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MD2 Neuro > Approach to Seizures and Epilepsy > Flashcards

Approach to Seizures and Epilepsy Flashcards

1
Q

Define seizure

A

Intermittent, stereotyped disturbance of consciousness, behaviour, emotion, motor or sensory function resulting from abnormal cortical neuronal discharges

Simply: abnormal hypersynchronous neural activity

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2
Q

List 2 non-epileptic causes of seizure

A

Alcohol withdrawal

Hypoglycaemia

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3
Q

List 2 seizure syndromes unrelated to epilepsy

A

Single seizures

Childhood febrile seizures

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4
Q

SUDEP

A

Sudden unexpected death in epilepsy

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5
Q

List 4 risk factors for epilepsy

A

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)

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6
Q

Distinguish between focal and primary generalised seizures

A

Focal: unilateral networks at onset

Primary generalised: bilateral networks at onset

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7
Q

List 3 types of focal seizures

A

Simple focal

Focal dyscognitive (PKA complex partial; affects consciousness)

Secondary generalised tonic clonic

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8
Q

List 4 types of primary generalised seizures

A

Absence

Myoclonic/atonic

Tonic

Primary generalised tonic clonic (GTCS; often all seizures are called this; important to clarify this is actually the case)

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9
Q

Focal seizures

A

Seizure starts (symptoms due to ictal areas)

Seizure discharges may spread enough to impair awareness

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10
Q

Where do focal seizures most commonly start?

A

Temporal lobe

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11
Q

List 5 early temporal lobe seizure symptoms

A

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)

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12
Q

Later symptoms of temporal lobe seizures

A

Automatisms; can look at predominant side involved to estimate the lateralisation of the seizure

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13
Q

What are 4 distinctive clinical features of frontal lobe seizures?

A

Bizarre stereotyped movements, often from sleep

More rapid recovery than temporal lobe seizures

Often fully aware throughout

Sudden onset and offset

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14
Q

What are the main symptoms of occipital lobe seizures?

A

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)

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15
Q

How can visual hallucinations caused by migraine be differentiated from those caused by occipital lobe seizure?

A

Migraine: black and white

Occipital: colour

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16
Q

What is the main symptom of parietal lobe seizures?

A

Somatosensory symptoms (often with neuropathic characteristics; tend to travel from periphery centrally)

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17
Q

What is one of the activating states for seizures?

A

Hyperventilation

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18
Q

How long do absence seizures last?

A

Often extremely frequent and extremely brief (several seconds)

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19
Q

When is the commonest age for onset of absence seizures?

A

Childhood (very unlikely after mid-20s)

Usually 4-8 years but can be up to age 12

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20
Q

List 3 features of absence seizures

A

Eye-flickering

Behavioural arrest

Can have minor automatisms but no loss of postural tone

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21
Q

How can absence seizures be distinguished from focal dyscognitive seizures?

A

Focal dyscognitive longer, pt feels tired afterward

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22
Q

Describe the typical progression of a primary generalised tonic clonic seizure

A

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

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23
Q

Differential diagnosis of blackout/collapse

A

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)

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24
Q

List 4 causes/types of syncope

A

Neurally mediated/vasovagal

Orthostatic hypotension

Cardiac arrhythmias

Structural cardiopulmonary (e.g. AS)

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25
Is EEG a useful diagnostic tool for epilepsy?
No; can be normal Best diagnostic tool is a good history (including witness history)
26
What 5 aspects are important when assessing a paroxysmal episode of collapse?
Background to pt Setting Prodrome Event Recovery
27
Syncope vs seizure: background
Syncope: previous syncope Seizure: PMHx or FHx of epilepsy
28
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
29
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
30
Syncope vs seizure: attack
Syncope: pallor, motionless collapse Seizure: tongue biting, head turning, unusual posturing, cyanosis, urinary incontinence in bed
31
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)
32
Pseudoseizure
Arching of the trunk common Attacks tend to be prolonged (20-30 mins), wax and wane, multiple attacks common, very variable in semiology
33
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
34
Migraine vs seizure?
Migraine: flickering, uncoloured zigzags, central zigzags, may leave scotoma
35
How does a myoclonic seizure present?
Sudden shock-like jerk
36
How does an atonic seizure present?
Sudden relaxation which may impair posture
37
How does a tonic seizure present?
Usually whole body stiffening, pt can fall over
38
Why are episodes of syncope often mistaken for seizure?
Because jerks, stiffness and sometimes automatism-like gestures can occur in syncope
39
What might focal occipital lobe seizures mimic?
Migrainous visual aura
40
What type of seizure might mimic a TIA?
Focal seizure, esp focal occipital seizure with negative symptoms
41
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)
42
What type of seizure might mimic tinnitus?
Lateral temporal seizures with auditory aura
43
Define ictus
Sudden neurological event
44
Define epilepsy
Tendency to repeated, spontaneous seizures
45
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
46
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
47
Compare the duration of a generalised tonic clonic seizure to that of an absence seizure
Tonic clonic: 1-5 mins Absence: 2-10 secs
48
What is myoclonus?
Sudden, involuntary muscle twitch not specific to seizure (hypnagogic myoclonus occurs normally)
49
In what condition is myoclonus common?
Metabolic encephalopathy
50
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)
51
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
52
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
53
What subsyndromes are seen in genetic generalised epilepsies?
Childhood absence epilepsy Juvenile myoclonic epilepsy Juvenile absence epilepsy Epilepsy with tonic-clonic seizures alone
54
What proportion people who have had a single seizure as an adult will not develop epilepsy?
50%
55
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
56
What kinds of seizures can appear as a prodrome to GTCS?
Myoclonic seizures
57
What seizure subsyndrome presents with myoclonus that is more prominent in the morning?
Juvenile myoclonic epilepsy
58
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
59
What seizure types are seen in genetic generalised epilepsies?
GTCS Absence Myoclonic
60
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
61
What are the clinical features of childhood absence epilepsy?
40-50 seizures/day No fatigue or weakness after each episode Can induce by hyperventilating
62
Childhood absence epilepsy PKA?
Petit mal
63
What seizure types are seen in childhood absence epilepsy?
Absence seizures (many/day) 40% also experience GTCS
64
Describe the natural Hx of childhood absence epilepsy
20% continue having absences and develop juvenile absence epilepsy 20% develop juvenile myoclonic epilepsy 60% resolve
65
What is the onset of juvenile absence epilepsy and what seizure types are seen?
Onset in adolescence GTCS and (infrequent) absence seizures
66
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
67
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%
68
What are the clinical features of juvenile myoclonic epilepsy?
Photosensitive Related to sleep-wake cycle (more common after wakening)
69
What is the prognosis of juvenile myoclonic epilepsy?
Not often refractory Spontaneous remission rare
70
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
71
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
72
List 5 predisposing factors and 4 triggers for syncope
Dehydration Anti-HTNs Prolonged standing Stressful situation Recent awakening Triggers: emotional, valsalva, pain, postural change
73
3 features of pre-syncope
"Dizziness" Feeling of distance Visual disturbance: silver flickers, greying of vision
74
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)
75
Describe features seen during recovery from syncope
Awaken rapidly: on the ground rather than in the ambulance (beware head injury) Often tired Not confused
76
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
77
List 3 predisposing factors/triggers for seizure
Sleep deprivation Hangover or abrupt abstinence from EtOH Flicker (photosensitivity)
78
What medications may trigger seizure?
Clozapine Tramadol
79
What is TIA?
Sudden, focal neurological deficit LOC exceptional (posterior circulation TIA almost always focal)
80
List 6 common features of psychogenic pseudoseizure
Fluctuating intensity Very long Eyes closed (pseudo-sleep) Non-anatomical tremor Reactive Consciousness retained (usually denied)
81
Distinguish between seizure and pseudo-seizure in terms of EEG findings
Seizure: almost always abnormal Pseudo-seizure: perfect
82
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)
83
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
84
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
85
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
86
How is epilepsy diagnosed?
Hx of minor seizures (focal or myoclonus) Await recurrence Epileptiform EEG Epileptogenic MRI lesion
87
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
88
What criterion must be fulfilled in order for a patient with epilepsy to be able to drive?
6-12 months seizure free
89
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
90
What drug options are there for treatment of genetic generalised epilepsy?
Ethosuxamide
91
5 broad-spectrum treatments for epilepsy
Valproate (but teratogenic) Levetiracetam Lamotrigine Zonisamide Topiramate
92
8 treatments for focal epilepsy (lesional and non-lesional)
Carbamazepine Phenytoin Oxcarbazepine Lacosamide Gabapentin Pregabalin Vigabatrin Tiagabine
93
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)

MD2 Neuro (9 decks)

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