Epilepsy Flashcards

(133 cards)

1
Q

What is the incidence and prevalence of epilepsy?

A

Incidence: 5 per 10,000 per year
• Prevalence: 7.5 per 1,000

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2
Q

Among patients with suspected “first seizures,” what are common alternative diagnoses?

A

• Most have syncope
• Many have provoked seizures (e.g., alcohol-related)

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3
Q

Among patients prescribed AEDs for recurrent episodes, what percentage may not actually have epilepsy?

A

20%, most often due to psychogenic non-epileptic attacks

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4
Q

What features suggest a true epileptic seizure?

A

• Stereotyped, unprovoked events
• Aura (characteristically “indescribable”)
• Automatisms, posturing, convulsions
• Lateral tongue biting
• Post-ictal confusion

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5
Q

What are key features of vasovagal syncope?

A

• Situational triggers (bathroom, restaurant, airplane)
• Prodrome: hot, prickly, nausea, visual darkening, pallor
• Brief loss of consciousness (with/without jerks), rapid orientation, prolonged fatigue
• Variants: cough syncope, micturition syncope
• May mimic seizures: myoclonic jerks, head turning, automatisms, incontinence

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6
Q

What suggests cardiac syncope?

A

• Cardiac symptoms or abnormal ECG
• Abrupt, unprovoked collapse
• Brief unconsciousness with rapid recovery

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7
Q

What other types of syncope should be considered?

A

• Orthostatic syncope (autonomic failure, elderly, anti-parkinsonian meds)
• Carotid sinus syncope (typically elderly)

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8
Q

What are features of psychogenic episodes?

A

• Panic attacks: slow onset, anxiety, breathlessness, tingling, blurred vision, tearfulness, long duration
• Dissociative convulsions (pseudoseizures): often start with panic, prolonged convulsion, flailing, closed eyes/mouth, resist eye opening, rapid/abnormal breathing, tearfulness

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9
Q

What other conditions may mimic seizures?

A

• Parasomnias: resemble frontal lobe seizures, single events, occur early in night
• Migraine: gradual onset, may cause LOC with typical migraine features
• Hypoglycaemia: especially sleep-related, pre-meal, post-exercise, in diabetics; may cause abnormal behavior and AED unresponsiveness

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10
Q

When do parasomnias usually occur?

A

Earlier in the night

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11
Q

How do parasomnias differ from frontal lobe seizures?

A

Parasomnias usually consist of single events, whereas frontal lobe seizures may be multiple events

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12
Q

Can migraine cause loss of consciousness?

A

Yes, typically with gradual onset

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13
Q

What symptoms accompany migraine-related loss of consciousness?

A

Typical migraine symptoms (e.g., headache, aura).

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14
Q

When should hypoglycaemia be considered as a seizure mimic?

A

In sleep-related episodes, before meals, after exercise, or in diabetics on blood glucose-lowering drugs

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15
Q

What features suggest hypoglycaemia rather than epilepsy?

A

Abnormal behaviour and AED-unresponsiveness.

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16
Q

What is essential before starting a seizure history?

A

Allocate adequate time; there is no shortcut to comprehensive history taking.

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17
Q

Why should you obtain a witness account?

A

Witnesses can provide details the patient may not recall, even if you need to call someone from the clinic.

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18
Q

What should you review before history taking?

A

Previous notes and investigations, including EEGs performed before medication initiation

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19
Q

How can you identify subtle or minor seizures?

A

Ask direct questions about myoclonus, minor seizures, or sleep-related events (e.g., blood on pillow, bitten tongue)

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20
Q

Why assess the patient’s medication history?

A

To check for:
• Epileptogenic drugs (e.g., tramadol, neuroleptics)
• Drugs causing syncope (e.g., vasodilators, drugs prolonging QT interval)

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21
Q

What aspects of past medical history are important?

A

Early life events (gestation, birth history, birth weight, incubator use), febrile seizures, cerebral infections, head injury, psychiatric history (depression, panic disorder, overdose, self-harm).

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22
Q

Why is family history important?

A

To identify seizures, faints, blackouts, or sudden/early deaths, which may suggest cardiac mimics.

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23
Q

What lifestyle factors should be explored?

A

Driving, alcohol use, relationships, education, occupation, leisure activities, pregnancy, and contraception.

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24
Q

Does physical examination usually reveal the cause in patients with blackouts?

A

Often adds little, but can provide additional history and reassurance.

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25
What skin findings are important during examination?
Signs of: • Tuberous sclerosis • Café-au-lait patches • Hemangiomas • Craniotomy scars • Evidence of previous self-harm (e.g., wrist scars)
26
What should be assessed in the cardiovascular exam?
Irregular pulse or other findings suggesting cardiovascular causes of blackouts.
27
What are key elements of the neurological examination?
• Visual fields (e.g., upper homonymous quadrantanopia → temporal lobe tumor) • Fundi examination and lateralizing signs • Hemi-smallness (e.g., thumb/nail size differences → subclinical hemiparetic cerebral palsy) • Cranial bruits (suggest intracranial vascular malformation)
28
Why is direct observation of seizures important?
It greatly aids accurate diagnosis
29
How can patients or caregivers help in observing seizures?
Encourage them to record events using video or mobile phones.
30
How are seizures categorized?
Generalized, focal, or unclassified, based on clinical and EEG findings.
31
What terms are used for focal seizures regarding awareness?
• Simple partial: retained awareness • Complex partial: loss of awareness
32
Do the terms simple and complex partial always perfectly indicate awareness?
No, there is overlap in ictal consciousness retention.
33
What are secondarily generalized tonic-clonic seizures?
Seizures that start as focal and then spread to involve both hemispheres, causing generalized convulsions.
34
Are most generalized convulsions in adults primary or secondary generalized?
Most are secondarily generalized
35
When do secondarily generalized seizures commonly occur?
During sleep
36
When are primary generalized convulsions more likely?
Upon awakening
37
Temporal Lobe Seizures What does a slow head turn at seizure onset suggest?
Ipsilateral seizure focus.
38
Temporal Lobe Seizures What does forced head turning later in the seizure indicate?
Contralateral (adversive) focus.
39
Temporal Lobe Seizures Are automatisms lateralizing?
Yes, they are ipsilateral to the seizure focus.
40
Temporal Lobe Seizures What about dystonic limb posturing?
Contralateral to the seizure focus.
41
Temporal Lobe Seizures Is nose wiping lateralizing?
No, it suggests mesial temporal involvement but is non-lateralizing.
42
Temporal Lobe Seizures What behaviors suggest nondominant temporal lobe involvement?
Ictal spitting, vomiting, coughing, peri-ictal water drinking.
43
Temporal Lobe Seizures What does unilateral eye blinking suggest?
Ipsilateral medial temporal focus (rare).
44
Temporal Lobe Seizures In secondarily generalized seizures, the final limb jerk is usually on which side?
Ipsilateral to the seizure focus.
45
46
Frontal Lobe Seizures What is characteristic of Jacksonian seizures?
“March” of limb jerking, often starting from the thumb
47
Frontal Lobe Seizures What is Todd’s phenomenon?
Post-ictal transient focal weakness after a seizure.
48
Frontal Lobe Seizures What are adversive seizures?
Forced head and eye turning away from seizure focus; arm jerking or “fencing” posturing contralateral to focus.
49
Frontal Lobe Seizures What are features of Supplementary Motor Area (SMA) seizures?
• Brief (<30 sec), often during sleep • Retained consciousness • Hypermotor phenomena: running, punching, shouting, cycling • Surface EEG may appear normal (deep midline onset) • Speech arrest/dysphasia → dominant hemisphere involvement • Clear ictal speech → non-dominant hemisphere
50
Occipital Lobe Seizures What is the hallmark feature of occipital lobe seizures?
Contralateral visual hallucinations (e.g., lights, colors)
51
Occipital Lobe Seizures How does eye deviation present in occipital lobe seizures?
Ipsilateral eye deviation toward the seizure focus
52
Occipital Lobe Seizures What condition can occipital lobe seizures overlap with clinically?
Migraines
53
How do parietal lobe seizures typically present?
Lateralized positive sensory disturbances (e.g., contralateral tingling or pain).
54
What two main factors determine epilepsy classification?
1. Site of seizure onset – generalized, focal, or unclassified 2. Presumed etiology – symptomatic, probable symptomatic (cryptogenic), or idiopathic
55
What defines symptomatic epilepsy?
Known structural cause.
56
What defines probable symptomatic (cryptogenic) epilepsy?
Presumed structural cause, but not identifiable
57
What defines idiopathic epilepsy?
Presumed genetic cause, age-specific onset/offset, normal brain imaging, good AED response.
58
What is Juvenile Myoclonic Epilepsy (JME)?
Idiopathic generalized epilepsy with: • Morning myoclonus • Generalized tonic-clonic seizures on awakening • Absences • Photosensitivity
59
When does JME typically begin and how long does it persist?
Begins in adolescence and tends to persist lifelong.
60
What EEG pattern is typical for JME?
Inter-ictal generalized polyspike-and-wave activity.
61
Name other idiopathic generalized epilepsy syndromes
• Juvenile absence epilepsy • Generalized tonic-clonic seizures on awakening • Eyelid myoclonia with absences
62
What is the most common cause of adult focal epilepsy?
Hippocampal (Mesial Temporal) Sclerosis.
63
What is the typical history for hippocampal sclerosis?
Early-life cerebral insult (e.g., prolonged febrile seizures), latent interval, then later onset of complex partial seizures with epigastric aura.
64
Name other causes of symptomatic focal epilepsy.
• Head injury (frontal/temporal lobes) • Tumors (low-grade cortical, often treatment-resistant simple partial seizures) • Cortical dysplasias (minor focal to generalized, variable intellectual disability) • Arteriovenous malformations and cavernous malformations
65
What are examples of benign childhood focal epilepsies?
• Benign childhood epilepsy with centrotemporal spikes • Benign occipital epilepsy
66
Are benign childhood focal epilepsies usually treatable?
Yes, easily treated and often self-remitting.
67
Name examples of monogenic focal epilepsies.
• Autosomal dominant nocturnal frontal lobe epilepsy • Familial temporal lobe epilepsy with variable severity
68
Symptomatic and Cryptogenic Generalized Epilepsies What are common examples?
Severe childhood-onset epilepsies often associated with intellectual disability, e.g.: • Lennox-Gastaut syndrome • Myoclonic astatic epilepsy
69
Should all new-onset unprovoked seizures be investigated?
Yes; allowing even a single seizure is considered unsafe
70
Who requires brain imaging?
All adults with new-onset unprovoked seizures.
71
When is CT scan used?
More accessible; suitable for initial investigation.
72
When is MRI preferred?
More sensitive for structural causes (e.g., hippocampal sclerosis, cortical malformations, benign tumors).
73
What MRI finding is more significant in hippocampal sclerosis?
Hippocampal volume loss rather than signal change.
74
What is current best practice for MRI in adult-onset epilepsy?
MRI for all adults unless idiopathic generalized epilepsy is clinically definite.
75
What is the role of functional imaging?
Techniques: fMRI, MR spectroscopy, magnetoencephalography; • Identify resectable abnormalities in MRI-negative patients • MR tractography maps visual pathways for safer surgery
76
What is the role of standard inter-ictal EEG?
Indicates epilepsy tendency; adjunct to diagnosis, especially useful in children/adolescents.
77
When is the first EEG most valuable?
Before starting treatment
78
How can EEG sensitivity be enhanced?
Longer recordings, testing within 72 hours of events, sleep deprivation.
79
What is the gold standard for capturing seizures?
Prolonged video EEG
80
Why may surface EEG appear normal?
In deep-seated seizure foci.
81
When should ECG be performed in patients with blackouts?
• All undiagnosed blackouts • Syncope presented to neurologists • Resistant epilepsy, especially with normal imaging and EEG
82
What should neurologists systematically assess on an ECG?
QTc interval and signs of rare but fatal cardiac disorders (e.g., long QT syndrome, hypertrophic cardiomyopathy)
83
What is the main goal of epilepsy treatment?
Seizure freedom without adverse drug effects
84
Is long-term follow-up necessary in seizure-free patients?
Yes, long-term follow-up is essential
85
Should AEDs be started immediately after a first seizure?
Usually not recommended; avoid lifelong medication without definitive diagnosis.
86
Who decides on long-term AED treatment?
Patient and epilepsy specialist jointly, after discussion
87
Which AED is first choice for focal epilepsy?
Lamotrigine
88
Which AED is first choice for generalized epilepsy?
Valproic acid
89
Can some AEDs worsen certain seizure types?
Yes, e.g., carbamazepine may worsen myoclonus and absences.
90
Why do AED choices differ between men and women?
Effects on oral contraceptives and pregnancy
91
What is the preferred treatment approach for AEDs?
Monotherapy; sequential monotherapy if first fails (response rates: 47% → 13% → 4%)
92
What are common short-term adverse effects of AEDs?
Sedation
93
Give an example of a long-term adverse effect.
Vigabatrin can cause visual field defects
94
Which AEDs interact with contraceptive pills?
Enzyme inducers like carbamazepine and phenytoin
95
What is important for rational AED prescribing?
Use different mechanisms for sequential AEDs; avoid polytherapy with similar mechanisms
96
How should AEDs ideally be dosed?
Once or twice daily
97
Are blood levels necessary for all AEDs?
Generally unnecessary, except for phenytoin
98
What affects medication concordance?
Fear of side effects, inadequate understanding, or complacency after seizure freedom
99
How is AED withdrawal approached in children?
Straightforward after two seizure-free years
100
How about AED withdrawal in adults?
More difficult due to seizure-free pressures (e.g., driving); recurrence risk guides decision
101
What defines status epilepticus (SE)?
Seizures lasting >30 minutes without recovery of consciousness.
102
When do tonic-clonic seizures become “status in evolution”?
Lasting >5 minutes; occurs in ~5% of patients and requires urgent intervention.
103
What labs should be checked immediately in SE?
Blood glucose, biochemistry, toxicology, and AED levels (without delaying treatment).
104
What important condition can mimic SE?
Status pseudoepilepticus (up to 50% of apparent cases in adult ICU).
105
What is the initial patient assessment?
Airway, breathing, circulation (ABC) management
106
What supportive drugs may be given immediately?
• IV thiamine 100 mg (if alcoholism suspected) • IV 50% glucose (if hypoglycemia)
107
Early Phase (1–10 minutes) Q7: First-line treatment in the community? Q8: First-line treatment in hospital?
A7: Buccal midazolam 0.2–0.4 mg/kg A8: IV lorazepam 0.1 mg/kg, repeat after 2 minutes if needed
108
Established Phase (5–30 minutes) Q9: What is the treatment for established SE?
IV phenytoin 15–20 mg/kg over 20–30 min with cardiac monitoring
109
Refractory Phase (30–90 minutes, ICU) Q10: What drugs are used for refractory SE?
• IV phenobarbital 20 mg/kg at 100 mg/min • General anesthesia with intubation (e.g., thiopentone, midazolam, propofol)
110
What is the monitoring goal in refractory SE?
EEG burst suppression or deeper monitoring; wake patients every 2–4 hours to check seizure remission
111
How should patients be involved in their epilepsy care?
Provide verbal and written information, encourage joint decision-making, and support self-management.
112
Should suboptimal seizure control or adverse AED effects be accepted?
No; challenge assumptions and explore additional treatment options.
113
Are lifestyle restrictions absolute for epilepsy patients?
Most activities are negotiable except driving, which requires tailored advice.
114
What are the UK rules for ordinary license (Group 1) seizure freedom?
1 year seizure-free or 3 years if seizures occur only in sleep.
115
What about commercial license (Group 2)?
10 years seizure-free and off AEDs.
116
What should guide AED choice in pregnancy?
Fetal safety, using observational data (e.g., UK Epilepsy and Pregnancy Register).
117
What supplement is recommended for women on AEDs planning pregnancy?
Folate 5 mg daily
118
How should sleep be managed in epilepsy?
Maintain regular sleep patterns, especially in idiopathic generalized epilepsy.
119
Is alcohol completely prohibited?
No, moderate consumption (2–4 units in 24 hours) is acceptable; excess lowers seizure threshold.
120
Should all patients avoid flashing lights?
No; light avoidance is only necessary for photosensitive epilepsy.
121
What is SUDEP and how should it be discussed?
Sudden Unexplained Death in Epilepsy; rare, preventable factors include AED adherence and avoiding excess alcohol.
122
How does epilepsy affect disability benefits?
Eligibility varies due to intermittent seizure patterns; payments may present conflicts of interest.
123
Are genetic tests routinely useful?
Monogenic epilepsies exist, but practical testing is limited currently.
124
When is lesional epilepsy surgery indicated?
For structural lesions such as hippocampal sclerosis or benign tumors.
125
What are the outcomes of lesional epilepsy surgery?
Up to 80% seizure-free, and half may withdraw AEDs.
126
What is required before surgery?
Prolonged presurgical evaluation for safety (memory, speech, functional mapping).
127
What is corpus callosotomy used for?
Prevents bilateral spread of generalized seizures, especially atonic seizures.
128
When is hemispherectomy indicated?
Children with hemiplegia and refractory seizures.
129
What are multiple subpial transections (MST)?
Isolate cortical blocks by interfering with horizontal seizure transmission.
130
What is gamma knife radiosurgery used for?
Small AVMs, tumors, metastases, or hippocampal sclerosis.
131
What is the efficacy of VNS?
Comparable to adding a new AED; 30–50% achieve >50% seizure reduction.
132
What are common adverse effects of VNS?
Pain, hoarseness, and swallowing difficulties.
133
Does VNS have drug interactions?
No significant drug interactions.