blackout or whiteout) at onset -25%

22
Q

What anti-epileptic drugs make myoclonic jerks ad absences worse?

A

phenytoin, carbamazepine, gabapentin, pregabalin

23
Q

Which patients do you scan?

A

Jacksonian motor or sensory seizures
Patients with focal neurological deficit

Alcohol withdrawal seizure; only scan if subdural haematoma suspected

24
Q

What is Epileptogenesis

A

the process by which parts of a normal brain are converted to a hyperexcitable brain

25
Q

What is an epileptic seizure?

A

an explosion of synchronous activity by lots of neurons at once that has a tendency to spread throughout the cerebral cortex causing an ‘electrical brain-storm’

a brief change in behaviour caused by the synchronous and rhythmic firing of action potentials by populations of neurons in the CNS

26
Q

Why is the brain prone to seizure activity?

A

action potentials are regenerative events relying on positive feedback: inherently unstable

a single neuron can fire a train (or trains) of action potentials spontaneously, without any external stimulation (intrinsic excitability)

thus, a network of excitatory neurons connected together in convergent and divergent pathways is potentially explosive:
Stimulation of any one cell can lead to a chain reaction due to the progressive spread of activity over a large area

to avoid this ‘explosion’, the brain requires at least as much inhibition as excitation, by means of inhibitory synapses

Epilepsy represents a failure of inhibitory regulation, either focally (e.g. motor cortex, temporal cortex) or generally (whole cortex at once)

27
Q

Describe what happens when Na+ channels are too slow to close

A

e.g., generalized epilepsy with febrile seizures (fever-induced convulsions in infants or small children)
point mutation in part of Na+ channel (β subunit)  abnormally slow inactivation
action potential repolarization impaired

28
Q

Describe the reduction in the number of functional K+

A

e.g., benign familial neonatal convulsions
defect in KCNQ2 or KCNQ3 K+ channel subunit (K+ channels are tetramers of 4 α subunits) leads to impaired activation
action potential repolarization impaired

29
Q

What happens to an EEG during epilepsy

A

rather like an ECG, recording with an array of electrodes attached to the scalp gives information about the electrical activity of very large numbers of neurons in the cerebral cortex
paradoxically, the largest potentials are recorded when the brain is at rest
when left alone and without sensory inputs the various neural networks feedback upon themselves, leading to rhythmic oscillations
when aroused, neuronal activity becomes desynchronized
the hyperexcitation of seizure leads again to synchronous activity on the EEG
EEG can help with determining the localization of a seizure

30
Q

Where do focal seizures originate and spread to?

A

Focal (partial) seizures originate within a small group of about 1000 neurons: the seizure focus
(temporal lobe seizures, focal motor convulsions)

synchronized ‘paroxysmal depolarizing shift’ (PDS, 20 to 40 mV, lasting 50 to 200 ms) overcomes inhibition
increased extracellular K+ due to neuronal damage or reduced uptake by the astrocytes as well as glutamate release from neurons or astrocytes contribute to PDS
during the PDS trains of action potentials occur
hippocampal neurons have similar responses under normal conditions, making the hippocampus more prone to seizures than the neocortex
Focal seizures may spread to other brain regions along the normal neuronal pathways and may also show secondary generalization if the activity spreads
to the thalamus (tonic clonic seizure)

31
Q

Where do primary generalized seizures spread to?

A

Primary generalized seizures reach the cerebral cortex via normal neuronal pathways from the thalamus (e.g. tonic clonic seizure; absence; juvenile myoclonic epilepsy)
pathways originate in the brainstem and are normally involved in regulating the sleep/wake cycle and arousal of the cerebral cortex
Ca2+ channels and inhibitory GABA receptors in thalamic neurons have been implicated in ‘spike and wave’ seizures, showing that inhibition (the wave) is preserved

32
Q

What are the antiepileptic drugs?

A

AEDs available today are actually not antiepileptic; that is, they do not prevent the development of epilepsy.
Most drugs work to prevent the spread of epileptic discharges.
Thus, they control epilepsy’s major symptom: the seizure, not the cause.

33
Q

How do drugs work to prevent the spread of epileptic discharges?

A

Increased activity in the brain may be attributable to:
Increased membrane excitability
Increased efficiency of excitatory synaptic transmission - glutamate
Decreased efficiency of inhibitory synaptic transmission – GABA

Treatments are be aimed at opposing these actions;
Sodium channel blockers and GABA enhancers were the first generation antiepileptic drugs

34
Q

How do sodium channel blockers work?

A

Many of the drugs that are used against partial seizures are effective at blocking repetitive firing of neurons by acting at ion channels (especially sodium channels).
Drugs that have selective actions at the channel may control seizures without affecting normal transmission
Normal neuronal firing is not impaired, thus there should be minimal effect on baseline functioning. When neuronal activity increases (as in a seizure), it is inhibited by the drugs, thereby preventing seizure spread.

35
Q

Name some Na+ channel receptors

A

Phenytoin
Lamotrogine
Carbamazepine/oxcarbazepine/eslicarbazepine
Zonisamide
Lacosamide enhances slow inactivation of sodium channels

36
Q

Describe how carbamazepine, oxcarbazepine and eliscarbazipine work?

A

Carbamazepine, oxcarbazepine and eslicarbazepine competitively inhibit the voltage gated sodium channel by binding with the receptor in its inactive state, prolonging the period between successive firings (prevents burst firing)

37
Q

What is perampanel?

A

non-competitive blockade of AMPA glutamate receptor
reduce spread / generalisation of seizure
well tolerated with improved alertness
role in LD with multiple seizure types not established for perampanel (or lacosamide)

38
Q

How is release of transmitter controlled?

A

Calcium channels are voltage-activated and require strong membrane depolarization for gating and are largely responsible for the regulation of calcium entry and neurotransmitter release from pre-synaptic nerve terminals.

Several anticonvulsant drugs (e.g. topiramate, gabapentin/pregabalin and probably lamotrigine/zonisamide) work this way. ** narrow vs broad spectrum

39
Q

List some anticonvulsant drugs

A 
sodium valproate (sodium channels)
benzodiazepines (clobazam, lorazepam)
barbiturates/primidone
tiagabine (inhibits re-uptake)
vigabatrin (inhibits GABA -T)
40
Q

What do anticonvulsant drugs do?

A

Facilitators of GABAergic transmission

41
Q

What is levetiracetam?

A 
high-affinity synaptic vesicle protein-2A ligand
modulates neurotransmitter release
rapidly titrated and is effective
Keeps patients alert but…
mood lowering/agitation side-effects
42
Q

What is the ideal antiepileptic drug?

A 
good efficacy, easy and rapid to titrate
no drug-drug interactions/liver enzyme induction
no cognitive side-effects/low sodium
no bone marrow suppression
no affective (mood)/drowsy side-effects
different routes of administration
cost effective
43
Q

Which drugs are used for primary generalized epilepsy

A

sodium valproate, lamotrigine first line
(also levetiracetam, topiramate, zonisamide)
broad spectrum antiepileptic drugs

44
Q

Which drugs are used for partial (focal onset) epilepsy

A

carbamazepine, lamotrigine first line

all other antiepileptic drugs have efficacy (all new antiepileptic drugs are tested first in partial epilepsy)

45
Q

Which drugs exacerbate generalized seizure types such as myoclonus and absences?

A
  • phenytoin- carbamazepine- gabapentin/pregabalin
46
Q

List the side effects of benzodiazepines

A 
Dose related  - (acute)
Drowsiness
Ataxia		
Hyperactivity
Personality Change
Cognitive impairment
  • long term
    Tolerance/dependence
47
Q

List the side effects of phenytoin

A

Dose related - (acute)
Ataxia
Diplopia
Nystagmus

long term

Gingival hyperplasia
Osteomalacia
Cerebellar atrophy

48
Q

Which drug interactions are present?

A

CYP450 liver enzymes most implicated
remember treatment is often long term

but not the only story! Check BNF; some antiepileptic drug blood levels can be measured

consider current and future co-morbidities; digoxin, theophylline, warfarin, OCP, rifampicin (TB), erythromycin, chemotherapy

** bones, heart

Module 202 Theme 1 (28 decks)

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