EPILEPSY Flashcards

1
Q

define seizure

A

signs or symptoms due to abnormal excessive or synchronous neuronal activity in the brain

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2
Q

define epilepsy

A

neurological disorder in which a person experiences recurring seizures

At least two unprovoked seizures occurring more than 24 hours apart

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3
Q

define status epilepticus

A

prolonged convulsive seizure lasting for 5 minutes or longer, or recurrent seizures one after the other without recovery in between

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4
Q

causes of epilepsy

A

structural - stroke, trauma, malformation

genetic - ie Dravet syndrome

infectious - meningitis, TB, cerebral malaria, HIV and Zika virus

Metabolic - porphyria, pryridoxine deficiency

immune

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5
Q

risk factors for epilepsy

A

Premature birth.

Complicated febrile seizures.

A genetic condition that is known to be associated with epilepsy, such as tuberous sclerosis or neurofibromatosis.

Brain development malformations

A family history of epilepsy or neurologic illness.

Head trauma, infections (for example meningitis, encephalitis), or tumours

Comorbid conditions such as cerebrovascular disease or stroke — more common in older people.

Dementia and neurodegenerative disorders (people with Alzheimer’s disease are up to ten times more likely to develop epilepsy than the general population).

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6
Q

complications of epilepsy

A

sudden unexpected death in epilepsy

injuries

depression and anxiety disorders

absence from school or work

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7
Q

how to assess a patient with seizure

A

Any subjective symptoms at the start of the seizure (aura) — suggestive of focal epilepsy; these may provide information on where the seizure might arise.

Any potential triggers, for example sleep deprivation, stress, light sensitivity, or alcohol use.

specific features about the seizure

Residual symptoms after the attack (post-ictal phenomena), such as drowsiness, headaches, amnesia, or confusion (usually occur only after generalised tonic and/or clonic seizures).

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8
Q

what are the specific features of the seizure

A

Short-lived (less than 1 minute), abrupt, generalised muscle stiffening (may cause a fall) with rapid recovery — suggestive of tonic seizure.

Generalised stiffening and subsequent rhythmic jerking of the limbs, urinary incontinence, tongue biting —suggestive of a generalised tonic-clonic seizure.

Behavioural arrest — indicative of absence seizure.

Sudden onset of loss of muscle tone — suggestive of atonic seizure.

Brief, ‘shock-like’ involuntary single or multiple jerks —suggestive of myoclonic seizure

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9
Q

what physical examination will one do for a patient who experienced a seizure

A

Cardiac, neurological, and mental state, and a developmental assessment if appropriate.

Examination of the oral mucosa to identify lateral tongue bites.

Identification of any injuries sustained during the seizure.

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10
Q

what blood tests will be done is you suspect epilepsy

A
  • FBC
  • U&Es
  • LFTs
  • glucose
  • calcium
  • (ECG).
  • blood gases
  • set up cardiac monitor and pulse oximetry
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11
Q

DD for epilepsy

A
  • Vasovagal syncope.
  • Cardiac arrhythmias.
  • Panic attacks with hyperventilation.
  • Non-epileptic attack disorders (psychogenic non-epileptic seizures, dissociative seizures, or pseudoseizures).
  • Transient ischaemic attack.
  • Migraine.
  • Medication, alcohol, or drug intoxication.
  • Sleep disorders.
  • Movement disorders.
  • Hypoglycaemia and metabolic disorders.
  • Transient global amnesia.
  • Delerium or dementia — altered awareness may be mistaken for seizure activity.
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12
Q

DD for epilepsy in children

A
  • Febrile convulsions.
  • Breath-holding attacks.
  • Night terrors.
  • Stereotyped/ritulistic behaviour — especially in those with a learning disability.
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13
Q

how do you manage someone with sus epilepsy

A

1) urgently refer if its first epileptic seizure
2) give info sheet - record future seizures
3) stop driving until confrim of diagnosis, dont do heaby machinery

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14
Q

what do you do if someone has a tonic clonic seizure less than 5 minutes

A

Look for an epilepsy identity card or jewellery.
Protect them from injury by:
Cushioning their head, for example with a pillow.
Removing glasses if they are wearing them.
Removing harmful objects from nearby, or if this is not possible, moving the person away from immediate danger.
Do not restrain them or put anything in their mouth.
When the seizure stops, check their airway and place them in the recovery position.
Observe them until they have recovered.
Examine for, and manage, any injuries.

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15
Q

what do you do if someone has tonic clonic seizure lasting more than 5 mins or 3 seizures within an hour

A

Treat with one of the following:
- Buccal midazolam as first-line treatment in the community.

  • Rectal diazepam if preferred, or if buccal midazolam is not available.
  • Intravenous lorazepam if intravenous access is already established and resuscitation facilities are available.
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16
Q

features of temporal lobe epilepsy (partial epilpesy)

frontal

parietal

occipital

A

Hallucinations (auditory/gustatory/olfactory)
Epigastric rising/Emotional
Automatisms (lip smacking/grabbing/plucking)
Deja vu/Dysphasia post-ictal)

Head/leg movements, posturing, post-ictal weakness, Jacksonian march

Paraesthesia

Floaters/flashes

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17
Q

what is jacksonian epilepsy

A

starts in one place and spreads

begin in the corner of mouth, the thumb, index finger or the great toe

then movements spreads on the face or ascend the limb (Jacksonian march)

the affected limb may remain temporarily weak (Todd’s paralysis)

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18
Q

what is epilpesia partialis continua

A

children under 3 months or adults over 18 years of age

rare condition involving recurrent and sometimes intractable focal onset seizures associated with retained awareness. EPC seizures can occur over hours, days, or even years. The disease can manifest in a variety of ways, a few of which include myoclonic epilepsy, localized myoclonus, Jacksonian epilepsy, or sensorimotor clonic seizures.

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19
Q

what is febrile convulsions

A

with fever

less than 15 mins

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20
Q

what is infantile spasms (West’s syndrome)
features
Ix
Mx

A

typically present in the 3-12 months of life
- more common in males

TRIAD

  • shock-like flexion of arms, head and neck with drawing up of the knees (salaam attaack)
  • multiple bursts of violent flexor spasms last 1/2 s but repeated maybe upto 50 times - baby cry
  • progressive learning dfifficulties

most undergo neurodegenerative neuro-encephelatic process.

Ix
EEG abnormality - hypsarrhythmia and burst suppression
CT - diffuse or localised brain disease

Mx
corticosteroids and vigabatrin PERIPHERAL VISUAL LOSS (first line if tuberous sclerosis)

  • poor prognosis
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21
Q

name of inhibitory neurotransmitter and receptor

A

GABA

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22
Q

types of generalised seizures

A
tonic - stiff flexed
atonic - relaxed
clonic - convulsions
tonic-clonic - stiff and they fit
myoclonic - short muscle twitches
absence - spaced out
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23
Q

what is generalised seizures

A

lose consciousness and involves both hemispheres

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24
Q

diagnosis of seizures

A

MRI
CT

EEG

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25
Q

management for west’s syndrome/ infantile spasms

A

corticosteroids or vigabatrin PERIPHERAL VISUAL LOSS (first line if tuberous sclerosis)

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26
Q

absence epilepsy in children

A

stare blank into space - eyes may flutter or roll up

characteristic EEG abnormalities - 3-Hz generalised, symmetrical spike-wave abnormalities

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27
Q

juvenile myoclonic epilepsy (Janz syndrome)

A
age of onset - 10-20
occurs after eaking
- myoclonic
- tonic-clonic
- absence

polyspike waves

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28
Q

causes of refractory epilepsy

A

non compliance
pseudoseizures/non epileptic attaks
ass structural brain disease - dev abnormlaitits
alcohol and lifestyle

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29
Q

when to stat antiepileptics after first seizure

A

after the first seizure if any of the following are present:

  • the patient has a neurological deficit
  • brain imaging shows a structural abnormality
  • the EEG shows unequivocal epileptic activity
  • the patient or their family or carers consider the risk of having a further seizure unacceptable
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30
Q

first line treatment for patients with tonic clonic generalised seizure

A

sodium valporate boys

lamotrigine women childbearing age

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31
Q

first treatment used for focal seizures

A

carbamzepine

32
Q

second line treatment for patients with generalised seizure

A

lamotrigine or carbamazepine

33
Q

management for myoclonic seizures

A

sodium valproate

second line: clonazepam, lamotrigine

34
Q

what type of seizures can carbamazepine exarcerbate

A

myoclonic

absence

35
Q

how to differentiate between a pseudo seizure and general seizure

A

Elevated serum prolactin 10 to 20 minutes after an episode in an actual seizure

36
Q

factors precipitating pseudoseizures

A
  • pelvic thrusting
  • family member with epilepsy
  • much more common in females
  • crying after seizure
  • don’t occur when alone
  • gradual onset
37
Q

what is lennox-gastaut syndrome

A

Difficult to treat - 1-3 years

Multiple seizure types

  1. most common atonic - mistaken for falls
  2. atypical (subtle) absences lasting 10s to several minutes - head nodding/rapid blinking
  3. tonic seizure may happen only at night

Poor prognosis e neurodevelopmental arrest or regression

slow generalised spike and wave (1-3Hz)

Mx - ketogenic diet

38
Q

what is benign rolandic epilepsy

A

common in children M>F -> 4-10yrs
outgrow it by puberty ‘benign’
seizures originate in the ‘rolandic’ region called centerotemporal

often start during sleep or when just about to wake up with:

  • feeling if tingling on one side of the mouth
  • may involve throat - speech inlcear/throaty/gurgling noises
  • can cause clonic or tonic to one side of mouth or face
  • can spread and affect the whole body

Ix
EEG - posterior sharp waves or occipital discharges

39
Q

features of absence seizures

A

absences last a few seconds and are associated with a quick recovery

seizures may be provoked by hyperventilation or stress

the child is usually
unaware of the seizure
they may occur many times a day
EEG: bilateral, symmetrical 3Hz spike and wave pattern

40
Q

Mx for absence seizures

A

sodium valproate and ethosuximide are first-line treatment

good prognosis - 90-95% become seizure free in adolescence

41
Q

causes of secondary epilepsy

A
tuberous sclerosis
neurofibroamtosis
brain tumor
stroke
hypoglycaemia
cerebral palsy mitochondrial diseases
42
Q

what is secondary epilepsy

A

when it starts off as a focal seizure then it becomes generalised

43
Q

other causes of seizures

A

febrile convulsions
alcohol withdrawal seizures
psychogenic non-epileptic seizures

44
Q

what is Psychogenic non-epileptic seizures

A

previously termed pseudoseizures, this term describes patients who present with epileptic-like seizures but do not have characteristic electrical discharges

REMAIN CONSCIOUS

NO POST ICTAL STATE

PSYCHIATRIC COMORBIDITIES

patients may have a history of mental health problems or a personality disorder

45
Q

features of alochol withdrawal seizures

A

ccur in patients with a history of alcohol excess who suddenly stop drinking, for example following admission to hospital

chronic alcohol consumption enhances GABA mediated inhibition in the CNS (similar to benzodiazepines) and inhibits NMDA-type glutamate receptors.Alcohol withdrawal is thought to be lead to the opposite (decreased inhibitory GABA and increased NMDA glutamate transmission)

the peak incidence of seizures is at around 36 hours following cessation of drinking

patients are often given benzodiazepines following cessation of drinking to reduce the risk

46
Q

when do you start antiepileptics

A

second epileptic seizure
the patient has a neurological deficit
brain imaging shows a structural abnormality
the EEG shows unequivocal epileptic activity
the patient or their family or carers consider the risk of having a further seizure unacceptable

47
Q

epilepsy and driving

A

generally patients cannot drive for 6 months following a seizure. For patients with established epilepsy they must be fit free for 12 months before being able to drive

48
Q

MOA of sodium valoprate

A

Increases GABA activity

49
Q

adverse effects of sodium valoprate

A
ncreased appetite and weight gain
alopecia: regrowth may be curly
P450 enzyme inhibitor
ataxia
tremor
hepatitis
pancreatitis
thrombocytopaenia
teratogenic (neural tube defects)
50
Q

MOA of carbamazepine

A

Binds to sodium channels increasing their refractory period

51
Q

SE of carbamazepine

A
P450 enzyme inducer
dizziness and ataxia
drowsiness
leucopenia and agranulocytosis
syndrome of inappropriate ADH secretion
visual disturbances (especially diplopia)
skin rash 
N/V
inactivates the OCP
52
Q

MOA of lamotrigine

A

Sodium channel blocker

53
Q

SE of lamotrigine

A
  • SJS
  • risk of interacting with other medications such as OCP
  • risk of rash
  • risk of harm to fetus if she falls pregnant
54
Q

MON of phenytoin

A

increase sodium uptake increasing refracotry period

55
Q

SE of phenytoin

A

Acute

  • initially: dizziness, diplopia, nystagmus, slurred speech, ataxia
  • later: confusion, seizures

Chronic
common: gingival hyperplasia (secondary to increased expression of platelet derived growth factor, PDGF), hirsutism, coarsening of facial features, drowsiness
megaloblastic anaemia (secondary to altered folate metabolism)
peripheral neuropathy
enhanced vitamin D metabolism causing osteomalacia
lymphadenopathy
dyskinesia

56
Q

non epileptic seizures

A

EEG normal

patients look like they having seizures

more frequent
no tongue biting or incontinence

57
Q

status epilepticus treatment

A
  • secure the airway, administer O2, support respiration if necessary
  • assess CVS status
  • obtain IV access
  • check glucose - if hypoglycaemic administer IV 50ml of 50% glucose
  • administer IV pabrinex - if alcoholism or malnutrition is suspected
  • bloods
  1. IV lorazepam 4mg, rate = 2mg/minute; repeat once after 15 minutes
  2. IV lorazepam - 10mg at a rate of 2-5mg/minute

after 10 minutes

  • IV phenytoin 20mg/kg by slow IV infusion at a max rate 50 mg/min with ECG monitoring
  • measure serum levels at 2h/4h

If no response (‘refractory status’) within 45 minutes from onset, then the best way to achieve rapid control of seizure activity is induction of general anaesthesia.

PR diaszepam IM midazolam

twice

ITU

58
Q

ABG on seizure

A

resp arrest - not much oxygen getting into body
lactate high

acidosis

59
Q

factors favouring pseudoseizures

A
  • pelvic thrusting
  • family member with epilepsy
  • much more common in females
  • crying after seizure
  • don’t occur when alone
  • gradual onset
60
Q

generalised tonic-clonic seizures Mx

A

sodium valproate

second line: lamotrigine, carbamazepine

61
Q

Myoclonic seizures**

MX

A

sodium valproate

second line: clonazepam, lamotrigine

62
Q

Focal seizures

MX

A

Focal seizures
1st line carbamazepine or lamotrigine
second line: levetiracetam, oxcarbazepine or sodium valproate

63
Q

which drug exacerbates absence and myoclonic seizures

A

carbamzepine

64
Q

what is idiopathic generalised epilepsy

A

A group of epileptic disorders that are believed to have a strong underlying genetic basis and so often have a family history of epilepsy.

Patients with IGE are typically otherwise normal and have no structural brain abnormalities.

IGE tends to manifest itself between early childhood and adolescence although it can be diagnosed later.

Seizure types include absence, myoclonus and primary generalized tonic-clonic.

65
Q

what increases the risk of fits in juvenile myoclonic/idiopathic generalised epilepsy

A

sleep deprivation and alcohol significantly increase the risk of fits

66
Q

First line Mx for Childhood absence epilepsy, juvenile absence epilepsy or other absence epilepsy syndromes

A

ethosuximide to girls

sodium valpoate for boys

67
Q

first line Mx of dravet syndrome

A

topiramate for girls

sodium valporate for boys

68
Q

apart from pharm Mx what other interventions are available

A
  • psychological intervention
  • vagus nerve stimualtion
  • > reduce frequency of seizures
69
Q

if someone is continually fitting a CT is needed what do u do

A

liase with anaesthetist to do CT under intubation

70
Q

Mx of cerebral mets causing fits

A

liase w oncologist/radiotherapist

administer IV dexamethasone and start oral steroid course to reduce cerebral oedema around lesions

introduce anti-convulsant meds

consider restaging of pt via CT or FDG PET

Analgesia as needed

71
Q

what is traumatic tap adn what is seen

A

when u do LP and than pt moves vigorously

shows raised CSF protein

72
Q

causes of status epilepticus

A

epilepsy
recent medication reduction/with- drawal
intercurrent illness metabolic derangement
progressive disease

73
Q

complications of status epilepticus

A

Cerebral oedema + i ICP
Cerebral damage secondary to hypoxia, seizure, or metabolic derangement
Cerebral venous thrombosis
Cerebral haemorrhage and infarction

Hyper/hypotension
Cardiac arrhythmias
Cardiogenic shock
Cardiac arrest
Hypoxia (often severe)
Aspiration pneumonia
Pulmonary oedema
Pulmonary embolism
Respiratory failure
Dehydration
Electrolyte derangement (especially d glucose,
d Na, d Mg, i K)
Metabolic acidosis
Hyperthermia
Rhabdomyolysis
Pancreatitis
Acute renal failure (often acute tubular necrosis)
Acute hepatic failure
Disseminated intravascular coagulation
Fractures
74
Q

what bloods are done for status epilepticus

A
U&Es
Calcium
glucose
Mg2+
FBC
clotting and blood cultures
75
Q

Adverse effects of sodium valproate

A
teratogenic 
P450 inhibitor
gastrointestinal: nausea
increased appetite and weight gain
alopecia: regrowth may be curly
ataxia
tremor
hepatotoxicity
pancreatitis
thrombocytopaenia
hyponatraemia
hyperammonemic encephalopathy: L-carnitine may be used as treatment if this develops
76
Q

Causes of seizures

A
epilepsy
alcohol intoxication
infections
head trauma
drugs -MAOI, illicit
hypoxia
degenerative disease
sickle cell crisis
metabolic disturbance
intracranial tumours 
toxins - CO