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54 CNS > Seizure & Epilepsy > Flashcards

Seizure & Epilepsy Flashcards

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1
Q

How is epilepsy defined?

A

Any one of:
- at least 2 unprovoked seizures >24h apart
- 1 unprovoked and probability of further seizures after 2 unprovoked seizures, occurring in the next 10 years
- diagnosis of epilepsy syndrome

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2
Q

What are acute symptomatic seizures?

A

Seizures that result from some immediately recognisable stimulus or cause (eg. about a week after acute brain injury)

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3
Q

What are remote seizures?

A

Seizures that occur longer than 1 week following a disorder (known to increase risk of developing epilepsy)

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4
Q

What re unprovoked seizures?

A

Seizures occurring in absence of a potentially responsible clinical condition OR beyond interval estimated (~1 week) for occurence of symptomatic

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5
Q

Metabolic causes of acute symptomatic seizures

A

Hyponatremia
Hypoglycemia
Hypocalcemia
Hypomagnesemia

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6
Q

Toxic/drug causes of acute symptomatic seizures

A

Illicit drugs (cocaine, amphetamines)
Drugs (tricyclic antidepressants, carbapenems, baclofen)
ETOH
Benzodiazepine withdrawal

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7
Q

Structural causes of acute symptomatic seizures

A

Stroke
Traumatic brain injury

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8
Q

Infection/inflammation causing acute symptomatic seizures

A

CNS infection
Febrile illness

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9
Q

Non-epileptic seizures

A

Not related to abnormal epileptiform discharges

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10
Q

What is the general pathophysiology for epilepsies?

A

Neuronal hyperexcitability and hypersynchronisation

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11
Q

What can result in neuronal hyperexcitability?

A
  • Voltage- or ligand-gated channels
  • Abnormalities in intra & extracellular substances
  • Excessive excitatory neurotransmitters
  • Insufficient inhibitory neurotransmitters
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12
Q

Which parts of the brain is associated with neuronal synchronisation?

A

Hippocampus, neocortex and thalamus

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13
Q

Focal onset

A

Seizure begins only in one hemisphere

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14
Q

Generalised onset

A

Seizure begins in both hemispheres

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15
Q

Secondary generalised

A

Seizure begins in one hemisphere, then spread to other

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16
Q

What do clinical characteristic of a seizure depend on?

A
  • Site of focus
  • Degree of irritability of the area surround the focus
  • Intensity of impulse
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17
Q

Phases of a seizure (in order)

A
  1. Prodromal
  2. Early ictal (“aura”)
  3. Ictal
  4. Postictal
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18
Q

Motor symptoms of focal onset (simple partial)

A
  • Clonic movements (twitching/jerking) of arm, shoulder, face, leg
  • Speech arrest
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19
Q

Desired outcomes of epilepsy treatment

A
  1. Absence of epileptic seizures
  2. Absence of ASM-related side effects
  3. Attainment of quality of life
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20
Q

What are some 1st generation ASMs?

A
  • Carbamazepine
  • Phenobarbitone/Phenobarbital
  • Phenytoin
  • Sodium Valproate
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21
Q

What are some 2nd generation ASMs?

A
  • Lamotrigine
  • Levetiracetam
  • Topiramate
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22
Q

1st line AEDs for generalised tonic-clonic

A
  • Carbamazepine
  • Sodium Valproate
  • Lamotrigine
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23
Q

1st line AEDs for tonic/atonic

A

Sodium Valproate

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24
Q

1st line AEDs for absence

A

Lamotrigine
Sodium Valproate

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25
1st line AEDs for focal
- Carbamazepine - Sodium Valproate - Lamotrigine - Levetiracetam
26
What are some problems with 1st generation ASMs?
- Poor water solubility - Extensive protein binding - Extensive oxidative metabolism - Multiple DDIs
27
What are the potential advantages of newer ASMs?
- Improved water solubility → predictable F - Negligible protein binding → no need to worry about hypoalbuminemia - Less reliance on CYP metabolism
28
Potent enzyme inducers in 1st generation ASMs
Carbamazepine: CYP (1A2, 2C, 3A4), UGTs Phenytoin: CYP (2C, 3A), UGTs Phenobarbital: CYP (1A, 2A6,2B,3A), UGTs
29
Potent enzyme inhibitors in 1st generation ASMs
Valproate: CYP2C9, UGTs
30
MOA of Carbamazepine
Blockade of voltage gated sodium channels → reduces repetitive firing of sodium dependent action potentials in depolarised neurons
31
Starting dose of Carbamazepine
Epilepsy: 100-200mg QD or BD Mania: 100-400mg in 2-4 divided dose Trigeminal neuralgia: 200-400mg QD
32
Indications of Carbamazepine
1. Epilepsy (NOT for absence!) 2. Acute mania 3. Trigeminal neuralgia (1st line)
33
Carbamazepine - renal
No renal adjustment required DO NOT use for moderate-severe impairment
34
Carbamazepine - elderly
Beer's list: Use with caution (likely due to neurological SEs)
35
Carbamazepine - hepatic
No hepatic adjustment required Consider dose reduction Hepatotoxicity is a concern
36
Carbamazepine - trigeminal
Elderly: 100mg BD
37
Carbamazepine - common SEs
GI effects - N/V/C/D, loss of appetite, stomach upset Hyponatremia - muscle cramps, weakness, mental status change Neurological - drowsy, lightheaded, headache, blurry or double vision
38
Carbamazepine - rare & serious SEs
SJS/TEN - monitor closely in first 3 months Liver failure Blood dycrasias
39
ASMs & pregnancy principles
Early planning with physicians - Evaluate concomitant medines + choose ASM with least risk - Gradually switch to one with lower risk before pregnancy - Or monitor and adjust accordingly
40
Carbamazepine - pregnancy
Teratogenic (major congenital malformations) If used, - Folic acid supplementation - Vit K during last period of pregnancy - TDM - Switch to levetiracetam, lamotrigine if possible
41
Carbamazepine - breastfeeding
Encouraged to continue, unless AEs in infants observed.
42
Carbamazepine - protein binding
75% protein bound; albuminuria increases free drug concentration
43
Carbamazepine - significant pK
Undergoes autoinduction (induces own metabolism): Stabilises in around 3 weeks Increase CL, decrease t1/2 → start low dose, titrate up, more frequent dosing
44
Carbamazepine - Initiation
Pharmacogenomic testing (HLA-B*1502) - To identify risk of SJS/TEN - Asian patients - If positive, avoid CBZ & phenytoin - If negative, continue to monitor patients (at risk of developing SCAR (DRESS))
45
Carbamazepine - DDI (1)
Macrolides (e.g. clarithromycin) - CYP3A4 inhibitor Reduce dose of CBZ
46
Carbamazepine - DDI (2)
OC (e.g. ethinyl estradiol) - CBZ induces CYP3A4-mediated metabolism of OC Consider CBZ alternatives, or use back up contraceptive during co-administration and at least 28 days after discontinuing CBZ
47
How does Carbamazepine induce hyponatremia
Increases ADH which cause increase expression of aquaporin 2 channels in renal tubules
48
Carbamazepine & hyponatremia
Serum Na <136mmol/L Acute onset <48h, associated with neurological complications
49
Management of hyponatremia when taking Carbamazepine
Symptomatic: stop CBZ and switch to levetiracetam) Asymptomatic: fluid restriction Chronic, asymtomatic: fluid restrict + oral salt tablets or loop diuretic Monitor: serum electrolytes
50
Carbamazepine - formulation
High oral F → oral formulation Poor solubility → does not have parenteral
51
Carbamazepine - monitoring
Baseline: - FBC, BUN, liver&kidney function, serum Na, ophthalmic test Follow up: - Drug concentrations, FBC, liver&kidney function
52
MOA of Phenytoin
Blockade of voltage-gated sodium channels → reduces repetitive firing of sodium-dependent action potentials in depolarised neurons
53
Indications of phenytoin
All types of seizures except absence seizure
54
Phenytoin - bioavailability
Complete but slow absorption Reduced at higher dose Reduced by interactions with enteral feeds - space apart by 2h
55
Phenytoin - protein binding
Highly protein bound - Low albumin = more free phenytoin
56
Phenytoin - pK
Zero-order kinetics (increase in dose =/= increase in concentration)
57
Phenytoin - pregnancy
Teratogenic
58
Phenytoin - monitoring
Labs measure total phenytoin level Corrected equation: Cobserved/[x(albumin/10)+0.1] x = 0.275 when CrCl≥10 x = 0.2 when CrCl<10
59
What drug class is phenobarbital?
Barbiturate
60
MOA of phenobarbital
Enhance GABA binding (GABA causes Cl- ion channels to open) → greater entry of Cl- → hyperpolarises neurons At different binding site from benzodiazepines
61
Which group of patient is phenobarbital mainly used for?
Neonates/paediatric (IV LD followed by PO/IV MD)
62
Phenobarbital - disadvantages
- Tendency to develop tolerance and dependance - Severe withdrawal symptoms
63
Valproate - dosage forms
Oral (tablet, syrup) Injection (solution, powder)
64
Valproate - dose
(Starting) Epilepsy Absence: 15mg/kg/day (1-4 divided dose) Complex partial: 10-15mg/kg/day (1-4 divided dose) GTC: 250mg/day
65
Valproate - common SEs
Dizziness - get up slowly from sitting/lying Drowsy Diarrhoea - drink more water N/V, stomach cramp Hirsutism Weight gain Slight tremors of hands and fingers when you first start
66
MOA of valproate
Blockade of voltage-gated sodium and calcium channels Inhibits GABA transaminase → increase GABA
67
Valproate - pregnancy
Teratogenic Major congenital malformations, decreased IQ, neurodevelopmental disorders
68
Valproate - breastfeeding
Encouraged
69
Valproate - renal
No dose adjustment necessary but closely monitor clinical response, tolerability, free valproic acid concentration
70
Valproate - liver
Mild to moderate: not recommended Severe: Contraindicated
71
Valproate - elderly
Lower initial and maintenance dose Monitor closely for AEs
72
Valproate - paediatric
Weight-based dosing
73
Valproate - DDIs (1)
CNS depressants - Strongly bound to plasma proteins, may displace other drugs
74
Valproate - DDIs (2)
Carbapenems - May decrease serum concentration of valproate
75
Valproate - DDIs (3)
Lamotrigine - May enhance AE & increase serum concentration of lamotrigine - Lamotrigine dose reduction required; increase monitoring for lamotrigine toxicity (rash, hematologic toxicities)
76
Valproate - Drug-disease interaction
Hepatotoxicity induced by sodium valproate Avoid concomitant use of salicylates

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