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stupid brain CA > seizure/epilepsy > Flashcards

seizure/epilepsy Flashcards

1
Q

what is a seizure

A

transient occurrence of S&s +/- symptoms due to abnormal excessive/synchronous neuronal activity in brain

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2
Q

what is epilepsy

A

disease of brain defined by any of

  • at least 2 unprovoked seizures happening > 24h apart
  • one unprovoked seizure and probability of further seizures similar to general recurrence risk after 2 unprovoked seizures occurring over the next 10 years
  • diagnosis of epilepsy syndrome
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3
Q

what is acute symptomatic seizure

A
  • immediately recognisable stimulus
  • occur in presence/closely timely association with acute brain insult
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4
Q

what is remote symptomatic seizure

A
  • absence of potentially responsible clinical condition
  • occur 1 wk after disorder that incrase risk of developing epilepsy
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5
Q

what is unprovoked seizure

A

no direct stimulus or acute seizure that last longer than normal

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6
Q

what are non-epileptic events

A
  • abnormal paroxysmal psychic, sensory, motor manifestations which resemble epileptic seizures but not abnormal epileptiform discharges
  • types

1) psychogenic non-epileptic seizures (PNES)

  • partial alteration in level of consciousness with partial preservation of awareness
  • caused by stressful psychological experiences or emotional trauma

2) physiological non-epileptic event

  • symptoms of paroxysmal systemic disorder
  • examples: convulsive syncope, hypoglycemia, migraine order, intoxication, panic attack
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7
Q

risk for recurrent seizure

A

1) lower risk: single seizure normal EEG, normal brain scan
2) higher risk: previous seizure, epileptiform EEG, abnormal brain scan

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8
Q

pathophysiology of seizure

A
  • synchronised paroxysmal discharges occuring in large population of neurons within cortex starting from defined regions (foci)
  • unbalanced excitatory & inhibitory receptor/ion channel function which favour depolarisation = dysregulated discharge
  • split into 2 components

1) hyperexcitability
2) hyper synchronisation

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9
Q

pathophysiology of seizure - hyperexcitability

A
  • enhanced predisposition of neurons to depolarise
  • causes

1) voltage gated K+, Na+, Ca2+, Cl- channels
2) abnormalities in intra/extracellular substances
3) excess excitatory neurotransmitters (e.g. glutamate bind to NMDA receptor -> open Ca2+ ion channel)
4) insufficient inhibitory neurotransmitters (GABA bind to GABA receptor = open Cl- ion channel)

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10
Q

pathophysiology of seizure - hyper synchronisation

A

hippocampal sclerosis

  • intrinsic reorganisation of local circuits (hippocampus, neocortex, thalamus)
  • contribute to synchronisation and promote generation of epileptiform activity
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11
Q

aetiology of acute seizure

A

1) metabolic

  • low Na, Ca, Mg, FBG

2) toxic substances/drugs

  • alcohol, drugs, benzodiazepine withdrawal

3) structural

  • stroke, traumatic brain injury

4) seizure triggers

  • hyperventilation, photo stimulation, physical/emotional stress, sleep deprivation, sensory stimuli, infection, hormonal change, drugs
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12
Q

classifications of seizures based on mode of onset

A

1) focal onset: 1 hemisphere
2) generalised onset: both hemisphere
3) secondary generalised: start with 1 hemisphere then spread to other

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13
Q

tldr phases of seizure onset

A

1) prodromal
2) early ictal (aura)
3) ictal
4) postictal

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14
Q

prodromal for seizure onset

A
  • before seizure
  • subjective feeling/sensation
  • symptoms: confusion, anxiety, irritability, headache, tremor, mood disturbances
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15
Q

early ictal (Aura) for seizure onset

A
  • not everyone w epilepsy experience aura
  • common symptoms
    ** bitter acidic taste, dejavu, dizzy, hallucination, psych problems, numbness, ringing/buzzing sound, vision problems
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16
Q

ictal for seizure onset

A

symptoms

  • stiffening, chewing, confusion, difficulty breathing, drooling, twitching in one direction, inability to move/speak, pupil dilation
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17
Q

postictal for seizure onset

A
  • recovery period after seizure
  • duration depends on seizure type, severity and regions of brain affected
  • common symptoms: arm/leg weakness, body sore, confusion, malaise, memory loss, HTN, headache, nausea, thirst
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18
Q

clinical presentation of focal onset

A

1) motor symptoms

  • clonic movement (twitch/jerk) of arm, shoulder, face, leg
  • speech arrest

2) sensory

  • numbness/tingling
  • visual disturbances (flashing lights)
  • rising epigastric sensation

3) autonomic symptoms

  • sweating, salivating, pallor, BP, HR

4) psychic (somatosensory) symptoms

  • flashback
  • visual, auditory, gustatory, olfactory hallucination
  • affective symptoms: fear, depression, anger, irritability
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19
Q

types of generalised seizures

A

1) tonic clonic (GTC, grand mal)
2) clonic
3) tonic
4) myoclonic
5) absence (pepti mal)
6) atonic
7) partial seizure

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20
Q

tonic clonic (GTC, grand mal) clinical presentation

A

1) tonic phase

  • stiffening of limbs
  • decrease/lack of breathing
  • cyanosis of nails/lips/face that returns during clonic phase

2) clonic phase

  • last 1 min
  • occur after brain hyperpolarised and insensitive to stimuli
  • possible symptoms
    ** incontinence
    ** biting of tongue/inside mouth
    ** noisy/laboured breathing

3) after

  • headache, lethargic, confused, sleepy
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21
Q

clonic clinical presentation

A
  • clonic jerking (asymmetrical, irregular)
  • most frequent in young
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22
Q

tonic clinical presentation

A
  • sudden loss of consciousness & rigid posture of entire body (10 - 20s)
  • characteristic of Lennox-Gaustat syndrome
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23
Q

myoclonic clinical presentation

A

rapid, brief contraction of bodily muscles (bilateral but can be unilateral)

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24
Q

absence (petit mal) clinical presentation

A
  • abrupt lapse in awareness, triggered by physical exertion, less erratic
  • mistaken as persistent staring
  • more common in children
  • only few seconds, no sfter effect
  • not preceded by aura
  • characteristic EEG pattern: 3Hz spike waves
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25
Q

partial seizure clinical presentation

A
  • simple: consciousness not impaired
  • complex: consciousness impaired
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26
Q

components of seizure diagnosis

A

1) history taking
2) neurologic examination
3) concomitant medical conditions

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27
Q

history taking for seizure diagnosis

A
  • onset, duration, symptoms
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28
Q

neurologic examination for seizure diagnosis

A

1) scalp EEG

  • epileptic discharges: generalised all regions affected, partial only some regions affected
  • limitations
    ** normal EEG X exclude possibility of epilepsy
    ** normal person can have abnormal EEG
    ** Expensive, labour intensive

2) MRI w gadolinium

  • indication: adult w first seizure, pt w focal neurologic deficit, suggestion of focal onset

3) biochemical/toxicology

  • rule out electrolyte abnormality
  • CK raised after GTC
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29
Q

tldr nonpharmaco for seizure treatment

A

1) ketogenic diet
2) vagus nerve stimulator (VNS)
3) responsive neurostimulator system (RNS)
4) epilepsy surgery
5) seizure diary

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30
Q

ketogenic diet for seizure treatment

A

1) indication

  • X tolerate or X respond to ASM treatment

2) low carbohydrates, high fat diet

  • induce ketosis, prevent seizures

3) limitations

  • challenging to adhere long term
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31
Q

vagus nerve stimulator for seizure trearment

A
  • indication: intractable focal seizure, X respond well to ASM
  • stimulator send electrical stimulus
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32
Q

responsive neurostimulator system (RNS) for seizure treatment

A
  • indication: pt w focal seizures who have
    1) undergone testing that localised ≤ 2 epileptogenic foci -> 2 foci causing seizure
    2) not responsive to ≥ 2 ASM
    3) frequent and disabling symptoms
  • continuously monitor electrical activity in brain -> deliver brief pulses of electrical stimulation when it detects epileptiform activity that can lead to a seizure
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33
Q

epilepsy surgery

A

indication

  • last line for focal seizure
  • early therapy for epileptic syndrome
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34
Q

seizure diary for seizure treatment

A
  • seizure frequency and type
  • how long each seizure last
  • changes in AED
  • AED SE
  • seizure triggers
35
Q

first aid for GTC

A
  • ease person to floor
  • turn person gently to side for them to breath
  • clear area of hards/sharps
  • put something soft under head
  • remove eyewear
  • loosen anything around neck
  • time seizure, call 995 if ≥ 5 mins
36
Q

aetiology for epilepsy

A

1) Structural

  • hippocampus sclerosis, brain tumour, vascular malformation, glial scarring (stroke, traumatic brain injury)

2) genetic/presumed genetic

  • Dravet syndrome with SCN1A mutations

3) neurodegenerative

  • Alzheimer

4) metabolic
5) infectious

37
Q

types of epileptic syndromes

A

1) electroclinical syndromes

  • infancy: West syndrome, Dravet syndrome
  • childhood: febrile syndrome plus, Lennox-gaustat syndrome, childhood absence epilepsy
  • adult: JME, PME, epilepsy w GTC seizures alone

2) distinctive constellation

  • mesial temporal lobe epilepsy w hippocampal sclerosis

3) epilepsies attributed to and organised by structural metabolic causes

  • malformation of cortical development tuberous sclerosis tumour trauma stroke

5) epilepsies of unknown causes

38
Q

treatment algorithm

A

1) diagnosis -> begin treatment with 1st ASD based on seizure type, comorbidities, SE
2) evaluate if seizure is controlled

2.1) if seizure is controlled check if can control SE

  • if can control SE then assess if optimal QoL
    ** optimal QoL: continue treatment, re-evaluate again in 2 yrs, if controlled then can consider removing ASD, if not controlled then (2)
    ** not optimal QoL: explore QoL issue, if cmi then (2)
  • if cannot control SE then decrease ASD dose and (2)

2.2) if seizure not controlled then check if can tolerate SE

2.2.a) can: increase ASD dose then repeat (2)
2.2.b) cannot: decrease 1st ASD dose then add 2nd ASD -> re-evaluate again if seizure free

  • if controlled: then remove 1st ASD and repeat (2)
  • if not controlled then check if can tolerate SE
    ** can tolerate SE: increase dose of 2nd ASD, check for interactions and compliance then (2.2b)
    ** cannot tolerate SE: remove least effective ASD, add another ASD and evaluate if seizure free, if seizure free then continue or (2.2.b), if not seizure free then check diagnosis/change treatment options
39
Q

phenytoin general

A
  • high interindividual variability
  • narrow therapeutic range so need TDM
40
Q

phenytoin indication

A

focal seizure

41
Q

phenytoin MOA

A

inhibit voltage gated Na+ channel

42
Q

phenytoin PK - absorption

A

completely absorbed (F=1) but slow

  • reduce F by

1) high dose > 400mg/dose
2) interaction with enteral feeds (nasogastric tube for delivery)

  • 2 hrs apart between enteral feed and phenytoin
43
Q

phenytoin PK - distribution

A
  • Vd = 0.7 L/kg
  • highly albumin bound
    ** increase phenytoin concentration when
    1) low albumin
    2) displace by drugs that are highly protein bound
44
Q

phenytoin PK - metabolism

A

CYP2C, CYP3A, UGT

45
Q

phenytoin PK - elimination

A

1) zero order kinetics

  • concentration increment not proportionate to dose increment

2) capacity limited clearance

  • CI inversely proportionate to concentration
46
Q

phenytoin serum concentration measurement

A

corrected phenytoin levels

  • corrected = observed/[albumin coefficient (albumin level/10) + 0.1]
  • albumin coefficient
    ** CrCl ≥ 10: x = 0.275
    ** CrCl > 10: x = 0.2
47
Q

phenytoin AE

A

1) dose/plasma concentration related

  • CNS: fatigue, headache, blurred vision, diplopia, ataxia
  • nystagmus

2) idiopathic/hypersensitivity related

  • SJS, TEN, rash
  • first few months of therapy

3) chronic/systemic

  • gingival hyperplasia, hirsutism
  • peripheral neuropathy: folate supplement
  • osteomalacia
    ** enzyme induced -> increased Vit D clearance -> secondary hyperparathryoidism -> increased bone turnover -> reduced bone density
  • hepatotox, macrocytic anemia

4) others

  • N/V, dyskinesia, teratogenic, suicidal
48
Q

phenytoin DDI

A

potent inducer of CYP2C, CYP3A, UGT

  • pharmacological classes affected: antidepressant, antipsychotic, immunosuppression, antiretroviral, chemo
  • potential physiological effect

1) women: reproductive hormones, sexual function, OC effectivness
2) men: sexual function, fertility
3) bone health
4) vascular risk

49
Q

phenytoin pharmacogenomic testing

A

HLA-B*1502 for hypersensitivity testing

50
Q

valproate indication

A

1st line for everything

51
Q

valproate MOA

A

1) reduce neuronal firing

  • inhibit voltage-gated Na+ channel
  • inhibit T-type Ca2+ channel

2) inhibit GABA transaminase -> increase inhibitory GABA concentrationva

52
Q

valproate PK

A

1) Absorption

  • F almost 1

2) Distribution

  • Vd = 0.15 L/kg
  • highly albumin bound
    ** saturable protein binding within therapeutic range (higher concentration = reduced protein binding)

3) metabolism

  • CYP2C9, UGT
53
Q

valproate AE

A

1) dose/plasma related

  • ataxia, tremor, hepatotoxicity, thrombocytopenia, pancreatitis, hyperammonemia

2) chronic/systemic

  • weight gain, alopecia, major malformation risk, affect neonatal cognition
54
Q

valproate DDI

A

potent inhibitor of CYP2C9, UGT

55
Q

carbamazepine MOA

A

inhibit voltage gated Na+ channel

56
Q

carbamazepine indication

A

focal, GTC

57
Q

carbamazpine PK

A

1) absorption

  • bioavailability about 0.8

2) distribution

  • Vd = 1.4 Lkg
  • highly albumin bound (low albumin = increase carbamazepine concentration)

3) metabolism, elimination

  • CYP3A4
  • autoinduction
    ** induce own metabolism
    ** increase clearance, shorter t1/2
    ** max autoinduction 2 - 3 wks after dose titration
    ** X start w desired dose at first, need titrate to initial dose
58
Q

carbamazepine AE

A

1) dose/plasma related

  • CNS: lethargy, headache, blurred vision, diplopia, unsteady, ataxia, incoordination
  • nystagmus
  • N/V

2) idiopathic/hypersensitivity related

  • rash, SJS, TEN

3) chronic (systemic)

  • hyponatremia, leukopenia, aplastic anemia, hepatotox, osteopenia/osteoporosis/osteomalacia, neuropathy
59
Q

carbamazepine DDI

A

potent inducer of CYP (1A2, 2C, 3A4), UGT

  • pharmacological classes to look out for: antidepressant, antipsychotic, immunosuppression, antiretroviral, chemotherapy
  • potential physiological effect
    ** women: reproductive hormone, sexual function, OC ineffective
    ** men: sexual function, fertility
    ** bone health
    ** vascular risk
60
Q

pharmacogenomic testing for carbamazepine

A

test HLA-B*1502 for hypersensitivity reaction

61
Q

types of benzodiazepine

A

clonazepam, diazepam, lorazepam

62
Q

benzodiazepine indication

A

status epilepticus

63
Q

benzodiazepine MOA

A

potentiate GABA binding to GABA receptor -> potentiate influx of Cl- ions into neuron -> hyperpolarisation -> more difficulty to reach threshold membrane potential

64
Q

benzodiazepine PK

A

long acting

65
Q

benzodiazepine AE

A

addictive

  • cause acute toxicity/overdose
  • respiratory depression +/- alcohol
  • drowsiness, confusion, anemia
  • impaired muscle coordination
  • tolerance & dependence
66
Q

management of dose/plasma related AE

A

1) monotherapy vs combination

  • monotherapy: higher concentration = more prominent
  • combination therapy: lower plasma concentration = more prominent (additive effect during initiation)

2) management

  • low dose -> titrate slowly
  • avoid large dose change
  • avoid combination if possible
  • adjust administration schedule
    ** largest dose at bedtime
    ** smaller, more frequent dose
    ** sustained release
    ** reduce total daily dose if clinically safe
67
Q

ASM choice for paediatric/neonatal

A

phenobarbital

  • IV loading dose +/- IV or oral maintenance
  • MOA: potentiate GABA mediated Cl- current at site distinct from benzodiazepine
  • disadvantages: severe withdrawal and tolerance, dose dependent CNS depression
68
Q

which drug choices for pregnant

A

1) lamotrigine
2) levetiracetam
3) NO VALPROATE

69
Q

lamotrigine for pregnant - indication

A

absent, GTC

70
Q

lamotrigine for pregnant - MOA

A

1) block voltage gated Na+ channel and high voltage gated Ca2+ channel
2) inhibit release of glutamate
3) impede sustained repetitive neuronal depolarisation

71
Q

lamotrigine for pregnant - PK

A
  • linear
  • t1/2
    ** shorter in children
    ** significantly reduced when + carbamazepine/phenytoin
    ** significantly increased w valproate
72
Q

lamotrigine for pregnant - AE

A
  • CNS: dizzy, headache, incoordination, tremor, somnolence
  • asthenia, N/V
  • rash, SJS, TEN, DRESS
73
Q

lamotrigine for pregnant - risk management for hypersensitivity reaction

A

avoid
1) high starting dose
2) rapid dose escalation
3) use with valproate

74
Q

levetiracetam for pregnant - indication

A

myoclonic

75
Q

levetiracetam for pregnant - MOA

A

bind to SV2A vesicles that contain glutamate in presynaptic neuron

76
Q

levetiracetam for pregnant - PK

A

linear, low intra/inter individual variability

77
Q

levetiracetam for pregnant - AE

A
  • CNS: somnolence, dizzy, coordination difficulties (4 wks after initiation, irritability, aggression)
  • asthenia
78
Q

lactation and ASM

A

safe

79
Q

indication for TDM

A

1) establish individual therapeutic range
2) assess lack of efficacy, potential toxicity, loss of efficacy

80
Q

what to monitor for TDM

A

1) seizure diary
2) SE, DDI
3) check and manage seizure trigger
4) be careful when swimming/driving

81
Q

treatment discontinuation for seizure

A

1) min 2 yrs wo seizure

  • longer if higher risk of recurrence or low frequency of seizure before remission

2) discuss risk benefit

82
Q

what is status epilepticus

A
  • failure of mechanism responsible for seizure termination or from initiation of mechanisms that lead to abnormally prolonged seizure
    ** prolonged seizure: GTC ≥ 5 mins
    ** long term consequences when GTC ≥ 30 mins
83
Q

treatment for status epilepticus

A

1) stabilisation phase: 0 - 5 mins

  • stabilise pt (ABC)
  • give O2, ECG monitoring
  • replenish glucose if glucose < 60 mg/dL (IV dextrose)
  • supportive care

2) initial therapy phase: 5 - 20 mins

  • if still seizure then IV lorazepam or diazepam

3) second therapy phase: 20 - 40 mins

  • if still seizure then IV phenytoin, valproic acid, levetiracetam

4) third therapy phase: 40 - 60 mins

  • if still seizure then repeat second therapy

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