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Laughing Your Way Neurology > Ch 3 - Epilepsy > Flashcards

Ch 3 - Epilepsy Flashcards

1
Q

Prior to 2010 classification as seizures was?

A

Generalized

  • Absence, atypical absence, tonic, tonic clonic, clonic, myoclonic, atonic

Partial

  • simple, complex, secondary generalized
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2
Q

Atypical absence vs absence seizures

A

Atypicals are slower Hz than absence seizures, last longer, and are most common in developmental delayed patients.

LL AA DD

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3
Q

Simple vs complex partial seizures

A

simple = patient is aware

complex = awareness is lost

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4
Q

common example of simple partial seizure?

A

Aura

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5
Q

Where do auditory/oflactory/visual auras technically come from?

A

Auditory = temporal

Olfactory = medial temporal

Visual = occipital

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6
Q

Symptomatic vs idiopathic vs cryptogenic seizures?

A

Symptomatic = there is a known lesion causing sz

Idiopathic - presumed to be genetic, MRI is nl

Cryptogenic - thought to be symptomatic, but unknown

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7
Q

Post 2010 classification of seizures?

A

Generalized, focal, or unknown

Focal = one hemisphere

Generalized = both

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8
Q

Types of generalized seizures?

A
  • Absence (normal, atypical)
  • Tonic
  • Tonic Clonic
  • Clonic
  • Myoclonic
  • Atonic
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9
Q

Infantile Spasms - features?

A
  • usually in first 3-7mo old
  • generalized tonic-myoclonic szs often called “Salaam” or Jacknife attacks
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10
Q

Triad of Infantile spasms:

A

West Syndrome

  • Hypsarrhythmia
  • Infantile Spasms
  • Developmental Delay

In the old West, when an infant seized, they all yelled ACTH and HID

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11
Q

Describe EEG pattern in Infantile Spasms

A

Hypsarrhythmia

Chaotic high amplitude, asynchronous slow activity with multifocal spikes

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12
Q

Treatment for infantile spasms? Second line?

A

ACTH

Topamax/Keppra

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13
Q

Treatment found effective in infantile spasms patients with tuberous sclerosis?

A

Vigabatrin

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14
Q

Triad of Lennox Gastaut Syndrome?

A
  • At least 2 different seizure types
  • EEG with 1.5-2.5 Hz spike and wave discharges
  • Developmental delay

Lenox (expensive dish company) had the GREATEST sale: buy one seizure, get one free!

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15
Q

Landau Kleffner Syndrome - features?

A

Also known as acquired epileptic aphasia

  • epileptic condition associated with language disturbances usually at 3-7 years of age.
  • patients develop word deafness, receptive>expressive aphasia (language disturbances).

Landau sounds like Lambeau (Packers Stadium), fans scream disturbing language and deafeningly loud!

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16
Q

Landau-Kleffner Syndrome (acquired epileptic aphasia) -EEG features?

A

epileptiform discharges over the parietal and temporal regions

During sleep, can show ESES (electrical status epilepticus of sleep)

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17
Q

Childhood Absence Epilepsy - features?

A

generalized epilepsy that starts at 4-8 yo with brief staring spells.

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18
Q

Childhood Absence Epilepsy - EEG?

A

3 Hz spike and slow wave discharges

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19
Q

Childhood Absence Epilepsy - treatment?

A

ethosuxamide is used for absence and is the best option

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20
Q

What is the best choice for patients with absence and generalized tonic clonic seizures (2)?

A

VPA or LTG

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21
Q

Juvenile Myoclonic Epilepsy - features?

A
  • GTCs at 13-20 years of age
  • typically myoclonic jerks (particularly in the AM) before the GTC
  • worsened with sleep deprivation, alcohol, and light stim.

JME patients Jerk More with the 3 E’s

Ethanol

Elimination of Sleep

Electric light (photic stim)

22
Q

Juvenile Myoclonic Epilepsy - EEG?

A

3.5 - 4.5 Hz spike/polyspike and wave discharges

23
Q

Most common form of benign partial epilepsy in childhood?

A

BREC
Benign Rolandic Epilepsy of Childhood

24
Q

BREC - typical age? features?

A

4-12 yo

nocturnal GTCs or nocturnal partial seizures associated with drooling or speech arrest

25
Q

BREC - EEG pattern?

A

Centro-temporal spikes bilaterally that increase in sleep

26
Q

Frontal Lobe Epilepsy - semiology?

A

brief seizures, typically at night with rapid recovery.

Can involve frenetic activity or pelvic thrusting

27
Q

Temporal Lobe Epilepsy - most common pathologic finding?

A

mesial temporal sclerosis/ Ammon’s horn sclerosis

28
Q

Temporal lobe epilepsy - classic aura?

A

epigastric rising, followed by automatisms

29
Q

occipital lobe epilepsy - most common syndrome?

A

Early onset benign epilepsy of childhood wih occipital paroxysms

30
Q

Semiology of Panayiotopoulos Syndrome (Occipital lobe epilepsy )?

A

2-8 years old, usually at night and can be prolonged. Vomiting and tonic eye deviation are seen and can be followed by hemiclonic activity/secondary generalization

31
Q

Gastaut Type Occipital Lobe Epilepsy?

A

Late onset benign epilepsy of childhood with occipital paroxysms

32
Q

Semiology of Gastaut type of occipital lobe epilepsy?

A

consist of visual symptoms - hemianopia, blindness, hallucinations - can secondary generalize.

Seizures can sometimes be triggered by light changes.

33
Q

Progressive Myoclonic Epilepsy - broad characteristics?

A

Typically consists of

  1. Seizures - GTCs
  2. myoclonic jerks
  3. Neurological decline - particularly cerebellar/cognitive.
34
Q

4 types of Progressive Myoclonic Epilepsy?

A

SLUMiN it!

Sialidoses

Lafora

Unverricht-Lundborg

MERRF

Neuronal Ceroid Lipofuscinoses

35
Q

Unverricht-Lundborg PME - due to a mutation in ?

A

Cystatin B on chromosome 21

36
Q

Unverricht-Lundborg PME - characteristics

A

stimulus sensitive myoclonic jerks

intellect is intact, cerebellar deterioration is late

37
Q

Unverricht-Lundborg PME - diagnosis?

A

membrane bound vacuoles in eccrine sweat glands.

(can also see high amplitude SSEPs)

38
Q

Lafora’s Disease PME - due to a mutation in

A

Laforin and malin on chromosome 6q/6p

39
Q

Lafora’s Disease PME - characteristics?

A

occipital seizures with visual hallucinations - progresses faster

40
Q

Lafora’s Disease PME - diagnosis?

A

Lafora bodies in various tissues (particularly sweat glands) - polyglucosan containing inclusions

41
Q

Neuronal Ceroid Lipofuscinoses (NCL) - mutation

A

AR lysosomal storage diseases with accumulation of multiple lipopigment particles

42
Q

Neuronal Ceroid Lipofuscinoses (NCL) PME - characteristics?

A

vision loss

43
Q

Neuronal Ceroid Lipofuscinoses (NCL) PME - diagnosis

A

Electon microscopy on skin/rectal/conjunctival tissue shows

  1. granular osmiphilic deposits
  2. curvilinear bodies
  3. fingerprint profiles
  4. rectilinear complexes

NCL= Norweigan Cruise Lines taking FINGERPRINTS for security, then take your cash DEPOSITS into COMPLEX slot machines, then bathe your CURVILINEAR body in the sun, but don’t get too much LIPOpigment from the sun or you could have VISION LOSS.

44
Q

Myoclonic Epilepsy with Ragged Red Fibers (MERRF) PME - mutation

A

maternally inherited mutation at position 8344 in mitochondrial genome

45
Q

Myoclonic Epilepsy with Ragged Red Fibers (MERRF) PME - characteristics

A

myoclonic epilepsy sometimes with deafness, optic atrophy, lipomas, short stature, myopathy/neuropathy

46
Q

Myoclonic Epilepsy with Ragged Red Fibers (MERRF) PME - diagnosis? labs elevated?

A

lactate and pyruvate elevated

ragged red fibers on muscle biopsy

47
Q

Sialidosis Type 1 - mutation

A

neuraminidase defect - which cleaves sialic acid from galactose

48
Q

Sialidosis Type 1 - characteristics

A

cherry red spots and cognitive deterioration

49
Q

Sialidosis Type 1 - diagnosis

A

sialyloligosaccharides in urine

50
Q
A

Laughing Your Way Neurology (6 decks)

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