Epilepsy Flashcards
What question should be asked in a history of a fit?
Amongst others
- Describe the seizure - generalised or focal?
- Prodrome, aura, precipitating event
- Loss of conscoiusness
- Incontinence
- Tongue biting
- Head trauma
- Preceding faint
- Nutrition status and any intoxication
What investigations for first fit?
B - ? urine dip, ECG, BM, ? LP, pregnancy test if about to start on AEDs
B - FBC, CRP, U+E, Glucose, LFT (chronic LD), drug levels and toxin screen
I - CT head, MRI,
O - EEG
First seizure - chance of recurrenc?
what is risk of after stroke?
When consider starting treatment?
- 3-5%
- Increased risk after stroke
- When ≥2 unprovoked, provided no obvious precipitant e.g. alcohol
What kinds of seizures are there?
Why does classification help?
- Partial onset (focal) - simple or complex if loss of consciousness
- Focal e.g. temporal lobe, frontal lobe
- Secondary generalised
- Jacksonian
- Generalised (usually start in childhood)
- Tonic clonic, myoclonic, absence
Helps with deciding on treatment, investiagations and prognosis
Mechanism of action?
Redress balance between excitatory and inhibitory signallg to reduce inappropriate impulses
- Voltage gated ion channels - e.g. L-type calcium and Na
- Reduce glutamate mediated excitation
- Enhance GABA mediated inhibition
WHat is first line for partial seizures? Additional drugs
First line for generalised? Additional?
What medication also works for absence?
LTG>CBZ>TPM
- Carbamazepine, Lamotrigine
- Levetiracetam, topiramate
VPA>TPM>LTG
- Valproate
- Lamotrigine, Topiramate, Levetiracetam
Ethosuximide
How start?
When consider 2nd medication?
What if >1 fails?
Start low and slow, titrate to effect and side-effects
Add second if fail to control fully with 1. COnsider removal of first medication if addition of second improves
Consider surgery
Lamotrigine
MOA?
Main side effects?
Any interactions?
Inhibits glutamate and sodium signalling. 55% protein bound
Blood - aplastic anasemia, rash (risk SJS), cerebellar dysfunction
OCP, AED, SSRI
Carbamazepine
MOA?
Main side effects?
Any interactions?
Enzyme inducer that can make myoclonic and absence worse; 75% protein bound
Sodium inhibition
Skin, diplopia, NH ataxia, SJS, pancytopaenia
OCP, warfarin, AED, erythromycin
Sodium Valproate
MOA?
Main side effects?
Any interactions?
Enzyme inhibitor 85% protein bound
Affects at GABA, Glu, Ca and Potassium
WG, hirsutism, gum hypertrophy, hair loss, GI, Hepatotxic, pancreatitis, encephalopathy
Increases plasma levels of other AEDs
Risk with salicylates and naproxen - displace form protein increasing toxicity risk
Risk to child bearing?
RIsk with OCP?
NTDefects and other major congenital malformations. Valproate had highest risk - mitigate by addition of 5mg folic acid and ? vitamin K before delivery (haemorrhage risk)
Reduce effectiveness so may need to double the dose. OCP may also enhance clearance of AEDs leading to risk of breakthrough seizures
Define Status
What is mortality
Causes?
Continuous seizure lasting >30 mins wihtout return to consciousness, or multiple seizure with no lucid return in between
20% (mainly due to hypoxia)
Multiple - e.g. alcohol, compliance, fialure to take mediaction, stroke, first presentation, glucose, trauma, tumour, SAH, infection, toxins, electrolytes
Mamnagement of Status
ABCDE
Bm - if glucose <4, give IV dextrose ±pabrinex/thiamine if alcoholic
- 4mg IV lorazepam (or 10mg buccal midazolam)
- Repeat afer 10 min if still fitting
- Expert support - Phenytoin infusion - 1000mg over 30 minutes NB not in same line as lorazepam
- ? Phenobarbital
- If remains refractory - generalised anaesthesia ITU
Stop any precipitants
Home with contraceptive device because of teratogenic effect of AEDs
Phenytoin
MOA?
Main side effects?
Any interactions?
Enzyme inducer 85% protein bound, narrow therapeutic window (may differ between patients) because zero order kinetics
Inhibits voltage-dependent sodium channels
IV - arrhythmia, Purple-glove syndrome, thrombophlebitis
Oral - rash, toxicity (dysarthryia, ataxia, lethargy), hirsutism, acne, macrocytosis
LT - cerebllar atrophy, peripheral neuropathy, OP, flate deficiency
Other AEDs, warfarin
Who to monitor?
- ? Non-adherence
- ? Toxicity
- Dose change
- Managing interactions
- Organ failure, pregnancy, status
When consider treatment withdrawal? How?
Who is at greater risk of relapse?
What do if relapse?
Fit-free fo ≥ 2 years; taper-off gradually e.g 10% every 2-8 weeks. One drug at a time
Can’t drive for 6 months
Childhood diagnosis, seizures on medicaiton, brain damage, EEG +ve diagnosis, >1 drug treatment, generalised TC or myoclonic
resume previous treatment if relapse
DVLA regulations
Other considerations?
- Can drive if seizure free for at least 1 year.
- Can’t drive for 6 months following withdrawal of meds.
- Short term licence - have to reapply every 3-5 years.
Avoidance of triggers, avaoidance of dangerous activities. THis can affect all aspects of daily living
