Peishieen Flashcards
State the features of tension type headache (6)
o No premonitory symptoms and aura
o Bilateral
o Constant, non-pulsatile tightness or pressure
o Mild/moderate intensity
o Gradual onset
o Not worse with activity but may improve with rest
State the features of migraine (6)
o May have premonitory symptoms and aura
o Unilateral or Bilateral
o Pulsating/ throbbing pain
o Moderate/severe intensity
o Worsened with, or caused by activity
o Presents with at least 1 other symptom (N/V or photophobia/phonophobia)
State the features of cluster headache (5)
o Unilateral (around the eye or along face)
o Variable pain
o Severe/ very severe intensity
o Causes restlessness or agitation when doing activities
o Presents with cranial autonomic symptoms on same side of headache (red, watery or swollen eye, nasal congestion/runny nose, sweating)
List the pharmacological agents that have demonstrated efficacy in the treatment of TTH (Acute vs Prophylaxis; 3 each)
o Acute
1) Paracetamol (alone or with caffeine)
2) Aspirin
3) NSAIDs: Ibuprofen, Naproxen, Diclofenac, Ketoprofen
o Prophylaxis
1) Amitriptyline (1st line) -> tricyclic antidepressant (TCA)
2) Mirtazapine (TCA)
3) Venlafaxine (SNRI)
What are the classification of tension type headahces?
o Infrequent episodic TTH: < 1 episode/month
o Frequent episodic TTH: 1-14 days/month
o Chronic TTH: 15 or more days/month
- More associated with Vitamin deficiencies
Describe the pathophysiology of migraine in relation to the various phases: premonitory, aura, headache, postdrome and interictal
o Prodrome
- Activation of the hypothalamus, as well as neuropeptides involved in homeostatic functions, may contribute to symptoms experienced during the prodrome phase (activation of the hypothalamus occurs prior to the onset of migraine pain)
o Aura
- Cortical spreading depression (CSD) is considered to be the primary pathophysiology behind the aura phase. CSD causes large wave of slow spreading depression in gray matter, inhibiting cortical activity -> causing changes to synaptic activity, extracellular ion concentrations, blood flow and metabolism + activate trigeminovascular system
o Headache (Ictal)
- Several neuropeptides (e.g CGRP) have been implicated in the sensitization of the central and peripheral trigeminovascular system, creating a state of hypersensitivity and contributing to both pain and non-pain symptoms during the headache phase.
o Postdrome
- There are a number of similarities in the symptoms experienced during the prodrome and postdrome phases. However, the precise pathophysiological events that underlie these symptoms remain uncertain.
o Interictal
- Some regions of the brain remain abnormally activated after headache cessation, including the olfactory regions, the midbrain, and the hypothalamus.
List the pharmacological agents that have established efficacy for acute (6) and preventive (3) treatment of migraine (and which are not established)
o Acute treatment
- NSAIDs ± other analgesics
- Triptans
- Ergotamine (Ergot Alkaloids; inferior to Triptan on outcome of headache relief at 2 hours)
- Opioids (not really established)
- Ditans (5-HT1F stimulator) and Gepants (CGRP receptor blocker; long term efficacy not determined)
o Preventive treatment
* Antiepileptics (e.g Topiramate, Valproate)
* Beta Blocker (e.g Propranolol, Metoprolol)
* Anti-CGRP antibody (Erenumab)
State the role of Triptans in migraine treatment
- Triptans are recommended for the acute treatment of migraine for patients for whom over the counter analgesics do not adequately relieve pain
- Most patients experienced pain relief within 2 hours
- Place in therapy:
o As a class, the triptans have largely replaced the ergot alkaloids, due to a better side effect profile
What are the contraindications of Sumatriptan? (8)
o Uncontrolled Arterial hypertension
o Coronary heart disease
o Raynaud’s disease -> spontaneous vessel constriction causing tissue necrosis
o History of ischaemic stroke
o Pregnancy and lactation
o Hypersensitivity to triptans,
o Concurrent administration with MAO inhibitors
o Myocardial infarct
Generally due to vasoconstrictive effects
State the potential targets for Anti-CGRP antibodies
Either target the CGRP protein (anti-CGRP), or the CGRP receptor (anti-CGRP receptor)
State what Erenumab targets
CGRP receptor
State the criteria in which a patient may be prescribed with Erenumab
Patients with episodic or chronic migraine who have not responded to at least 2 medical treatments, or who cannot use other preventative treatments because of comorbidities, side effects, or poor compliance
State the potential problem that may be caused by blocking CGRP activity
CGRP is a vasodilator.
CGRP might act as a ‘vasodilator safeguard’ during ischaemia therefore, mild and transient ischaemic events might be worsened in individuals who receive long term CGRP blockade treatment
State the ICHD-3 criteria for diagnosing Migraine without aura
At least 5 attacks that fulfil the following criteria:
* Headache attack duration: 4-72 hours (when untreated or unsuccessfully treated)
* Headache characteristics (≥ 2 of 4 characteristics)
o Unilateral location
o Pulsating quality
o Moderate to severe pain intensity
o Aggravation by or causing avoidance of routine physical activity (e.g walking or climbing stairs)
* At least 1 other symptom during headache
o N/V
o Photophobia and phonophobia
* Not better accounted for by another ICHD-3 diagnosis
State the ICHD-3 criteria for diagnosis of Migraine with aura
At least 2 attacks fulfilling the following criteria:
* Presence of fully reversible aura symptoms (at least 1)
o Visual
o Sensory
o Speech and/or language
o Motor
o Brainstem
o Retinal
* Characteristics (≥ 3 of 6)
o At least 1 aura symptom spreads gradually over ≥ 5 minutes
o 2 or more aura symptoms occur in succession
o Each individual aura symptom lasts 5-60 minutes
o Aura symptom (≥ 1 symptom) is unilateral
o Aura symptom (≥ 1 symptom) is positive
o Aura is accompanied or followed within 60 mins, by headache
AND not better accounted for by other ICHD-3 diagnosis
State the classifications of migraine and state what counts as MMD and MHD
o Episodic: < 15 MMD or MHDs
- In lifetime, must have experienced ≥ 5 migraine attacks lasting 4-72 hours
o Chronic: ≥ 15 MHD, of which ≥ 8 are MMD
- At least 3 months
o MMD = Monthly migraine days
≥ 2 migraine characteristics (see above)
If no aura, ≥ 1 symptom (see above)
o MHD = Monthly headache days
A day with migraine-type or tension type headache
What is the criteria for migraine prophylaxis to be considered?
- Generally based on the number of headache days per month and the degree of disability caused by the attacks (at least 2 days a month and some moderate disability caused to be considered)
See notes for exact days and severity of disability
Describe what is medication overuse headache
Diagnosis Criteria:
* Headache on ≥15 days/month in patient with pre-existing headache disorder
* Regular overuse of acute and/or prophylactic headache drugs for > 3 months
o Anything not simple analgesic/ NSAID or combi is at least 10 day/mth
o Anything that is simple analgesic/ NSAID at least 15 day/mth
* Headache cannot be better accounted for by another ICHD-3 diagnosis
What are non-pharmacological therapies for TTH? (7)
o Patient education and identify triggers (Headache diary)
o CBT (Cognitive Behavioural Therapy; decrease stress level and depressive symptoms), biofeedback, relaxation
o Physical and/or occupational therapy
o Lifestyle modification (include sleep hygiene)
What are red flags that may indicate secondary headache? (SNNOOP10)
1) Systemic symptoms including fever
* Potential infection
2) Neoplasm in history
* Pre-existing history of cancer; worried about brain metastases or oncological process causing more serious conditions that mimic headache
3) Neurologic deficit or dysfunction
* Unless inborn, should not have any form of asymmetry
4) Onset of headache is sudden or abrupt
5) Older age (over 50 years)
* Exposed to more chronic disorders; risk profiling may change over time
6) Pattern change or recent onset of headache
7) Positional headache
8) Precipitated by sneezing, coughing or exercise
9) Papilledema (swelling at back of eye)
10) Progressive headache with atypical presentation
11) Pregnancy or puerperium (post-partum)
12) Painful eye with autonomic features
13) Post-traumatic onset of headache
* May be underlying bleed or structural issues
14) Pathology of immune system such as HIV/ immunocompromised
15) Painkiller overuse or new drug at onset of headache (Medication overuse headache)
State how headache treatment efficacy is monitored and what is monitored (3)
o Headache diary
o Disability assessment (e.g. MIDAS)
- Objective way to measure disability before and after treatment
o Adverse effect from medications
DDI of Sumatriptan (3)
1) Monoamine Oxidase Inhibitor (MAOi)
● Concurrent administration of MAOIs and sumatriptan is CONTRAINDICATED
● Sumatriptan must not be used within 2 weeks of discontinuation of therapy with MAOIs
2) Ergotamine
● Concomitant use of ergotamine (eg Caffox, Cafergot) or derivatives of ergotamine (including methysergide, dihydroergotamine) is CONTRAINDICATED
● Avoid taking sumatriptan within 24 hours after taking these medications
3) Other Triptans or Triptan Combination Products
● Avoid taking different triptans or triptan combination products (e.g. zolmitriptan, naratriptan, etc.) within 24 hours after taking sumatriptan
Define acute symptomatic seizures, dissociative (non-epileptic) seizures and unprovoked seizures
Acute symptomatic seizure: Seizures that result from some immediately recognizable stimulus or cause, i.e. that occur in the presence or close timely association (about a week) with an acute brain insult (metabolic, toxic, structural, infectious, hypoxic, etc.)
Unprovoked seizure: Seizures occurring in the absence of a potentially responsible clinical condition (cryptogenic) or beyond the interval estimated for the occurrence of acute symptomatic seizures (remote symptomatic seizure)
Dissociative (non-epileptic) seizure: Abnormal paroxysmal psychic, sensory and/or motor manifestations which resemble (at least in part) epileptic seizures but are not related to abnormal epileptiform discharges -> no abnormal discharges = normal EEG
Define Psychogenic non-epileptic “seizures” (PNES)
o Partial alteration of level of consciousness with a partial preservation of awareness.
o Caused by stressful psychological experiences or emotional trauma
o Involuntary -> when stresses come, body reacts in this manner
Define epilepsy
Disease of the brain defined by any of the following conditions:
* At least two unprovoked seizures occurring > 24h apart
* One unprovoked seizure and a probability of further seizures similar to the general recurrence risk (at least 60%) after two unprovoked seizures, occurring over the next 10 years
* Diagnosis of an epilepsy syndrome
Describe the underlying pathophysiology processes in seizures and epilepsy
o Hyperexcitability
- Occurs because there is an enhanced predisposition of a neuron to depolarize
o Hypersynchronisation
- Under abnormal circumstances, intrinsic reorganisation of local circuits lead to synchronisation and promotion of epileptiform activity generation.
State the clinical presentation of GTC seizures (6)
- Begins with stiffening of the limbs (tonic phase), followed by jerking of limbs and face (clonic phase)
- During tonic phase, breathing may decrease or cease altogether -> cyanosis of nail beds, lips & face; typically returns during clonic phase but may be irregular
- Limb stiffen such that it forms figure of 4 (see image below)
- Clonic phase usually lasts 1 minute, after which the brain is extremely hyperpolarised and insensitive to stimuli
- Incontinence may occur, along with biting of the tongue or inside of the mouth; breathing may be noisy and appear to be laboured
- Following the seizure, patient may have a headache and appear lethargic, confused or sleepy
State the clinical presentation of focal onset (with no dyscognitive features i.e no altered consciousness) seizures (4 types of symptoms)
Motor
- Clonic movements (e.g twitching or jerking) of the arm, shoulder, face, or leg
- Speech arrest (involve muscles of articulation; dysarthria)
Sensory
- Feelings of numbness or tingling
- Visual disturbances flashing lights
- Rising epigastric sensation
Autonomic
- Sweating, salivation, or pallor
- ↑BP, HR
Psychic (or somatosensory symptoms)
- Flashbacks, dé j à vu (memory
- Visual, auditory, auditory, gustatory or olfactory hallucinations
- Affective symptoms include fear (most common), depression, anger and irritability
Does normal EEG mean no epilepsy?
No
State the laboratory tests/investigations that may be used to diagnose Epilepsy (4) state their purpose and limitations if any
1) Scalp Electroencephalography (EEG)
* Essential tool for diagnosis and classification of seizures and epileptic syndromes
* If diagnosis of seizures or epilepsy is considered, epileptiform discharges on EEG confirm diagnosis
* A normal EEG DOES NOT exclude possibility of epilepsy
* Limitations:
o Not all Epileptic patients have an abnormal EEG
- 50% chance of showing epileptiform activity in a first awake EEG.
- 80-90% sensitivity with repeated awake sleep EEGs.
o EEG can be abnormal in normal persons
- False positive epileptiform discharges on EEG in asymptomatic adults: 0.5-1%
2) Video EEG
* Video recording concurrent with EEG -> can see outward manifestation and what’s going on inside the brain
* Cons:
o Can be expensive and labor intensive
o Its use typically limited to diagnostic problems that cannot be resolved easily in the routine EEG laboratory
3) Magnetic resonance imaging with gadolinium
* Ordered for: adult patient who presents with first seizure, especially for patients with focal neurologic deficits, suggestion of focal onset seizure
* To identify focal lesions (structural reasons for seizure episode)
4) Biochemical/toxicology (even if diagnosed with epilepsy, still need to run)
* Helps to rule out electrolyte abnormalities (contributory factors)
* Serum prolactin -> considerable variability, not used routinely
* Creatine kinase (CK) -> raised after GTC (violent contractions may cause muscle breakdown)
What is the ILAE Seizure Classification based on? (3)
1) Mode of onset
2) Impairment of consciousness
3) Other features of the seizure
What are the 3 modes of seizure onset?
1) Focal onset: seizures begin only in one hemisphere
o May spread to the contralateral hemisphere = “focal seizures evolving to a bilateral convulsive seizure” (previously termed “secondarily generalized”)
2) Generalized onset: seizures begin in both hemispheres
o Can be clonic, tonic, myoclonic, absence or atonic
3) Secondarily generalized: being in one hemisphere, then spread to the other
Explain what is meant when a seizure is described as:
a) Simple
b) Complex
c) With dyscognitive features
o Simple = no loss of consciousness
o Complex = loss of consciousness
o With dyscognitive features = impairment of consciousness
Describe appropriate first aid for a person with seizures (7)
- Ease person to floor
- Turn person gently to one side to help breathe
- Clear area of anything hard or sharp
- Put something soft and flat under person’s head e.g folded jacket
- Remove eyeglasses
- Loosen ties or anything around neck to help breathe
- Time the seizure. If anything longer than 5 mins, call 995.
What are available non-pharmacological ways to treat epilepsy (4) and state when each may be indicated
1) Ketogenic diet
- Ketogenic diet may be used for patients who cannot tolerate or have not responded well to ASM treatment
- Comprises low carbohydrate, high fat diet (cause body to burn fat to produce ketone which is used as energy, instead of glucose, by the brain; challenging to adhere to)
2) Vagus Nerve (Cranial nerve X) stimulation
- Indicated only for intractable focal seizures
- Stimulator delivers cyclical stimulation (pacemaker for the brain) to maybe influence neurotransmitter release
- During a seizure, ‘on demand’ stimulation can be achieved by placing a magnet next to subcutaneously implanted stimulator
3) Responsive neurostimulator system (RNS)
- More invasive compared to Vagus nerve stimulator (RNS implanted in brain)
- New adjunctive therapy to help reduce the frequency of with partial-onset seizures, in patients who:
* Have undergone diagnostic testing that localized ≤ 2 epiloptogenic foci (found the area in the brain where got problem)
* Are refractory to ≥ 2 antiepileptic medications
* Have frequent and disabling symptoms
4) Surgery
* Involves identification of the lesions that causes seizure and remove it
* Also considered as a last option (vs continued drug therapy) for certain refractory cases
- Cons:
* Will have collateral damage -> need time to recover post-surgery
Starting pharmacological treatment after 1st seizure _______ (3)
o Reduced risk of 2nd seizure
o No effect on long term prognosis
o No evidence of higher risk of death, injuries, or status epilepticus in patients allocated to deferred treatment
Which patients are at higher risk for seizure recurrence? (4)
- Epileptiform abnormalities on EEG
- Prior brain insult (e.g. stroke, brain trauma)
- Structural abnormality in brain imaging
- Nocturnal seizure
What are the factors that influence choice of Antiseizure medications in a patient? (5)
1) Efficacy and effectiveness (Seizure type, epilepsy syndrome)
2) Tolerability [Drug profile effect on comorbidity, other medications and tolerability in special groups (women with childbearing potential, older people, learning disabilities)]
3) PK (DDI, hormonal effects, renal or liver failure)
4) Personal preference (Formulation, dosing frequency)
5) Nation-specific factors (Guidelines, availability, costs, insurance coverage)
For 1st gen ASM, state which are enzyme inducers and which ones are enzyme inhibitors
Inducers: Carbamazepine, Phenytoin, Phenobarbital
Inhibitors: Valproic acid
In general, which enzymes do first gen ASMs affect?
CYP, UGTs
- Carbamazepine -> CYP (1A2, 2C, 3A4), UGTs
- Phenytoin -> CYP (2C, 3A), UGTs
- Phenobarbital/Primidone -> CYP (1A, 2A6, 2B, 3A), UGTs
- Valproate -> (CYP2C9, UGT)
State which formulation of Phenytoin contains 100% phenytoin
Oral suspension
- Capsules (30mg, 100mg) Phenytoin sodium (92% phenytoin)
- Injection IV Phenytoin sodium (92% phenytoin)
State the ways in which absorption of Phenytoin may be affected and how to mitigate it (2).
1) Absorption reduced at higher doses > 400mg/dose
o Split up the dose to prevent delayed absorption
2) Reduced by interaction with enteral feeds
o Some patients are unable to swallow and may require the use of nasogastric tube for delivery of enteral feeds and medications
o Recommend: space apart by 2 hours between enteral feeds & phenytoin
State potential ways free ASM level may increase for 1st gen
- Low albumin
- Uremia, other drugs
o Also may cause displacement reactions
State what order kinetics phenytoin follows and what is the implication
Follows Zero-order kinetics
* Unlike first order kinetics, concentration increment is NOT proportional to dose increment -> linear increase up to point where enzymes are saturated but this often occurs within therapeutic window of drug + different people different enzyme level so different point of saturation -> Phenytoin hard to dose
State at what levels of albumin does Phenytoin correction need to be calculated and how it is calculated
Albumin < 40g/L
Ccorrected = Cobserved/[x.(Alb/10)+ 0.1]
x = 0.275 for CrCl >= 10
x = 0.2 for CrCl < 10, on HD
State which proteins do CBZ usually bind to (2)
Albumin, α1-acid glycoprotein
State which Carbamazepine metabolite is still active
Carbamazepine-10,11-epoxide
State how Carbamazepine affect metabolism and how to deal with this issue
Undergoes autoinduction (induces its own metabolism)
* Over time, after the first dose, clearance increase and half-life shorten -> carbamazepine concentration decline and stabilize in accord with the new clearance and half life
* Maximal autoinduction usually occurs 2-3 weeks after dose initiation
Management:
* Do not start with desired maintenance dose at the first dose, but gradually increase over the initial few weeks -> allow patient to manage the ADRs better and improve adherence
Which ASMs have little to no effect on CYP? (3)
Gabapentin, Levetiracetam (Keppra; does not affect CYP i.e lesser DDI and also follow 1st order kinetics so easy to use), Pregabalin
ASMs are commonly associated with DDIs with which pharmacological classes? (5)
o Antidepressants & antipsychotics
o Immunosuppressive therapy
o Antiretroviral therapy
o Chemotherapeutic agents
o Statins
What are unique side effects of Phenytoin? (2)
1) Gingival hyperplasia
2) Hirsuitism
What are unique side effects of Valproate? (3)
Alopecia, weight gain, Pancreatitis
Which ASM is associated with Aplastic anemia?
Carbamazepine
Which ASMs are associated with weight loss and anorexia? (2)
Topiramate and Felbamate
Which ASMs are associated with osteopenia/osteoporosis, megaloblastic anemia, peripheral neuropathy?
Carbamazepine, Phenobarbital, Phenytoin
State what problems enzyme inducing ASMs may cause (6)
1) De-induction Interactions
o Other drugs that may be affected by enzymes may have been dose adjusted before or after ASM was started when enzyme affecting ASM is discontinued, activity of affected enzymes return to baseline.
o Hence when discontinuing ASM, need to dose adjust the other drugs.
2) DDIs especially with the following Pharmacological classes:
o Antidepressants & antipsychotics
o Immunosuppressive therapy
o Antiretroviral therapy
o Chemotherapeutic agents
3) Direct impact on reproductive hormones, sexual function, OC in women (ASM are not specific for drugs or hormones)
4) Sexual function & fertility in men
5) Affect Bone health as well
o At increased risk of osteopenia or osteoporosis if Vit D and Calcium not supplemented properly
o More likely to occur with longer drug use i.e older patients
6) Vascular risk (due to effect on cholesterol metabolism + DDI with statin)
What increases risk of SJS/TEN when using Lamotrigine? (3) State how to mitigate the risk of this ADR
High starting doses, rapid dose escalation, concomitant valproate (DDI)
Following dosing guidance (slow titration)
State the potential mechanism of cross-reactivity reactions of ASM in causing skin reactions and how to mitigate risk
Involves formation of arene oxide intermediate for those with aromatic ring -> switch to ASMs that do not contain benzene ring.
Hepatotoxicity is associated with which 1st gen ASMs?
Carbamazepine, Valproate, Phenytoin
State what to do for patients on ASM with suicidal ideation
o The risk of stopping ASMs or refusing to start ASMs is significantly worse and can actually result in serious harm including death to the patient. Suicidality in epilepsy is multifactorial, and different variables are operant.
o No changes to ongoing therapy without first discussing with physician
o Closer monitoring of symptoms
What are the indications for TDM? (4)
1) To establish an individual’s “therapeutic” range
o “Reference range” may not be effective for all
o Once stable -> to document effective level which controls seizures while minimising side effects
o Helps in subsequent changes (e.g. anticipated pharmacokinetic changes, drug interactions, medical conditions)
2) To assess lack of efficacy
o “Fast metabolizers”?
o Adherence issues?
o Other problems?
o To aid in deciding when to change drugs vs need to rework-up diagnosis right drug for right disease?
3) To assess potential toxicity
o Changing physiology?
o “Slow metabolisers”?
o Changes in disease / drugs?
- Renal (uremia, hypoalbuminemia)
- Liver (CYP enzymes)
- New drugs / interactions
o Danger levels! (concentration-dependent adverse effects)
4) To assess loss of efficacy (manifest as breakthrough seizures)
o Changes in physiology
o Age, pregnancy
o Changes in pathology
o Changed formulation brand vs generic, dosage forms
o Drug interactions
State what needs to be done for women with childbearing potential before starting ASMs (3)
1) Women with epilepsy should be referred to specialist care
o Discussion on fertility, contraception, family planning issues
o Early discussion on family planning
2) Discuss use of Contraception
o Use of oral contraceptives
- Potent enzyme inducers may render OC ineffective, alternative methods required
- For patients on lamotrigine, OC may lower lamotrigine concentrations, resulting in breakthrough seizures
3) Valproate is contraindicated in women of childbearing potential, unless the conditions of the pregnancy prevention programme are fulfilled
State potential contraceptive options for women of childbearing potential and starting ASM (3)
1) IUD
2) Medroxyprogesterone depot injection q10-12 wks + barrier method
3) Continuous cycle COC (high dose estrogen required; at least 50 mcg) + Barrier method
State principles of ASM use in pregnancy (3)
o Levetiracetam and lamotrigine are safer options for use during pregnancy
o Valproate should not be used in female children and women of childbearing potential unless other treatments are ineffective or not tolerated
o For women of childbearing potential currently using valproate:
* Prescriber to review alternative if possible
* Ensure communication of risks and need for contraception
Can breastfeeding women on ASM continue breastfeeding?
Yes. All breastfeeding women on ASM therapy should be encouraged to breastfeed
Describe clinical definition of status epilepticus
A condition resulting either from failure of mechanisms responsible for termination of seizure or from initiation of mechanisms leading to abnormally prolonged seizures for > 5mins.
What is/are the 1st line drug(s) for Status Epilepticus?
Parenteral benzodiazepine.
IM Midazolam (10mg for > 40kg, 5mg for 13-40kg)
IV Diazepam (4mg/dose, may repeat once)
IV Lorazepam (10mg/dose, may repeat once)
What are alternative 1st line for SE?
- IV Phenobarbital
- Rectal Diazepam (widely available and given to patients with seizure clusters; but not ideal dosage form)
Which ASM can be used for refractory seizures in both focal onset and generalised tonic-clonic?
Clobazam
What are 1st line ASMs for new onset Focal onset epilepsy?
- Carbamazepine (ILAE Level A)
- Levetiracetam (ILAE Level A)
- Lamotrigine (ILAE Level A, elderly)
What is drug of choice for focal onset epilepsy in elderly?
Lamotrigine
Which ASMs can be used for both focal onset and GTC (new onset)?
Lamotrigine, Carbamazepine, Valproate
State general procedure if patient has no response to first anti-epileptic agent
If patient does not respond to 1st agent chosen for new onset epilepsies, can choose the other agents that were not used amongst the level A or B agents before moving on to refractory drugs if they still don’t work.
State when can ASM be considered to be removed and when a patient’s epilepsy is considered to be resolved.
Drug discontinuation may be considered after a minimum of two years without a seizure (wait longer for those with high risk of recurrence or those with low incidence of less than one a year)
Epilepsy is considered to be resolved for individuals who had an age dependent epilepsy syndrome but are now past the applicable age or those who have remained seizure free for the last 10 years, with no seizure medicines for the last 5 years.
What is recorded in seizure diary? (5)
- Seizure frequency and types
- How long they last
- Changes in ASMs
- ASM side effect
- Seizure triggers
State unique side effects of Topiramate (4)
Renal stone
Glaucoma
Speech fluency affected
Anorexia and weight loss
Which ASM most associated with behavioural disturbance (increased irritability)?
Levetiracetam
