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PR3136 PT IV > Epilepsy WPS > Flashcards

Epilepsy WPS Flashcards

1
Q

What is the epidemiology of epilepsy in Singapore?

A
  • estimated prevalence of 3.5-5.0 per 1000 population
  • mean age of 1st seizure onset 11.1 yrs
  • Chinese: 5.2/ 1000 persons
  • Malays: 2.8/ 1000 persons
  • Indians: 6.4/ 1000 persons
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2
Q

What is the mortality risk of epilepsy? How high is the risk of premature death amongst ppl with epilepsy?

A
  • mortality risk inc 2- to 3-fold
  • highest within the 1st 12 months of diagnosis (the first year)

Epilepsy-related mortality risk:

  • sudden unexplained death in epilepsy (SUDEP)
  • Status epilepticus
  • Unintentional injuries (drowning, head injuries, burns)
  • suicide
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3
Q

What is the incidence of sudden unexplained death in epilepsy (SUDEP) and when does it usually occur and what are some risk factors?

A

Incidence: 1-2/ 1000 person-years; peak for those aged 20-40yo

Mostly unwitnessed and sleep-related:
many ind with SUDEP are found in prone position with evidence of having had a recent seizure;

rare cases occurring during video-EEG monitoring suggest that SUDEP is preceded by a convulsion followed shortly by apnoea and then asystole

Risk factors: presence and frequency of generalised tonic-clonic seizures; Nocturnal seizures; Lack of seizure freedom

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4
Q

What is the difference between seizures and epilepsy?

A

Seizure: transient occurrence of signs and/or smx due to abnormal excessive or synchronous neuronal activity in the brain

Epilepsy (any of the following):

  1. at least 2 unprovoked seizures occurring >24h apart
  2. One unprovoked seizure and a probability of further seizures similar to the general recurrence risk (At least 60%) after 2 unprovoked seizures, occurring over the next 10 years
  3. Diagnosis of an epilepsy syndrome

Epilepsy is a brain disorder characterised by an enduring predisposition to generate epileptic seizure

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5
Q

What are provoked seizures?

A

Acute Symptomatic Seizure

Interval between insult and seizure may vary according to underlying condition

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6
Q

What causes provoked seizures?

A
  1. events occuring in close temporal relationship with an acute CNS insult: Metabolic, Toxic, Structural, Infectious, Inflammation
  2. Electrolyte imbalances: HypoNa, HypoCa, HypoMg, Hypoglycaemia
  3. Toxic subs/drugs: illicit drugs (e.g. cocaine, amphetamines); drugs (e.g. TCAs, carbapenems, baclofen) –> lowers seizure threshold; EtOH (withdrawal and intoxication); Benzodiazepine withdrawal
  4. Traumatic brain injury
  5. Stroke
  6. CNS infection
  7. Febrile illness
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7
Q

What is the pathophysiology of epilepsy?

A

Key concept: Hyperexcitability and Hypersynchronisation

  • instability in a single neuronal cell membrane or group of cells around it
  • seizure activity us characterised by synchronised paroxysmal discharges occurring in a large population of neurons within the cortex
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8
Q

What does hyperexcitability mean?

A
  • Hyperexcitability: enhanced predisposition of a neuron to depolarise
  • voltage- or ligand-gated K+, Na+, Ca2+, and Cl- ion channels
  • Abnormalities in intra- & extracellular substances (e.g. Na+, K+, O2, glucose, etc)
  • Excessive excitatory neurotransmitters (E.g. glutamine, acetylcholine, histamine, cytokines, etc.)
  • Insufficient inhibitory neurotransmitters (e.g. GABA, dopamine)
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9
Q

What does hypersynchronisation mean?

A

Intrinsic organisation of local circuits - hippocampus, the neocortex, and the thalamus: contribute to synchronisation and promote generation of epileptiform activity

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10
Q

What is the aetiology (causes) of individuals getting epilepsy?

A
  • Genetic: gene/chromosone, E.g. FMRI (Fragile X Syndrome)
  • Structural: e.g. traumatic brain inj, tumours, hypoxic-ischemic abnormalities, vascular malformation
  • Metabolic: e.g. Mitochondrial disorders, GLUT1 deficiency
  • Immune: e.g. AB mediated
  • Infectious: e.g. bacterial meningitis, HIV, meningo-TB
  • Unknown
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11
Q

How to classify epilepsy?

A
  • Based on mode of onset:
    1. Focal onset: seizures begin only in one hemisphere; may spread to the contralateral hemisphere - “focal seizures evolving to a bilateral convulsive seizure”
    2. Generalised onset: seizures begin in both hemispheres
  • Impairment of consciousness: loss of awareness of external stimuli or inability to respond to external stimuli in a purposeful and appropriate manner; described as ‘with or without dyscognitive features’
  • significance: fundamental characteristic by which to classify seizures; treatment and prognostic implications
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12
Q

What are some categories of epilepsy?

A
  1. generalised onset (loss of consciousness)
    - -> (motor) tonic clonic (grand mal)
  • -> (non-motor) absence (petit mal)
  • -> myoclonic (muscle jerking)
  • -> atonic (motor) (paralytic; sudden loss of muscle strength)
  1. Focal onset
    - -> simple partial seizures (consciousness not impaired; without dyscognitive features)
    - -> complex partial seizures (consciousness impaired; with dyscognitive features)
  2. Unknown onset (motor and non-motor)
  3. Unclassified
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13
Q

What are the 3 key features that helps to group the type of seizures?

A
  • where seizures begin in the brain
  • level of awareness during the seizure
  • other features of the seizure
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14
Q

What are some epileptic syndromes that cause epileptic disorders? (idk how to phrase it)

A
  • epileptic disorder characterised by a cluster of S&S; e.g. type of seizure, aetiology, anatomy, precipitating factors, age of onset, severity, chronicity
    1. Electroclinical Syndromes (and common examples arrange by age at onset)
    2. Distinctive Constellations (And common examples): Mesial Temporal Lobe Epilepsy with Hippocampal Sclerosis
    3. Epilepsies Attributed to and Organised by Structural -Metabolic Causes (and common examples): Malformation of Cortical Development Tuberous Sclerosis Tumour Trauma Strokes
    4. Epilepsies of unknown cause
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15
Q

What are the clinical presentation of epilepsy depended on?

A
  • site of focus
  • degree of ‘irritability’ of the areas of the brain surrounding the focus
  • intensity of the impulse
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16
Q

FYI What are the clinical presentation of focal onset (w/o dyscognitive features)/ simple partial seizures?

A
  • Motor smx: clonic movements, speech arrest
  • Sensory: feelings of numbness/tingling; Visual disturbances (flashing lights); rising epigastric sensation
  • Autonomic smx: sweating, salivation/pallor; BP, HR
  • Psychic (somatosensory smx): flashbacks, de ja vu; Visual, auditory, gustatory or olfactory hallucinations
  • affective smx include fear (most common), depression, anger and irritability
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17
Q

What are the clinical presentation of focal onset (w dyscognitive features)/ complex partial seizures?

A
  • Aura: manifestations as described in focal non-dyscognitive seizures; usually last for few seconds
  • Impaired consciousness: Amnesia to the event
  • Automatisms: e.g. lip smacking, chewing, or picking at their clothing unpurposefully
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18
Q

What are the clinical presentation of generalised onset tonic-clonic ‘grand mal’ seizures?

A
  • most common and best known type
  • begins with stiffening of the limbs (tonic phase), followed by jerking of limbs and face (clonic phase)
  • During tonic phase, breathing may dec or cease altogether
  • Cyanosis of nail beds, lips and face; typically returns during clonic phase but may be irregular
  • Clonic phase usually lasts 1 min, after which the brain is extremely hyperpolarised and insensitive to stimuli
  • Incontinence may occur, + biting of the tongue or inside of mouth; breathing may be noisy and appear to be labours
  • Following the seizure, pt may have HA and appear lethargic, confused or sleepy
  • Full recovery takes several min to hours
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19
Q

FYI What are the clinical presentation of generalised onset clonic seizures?

A
  • Clonic jerking, often asymmetrical and irregular

- most frequent in neonates, infants or young children

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20
Q

FYI What are the clinical presentation of generalised onset tonic seizures?

A
  • Sudden loss of consciousness and rigid posture of entire body, last 10-20sec
  • Occur at all ages in setting of diffuse cerebral damage and learning disability, and are invariably assoc w other seizure types
  • Characteristic and defining seizure type in Lennox - Gastaut syndrome
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21
Q

FYI What are the clinical presentation of generalised onset myoclonic seizures?

A
  • Involves rapid, brief contractions of bodily muscles, usually occurring on both sides of the body concurrently
  • On occasion, may involve just one arm or one foot
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22
Q

What are the clinical presentation of generalised onset absence ‘petit mal’ seizures?

A
  • usually manifests as basic lapse in awareness that begins and ends abruptly
  • sometimes mistaken as persistent staring
  • lasts only a few sec - no warning, no after-effects
  • often undetected even if there 50-100 attacks per day
  • more common in children than in adults
  • first onset usually occurs 4-12yo; rarely after 20yo
  • may be mistaken for complex partial seizures - implication in wrong choice of medication prescribed
  • Absence seizures differ from complex partial seizures in that they:
    1. are never preceded by auras
    2. last seconds (rather than minutes)
    3. begin frequently and end abruptly

4. produce characteristic EEG pattern “3Hz spike waves”

23
Q

What are the clinical presentation of generalised onset atonic seizures?

A
  • most severe form is the classic drop attack (astatic seizure) in which all postural tone is suddenly lost, causing collapse to the ground like a rag doll
  • short episode and followed by immediate recovery
  • occur at any age, and are always associated with diffuse cerebral damage and learning disability
  • Common in severe symptomatic epilepsies (esp in Lennox-Gastaut syndrome and in myoclonic astatic epilepsy)
24
Q

how do we diagnose the correct type of epilepsy condition for a patient?

A
  1. Hx taking IMPT
    - -> description of onset, duration, characteristics of a seizure
    - -> accurate hx is best provided by person who has observed the events
    - -> patient is useful in describing details of aura, preservation of consciousness, and post-ictal state

(The postictal state is the abnormal condition occurring between the end of an epileptic seizure and return to baseline condition.)

  1. neurologic examination
  2. concomitant medical conditions
25
Q

what are the positive identification of the classical characteristics of an epilepsy condition when diagnosing someone?

A
  • aura
  • cyanosis
  • loss of consciousness
  • motor manifestation
  • generalised stiffness of limbs and body (tonic)
  • jerking of limbs (clonic)
  • tongue biting
  • urinary incontinence
  • post-ictal confusion
  • muscle soreness
26
Q

what are the differential diagnosis that resemble epilepsy?

A
  • syncope (fainting) - ‘fit’ vs ‘faint’ dilemma
  • transient ischemic attack (symptoms similar to a stroke)
  • migraine
  • psychogenic nonepileptic seizures (someone who has a formal diagnosis of epilepsy, but doesn’t have seizure under the EEG but looked like the patient had a seizure)
27
Q

why is an electroencephalography (EEG) important?

A
  • tool for diagnosis and classification of seizures and epileptic syndromes
  • if diagnosis of seizures or epilepsy is considered, epileptiform EEG confirms diagnosis
  • a normal EEG does NOT exclude possibility of epilepsy
28
Q

what are the limitation of a scalp EEG?

A
  • 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
  • EEG can be abnormal in normal persons
  • -> false positive epileptiform EEG in asymptomatic adults: 0.5-1%
29
Q

difference between a focal onset epilepsy and a generalised onset epilepsy

A

EEG in focal onset epilepsy: only one hemisphere have epileptiform reading

EEG in generalised onset epilepsy: both hemisphere have epileptiform reading

30
Q

EEG is now increasingly used for what type of seizures?

A

patients with suspected psychogenic non-epileptic seizures

EEG + video recording done - to see for correlation

31
Q

what other investigation tests we do to diagnose/classify epilepsy other than EEG?

A
  1. Magnetic resonance imaging (MRI) with gadolinium
    - -> ordered for: adult pt who present with first seizure, pts with focal neurologic deficits, suggestion of focal onset seizure
    - -> identify focal lesions:
    - mesial temporal sclerosis
    - focal cortical dysplasia
    - remote injury (old stroke etc)
    - tumor
    - vascular malformation
  2. Biochemical/toxicology
    –> helps rule out electrolyte abnormalities
    –> serum prolactin - considerable variability - not used routinely
    –> creatine kinase (CK) - raised after GTC
    (GTC = generalised tonic-clonic seizure)
32
Q

how do we approach to diagnose a patient with epilepsy if they had their first seizure? what questions do we ask when diagnosing a patient?

A
  1. was it a seizure?
  2. was it the first seizure?
  3. was it a provoked seizure? (consider drug or medical conditions)
  4. if not, what is the likely cause (etiology)?
  5. Does the patient need anti-seizure med (AED)
    - what is the risk of seizure recurrence
    - patient factors
    - which AED to give?
33
Q

IMPT

what is the risk of seizure recurrence?

A

risk of second seizure:
- within next 5 yrs -30%, higher in the 1st 2 years

  • higher in presence of:
  • -> epileptiform abnormalities on EEG
  • -> prior brain insult (e.g. stroke, brain trauma)
  • -> structural abnormality in brain imaging MRI
  • -> nocturnal seizure

risk of recurrent seizures after TWO unprovoked seizures at 4yrs ~70%

34
Q

IMPT

when do we start treatment in patients who had seizures?

A
  • after a single unprovoked seizure, recurrence is low ~30% –> 80-90% had second seizure within 2 years
    (but dont start cause, even with evidence showing AED will reduce risk of 2nd seizure, there’s no effect on long-term prognosis and no evidence of higher risk of death, injuries, or status epilepticus; risk > benefits)

BUT only start when:
1. two unprovoked nonfebrile seizures (risk of recurrence ~70%)
OR
2. one seizure + either of the 4 conditions mentioned in slide 42

35
Q

what could be other determinants to start treatment?

A
  • work, need for driver license (in sg if diagnosed w epilepsy, cannot drive), desire to bear children
36
Q

what are the treatment goals for epilepsy?

A
  • absence of epileptic seizure
  • absence of anti-epileptic drug (AED)-related SE
  • attain optimal QoL
  • about 2/3 of patients able to achieve seizure-freedom w approp treatment
37
Q

what are the different treatment for epilepsy?

A
  1. pharmacological (mainstay)
  2. non-pharmacological
    - ketogenic diet
    - vagus nerve stimulation (VNS)
    - responsive neurostimulator system (RNS)
    - surgery
38
Q

what are the factors influencing AED choice?

A

treatment has to be individualized based on:

  1. seizure type, epilepsy syndrome
    - -> whether rapid titration is required: e.g. lamotrigine and topiramate requires slow titration; carbamazepine undergoes autoinduction
  2. co-medication and co-morbidity
    - -> e.g. migraine - consider topiramate, valproate
    - -> depression/anxiety: use levetiracetam with caution
    - -> DDI: e.g. patient on HIV med, immunosuppressants
    - -> route of elimination: renal or liver impairment
    - -> special precaution: women of childbearing potential - avoid valproate, consider levetiracetam/lamotrigine
39
Q

how do we start patients on AED? (start w one or two med?)

A
  • monotx preferred

advantages of monotx:

  • lower incidence of adverse effect
  • absence of drug interactions
  • reduced risk of birth defects
  • lower cost
  • easier to correlate response and adverse effects
  • better adherence
40
Q

at what dose do we start on patient w epilepsy?

A
  • start low dose of first line AED for the particular seizure type
  • if seizure continue but no SE occurs: gradually increase dose of AED
  • if seizure continues despite max tolerated dose of first line AED:
  • -> diagnosis to be reviewed

–> ensure patient has receive the appropriate drug for their seizure type/epileptic syndrome

–> check for adherence (pt need to understand dosing instruction, able to execute, SE, inconvenient regimen, financial issues etc)

41
Q

IMPT

how can we ensure seizure freedom for our patients?

A
  • chance of seizure freedom after failure of first AED is low ~16%
  • -> thus many pt with epilepsy will require combination(adjunctive( therapy
  • there is no evidence whether subsititution monotx or combination(adjunctive) therapy is better
    THUS
  1. if first AED produces an adverse drug rxn or is not tolerated at low dose or does not improve seizures: consider SUBSTITUTION
  2. if patient tolerates the first or second AED but with a suboptimal response: consider COMBINATION therapy
42
Q

what are the factors to consider when combining AED?

A
  • patient’s previous clinical response to each drug alone
  • drugs MOA (to widen the spectrum, choose another AED with another MOA)
  • drugs tolerability profile
  • drugs PK profile (e.g. whether it will interact with other med in patients w pre-existing condition)
43
Q

what is the seizure freedom percentage like for patients?

A
  • about 50% patients with new onset focal or generalised seizure achieve seizure freedom while taking the first appropriately selected and dosed first line antiepileptic drug (just one drug)
  • about 30% patients have drug resistant epilepsy: failure of two tolerated appropriately chosen and used antiepileptic schedules (whether monotx/substitution or combination) to achieve sustained seizure freedom
44
Q

what are the non-pharmacological treatment for epilepsy?

A
  1. ketogenic diet
    - in young children
    - who cannot tolerate/ not responded to AED treatment
    - low carb, high fat in diet
    - hard to adhere long term
    - induction of ketosis
  2. vagus nerve stimulator (VNS)
    - for intractable focal seizures (seizure that doesnt come under control with treatment)
  3. responsive neurostimulator system (RNS)
    - not yet in sg
    - stimulator implanted in skull
    - reduce freq of partial-onset seizures
    - refractory to >= 2 antiepileptic med
  4. epilepsy surgery
    - early therapy for some specific epileptic syndromes
45
Q

what are the psychosocial issues of someone having epilepsy

A
  1. social stigma
    - marriage, starting a family
  2. employment
    - more time away from work for medical follow-up
    - higher medical cost borne by employer
  3. prohibited from driving
    - SG: prohibited from driving regardless of whether they have been seizure-free for >2yrs
  4. caregiver burden
46
Q

what is the attitude toward patients w epilepsy like?

A

better awareness and more acceptance

47
Q

what are the comorbidities in people w epilepsy?

A
  • physical and psychiatric comorbidities in people with epilepsy assoc w:
  • -> poorer health outcomes
  • -> increased healthcare needs
  • -> decreased QoL
  • -> greater social exclusion
  • most common psychiatric comorbidities: depression and anxiety
  • intellectual disability is the most common comorbidity in children with epilepsy
48
Q

what do we educate the epilepsy patient

A
  • avoid preventable seizure triggers
  • AEDs: SE, drug interactions (e.g warfarin)
  • activities
  • -> driving, firearms, swimming
  • community resources
49
Q

what are some seizure triggers?

A
  • hyperventilation
  • photostimulation
  • physical and emotional stress
  • sleep deprivation
  • electrolyte imbalance (hypoglycemia, hyponatremia/hypernatremia, hypocalcemia, hypomagnesemia)
  • sensory stimuli
  • infection
  • hormonal changes (time of menses, puberty, or pregnancy)
  • drugs (theophylline, alcohol, high-dose phenothiazines (chlorpromazine), antidepressant (esp bupropion, tramadol, carbapenems)
50
Q

what to write in a seizure diary?

A
  • seizure freq and types
  • how long they last
  • changes in AEDs
  • AED SE
  • seizure triggers
51
Q

what is the seizure first aid

A

for generalised tonic-clonic seizures:

  • turn person gently onto one side, helps them breathe
  • put something soft and flat
  • remove eyeglasses
  • loosen ties or anything around neck
  • clear any sharp hard objects
  • time the seizure. Call 911 if seizure last longer than 5 min
  • dont put anything in person’s mouth
  • dont give cpr
  • dont offer water or food
52
Q

SUMMARY

are all patients presenting with seizures given a clinical diagnosis of epilepsy?

A

No

53
Q

KEY TAKEWAY POINTS

A
  • not all pts who present with seizures are given the clinical diagnosis of epilepsy
  • neuronal hyperexcitability and hypersynchronisation of local circuits promote generation of epileptiform activity
  • clinical manifestation of a seizure episode is dependent on the area affected
  • diagnosis: accurate Hx taking is key, EEG confirmatory
  • ILAE classification - provides guidance to prognostication and treatment
  • Ppl w epilepsy (PWE): unique psychosocial challenges
  • treatment: pharmacological (MAINSTAY) + non-pharm options (keto, VNS, RNS, surgery)

PR3136 PT IV (17 decks)

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