Approach to Seizures and Epilepsy Flashcards
Define seizure
Intermittent, stereotyped disturbance of consciousness, behaviour, emotion, motor or sensory function resulting from abnormal cortical neuronal discharges
Simply: abnormal hypersynchronous neural activity
List 2 non-epileptic causes of seizure
Alcohol withdrawal
Hypoglycaemia
List 2 seizure syndromes unrelated to epilepsy
Single seizures
Childhood febrile seizures
SUDEP
Sudden unexpected death in epilepsy
List 4 risk factors for epilepsy
FHx
Childhood febrile seizures (small increased risk, esp if convulsive status epilepticus)
Perinatal event or abnormal early development
Other previous brain insult (e.g. significant head trauma, stroke, meningitis, encephalitis)
Distinguish between focal and primary generalised seizures
Focal: unilateral networks at onset
Primary generalised: bilateral networks at onset
List 3 types of focal seizures
Simple focal
Focal dyscognitive (PKA complex partial; affects consciousness)
Secondary generalised tonic clonic
List 4 types of primary generalised seizures
Absence
Myoclonic/atonic
Tonic
Primary generalised tonic clonic (GTCS; often all seizures are called this; important to clarify this is actually the case)
Focal seizures
Seizure starts (symptoms due to ictal areas)
Seizure discharges may spread enough to impair awareness
Where do focal seizures most commonly start?
Temporal lobe
List 5 early temporal lobe seizure symptoms
Olfactory and gustatory hallucinations (typically noxious)
Changes in speech (esp if seizure starts on dominant hemisphere; impt to distinguish from TIA)
Deja vu
Autonomic phenomena (e.g. butterflies in stomach)
Auditory hallucinations (less common; esp hallucinations of reverberating machine-like noise)
Later symptoms of temporal lobe seizures
Automatisms; can look at predominant side involved to estimate the lateralisation of the seizure
What are 4 distinctive clinical features of frontal lobe seizures?
Bizarre stereotyped movements, often from sleep
More rapid recovery than temporal lobe seizures
Often fully aware throughout
Sudden onset and offset
What are the main symptoms of occipital lobe seizures?
Visual symptoms (commonly simple hallucinations, e.g. coloured circles and patterns)
Occasionally negative phenomena (i.e. blindness)
Headache after occipital lobe seizures (can be confused with migraine)
How can visual hallucinations caused by migraine be differentiated from those caused by occipital lobe seizure?
Migraine: black and white
Occipital: colour
What is the main symptom of parietal lobe seizures?
Somatosensory symptoms (often with neuropathic characteristics; tend to travel from periphery centrally)
What is one of the activating states for seizures?
Hyperventilation
How long do absence seizures last?
Often extremely frequent and extremely brief (several seconds)
When is the commonest age for onset of absence seizures?
Childhood (very unlikely after mid-20s)
Usually 4-8 years but can be up to age 12
List 3 features of absence seizures
Eye-flickering
Behavioural arrest
Can have minor automatisms but no loss of postural tone
How can absence seizures be distinguished from focal dyscognitive seizures?
Focal dyscognitive longer, pt feels tired afterward
Describe the typical progression of a primary generalised tonic clonic seizure
Sudden stiffening often in association with ictal cry
Stiffen usually in fully extended position, arms and/or legs may be flexed (can have fractures, dislocations in this phase)
No ventilation during this time, pt will be cyanosed
After 15-20 seconds, low amplitude high frequency vibration movements
As seizure progresses, movements become higher in amplitude and lower in frequency before seizure ceases
Differential diagnosis of blackout/collapse
Syncope
Functional attacks (pseudo-seizures)
Migrainous visual aura
TIA (usually negative symptoms)
Metabolic dysfunction (e.g. hypoglycaemia; distinguish from focal seizures
Tinnitus (distinguish from lateral temporal seizures with auditory aura)
Physiological deja vu (distinguish from mesial temporal seizures)
Parasomnias (distinguish from frontal seizures; quite complex but good literature about how to do it)
Movement disorders (e.g. hemiballismus, paroxysmal dyskinesias; distinguish from frontal seizures)
List 4 causes/types of syncope
Neurally mediated/vasovagal
Orthostatic hypotension
Cardiac arrhythmias
Structural cardiopulmonary (e.g. AS)
Is EEG a useful diagnostic tool for epilepsy?
No; can be normal
Best diagnostic tool is a good history (including witness history)
What 5 aspects are important when assessing a paroxysmal episode of collapse?
Background to pt
Setting
Prodrome
Event
Recovery
Syncope vs seizure: background
Syncope: previous syncope
Seizure: PMHx or FHx of epilepsy
Syncope vs seizure: setting
Syncope: rising, prolonged standing, pain/fright/needles, cough, micturition, hairbrushing, after exercise (favours vasovagal), during exercise (favours cardiogenic syncope)
Seizure: stress, sleep deprivation, photic triggers, drug withdrawal
Syncope vs seizure: prodrome
Syncope: nausea, palpitations, dyspnoea, pallor, warm sensation, sweating, light-headedness, greying of vision, hearing becomes distant
Seizure: aura may reflect ictal focus
Syncope vs seizure: attack
Syncope: pallor, motionless collapse
Seizure: tongue biting, head turning, unusual posturing, cyanosis, urinary incontinence in bed
Syncope vs seizure: recovery
Syncope: nausea, rapid recovery to orientation
Seizure: headache, confusion, post-ictal amnesia, slow recovery to orientation (ask what was the first thing the pt remembers after their episode)
Pseudoseizure
Arching of the trunk common
Attacks tend to be prolonged (20-30 mins), wax and wane, multiple attacks common, very variable in semiology
Seizures vs pseudoseizures
Pseudoseizures: often background abuse, may be other medically unexplained symptoms (e.g. pain), attacks variable, often wax and wane, flurries of attacks common, attacks often prolonged (e.g. 20 mins)
Seizures: may be background brain injury or FHx epilepsy, attacks stereotyped, attacks evolve then stop, attacks usually 1-2/day (except absences, NFLE), attacks >4 mins uncommon
Migraine vs seizure?
Migraine: flickering, uncoloured zigzags, central zigzags, may leave scotoma
How does a myoclonic seizure present?
Sudden shock-like jerk
How does an atonic seizure present?
Sudden relaxation which may impair posture
How does a tonic seizure present?
Usually whole body stiffening, pt can fall over
Why are episodes of syncope often mistaken for seizure?
Because jerks, stiffness and sometimes automatism-like gestures can occur in syncope
What might focal occipital lobe seizures mimic?
Migrainous visual aura
What type of seizure might mimic a TIA?
Focal seizure, esp focal occipital seizure with negative symptoms
What type of seizure might mimic metabolic dysfunction (e.g. hypoglycaemia)?
Focal seizures
Physiological deja vu (distinguish from mesial temporal seizures)
Parasomnias (distinguish from frontal seizures; quite complex but good literature about how to do it)
Movement disorders (e.g. hemiballismus, paroxysmal dyskinesias; distinguish from frontal seizures)
What type of seizure might mimic tinnitus?
Lateral temporal seizures with auditory aura
Define ictus
Sudden neurological event
Define epilepsy
Tendency to repeated, spontaneous seizures
Describe the typical progression of a tonic clonic seizure
Tonic phase: arms down, eyes open, cry
Clonic phase: low amplitude high frequency vibratory movements (amplitude increases and frequency decreases until this ceases)
Apnoea: cyanosis or plethora
Aftergoing confusion
Usually lasts 1-5 mins, minor injury is common
What are the main features of an absence seizure?
Alteration of consciousness but with no loss of postural tone: pt stays upright, no warning, difficult to detect
Facial twitch: 3Hz blink with oral myoclonias, eyes often drift open
Compare the duration of a generalised tonic clonic seizure to that of an absence seizure
Tonic clonic: 1-5 mins
Absence: 2-10 secs
What is myoclonus?
Sudden, involuntary muscle twitch not specific to seizure (hypnagogic myoclonus occurs normally)
In what condition is myoclonus common?
Metabolic encephalopathy
Distinguish between simple focal seizures and focal discognitive seizures
Simple: no alteration of consciousness, features depend on location (e.g. temporal may cause deja-vu), usually brief
Focal discognitive: alteration of consciousness due to bilateral involvement of the temporal lobe (effects are localised)
How do focal dyscognitive seizures differ from absence seizures?
Longer (>30 secs)
Less distinct offset
Automatisms (more florid than in absence)
Less frequent
Preceding simple focal seizure
What features are important for defining an epilepsy syndrome?
Seizure type (determined by clinical characteristics of seizure and patient, and EEG features)
Age
Clinical course
Interictal EEG
MRI
+/- genetics
What subsyndromes are seen in genetic generalised epilepsies?
Childhood absence epilepsy
Juvenile myoclonic epilepsy
Juvenile absence epilepsy
Epilepsy with tonic-clonic seizures alone
What proportion people who have had a single seizure as an adult will not develop epilepsy?
50%
Distinguish between disease vs. syndrome in the context of epilepsy
Disease: illness with shared aetiology, pathology, progression and presentation, and with a known cause
Syndrome: collection of clinical features that present together, clinical first step to defining a disease
There are a variety of causes which may produce the same seizure syndrome
What kinds of seizures can appear as a prodrome to GTCS?
Myoclonic seizures
What seizure subsyndrome presents with myoclonus that is more prominent in the morning?
Juvenile myoclonic epilepsy
DDx for seizure syndrome in a generalised convulsion
Primary GTCS
Late stage focal seizure
Because recognisable partial phase is variable so the two syndromes may be indistinguishable
What seizure types are seen in genetic generalised epilepsies?
GTCS
Absence
Myoclonic
What are the clinical features of genetic generalised epilepsies?
No clinical, radiological or EEG evidence of brain damage
Epileptiform discharges 3 Hz or faster
Response to therapy is usually good
What are the clinical features of childhood absence epilepsy?
40-50 seizures/day
No fatigue or weakness after each episode
Can induce by hyperventilating
Childhood absence epilepsy PKA?
Petit mal
What seizure types are seen in childhood absence epilepsy?
Absence seizures (many/day)
40% also experience GTCS
Describe the natural Hx of childhood absence epilepsy
20% continue having absences and develop juvenile absence epilepsy
20% develop juvenile myoclonic epilepsy
60% resolve
What is the onset of juvenile absence epilepsy and what seizure types are seen?
Onset in adolescence
GTCS and (infrequent) absence seizures
What is absence status?
Absence status epilepticus, is marked by a generalised seizure affecting the whole brain resulting in episodes characterized by a long-lasting stupor, staring, and unresponsiveness
What is the typical age of onset for juvenile myoclonic epilepsy (Janz syndrome) and what seizure types are seen in juvenile myoclonic epilepsy?
Onset: 12-18 years
Seizure types: myoclonus, GTCS, absences in 30%
What are the clinical features of juvenile myoclonic epilepsy?
Photosensitive
Related to sleep-wake cycle (more common after wakening)
What is the prognosis of juvenile myoclonic epilepsy?
Not often refractory
Spontaneous remission rare
What are the clinical characteristcs and EEG features of an absence seizure?
Clinical characteristics: brief lapse of attention (~5 secs), otherwise normal patient
EEG features: run of 4Hz spike-wave
Describe the age of onset, typical clinical course and appearance on MRI of childhood absence epilepsy
Onset: 5 years
Clinical course: response to valproate, often remission at 14 years
MRI: normal
List 5 predisposing factors and 4 triggers for syncope
Dehydration
Anti-HTNs
Prolonged standing
Stressful situation
Recent awakening
Triggers: emotional, valsalva, pain, postural change
3 features of pre-syncope
“Dizziness”
Feeling of distance
Visual disturbance: silver flickers, greying of vision
Describe features seen during syncope
Pale
Eye elevation
Collapse (may be described as stiff)
Convulse: brief (<30 secs), asymmetric, no tonic, often delayed
Often incontinent
Injury not uncommon
May be prolonged if held upright (e.g. if LOC in toilet cubicle)
Describe features seen during recovery from syncope
Awaken rapidly: on the ground rather than in the ambulance (beware head injury)
Often tired
Not confused
Distinguish between the prodrome and post-ictal state of GTCS vs syncope
Prodrome: presence/absence of syncopal triggers, posture (syncope while supine is more concerning), pre-syncope vs aura
Ictal state: tongue-biting more common in GTCS (may be incontinence in either syncope or GTCS)
Post-ictal state: speed of recovery
List 3 predisposing factors/triggers for seizure
Sleep deprivation
Hangover or abrupt abstinence from EtOH
Flicker (photosensitivity)
What medications may trigger seizure?
Clozapine
Tramadol
What is TIA?
Sudden, focal neurological deficit
LOC exceptional (posterior circulation TIA almost always focal)
List 6 common features of psychogenic pseudoseizure
Fluctuating intensity
Very long
Eyes closed (pseudo-sleep)
Non-anatomical tremor
Reactive
Consciousness retained (usually denied)
Distinguish between seizure and pseudo-seizure in terms of EEG findings
Seizure: almost always abnormal
Pseudo-seizure: perfect
What are interictal EEG findings useful for? What are the limitations?
Dx of epilepsy syndrome (not seizure) and prognosis
Limitations: not very sensitive (most abnormal patterns also seen in normals; most helpful for distinguishing between focal and generalised patterns)
What is the role of CTB in epilepsy Dx?
Good for detecting certain conditions which may trigger seizure, including tumour, haemorrhage, neurocysticercosis (can visualise calcified cysts; this is one of the commonest causes of epilepsy in the world but not necessarily Aus)
Bad for almost everything else
What does this MRI show? Describe the cliinical features and pathophysiology of this disorder

Double cortex or band heterotopia
Form of diffuse grey matter heterotopia affecting almost only women; refractory epilepsy is present in nearly all affected patients, with partial complex and atypical absence epilepsy being the most common syndromes
Precursor cells which make the cortex must migrate up a scaffold of glial cells; in some genetic disorders they stall because of a lack of appropriate machinery
Can early treatment of seizure change prognosis? (In terms of longterm epilepsy rates)
Large randomised trial which provided treatment after either the first or second seizure found that there was better early seizure freedom if treated early but by five years the outcome was identical
How is epilepsy diagnosed?
Hx of minor seizures (focal or myoclonus)
Await recurrence
Epileptiform EEG
Epileptogenic MRI lesion
What activities should patients with epilepsy be counselled on in the interests of safety?
Swimming: should have showers not baths, have a swimming partner
Heights (including ladders)
Work
Driving
Avoiding triggers: alcohol, inadequate sleep, stress
What criterion must be fulfilled in order for a patient with epilepsy to be able to drive?
6-12 months seizure free
Mx of acute seizures
In the acute setting: benzodiazepenes for seizure termination, benzodiazepines or phenytoin (levetiracetam, valproate) for acute prophylaxis
In the long term setting: don’t treat - almost always self-limiting, only need to treat if prolonged or recurrent
What drug options are there for treatment of genetic generalised epilepsy?
Ethosuxamide
5 broad-spectrum treatments for epilepsy
Valproate (but teratogenic)
Levetiracetam
Lamotrigine
Zonisamide
Topiramate
8 treatments for focal epilepsy (lesional and non-lesional)
Carbamazepine
Phenytoin
Oxcarbazepine
Lacosamide
Gabapentin
Pregabalin
Vigabatrin
Tiagabine
What is SUDEP?
Sudden Unexpected Death in Epilepsy: high rate of sudden death in epilepsy (1-2 per 1000 patient years, 20-fold increase in 18-35 years), likely due to cardio-respiratory arrest (often in sleep)
Related to seizure frequency (risk is much reduced by seizure freedom; 6-9 per 1000 patients years in refractory focal epilepsy)