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Epilepsy 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 (Generally congenital and young)
Partial Epilepsy (Any age, due to focal brain damage)

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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

Treatment for epilepsy
Describe all first line drugs for generalized, focal and absence [3]
In which instances are abortive drugs used? [1] State what drugs these are [1]
Describe second line drugs for generalized and partial [2]

A

1st line:

  • Sodium Valproate (Anti-convulsant) for Generalised
  • Carbamazepine (Anti-convulsant) for Focal
  • Ethosuximide for Absence seizures

Abortive drugs such as lorazepam are used in generalised and status epileptics

2nd line:

  • Generalised: topiramate
  • Focal: sodium valproate
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22
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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23
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

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24
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.

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25
Alternative uses for carbamazepine [1]
As well as being an anticonvulsant it treats nerve pain in conditions such as Trigeminal Neuralgia
26
Partial seizure Frontal lobe seizures State 2 types Explain Todd's paralysis [1]
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]
27
Partial seizure Point of origin in cortex [1] Parietal lobe seizures Presentation [2]
Arising in sensory cortex Paresthesia in extremity or on face Distortion of body image
28
Why are frontal and parietal seizures indicate structural brain disease
Frontal and parietal seizures indicate structural brain disease
29
Partial seizure | Temporal lobe seizure
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
30
Partial seizure | Occipital lobe seizure
Visual hallucination eg line or flash | Tonic clonic seizure
31
Explain underlying pathogenesis of secondary generalized seizures [2] Why is there a risk of death in these type of seizures? [1]
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
32
Absent seizures Main features [2] Frequency [1] Trigger [2]
The patient (usually a child) stares vacantly, eyes may blink Many times a day with duration 5-15s Trigger: hyperventilation, photic stimulation
33
Generalized tonic-clonic seizures Main features [2] Explain why there are 2 phases Describe typical history from a secondary generalized seizure [5]
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 ```
34
Triggers for epilepsy [7]
``` Forgetting epilepsy medicine Feeling tired, stressed Sleep deprivation Alcohol Photic stimulation Menstruation Missing meals ```
35
MOA of sodium channel blockers ie the anticonvulsants on epilepsy Give examples [5]
Sodium channel blockers reduce opportunity for depolarisation * Phenytoin * Carbamazepine * Lamotrigine * Lacosamide * Rufinamide
36
Name other drugs that are used in epilepsy (besides sodium channel blockers) [4]
GABA-receptor agonist T-type CCB ie ethosuximide Glutamate blocker Levetiracetam
37
Give examples of a GABA receptor agonist [2]
Lorazepam | Valproate
38
Give an example of a glutamate blocker [1] | Which group of patients are they well suited to
Topiramate | Obese patients as weight loss inducing effect
39
# Epilepsy Give 4 example of an anti-epileptic that works on calcium channels
Ethosuximide Lamotrigine Topiramate Gabapentin
40
Give an example of an anti-epileptic that works on potassium channels
Direct activation limits the firing of action potentials by hyperpolarising the neural membrane.
41
Give an example of an anti-epileptic that works on potassium channels
Direct activation limits the firing of action potentials by hyperpolarising the neural membrane. Retigabine
42
Give an example of an anti-epileptic that works on potassium channels
Direct activation limits the firing of action potentials by hyperpolarising the neural membrane. Retigabine
43
Give an example of an anti-epileptic that works on potassium channels
Direct activation limits the firing of action potentials by hyperpolarising the neural membrane. Retigabine
44
Secondary epilepsy Name 5 recognised insults
* 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.
45
Identify 3 mechanisms of cerebral structural damage that lower seizure threshold: This is why we give prophylactic keppra for 10 days in some patients.
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.
46
Classification of Epilepsy What are the 3 broad categories? How is focal seizure classified?
46
Give an example of an anti-epileptic that works on potassium channels
Direct activation limits the firing of action potentials by hyperpolarising the neural membrane. Retigabine
47
Give an example of an anti-epileptic that works on potassium channels
Direct activation limits the firing of action potentials by hyperpolarising the neural membrane. Retigabine
48
Give an example of an anti-epileptic that works on potassium channels
Direct activation limits the firing of action potentials by hyperpolarising the neural membrane. Retigabine
49
# First line anti-epileptics Generalised seizures: Tonic clonic Absence Myoclonic Tonic/atonic
All sodium valproate
50
# First line anti-epileptics Focal seizures
Carbamazepine or lamotrigine
51
# Management of epilepsy in pregnancy Which anti-epileptics are contraindicated in pregnancy? Which anti-epiletics are used in pregnancy?
* 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.
52
# 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
* 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.
53
Give an example of an anti-epileptic that works on potassium channels
Direct activation limits the firing of action potentials by hyperpolarising the neural membrane. Retigabine
54
Give an example of an anti-epileptic that works on potassium channels
Direct activation limits the firing of action potentials by hyperpolarising the neural membrane. Retigabine
55
Give an example of an anti-epileptic that works on potassium channels
Direct activation limits the firing of action potentials by hyperpolarising the neural membrane. Retigabine
56
Give an example of an anti-epileptic that works on potassium channels
Direct activation limits the firing of action potentials by hyperpolarising the neural membrane. Retigabine
57
Give an example of an anti-epileptic that works on potassium channels
Direct activation limits the firing of action potentials by hyperpolarising the neural membrane. Retigabine
58
Give an example of an anti-epileptic that works on potassium channels
Direct activation limits the firing of action potentials by hyperpolarising the neural membrane. Retigabine
59
Give an example of an anti-epileptic that works on potassium channels
Direct activation limits the firing of action potentials by hyperpolarising the neural membrane. Retigabine
60
Give an example of an anti-epileptic that works on potassium channels
Direct activation limits the firing of action potentials by hyperpolarising the neural membrane. Retigabine
61
Give an example of an anti-epileptic that works on potassium channels
Direct activation limits the firing of action potentials by hyperpolarising the neural membrane. Retigabine
62
Give an example of an anti-epileptic that works on potassium channels
Direct activation limits the firing of action potentials by hyperpolarising the neural membrane. Retigabine
63
Give an example of an anti-epileptic that works on potassium channels
Direct activation limits the firing of action potentials by hyperpolarising the neural membrane. Retigabine
64
Give an example of an anti-epileptic that works on potassium channels
Direct activation limits the firing of action potentials by hyperpolarising the neural membrane. Retigabine
65
Give an example of an anti-epileptic that works on potassium channels
Direct activation limits the firing of action potentials by hyperpolarising the neural membrane. Retigabine
66
Give an example of an anti-epileptic that works on potassium channels
Direct activation limits the firing of action potentials by hyperpolarising the neural membrane. Retigabine
67
Give an example of an anti-epileptic that works on potassium channels
Direct activation limits the firing of action potentials by hyperpolarising the neural membrane. Retigabine

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