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Neurology > Epilepsy > Flashcards

Epilepsy Flashcards

1
Q

What are important features when taking a history from a patient with suspected epilepsy?

A

Onset - what were they doing? Light-headed or other syncopal symptoms? What did they look like? (breathing, posture, head turning)
Event itself - type of movements (tonic, clonic, rigor), responsiveness and awareness throughout
Afterwards - speed of recovery, sleepiness/disorientation, deficits

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2
Q

What are some risk factors for epilepsy that need to be asked about in a history?

A

Birth, development, seizures in past, head injury, family history, drugs and alcohol

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3
Q

How is a patient with suspected epilepsy examined?

A

Don’t usually examine in 1st seizure clinics - history is most important.
If diagnosis of syncope - cardiovascular examination and lying + standing BP important

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4
Q

How is patient presenting with a fall investigated?

A

ECG - mandatory!
Imaging - MRIb vs CTb
Electroencephalogram (EEG)

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5
Q

When does a patient get a CT scan acutely?

A

Clinical or radiological skull fracture, deteriorating GCS, focal signs, head injury with seizure, failure to be GCS 15/15 4 hours after arrival, suggestion of other pathology e.g. SAH

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6
Q

Why is EEG used?

A

Classification of epilepsy, confirmation of non-epileptic attacks, surgical evaluation, confirmation of non-convulsive status

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7
Q

What are the laws surrounding driving and a patient’s 1st ever seizure?

A

6 month ban from driving a car

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8
Q

What is the law for driving a car in a patient with diagnosed epilepsy?

A

Must be seizure free for 1 year or 3 years if the seizure was during sleep

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9
Q

What is an epileptic seizure?

A 
Abnormal synchronisation of neuronal activity - usually excitatory with high frequency action potentials, sometimes predominantly inhibitory i.e. either too much excitation or too little inhibition
Interruption of normal brain activity - focal or generalised
Usually brief (secs-mins)
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10
Q

How common is epilepsy and in what age group is it most common?

A

Incidence 50-80/100,000

Any age but most common in infancy and old age

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11
Q

What does this diagram represent in terms of epilepsy?

A

Demonstrates that a generalised seizure could start at different points in the network and engage bilaterally distributed networks.
Key point = generalised seizures can start from a focal point

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12
Q

How are partial epileptic seizures classified?

A

Simple - without impaired consciousness

Complex - with impaired consciousness

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13
Q

How are generalised epileptic seizures classified?

A

Absence, myoclonic, atonic, tonic, tonic clonic

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14
Q

What are the motor symptoms associated with partial seizures?

A

Rhythmic jerking, posturing, head and eye deviation, other movements e.g. cycling, automatisms e.g. plucking, vocalisation

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15
Q

What are the sensory symptoms associated with partial seizures?

A

Somatosensory, olfactory, gustatory, visual and auditory

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16
Q

What are the psychic symptoms associated with partial seizures?

A

Memories, deja vu, jamais vu, depersonalisation, aphasia, complex visual hallucinations

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17
Q

When does generalised epilepsy typically present and what is the underlying mechanism?

A

Present in childhood and adolescence.
Generalised spike-wave abnormalities on EEG
Most have genetic predisposition

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18
Q

How is primary generalised epilepsy treated?

A

Sodium valproate is treatment of choice but is teratogenic, lamotrigine is an alternative

19
Q

Name an example of primary generalised epilepsy

A

Juvenile myoclonic epilepsy - early morning jerks, generalised seizures, sleep deprivation is a risk factor

20
Q

When does focal onset epilepsy typically present and what is the underlying mechanism?

A

Onset at any age.
Underlying structural cause
Focal onset, can then generalise

21
Q

What are the features of focal onset epilepsy and how is it treated?

A

Frequent - complex partial seizures with hippocampal sclerosis
Treatment - carbamazepine or lamotrigine (sodium valproate is not first line due to side effects)

22
Q

Some AEDs target voltage-gated Na channels because Na influx increases excitability and drives APs. Name some examples of these drugs

A

Na channel antagonists - carbamazepine, oxcarbazepine, phenytoin, lamotrigine, topiramate, zonisamide

23
Q

Some AEDs target voltage-gated K channels because K efflux reduces neuronal excitability. Name some examples of these drugs

A

K channel agonists - retigabine

24
Q

Some AEDs target voltage-gated Ca channels because Ca influx triggers neurotransmitter release. Name some examples of these drugs

A

Ca channel antagonists - pregabalin and gabapentin (also ethosuximide)

25
Q

Some AEDs target SV2A as it is required for release of neurotransmitter from vesicles. Name the drug that inhibits SV2A

A

Levetiracetam

26
Q

Some AEDs target the GABAa receptor as it reduces neuronal excitability. Name some examples of these drugs

A

GABAa receptor agonists - benzodiazepines, barbituates, topiramate, felbamate

27
Q

Some AEDs target the GABA transporter as it removes GABA from the synapse. Name the drug that inhibits the GABA transporter

A

GABA transporter antagonist - tiagabine - elevated GABA levels

28
Q

Name the drug that inhibits GABA transaminase and describe it’s mode of action

A

Vigabatrin - elevates GABA levels by inhibiting GABA transaminase

29
Q

Which drug enhances GABA synthesis?

A

Sodium valproate

30
Q

What is the initial treatment of partial seizures?

A

Carbamazepine or lamotrigine are the main 1st line drugs

31
Q

Name some add-on drugs used in partial seizures

A

Gabapentin, pregabalin, zonisamide

32
Q

What is used to treat generalised absence seizures?

A

Sodium vaproate, ethosuximide (topiramate, levetiracetam)

33
Q

What is used to treat generalised myoclonic seizures?

A

Sodium valproate, levetiracetam, clonazepam (lamotrigine, topiramate)

34
Q

What is used to treat atonic tonic and generalised tonic clonic seizures?

A

Sodium valproate (levetiracetam, topiramate, lamotrigine)

35
Q

When is phenytoin used?

A

For acute management only, rapid loading possible

36
Q

What are some of the side effects of sodium valproate?

A

Weight gain, teratogenic, hair loss, fatigue

37
Q

When is carbamazepine used and when is it NOT used?

A

Focal onset seizures

Can make primary generalised epilepsies worse

38
Q

When are drugs administered for epilepsy?

A

If a diagnosis of epilepsy is made, if the patient had a single seizure but was at a high risk of recurrence, only id the patient wants the drug!

39
Q

What is the issue with women and anti-convulsant therapy?

A

Some anti-convulsants induce hepatic enzymes e.g. carbamazepine, phenytoin, topiramate
This can alter the efficacy of the COC pill
Shouldn’t use progesterone only pill (ineffective)
Morning after pill dose is not adequate if taking enzyme inducing AEDs

40
Q

What is status epilepticus?

A

Recurrent epileptic seizures without full recovery of consciousness.
Continuous seizure activity lasting more than 30 minutes

41
Q

What are the types of status epilepticus?

A

Generalised convulsive status epilepticus
Non-convulsive status - conscious but in altered state
Epilepsia partialis continua - continual focal seizures, consciousness preserved

42
Q

What can precipitate status epilepticus?

A 
Severe metabolic disorders e.g. hyponatraemia
Infection
Head trauma
Sub-arachnoid haemorrhage
Abrupt withdrawal of anti-convulsants
Treating absence seizures with CBZ
43
Q

What are the potential consequences of status epilepticus?

A

Generalised convulsions without cessation -> excess cerebral energy demand and poor substrate delivery causes lasting damage -> respiratory insufficiency + hypoxia, hypotension, hyperthermia, rhabdomyolysis

44
Q

How is status epilepticus managed?

A

ABC!
Must identify cause - emergency blood tests +/- CT
Anti-convulsants - phenytoin, valproate, benzodiazepines

Neurology (18 decks)

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