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Neurology > Epilepsy: seizures and differentials > Flashcards

Epilepsy: seizures and differentials Flashcards

1
Q

What questions must be asked about the onset of a fall?

A
  • What were they doing? Environment etc
  • Light-head or other syncopal symptoms
  • what did they look like?
    • pallor, breathing
    • posturing of limbs, head turning
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2
Q

What must be asked about the event of a seizure?

A
  • type of movements
    • tonic phase, clonic movements
    • corpopedal spasms, rigor
  • responsiveness and awareness thoughout
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3
Q

What must be asked about the events after a seizure?

A
  • speed of recovery
  • sleepiness/disorientation
  • deficits
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4
Q

What are the epilepsy risk factors?

A
  • birth
  • development
  • seizures in past (including febrile fits)
  • head injury (including LOC)
  • family history
  • drugs
  • alcohol
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5
Q

What examination is important if a patient develops syncope?

A

Cardiovascular examination and L&S BP

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6
Q

What investigations should be carried out in someone who has fallen?

A

ECG

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7
Q

Which patients get a CT scan acutely?

A
  • clinical or radiological skull fracture
  • deteriorating GCS
  • focal signs
  • head injury with seizure
  • faiulre to be GCS 15/15 5 hours after arrival
  • suggestion og other pathologh e.g. SAH
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8
Q

Which imagins can be undertaken in someone who has fallen?

A

MRIb or CTb

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9
Q

What is the advice regarding 1st seizures and driving?

A

6 months, 5 years for HGV/PCV

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10
Q

What is the advice for driving with epilepsy

A

1 year or 3 years (if during sleep), 10 years off medication for HGV/PCV

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11
Q

Describe generalised epilepsy?

A
  • Most have genetic predisposition
  • Present in childhood and adolescence, generalised spike wave abnormalities on EEG
  • Tonic clonic, absence, myoclonic, clonic, tonic and atonic
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12
Q

When does primary generalised epilepsy present?

A

Childhood or teens

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13
Q

What is the treatment of choice for primary generalized epilepsy?

A

Sodium valproate

Lamotrigine if female of child bearing age

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14
Q

Juvenile myoclonic epilepsy presents with _____ _______ jerks, _________ seizures. The risk factors are _____ _______ and ______ ______

A

Juvenile myoclonic epilepsy presents with early morning jerks, generalised seizures. The risk factors are sleep deprivation and flashing lights

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15
Q

What is EEG useful for?

A

Identifying type of epilepsy

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16
Q

What is the underlying cause of focal onset epilepsy?

A

Underlying structural cause

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17
Q

Describe the progression of focal onset epilepsy?

A

Focal onset and can then generalise to secondary generalisation

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18
Q

What is the age of onset and treatment of focal onset epilepsy?

A

Onset at any age

Carbamazepine or lamotrigine (sodium valproate works as well)

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19
Q

What is often the result of focal onset epilepsy?

A

Complex partial seizures with hippocampal sclerosis

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20
Q

Describe the use of lamotrigine

A

Well tolerated in generalised and focal epilepsies

Takes a long time to titrate up

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21
Q

Describe the use of levetiracetam?

A

Very popular

Few interactions with other medications

Can cause mood swings

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22
Q

Descibe the use of topiramate

A

Sedation, dysphasia as side effects

Weight loss

Effective but not well tolerated

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23
Q

What anticonvulsants are more commonly used for neuropathic pain?

A

Gabapentin, pregabalin

24
Q

Which anticonvulsants induce hepatic enzymes?

A

Carbamazepine, oxcarbazepine, phenobarbitol, phenytoin, primidone, topiramate

25
Q

What is the issue with anticonvulsants that induce hepatic enzymes?

A

Can alter efficacy of combined oral contraceptive pill

Cannot use progesterone only pill

Morning after pill not adequate

26
Q

What must be taken by epileptic women looking to conceive?

A

Folic acid and vitamin K

Balance risk of uncontrolled seizures vs teratogenicity

27
Q

What is status epilepticus?

A

Recurrent epileptic seizures without full recovery of consciousness

Continuous seizure activity lasting more than 30 minutes

28
Q

What are the types of status epilepticus?

A
  • Generalised convulsive status epilepticus
  • Non convulsive status
    • Concious but in altered state
  • epilepsia partialis conntinua
    • continual focal seizures, consciousness preserved
29
Q

What are the precipitants of status?

A
  • severe metabolic disorders
    • hyponatraemia, pyridoxine deficiency
  • infection
  • head traume
  • sub-arachnoid haemorrhage
  • abrupt withdrawal of anti-convulsants
  • treating absence seizures with CBZ
    *
30
Q

Describe convulsive status

A

Generalised convulsions without cessation

31
Q

How does convulsive status cause damage?

A

Excess cerebral demand and poor substrate delivery causes lasting damage

  • respiratory insufficiency and hypoxia
  • hypotension
  • hyperthermia
  • rhabdomyolysis
32
Q

What is the management of convulsive status epilepticus?

A
  • Stabilise patient
    • ABC
  • Must identify cause
    • emergency blood tests +/- CT
  • Anti-convulsants
    • phenytoin (check levels)
    • levatiracetam (keppra)
    • valproate
    • benzodiazepines
      • if given need to go to ITU
33
Q

What conditions are commonly confused with epilepsy?

A
  • syncope
  • non-epileptic attack disorder (pseudoseizures, psychogenic non-epileptic attacks)
  • panic attacks/hyperventilation attacks
  • sleep phenomena
34
Q

List some DDx for epilepsy?

A

TIA

migraine

hypoglycaemia

Parasomnia

Paroxysmal movement disorder

cataplexy

periodic paralyses

tonic spasms of MS

35
Q

What is an epileptic seizure?

A

Abnormal synchronisation of neuronal activity

  • usually excitatory with high frequency action potentials
  • sometimes predominantly inhibitory

Interruption of normal brain activity

  • focal
  • generalised
36
Q

Why do epileptic seizures occur?

A

- too much excitation

- too little inhibition

changes;

  • cell numbers/types
    • connectivity*
    • synaptic function*
    • voltage gated ion channel function*

Genetic, acquired brain, metabolic, toxic and environmental factors

37
Q

What are the types of partial epileptic seizures?

A

Simple: without impaired consciousness

Complex: with impaired consciousness

38
Q

What are the types of generalised seizures?

A
  • absence
  • myoclonic
  • atonic
  • tonic
  • tonic clonic
39
Q

Describe the motor semiology of partial seizures?

A

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

40
Q

Describe the sensory semiology of partial seizures?

A

Somatosensory, olfactory, gustatory, visual, auditory

41
Q

Describe the psychic semiology of partial seizures?

A

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

42
Q

about __% are seizure free on monotherapy

about __% are seizure free with polytherapy

about __% have drug resistant epilepsy

A

about 55% are seizure free on monotherapy

about 10% are seizure free with polytherapy

about 35% have drug resistant epilepsy

43
Q

Activity of _____-_____ ___ channels is inhibited by many AEDs, reducing pre-synaptic excitability and the ability of action potentials to spread.

Drugs include (10)

A

Activity of voltage-gated Na+ channels is inhibited by many AEDs, reducing pre-synaptic excitability and the ability of action potentials to spread.

  1. carbamazepine
  2. oxcarbazine
  3. esilcarbazepine
  4. phenytoin
  5. felbamate
  6. lacosamide
  7. lamotrigine
  8. rufiramide
  9. topiramate
  10. zonisamide
44
Q

Activity of _____-_____ __ channels is enhanced by the AED ________, which opens these channels and stabilises the neurone- reducing excitability.

A

Activity of voltage-gated K+ channels is enhanced by the AED retigabine, which opens these channels and stabilises the neurone- reducing excitability.

45
Q

Activity of the N-type ______-_____ ____channels that trigger neurotransmiter release is inhibited by the AEDs ______ and _______, and T-type ____ channels are inhibited by the AED ________.

A

Activity of the N-type voltage-gated Ca2+ channels that trigger neurotransmiter release is inhibited by the AEDs gabapentin and pregabalin, and T-type Ca2+ ​channels are inhibited by the AED ethosuximide.

46
Q

The AED levetiracetam acts by binding to _____, interfering with _____ vesicles and inhibiting neurotransmitter ______.

A

The AED levetiracetam acts by binding to SVA2, interfering with synaptic vesicles and inhibiting neurotransmitter release.

47
Q

Which AEDs enhance the response of GABAA receptor to GABA

A

Benzodiazepines, barbiturates, felbamate, topiramate

48
Q

Which AEDs increase GABA levels

A

Tiagabine inhibits the GABA transporter, and vigabatrin is thought to inhibit GABA transaminase

49
Q

What is the initial treatment for partial seizures?

A

Carbamazepine

Lamotrigine

Oxcarbazepine

Levetiracetam

Topiramate

Sodium Valproate

50
Q

What are the add on drugs for partial seizures?

A

Gabapentin

Tiagabine

Pregabalin

Zonisamide

Vigabatrin

Clonazepam

Clobazam

51
Q

What are the older drugs not commonly used for partial seizures?

A

Phenytoin

Phenobarbitone

Primidone

52
Q

What is the treatment for generalised absence seizures?

A

Sodium Valproate

Ethosuximide

add on;

  • topiramate
    • levetiracetam*
53
Q

What is the treatment for myoclonic generalised seizures?

A

Sodium valproate

Levetiracetam

Clonazepam

add on;

  • lamotrigine
    • topiramate*
54
Q

What is the treatment for generalised atonic, tonic, generalised tonic clonic seizures?

A

sodium valproate

  • levetiracetam
  • topiramate
  • lamotrigine
55
Q

What is phenytoin used for?

A

For acute management only

56
Q

Which drug used for focal onset seizures can make primary generalised epilepsies worse?

A

Carbamazepine

57
Q

When do we give the drugs?

A

If the patient has epilepsy

If the patient had a single seizure but was at a high risk of recurrence

Only if the patient wants the drugs

Neurology (41 decks)

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