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EPILEPSY Flashcards

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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
management for west's syndrome/ infantile spasms
corticosteroids or vigabatrin PERIPHERAL VISUAL LOSS (first line if tuberous sclerosis)
26
absence epilepsy in children
stare blank into space - eyes may flutter or roll up characteristic EEG abnormalities - 3-Hz generalised, symmetrical spike-wave abnormalities
27
juvenile myoclonic epilepsy (Janz syndrome)
``` age of onset - 10-20 occurs after eaking - myoclonic - tonic-clonic - absence ``` polyspike waves
28
causes of refractory epilepsy
non compliance pseudoseizures/non epileptic attaks ass structural brain disease - dev abnormlaitits alcohol and lifestyle
29
when to stat antiepileptics after first seizure
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
30
first line treatment for patients with tonic clonic generalised seizure
sodium valporate boys lamotrigine women childbearing age
31
first treatment used for focal seizures
carbamzepine
32
second line treatment for patients with generalised seizure
lamotrigine or carbamazepine
33
management for myoclonic seizures
sodium valproate second line: clonazepam, lamotrigine
34
what type of seizures can carbamazepine exarcerbate
myoclonic absence
35
how to differentiate between a pseudo seizure and general seizure
Elevated serum prolactin 10 to 20 minutes after an episode in an actual seizure
36
factors precipitating pseudoseizures
- pelvic thrusting - family member with epilepsy - much more common in females - crying after seizure - don't occur when alone - gradual onset
37
what is lennox-gastaut syndrome
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
what is benign rolandic epilepsy
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
features of absence seizures
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
Mx for absence seizures
sodium valproate and ethosuximide are first-line treatment | good prognosis - 90-95% become seizure free in adolescence
41
causes of secondary epilepsy
``` tuberous sclerosis neurofibroamtosis brain tumor stroke hypoglycaemia cerebral palsy mitochondrial diseases ```
42
what is secondary epilepsy
when it starts off as a focal seizure then it becomes generalised
43
other causes of seizures
febrile convulsions alcohol withdrawal seizures psychogenic non-epileptic seizures
44
what is Psychogenic non-epileptic seizures
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
features of alochol withdrawal seizures
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
when do you start antiepileptics
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
epilepsy and driving
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
MOA of sodium valoprate
Increases GABA activity
49
adverse effects of sodium valoprate
``` ncreased appetite and weight gain alopecia: regrowth may be curly P450 enzyme inhibitor ataxia tremor hepatitis pancreatitis thrombocytopaenia teratogenic (neural tube defects) ```
50
MOA of carbamazepine
Binds to sodium channels increasing their refractory period
51
SE of carbamazepine
``` 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
MOA of lamotrigine
Sodium channel blocker
53
SE of lamotrigine
- SJS - risk of interacting with other medications such as OCP - risk of rash - risk of harm to fetus if she falls pregnant
54
MON of phenytoin
increase sodium uptake increasing refracotry period
55
SE of phenytoin
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
non epileptic seizures
EEG normal patients look like they having seizures more frequent no tongue biting or incontinence
57
status epilepticus treatment
- 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
ABG on seizure
resp arrest - not much oxygen getting into body lactate high acidosis
59
factors favouring pseudoseizures
- pelvic thrusting - family member with epilepsy - much more common in females - crying after seizure - don't occur when alone - gradual onset
60
generalised tonic-clonic seizures Mx
sodium valproate | second line: lamotrigine, carbamazepine
61
Myoclonic seizures** | MX
sodium valproate | second line: clonazepam, lamotrigine
62
Focal seizures | MX
Focal seizures 1st line carbamazepine or lamotrigine second line: levetiracetam, oxcarbazepine or sodium valproate
63
which drug exacerbates absence and myoclonic seizures
carbamzepine
64
what is idiopathic generalised epilepsy
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
what increases the risk of fits in juvenile myoclonic/idiopathic generalised epilepsy
sleep deprivation and alcohol significantly increase the risk of fits
66
First line Mx for Childhood absence epilepsy, juvenile absence epilepsy or other absence epilepsy syndromes
ethosuximide to girls sodium valpoate for boys
67
first line Mx of dravet syndrome
topiramate for girls sodium valporate for boys
68
apart from pharm Mx what other interventions are available
- psychological intervention - vagus nerve stimualtion - > reduce frequency of seizures
69
if someone is continually fitting a CT is needed what do u do
liase with anaesthetist to do CT under intubation
70
Mx of cerebral mets causing fits
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
what is traumatic tap adn what is seen
when u do LP and than pt moves vigorously shows raised CSF protein
72
causes of status epilepticus
epilepsy recent medication reduction/with- drawal intercurrent illness metabolic derangement progressive disease
73
complications of status epilepticus
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
what bloods are done for status epilepticus
``` U&Es Calcium glucose Mg2+ FBC clotting and blood cultures ```
75
Adverse effects of sodium valproate
``` 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
Causes of seizures
``` epilepsy alcohol intoxication infections head trauma drugs -MAOI, illicit hypoxia degenerative disease sickle cell crisis metabolic disturbance intracranial tumours toxins - CO ```

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