Epilepsy Flashcards

1
Q

What is epilepsy?

A

A disorder of the brain function caused by the repeated and unpredictable occurrence of epileptic seizures.

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2
Q

Define the meaning of seizure?

A

a sudden alternation of behaviour due to a transient burst of abnormal, synchronous, rhythmic, high frequency firing of populations of brain neurones (‘electrical activity’)

not all seizures are epileptic

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3
Q

Explain the meaning of a tonic-clonic seizure and tonic seizure?

A

tonic seizures is when the fall backwards to the ground after going stiff. Lasts for about a minute. While tonic-clonic seizures last for about 1-3 mins and involves the person having jerky movements, cry for help, tongue-biting and incontinence of bowels and bladder.

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4
Q

What are the 5 main types of generalised seizures and explain each one?

A

Tonic: 1 minuteperson may fall backwards after going stiff
Tonic-clonic: 1-3 minutes - person goes stiff and has jerky movements, bladder and bowel inconsistence , cry for help
Absent: a few seconds - a very short loss of consciousness where they stare into space, a person may have 100s of absent seizures a day
Atonic: 15 seconds - person body goes floppy and they usually fall forward
Myoclonic: jerk sharply and uncontrollably. they may even drop items

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5
Q

What are the two types of epilepsy and explain each classification?

A

Partial/focal seizures: discharge begins locally ‘the focus’ and often remains localized (sometimes 2oary generalization)
Simple partial (focal aware seizure /conscious)
Complex partial (focal impaired awareness seizure/ unconscious): impaired or loss of consciousness as spreads to brain stem reticular formation

Generalized seizures: A rise simultaneously from both cerebral hemispheres of the brain leading to an immediate loss of consciousness

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6
Q

Why are continued seizures life threatening to a patient?

A

Causes excitotoxicity – when repeated epilepsy discharge causes neuronal cell death
Status epilepticus: A potential life-threatening state of continuous seizures without recovery. Repeated epileptic discharge can cause neuronal cell death (excitotoxicity)

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7
Q

What part of the brain is affected in localised seizures?

A

Temporal lobe

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8
Q

What is the purpose of electroencephalograms (EEGs)? Why is it performed?

A

EEGs are used to record the changes in electrical potentials during and after a seizure.

Two types of abnormal signals looked for in a seizure that EEGs record

Ictal spikes occur during a seizure.

Interictal occur between seizures.

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9
Q

What clinical regions can we expect from the brain regions: motor, frontal lobe, temporal lobe parietal lobe and occipital lobe?

A

Motor - focal motor jerking
frontal lobe - complex motor jerking
Temporal lobe - auditory and memory disturbances
Occipital lobe - transient visual symptoms including flashing lights
Parietal lobe - transient sensory symptoms

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10
Q

What are the causes of epilepsy?

A

Most cases are unknown. However there is a 30% likelihood of genetic links.

Non structural metabolic causes – alcohol abuse, hypoglycaemia, photosensitive.

Structural causes – trauma (e.g. at birth), ischaemia, stroke, tumour, developmental, neurodegenerative diseases, infection e.g. meningitis

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11
Q

Explain the pathogenesis of epilepsy.

A

In epileptic patients, there is an increase in the stimulatory pathway and a decrease in the inhibitory pathway. There is an increase in glutamate production or an increase in glutamate activity on the NMDA receptors and the AMPA receptors on the post synaptic neurone. When glutamate binds to these receptors it allows cations such as Mg2+, Ca2+, and Na+ to enter the cell. When this occurs, the positive charge from the cations in the neurone activates voltage gated channels on the neurone. This propagates depolarisation and therefore an action potential. This increases more glutamate release.

In addition, the GABA-R receptors become dysfunctional and do not respond to GABA. In normal function, the GABA would act on GABA-R receptors causing the release of negative chloride ions. The release of Cl- negative charges would be enough to inhibit the activity of an action potential in the cell.

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12
Q

When does one become epileptic free?

A

Epilepsy is defined as resolved in individuals who are seizure-free for >10 years, with no anti-epileptic medicines (AEMs) and have not needed AEMs for the past 5 years.

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13
Q

What are the different treatments for epilepsy?

A

Surgery (last resort if drugs cannot sufficiently control seizures)

Drug therapy (AEMs)

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14
Q

When can you use AEM/ What type of epilepsy?

A

All types of epilepsy

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15
Q

What are refractory seizures?

A

Seizures that are hard to treat with epileptic drugs

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16
Q

What class of medicines are used to treat epilepsy?

A

benzodiazepines

17
Q

What are the first-line use dependent drugs for epilepsy? Which ones make absence seizures worse?

A

carbamazepine, valproate and phenytoin. Carbamazepine and phenytoin make absence seizures worse

18
Q

How do benzodiazepines work to inhibit epileptic seizures?

A

Increase the affects of Gaba

19
Q

How does tiagabine work to increase GABA?

A

Inhibits GABA transporters

20
Q

What interactions are most common with epileptic drugs?

A

Alcohol

21
Q

How do we stop treatment of AEMs?

A

Consider when patients have been seizure free for more than 2 years

22
Q

What are the three mechanisms of actions of AEMs?

A
  1. Blocks sodium voltage gated channels in the inactive state so drug becomes more potent if the channel is in this state more during high firing frequency.
  2. inhibiting T-type Ca channels (important during absence seizures)
  3. Increase the amount of GABA by inhibiting the reuptake of GABA from the receptors and inhibiting GABA metabolism. This will allow the release of chloride ions to inhibit the release of an action potential.
23
Q

What is the first line treatment for the 1st mechanism of action?

A

Carbamazepine, sodium valproate, and phenytoin

24
Q

What is the first line treatment for the mechanism important for absence seizures?

A

Valproate, ethosuximide, and clonazepam

25
Q

How do benzodiazepines work to inhibit neuronal activity?

A

Diazepam, midazolam, clonazepam, lorazepam

26
Q

How do you provide emergency treatment in patients who have convulsive status epilepticus?

A

Emergency treatment plan

If no plan:
Community – a benzodiazepine
Hospital – intravenous lorazepam

27
Q

What are the major side effects of benzodiazepines?

A

sedation, impaired alertness, ataxia, memory

28
Q

LOs:
Describe epilepsy in terms of pathology and pathophysiology including risk factors and diagnosis

How do classes of anti-epileptic medication (AEM) work (mechanism of action)?

What classes of medication (AEM) are licenced for epilepsy disorders (Clinical indication)?

What are the major pharmacokinetic, chemical and pharmaceutical features of anti-epileptic medicines (AEMs)?

What are the important common adverse reactions to anti-epileptic medicines (AEMs)?

Are there any major drug interactions associated with anti-epileptic medicines (AEMs)?

A
29
Q

What drugs can we use if we are trying to avoid drug dependence to GABA?

A

Tiagabine, gabapentin/pregabalin

30
Q

What AEMs need TDM?

A

phenytoin and carbamazepine. However no strict time scale once stabilised. Stabilised patients may only be seen 1 or 2 times a year.