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My MRCP > Epilepsy & Seizures > Flashcards

Epilepsy & Seizures Flashcards

1
Q

What can cause a blackout? [5]

A
  • Vasovagal Syncope
  • Hypoxic Seizure
  • Concussive Seizures
  • Cardiac Arrhythmia
  • Non-epileptic attacks
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2
Q

Define Vasovagal syncope [3]

Symptoms [5]

A

Syncope may be defined as a transient loss of consciousness [1] due to global cerebral hypoperfusion [1] with rapid onset, short duration and spontaneous complete recovery [1].

  • Light headed
  • Nausea
  • Hot/Sweating
  • Tinnitus
  • Tunnel Vision
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3
Q

What could trigger vasovagal syncope? [5]

A
  • Prolonged Standing or standing up too fast
  • Trauma
  • Venepuncture
  • Urination
  • Coughing
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4
Q

Whats the difference between a seizure and syncope?

A
  • Syncope tends to happen when your upright
  • Pallor is common in syncope
  • Syncope has a gradual onset vs a sudden onset seizure
  • Injury & incontinence are rare in syncope
  • Recover rapidly from syncope but not seizure
  • Syncope is triggered, precipitants for seizures are rare
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5
Q

How does a hypoxic seizure occur? Which setting would this most commonly occur? [2]

A

People who faint and then are kept upright keep fainting and dont breath –> Seizure

Occurs a lot in aircraft where people cant end up lying down

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6
Q

What is a non-epileptic attack? [1]
Gender epidemiology [1]
Links [3]
Management [1]

A

F > M
‘pseudoseizures’

They are often linked to:

  • Stress
  • Past abuse
  • History of medically unexplained symptoms

Require psychological input not AEDs

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7
Q

When you have a patient who blacked out what do you want to know?

A
  • What they were doing
  • Any warning feelings or Aura
  • Similar previous history
  • Any injury or incontinence
  • How responsive are/were they, what collour did they go, did they move or make sound
  • Whats their pulse like
  • Past medical, psych, alcohol/drug and family history
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8
Q

If someone’s had their first seizure how would you investigate? [4]

A
  • Bloods - metabolic causes e.g., hyponatraemia
  • Brain imaging
  • CSF exam if systemic illness - HSV, autoimmune encephalitis
  • EEG
  • Advanced functional imaging can localise seizure focus
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9
Q

What features on a first seizure would suggest generalized epilepsy [3]
What features on a first seizure would suggest focal epilepsy [3]

A

Primary Generalised Epilepsy:

  • History of myoclonic jerks (particularly in morning)
  • Absences
  • Feeling strange +/- flickering lights

Focal Onset Epilepsy:

  • Deja Vu
  • Rising in abdomen
  • Episodes where they look blank and smack lips
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10
Q

How would you advise someone who’s just had their first seizure? [3]

A
  • Driving Regulations
  • Inquire about employment or potentially dangerous activities
  • Refer to epilepsy clinic for routine follow up
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11
Q

Define Epilepsy [3]

A
  • A neurological disorder marked by sudden recurrent episodes [1] of sensory disturbance, loss of consciousness, or convulsions, [1] associated with abnormal electrical activity in the brain. [1]
  • Caused by predisposition to neuronal hyperexcitability
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12
Q

Epilepsy epidemiology [1]

Causes of epilepsy [5]

A

More common in extremes of age

  1. 6 in 10 unknown cause
  2. Difficult birth
  3. Brain infection
  4. Stroke
  5. Serious brain injury
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13
Q

In what groups is epilepsy more common? [1]

A

People with learning difficulties (22% of people with LD)

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14
Q

What are the classifications of Epilepsy [2]

A

Generalised Epilepsy (metabolic causes)
Focal Epilepsy (structural abnormalities)

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15
Q

What are the types of Primary Generalised Epileptic Seizure [6]

A
  • Tonic Clonic (Tense-Jerky)
  • Myoclonic (Very brief twitch contractions)
  • Clonic
  • Tonic
  • Atonic (Very rapid collapse to floor)
  • Absence (most common in kids, tends to grow out by age 12)
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16
Q

How are focal onset seizures different? [2]
Name the 3 subtypes
In which type of seizure classification is family history relevant? [1]

A

They vary by which area of the brain is affected. May come with aura which may localise where the seizure is happening in the brain.

They may retain awareness/responsiveness (Simple) OR may have impaired awareness (Complex)

Can develop into a secondary generalized seizure
called ‘Focal to Bilateral seizure’ or secondary generalized seizure

Family history association in generalized but not in focal epilepsy

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17
Q

How does an EEG change between focal/partial and generalized epileptic seizures?
What could an MRI/CT show us to differentiate between focal and generalized?

A

An EEG would show generalised vs focal abnormalities of brain waveform

An MRI or CT may show a physical cause in a focal epileptic but not primary generalised

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18
Q

How would you make epilepsy visible in order to test with an EEG? [3]

A

Hyperventilation
Photic Stimulation
Sleep Deprivation

Will show up best in Generalised Epilepsy

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19
Q

What other test can be done for epilepsy if you didn’t find anything on EEG? [2]

A

Video-Telemetry

Basically an EEG with a camera over several days

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20
Q

What are the rules for driving with epilepsy?

A

Normal licenses:

  • Seizure Free for a year Or had seizures but only from sleep.
  • If you have a daytime seizure ever then you will need 3 yrs of none or purely nocturnal seizures

HGV/PSV:
- Seizure and medication free for 10yrs

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21
Q

Side effects of Sodium valproate [4] and Carbamezapine [4]?

A

Sodium Valproate:

  • Tremor/Ataxia
  • Weight Gain
  • Hair Loss
  • Pancreatitis/Hepatitis

Carbamazepine:

  • Ataxia
  • Low Serum Na
  • Severe Skin rash
  • Nystagmus/Blurred Vision
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22
Q

What is Status Epilepticus? [1]
Whats the most common type?
Aetiology [4]
Sequelae [1]

A

A prolonged or recurrent seizure that lasts for 5 mins with no recovery period in between

(Most common type is TCSE - Tonic Clonic Status Epilepticus)

Usually caused by stroke, tumour, haemorrhage or alcohol and 90% of deaths are due to the underlying cause not the seizure itself

Can lead to neuro problems (brain damage) in children

23
Q

How do we treat TCSE?

A

1st line - IV lorazepam 4mg, midazolam buccal/IM/IV, diazepam oral/rectal/IV.
2nd line - Phenytoin slow infusion 15-18mg/kg at 50mg/min
3rd line - GA e.g. propofol

NPA airways may be more practical than oral airways.

24
Q

Alternative uses for carbamazepine [1]

A

As well as being an anticonvulsant it treats nerve pain in conditions such as Trigeminal Neuralgia

25
Q

Partial seizure
Frontal lobe seizures
State 2 types
Explain Todd’s paralysis [1]

A

Jacksonian motor seizures - ‘march’ of involuntary movement from one muscle group and then spreads [1]
Adverse seizure - patient’s eyes and head turn away from the site of the focal origin [1]
Todd’s paralysis is common after motor seizure - affected limb remains weak for some hours after [1]

26
Q

Partial seizure
Point of origin in cortex [1]
Parietal lobe seizures
Presentation [2]

A

Arising in sensory cortex
Paresthesia in extremity or on face
Distortion of body image

27
Q

Why are frontal and parietal seizures indicate structural brain disease

A

Frontal and parietal seizures indicate structural brain disease

28
Q

Localisation of features of focal seizures

Partial seizure

Temporal lobe seizure

A

Visceral disturbance: taste, smell hallucinations, lip smacking, epigastric fullness, choking sensation
Memory disturbance: deja vu, jamais vu (unfamiliarity), depersonalization
Motor disturbance: fumbling movement, rubbing, chewing
Affective disturbance: displeasure, elation, fear

29
Q

Partial seizure

Occipital lobe seizure

A

Visual hallucination eg line or flash

Tonic clonic seizure

30
Q

Explain underlying pathogenesis of secondary generalized seizures [2]
Why is there a risk of death in these type of seizures? [1]

A

Seizure discharges have capacity to spread from point of origin and excite deeper subcortical structures eg thalamus
Their excitation releases discharge spreading back to both hemispheres

Sudden death may occur (rare) from cardiac arrhythmia

31
Q

Absence seizures
Main features [2]
Frequency [1]
Trigger [2]
Management [2]
Prognosis

A

The patient (3-10 y/o stares vacantly, eyes may blink, ‘petit mal’
Many times a day with duration 5-15s
No awareness
Trigger: hyperventilation, photic stimulation
Mx: sodium valproate and ethosuximide are first-line treatment
Prognosis: good prognosis - 90-95% become seizure free in adolescence

32
Q

Generalized tonic-clonic seizures
Main features [2]
Explain why there are 2 phases
Describe typical history from a secondary generalized seizure [5]

A

Occur without warning or aura, ALL unconscious

Tonic phase associated with rapid neuronal discharge
Clonic phase begins as neuronal discharge slow

LOC > fall to ground
Tonic phase 10s
Clonic phase 1-2 min
Unrousable sleep, stertorous respiration
Muscle ache, exhaustion post-ictal
33
Q

Triggers for epilepsy [7]

A 
Forgetting epilepsy medicine
Feeling tired, stressed
Sleep deprivation
Alcohol
Photic stimulation
Menstruation
Missing meals
34
Q

MOA of sodium channel blockers ie the anticonvulsants on epilepsy

Give examples [5]

A

Sodium channel blockers reduce opportunity for depolarisation
* Phenytoin
* Carbamazepine
* Lamotrigine
* Lacosamide
* Rufinamide

35
Q

Name other drugs that are used in epilepsy (besides sodium channel blockers) [4]

A

GABA-receptor agonist
T-type CCB ie ethosuximide
Glutamate blocker
Levetiracetam

36
Q

Give examples of a GABA receptor agonist [2]

A

Lorazepam

Valproate

37
Q

Give an example of a glutamate blocker [1]

Which group of patients are they well suited to

A

Topiramate

Obese patients as weight loss inducing effect

38
Q

Epilepsy

Give 4 example of an anti-epileptic that works on calcium channels

A

Ethosuximide
Lamotrigine
Topiramate
Gabapentin

39
Q

Give an example of an anti-epileptic that works on potassium channels

A

Direct activation limits the firing of action potentials by hyperpolarising the neural membrane.

40
Q

Give an example of an anti-epileptic that works on potassium channels

A

Direct activation limits the firing of action potentials by hyperpolarising the neural membrane.
Retigabine

41
Q

Give an example of an anti-epileptic that works on potassium channels

A

Direct activation limits the firing of action potentials by hyperpolarising the neural membrane.
Retigabine

42
Q

Give an example of an anti-epileptic that works on potassium channels

A

Direct activation limits the firing of action potentials by hyperpolarising the neural membrane.
Retigabine

43
Q

Secondary epilepsy
Name 5 recognised insults

A
  • Metabolic, e.g. electrolyte/glucose disturbance.
  • Infectious, e.g. meningitis, encephalitis.
  • Autoimmune, e.g. vasculitis, limbic encephalitis, Rasmussen’s encephalitis (affecting a single cerebral hemisphere and characterised by frequent and severe seizures, hemiparesis, encephalitis and
    dementia).
  • Cerebral structural damage: lowers seizure threshold.
44
Q

Identify 3 mechanisms of cerebral structural damage that lower seizure threshold:
This is why we give prophylactic keppra for 10 days in some patients.

A

Surgery, trauma, subarachnoid/subdural haemorrhage, abnormal vasculature, e.g. AVM, cavernoma:
- blood is particularly epileptogenic, especially when it contacts the cortical surface.

Tumours: benign and malignant, whether primary or metastatic.

Demyelination.

45
Q

Give an example of an anti-epileptic that works on potassium channels

A

Direct activation limits the firing of action potentials by hyperpolarising the neural membrane.
Retigabine

46
Q

Give an example of an anti-epileptic that works on potassium channels

A

Direct activation limits the firing of action potentials by hyperpolarising the neural membrane.
Retigabine

47
Q

Give an example of an anti-epileptic that works on potassium channels

A

Direct activation limits the firing of action potentials by hyperpolarising the neural membrane.
Retigabine

48
Q

First line anti-epileptics

Generalised seizures:
Tonic clonic
Absence
Myoclonic
Tonic/atonic

A

All sodium valproate

49
Q

First line anti-epileptics

Focal seizures

A

Carbamazepine or lamotrigine

50
Q

Management of epilepsy in pregnancy

Which anti-epileptics are contraindicated in pregnancy?
Which anti-epiletics are used in pregnancy?

A
  • Sodium valproate is most strongly associated with malformations and neurodevelopmental problems and, as such, should be a drug of last resort in fertile women.
  • Phenytoin, carbamazepine and phenobarbital are all associated with a significantly increased risk of teratogenicity - older anti-epileptics
  • Lamotrigine has been well studied in pregnancy and, although it does still carry a small dose-dependent risk to the fetus, is generally the medication of choice.
  • Levetiracetam has less extensive pregnancy data, but appears to be safe.
51
Q

Management of epilepsy in pregnancy

What is important in the use of lamotrigine during pregnancy in terms of pharmacokinetics
Other medications you must ensure pregnant epileptic women is taking

A
  • Pregnancy can reduce serum lamotrigine levels, and these should therefore be monitored and the dose increased when necessary.
  • All women with epilepsy should be given daily folic acid during the preconception period and while pregnant to reduce the risk of neural tube defects.
  • Many anti-epileptic drugs induce infantile vitamin K deficiency, and the neonate should receive supplementation at birth and again at 28 days.
52
Q

Give an example of an anti-epileptic that works on potassium channels

A

Direct activation limits the firing of action potentials by hyperpolarising the neural membrane.
Retigabine

53
Q

Classification of Epilepsy
What are the 3 broad categories?
How is focal seizure classified?

A
54
Q

Alcohol withdrawal

symptoms, pathophysiology, treatment

A
  • can occur in patients who abruptly stop or significantly reduce their alcohol consumption.
  • tremors, anxiety, insomnia, and seizures.
  • pathophysiology of alcohol withdrawal involves changes in the brain’s neurotransmitter systems- gamma-aminobutyric acid (GABA) and glutamate.
  • Treatment typically involves benzodiazepines (chlordiazepoxide), which enhance GABA activity and help to prevent seizures and other complications.

My MRCP (43 decks)

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