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RITE PREP > Seizure > Flashcards

Seizure Flashcards

1
Q

Jeavon’s Syndrome

A
  1. Eyelid Myoclonia w/wo absence seizures

2. high-amplitude 3–6 Hz generalized discharges

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2
Q

Childhood absence epilepsy

types

A
  1. Absence

2. Generalized Tonic-Clonic (rare)

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3
Q

Childhood Absence epilepsy (age of onset)

A
  1. 4-10 years
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4
Q

Childhood Absence epilepsy (EEG)

A
  1. Normal background
  2. Occipital intermittent rhythmic delta activity
  3. 3-3.5Hz generalized spike-wave discharges
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5
Q

Juvenile Absence Epilepsy (seizure types)

A
  1. Absence
  2. Generalized Tonic-Clonic
  3. Myoclonic (rare)
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6
Q

Juvenile Absence Epilepsy (Age of onset)

A

Adolescence to early adulthood

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7
Q

Juvenile Absence Epilepsy (EEG)

A
  1. Normal background
  2. Polyspikes may be present
  3. 3-3.5Hz generalized spike-wave discharges
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8
Q

Epilepsy with generalized tonic clonic seizures alone (seizure type)

A
  1. Generalized tonic-clonic
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9
Q

Epilepsy with generalized tonic clonic seizures alone (Age of onset)

A
  1. childhood to mid-adulthood
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10
Q

Epilepsy with generalized tonic clonic seizures alone (EEG)

A
  1. Normal background

2. Generalized spike/polyspike-wave discharges

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11
Q

6 categories of seizure etiology

A
  1. Structural
  2. Genetic
  3. Infectious
  4. Metabolic
  5. Immune
  6. Unknown
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12
Q

Benign Familial Neonatal convulsions (inheritance)

A

Autosomal dominant (also a non-familial sporadic form)

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13
Q

Benign Familial Neonatal convulsions (Age of presentation)

A

5th day of life “5th Day Fits”

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14
Q

Benign Familial Neonatal convulsions (Gene)

A

KCNQ2

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15
Q

Benign Familial Neonatal convulsions (Prognosis/Seizure type)

A
  1. self-limiting

2. Focal/Generalized clonic seizures

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16
Q

Myoclonic epilepsy of infancy (Age)

A

4 months to 3 years

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17
Q

Myoclonic epilepsy of infancy (Seizure Type)

A
  1. myoclonic seizures, tonic spasms and partial seizures

2. May have “reflex seizures” triggered by startling noise or tactile stimulation (benign course)

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18
Q

Myoclonic epilepsy of infancy (EEG)

A

polyspike and waves with myoclonic jerks. Interictal EEG can be normal but can have a burst suppression pattern during sleep

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19
Q

Myoclonic epilepsy of infancy (AED for myoclonus)

A

Valproic acid is valuable in the management of myoclonic activity.

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20
Q

Ohtahara syndrome / Early infantile epileptic encephalopathy (EIEE) (Age and Presenting seizure)

A

Presents usually within the first 2 months of initially with tonic spasms, partial seizures and rarely myoclonic seizures. It frequently evolves into infantile spasms and/or West syndrome.

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21
Q

Myoclonic epilepsy of infancy (EEG)

A

EEG will show burst suppression

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22
Q

Myoclonic epilepsy of infancy (etiology)

A

Develops in patients with secondary brain insults such as brain malformations, metabolic syndromes, and mitochondrial disorders. Poor prognosis

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23
Q

Infantile spasms & West syndrome (Age/Seizure)

A

Presents in the first year of life (3-7 months) with brief episodes of axial flexion in clusters (spasms) which has an electrodecrement during the events if captured on EEG.

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24
Q

Infantile spasms & West syndrome (EEG)

A

EEG will show chaotic interictal high amplitude and arrhythmic delta activities with independent multifocal spike discharges and variable rhythm called hypsarrhythmia.

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25
Q

West Syndrome Triad

A
  1. Hypsarrhythmia
  2. developmental delay
  3. infantile spasms.
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26
Q

Aicardi Syndrome Triad

A
  1. Agenesis of corpus callosum
  2. chorioretinal lacunae
  3. infantile spasms.
    X-linked dominant.
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27
Q

Infantile spams (alternative etiologies)

A

Infantile spasms can also be seen with tuberous sclerosis, HIE, Menkes, MSUD, and PKU.

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28
Q

Infantile spasms & West syndrome (Treatment)

A

Treatment: ACTH, glucocorticoids
Vigabatrin used if spasms are associated with tuberous sclerosis.
Patients are poorly responsive to therapies and many go on to develop Lennox-Gastuat syndrome.

29
Q

Dravet syndrome (severe myoclonic epilepsy of infancy, SMEI) (Gene)

A

SCN1A gene mutation

30
Q

Dravet syndrome (severe myoclonic epilepsy of infancy, SMEI) (Treatment)

A

Stiripentol

31
Q

Dravet syndrome (severe myoclonic epilepsy of infancy, SMEI) (Presentation)

A

Presents within the first year of life. Severe epilepsy with multifocal and generalized spikes. 20% mortality, and high SUDEP frequency.

32
Q

Lennox-Gastaut syndrome

A
  1. Presents in the first years of life with developmental delay and generalized slow (1.5 Hz to 2.5 Hz) spike-and-wave activity with increasing disorganization during sleep.
  2. Patients will have multiple seizure types such as tonic, atypical absence, and atonic.
  3. Generalized paroxysmal fast activity (GPFA) can also be seen on interictal EEG.
    Tends to be refractory to treatment.
33
Q

Panayiotopoulos syndrome (presentation)

A

Presents in childhood (2-8 years) with vomiting, migraine features, autonomic symptoms, and acute loss of tone (ictal syncope) due to focal occipital lobe seizures.

34
Q

Panayiotopoulos syndrome (Interictal EEG)

A

Interictal EEG will show bilateral independent occipital spikes.

35
Q

Panayiotopoulos syndrome (May develop what)

A

Many children will go on to develop BECTS, but most will enter spontaneous remission within a couple years.

36
Q

Benign rolandic epilepsy (BRE)/ Benign epilepsy with centrotemporal spikes (BECTS) (Age)

A

Presents between 7-13 years of life with hemifacial twitching, excessive salivation, and inability to speak due to simple or complex partial seizures. Occasionally these seizures can generalize. Patients often outgrow the disorder.

37
Q

Benign rolandic epilepsy (BRE)/ Benign epilepsy with centrotemporal spikes (BECTS) (Inheritance/Gene)

A 
Autosomal dominant. 
Chromosome 15q14 (alpha-7 subunit of Ach receptor). Males > female.
38
Q

Benign rolandic epilepsy (BRE)/ Benign epilepsy with centrotemporal spikes (BECTS) (EEG)

A

EEG will show bilateral independent centrotemporal (i.e. “Rolandic” fissure) spikes during light sleep.

39
Q

Benign rolandic epilepsy (BRE)/ Benign epilepsy with centrotemporal spikes (BECTS) (Treatment)

A

Treatment: carbamazepine, but most resolve spontaneously in 5 years.

40
Q

Rasmussen encephalitis (chronic focal epilepsy, CFE) (age)

A

Presents between 18 months and 14 years of age with frequent focal seizures that can evolve to epilepsia partialis continua (EPC) and progressive neurologic deficits.

41
Q

Rasmussen encephalitis (chronic focal epilepsy, CFE) (Imaging)

A

MRI brain will show unilateral hemispheric changes in white matter and then atrophy. Treatment with hemispherectomy is often required.

42
Q

Rasmussen encephalitis (chronic focal epilepsy, CFE) (EEG)

A

EEG with focal and multifocal epileptiform discharges and slowing and progressive seizures over time.

43
Q

Rasmussen encephalitis (chronic focal epilepsy, CFE) (Gene)

A

Associated in some patients with GluRε2 (anti-NR2A) or GluR3 (AMPA receptor).

44
Q

Doose syndrome / Myoclonic astatic epilepsy (age)

A

primary generalized idiopathic disorder which presents in early childhood (2-5 years) in boys > girls.

45
Q

Doose syndrome / Myoclonic astatic epilepsy (seizure types)

A

Multiple seizure types including myoclonic, astatic, absence.

46
Q

Doose syndrome / Myoclonic astatic epilepsy (development)

A

Children often develop normally before the onset of seizures, then ~33% of patients decline to moderate-severe intellectual disability.

47
Q

Doose syndrome / Myoclonic astatic epilepsy (EEG)

A

EEG will initially be normal and will progress to brief bursts of 2-5 Hz spike and wave discharges.

48
Q

Febrile seizures (Age)

A

The most common seizure disorder in children.
Presents usually in the first 6 years of life in association with fever, without CNS infection or other definable causes, and without a history of previous afebrile seizures

49
Q

Febrile seizures (Prognosis)

A

While 3% of children under 6 years of age have febrile seizures, only a small percentage of these patients develop epilepsy (<5%).
AEDs are often not required

50
Q

Generalized epilepsy with febrile seizures + (GEFS+)

A

A genetic disease in which patients have recurrent febrile seizures beyond 6 years of age. Patients will also have afebrile generalized seizures (generalized tonic-clonic, myoclonic, absence and/or atonic).

51
Q

Generalized epilepsy with febrile seizures + (GEFS+) (Genes/Inheritance)

A

autosomal dominant mutation in the SCN1A or SNC1B gene which encodes sodium channel subunits

52
Q

Landau-Kleffner syndrome (age)

A

Onset between 2-12 years, AKA epileptic aphasia

53
Q

Landau-Kleffner syndrome (progression/development)

A

Patients are often developmentally normal prior to disease onset which includes language regression and focal seizures with impaired awareness.
Focal seizures can secondary generalize.

54
Q

Landau-Kleffner syndrome (EEG)

A

near continuous, diffuse sleep-activated spikes.

55
Q

Familial (autosomal dominant) nocturnal frontal lobe epilepsy (ADNFLE) (AgE)

A

Most begin in childhood but can present in infancy to adulthood.

56
Q

Familial (autosomal dominant) nocturnal frontal lobe epilepsy (ADNFLE) (Inheritance/Mutation)

A

An autosomal dominant disorder due to mutation of a nicotinic acetylcholine receptor

57
Q

Familial (autosomal dominant) nocturnal frontal lobe epilepsy (ADNFLE) (symptoms)

A

Fear is a dominant symptom for the patient during episodes. Paroxysmal events present similarly to parasomnia, panic attacks, and psychogenic non-epileptic seizures due to retained consciousness.

58
Q

Absence seizures / Pyknolepsy (age)

A

Presents between 5-15 years of life with staring spells of brief duration and lack of aura or postictal state. Can be triggered by hyperventilation.

59
Q

Absence seizures / Pyknolepsy (EEG)

A

3 Hz spike-and-wave discharges.
Discharges are enhanced with hyperventilation and hypoglycemia.
Seizure onset is associated with the thalamus.

60
Q

Absence seizures / Pyknolepsy (Treatment)

A
  • Treatment: Ethosuximide (T-type calcium channel blocker), or valproate
  • Absence seizures can be worsened by sodium channel drugs (phenytoin and carbamazepine) and GABA receptor drugs (vigabatrin).
  • Ethosuximide does not treat GTCs, so if also having GTCs, then valproic acid is indicated. Lamotrigine can also be used, despite the potential to worsen absence seizures.
61
Q

Absence seizures / Pyknolepsy (Genetics)

A

Associated with GABRG2, GABRA1, and CLCN2, which encode for the gamma 2 subunit of the GABA receptor, the alpha1 subunit of the GABAA receptor, and chloride channel protein 2.

62
Q

Progressive myoclonus epilepsy (PME) (Age/Symptoms)

A

A disease complex of different diagnostic etiologies which presents between 6 and 15 years of age characterized by progressive myoclonus, ataxia, and other neurologic deficits.

63
Q

Progressive myoclonus epilepsy (PME) (Syndromes)

A

Syndromes: Lafora body disease, Unverricht-Lundborg disease/Baltic Myoclonic epilepsy, myoclonic epilepsy with ragged-red fiber (MERRF) syndrome.

Lafora disease (Lafora progressive myoclonic epilepsy): Autosomal recessive. Round, targetoid Lafora body inclusions deposit throughout skin and organs, including the brain. Causes dementia, drop attacks, and seizures. It is progressive and fatal within 10 years.

64
Q

Juvenile myoclonic epilepsy (JME) (Age)

A

8-26

65
Q

Juvenile myoclonic epilepsy (JME) (semiology)

A

Presents with morning myoclonic jerks and generalized seizures.
33% also have absence seizures.
Myoclonus of fingers presents as “clumsiness” and dropping things.

66
Q

Juvenile myoclonic epilepsy (JME) (precipitating factors)

A

Seizures are often precipitated by sleep deprivation, drugs and/or alcohol.

67
Q

Juvenile myoclonic epilepsy (JME) (EEG)

A

Interictal EEG will show generalized 4-6 Hz polyspike and wave discharges. May see associated myoclonic jerks or runs of spikes brought on by photic stimulation.

68
Q

Juvenile myoclonic epilepsy (JME) (Treatment)

A

Treatment:

  • Valproic acid is the treatment of choice.
  • Lamotrigine is a second option for women of childbearing age.
  • Levetiracetam, topiramate and zonisamide are additional options.
  • Carbamazepine, phenytoin, gabapentin, pregabalin, tiagabine, and vigabatrin can worsen myoclonic seizures

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