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Elsa AACN > Ch 22 Epilepsy and Seizure Disorders > Flashcards

Ch 22 Epilepsy and Seizure Disorders Flashcards

1
Q

definition of seizure

A

transient occurrence of signs and sx due to abnormal excessive or synchronous neuronal activity in the brain

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2
Q

what is ictal semiology

A

clinical manifestation, behaviors exhibited during seizure

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3
Q

seizures are classified based on

A

observed behavior during the event

behavioral features at the onset is KEY to classification

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4
Q

what are the 3 classifications of seizure onset?

A

focal onset
generalized onset
unknown onset

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5
Q

focal seizure

A

onset originating in networks limited within one cerebral hemisphere
may be discretely localized within the hemisphere
widely distributed within the hemisphere or
originate in subcortical structure

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6
Q

seizures can be caused by acquired and congenital conditions

A

true

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7
Q

All conditions that cause seizure can lead to epilepsy, t or false

A

false, not all conditions may lead to epilepsy. some can be treated or resolved without recurrent seizures

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8
Q

epilepsy

A

recurrent seizures
implies underlying condition that is not related to transient factors and is an intrinsic property of the brain where there is enduring predisposition to generate epileptic seizures

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9
Q

diagnosis of epilepsy is made when there are

A

at least 2 unprovoked seizures
at least 24 hours apart
after a single unprovoked seizure when the risk for another is known to be high (>60%) based on other medical factors
epilepsy syndrome diagnosed in childhood

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10
Q

etiology of epilepsy

A 
structural
genetic
infectious
metabolic
immune 
unknown
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11
Q

seizure types

A

focal
generalized
unknown

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12
Q

epilepsy types

A

focal
generalized
combined generalized and focal
unknown

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13
Q

what is the mechanism of epilepsy?

A

fundamental disruption of the balance between inhibitory and excitatory neuronal activity
development of recurrent excitatory networks
disruption can be caused by acquired or congenital genetic conditions affecting the brain

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14
Q

epilepsy is a lifespan or acute disorder?

A

lifespan, may persist throughout lifespan

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15
Q

most common site of pathology in adults and adolescents with seizures?

A

temporal lobe (hippocampus)

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16
Q

seizures in temporal lobe would show

A

alteration of awareness = 2/3 of all cases

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17
Q

most common pathology in adults

A 
hippocampal sclerosis (HS)
65-75% of surgical cases
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18
Q

what is hippocampal sclerosis

A

histopathologically defined pattern of cell loss and astrogliosis in the hippocampal formation

commonly seen in temporal lobe epilepsy
can also be seen in dementia, hypoxic injury

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19
Q

astrogliosis

A

abnormal increase in the number of astrocytes due to the destruction of nearby neurons from central nervous system (CNS) trauma, infection, ischemia, stroke, autoimmune responses or neurodegenerative disease.

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20
Q

Hippocampal sclerosis has how many subtypes?

A

3 subtypes
Type 1 - 60-80%: prominent cell loss in hippocampal subfields
Type 2, 3 - less common: cell loss more limited to CA1 and CA 4

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21
Q

how is hippocampal sclerosis detected?

A

neuroimaging
appearance of atrophy
increased intensity on T2 and FLAIR

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22
Q

new onset epilepsy in adults - common or uncommon

A

uncommon

usually asociated with primary CNS neoplasm, neurovascular event, trauma, infection, autoimmune disorders

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23
Q

autoimmune mediated epilepsy may be related to

A

paraneoplastic syndrome

infectious etiology

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24
Q

underlying pathology in pediatric epilepsy is dependent on?

A

age
more variable
more unknown

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25
Q

neonatal seizures are usually associated with

A

hypoxic ischemic encephalopathy 35-45% of cases
infarction/hemorrhage
genetic or syndromic epilepsy
brain malformation

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26
Q

childhood onset epilepsy variable or stable?

A

variable

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27
Q

cause of childhood onset epilepsy?

A

genetic variants
autoimmune epilepsy
malformation of cortical development (MCD)
low grade brain tumors

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28
Q

Malformation of cortical development (MCD) is a frequent cause of

A

epilepsy

MCD can present in anywhere in the cerebral cortex

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29
Q

MCD vary in what ways?

A

origin

presentation can be macro or microscopic

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30
Q

MCD classification is based on

A

genetic
embryologic
pathologic, histologic, imaging criteria

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31
Q

4 classifications of MCD

A

MCD caused by abnormal neuronal and glial proliferation or apoptosis
MCD caused by abnormal neuronal migration
MCD caused by abnormal cortical organization
MCD not otherwise classified

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32
Q

neonatal period and epileptic syndromes

A

neonatal seizures
familial neonatal epilepsy
ohtahara syndrome
early myoclonic encephalopathy

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33
Q

infancy and epileptic syndromes

A 
febrile seizures
self limited infantile epilepsy
self limited familial infantile epilepsy
West syndrome
Dravet syndrome
Myoclonic epilepsy of infancy
Myoclonic encephalopathy in non progressive disorders
Epilepsy of infancy with migrating focal seizures
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34
Q

Childhood and epileptic syndromes

A

febrile seizures
early onset childhood occipital epilepsy
epilepsy with myoclonic atonic seizure
childhood absence epilepsy
self limited epilepsy with centrotemporal epilepsy
late onset childhood occipital epilepsy
autosomal dominant nocturnal frontal lobe epilepsy
epilepsy with myoclonic absences
lennox gastaut syndrome
epileptic encephalopathy with continuous spike and wave during sleeo
landau-kleffner syndrome

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35
Q

Adolescence/Adult and epileptic syndrome

A

juvenile absence epilepsy
juvenile myoclonic epilepsy
epilepsy with generalized tonic clonic seizures
autosomal dominant epilepsy with auditory features
other familial temporal lobe epilepsy

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36
Q

Variable at age of onset

A

familial focal epilepsy with variable foci
new onset refractory status epilepticus
febrile illness related epilepsy syndrome
progressive myoclonus epilepsy
reflex epilepsy

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37
Q

Distinctive constellations/surgical syndrome

A

mesial temporal lobe epilepsy with hippocampal sclerosis
rasmussen syndrome
gelastic seizure with hypothalamic hamartoma
hemiconvulsive hemiplegic epilepsy

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38
Q

epilepsy attributed to structural metabolic causes

A

MCD
neurocutaneous syndromes (tuberous sclerosis complex, Sturge weber)
tumor, infection, trauma, vascular, perinatal insults

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39
Q

Genes associated with epilepsy can be grouped into

A

monogenic
neurodevelopment-related genes
epilepsy related genes
potential epilepsy associated genes

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40
Q

of people worldwide have epilepsy

A

50 million people

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41
Q

majority of epilepsy occurs in what regions? developing or non developing

A

developing (possible 2/2 malaria, birth related injuries, lack of access to care)

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42
Q

USA incidence

A

50/100,000 individuals

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43
Q

prevalence of epilepsy

A

5-10/1000

more than 3 million

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44
Q

most common onset at what age?

A

younger than 5 years or over 65 years

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45
Q

majority of seizures with alteration of consciousness or awareness occur before

A

age 15

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46
Q

which population has the fastest growing number of new onset cases?

A

elderly population

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47
Q

causes for mortality of epilepsy

A 
neurological disease
neurovascular disease or neoplasm
SUDEP (suddenly unexplained)
unintentional injury
suicide
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48
Q

mortality rate increase in epilepsy for cases without a known cause OR in cases with symptomatic epilepsy

A

cases with symptomatic epilepsy

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49
Q

mortality risk factors higher for male or female?

A

same

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50
Q

mortality risk factors highest in which age group

A

younger

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51
Q

severity of epilepsy increases with

A

seizure recurrence

frequency

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52
Q

known risk factors for seizure recurrence

A

prolonged febrile convulsions that leads to

  • neurological injury
  • neoplasm
  • disorders of neuroblast migration
  • TBI
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53
Q

cognitive deficits related to seizures are determined by

A

localized brain regions associated with specific functions (e.g. memory in temporal lobe epilepsy)

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54
Q

generalized cognitive deficits (e.g. attention, psychomotor speed) associated with

A

seizures themselves

treatment of seizures with AED

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55
Q

which factor is the strongest determinant for cognitive impairment in epilepsy?

A

seizure frequency!

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56
Q

other determinants of cognitive impairment in epilepsy?

A

tumor, CNS infection, trauma
younger age of onset
no of AEDs

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57
Q

genetic epilepsy more associated with what kind of developmental disorders?

A

ASD

ID

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58
Q

temporal lobe epilepsy with hippocampal sclerosis is associated with a history of

A

infantile seizures as an infant or toddler

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59
Q

what are febrile seizures?

A

children aged 3 months to 6 years
who may have tonic-clonic seizures when they have a high fever
good outcomes

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60
Q

when there are recurrent episodes of febrile seizures, it presents a greater risk for

A

future development of temporal lobe epilepsy

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61
Q

increased risk for hippocampal sclerosis

A

history of perinatal complications
hypoxic ischemic injury
CNS infections
limbic encephalitis

62
Q

treatment of TLE

A

very difficult to treat - 1/3 of TLE patients develop medically intractable seizures

anticonvulsant medications
surgery (temporal lobectomy - remove epileptogenic temporal lobe and mesial temporal structures)
thermal laser ablation
neurostimulation system (neurospace)

63
Q

Behaviors associated with TLE

A

auras (mostly with GI symptoms, psychological phenomenon)
disorganized behaviors
repetitive movements of hands, tongue, mouth, lips, usually ipsilateral to size of seizure onset
post ictal confusion/fatigue (min to hours)
secondary generalization to tonic clonic seizure 50% of the time

64
Q

seizure onset of TLE characteristics

A

alteration of awareness
gradual alteration of awareness
may not have LOC

65
Q

Speech patterns and TLE

A

if pt can continue to speak clearly is associated with non language dominant temporal lobe onset in most cases

if patient is aphasic or has dysnomic speech after TLE, it’s usually lateralizing, meaning, it’s associated with language dominant TLE

66
Q

surgeries of TLE

A

standard temporal lobectomy
modified anterior temporal lobectomy
selective amygdalahippocampectomy

67
Q

risks of TLE surgery

A

cognitive morbidity

  • decreased efficiency in learning and memory
  • word finding
  • visual field deficits
68
Q

newer TLE treatment

A

thermal laser ablation applied to mesial temporal lobe structures

69
Q

childhood absence epilepsy

A

primary generalized epilepsy
widespread neural networks at seizure onset
self limiting, does not persist past adolescence

70
Q

Childhood absence epilepsy accounts for % of childhood seizures?

A

15%

71
Q

which is the most common epilepsy syndromes of childhood?

A

Childhood absence epilepsy

72
Q

imaging findings of Childhood absence epilepsy?

A

typically negative

73
Q

age of onset of Childhood absence epilepsy

A

3- 8 years

peak at 6 years

74
Q

neurological implications of Childhood absence epilepsy ?

A

neurologically normal usually

comorbid learning and attention problems

75
Q

Childhood absence epilepsy EEG characterized by ? Hz?

A

3 Hz spike wave discharges
lasts 5-10 seconds
as short as 3, or as long as 20 seconds

76
Q

untreated Childhood absence epilepsy?

A

very frequent seizures on a daily basis

77
Q

behaviors of Childhood absence epilepsy

A

sudden behavior arrest
alteration of awareness (STARING)
minor motor automatisms (eyelid fluttering, lip movements)
begin and end suddenly
usually pt unaware
briefly disoriented and need prompting to resume activity

78
Q

Medical tx of Childhood absence epilepsy failure rate

A

variably effective, but failure rate 47%

79
Q

common meds for Childhood absence epilepsy

A

lamotrigine
valporic acid
ethosucimide

80
Q

best meds for seizure relief in Childhood absence epilepsy?

A

Zarontin/ethosuximide

81
Q

Is Childhood absence epilepsy benign or malicious?

A

benign

82
Q

when do children with Childhood absence epilepsy have remission?

A

during adolescence most cases

15% persist into adolescence, adulthood, develop into juvenile myoclonic epilepsy

83
Q

other epilepsy syndromes

A

Landau Kleffner syndrome
Lennox Gastaut syndrome
Rasmussen syndrome

(Left-right-left)

84
Q

Landau Kleffner syndrome LKS

A

progressive encephalopathy
AFFECTS LANGUAGE
normal language prior to onset of seizures

85
Q

onset of Landau Kleffener

A

ages 3- 7 years

86
Q

deficits in Landau kleffner

A

progressive aphasia:

  • development of receptive language impairment
  • verbal auditory agnosia
  • then gradual development of expressive language deficits
general cognitive impairment
regression of IQ
deficits in attention
sociability
autistic behaviors
87
Q

cause of landau kleffner syndrome

A

no known cause

20% of cases show variation in GRIN2A

88
Q

localization of Landau kleffner syndrome

A

language dominant perisylvian region or bilateral

frontal lobe pathology

89
Q

recovery and treatment of landau kleffner syndrome

A

no sponatneous recovery of language
tx does not help with cognitive impairment
speech and language interventions are critical (or use sign language)

90
Q

Lennox Gastaut syndrome (LGS)

A

encephalopathic generalized epilepsy syndrome

progressive and severe cognitive impairment

91
Q

possible cause of lennox gastaut syndrome

A

possibly genetic

92
Q

clinical presentation of lennox gastaut syndrome

A

multiple seizure types

  • atypical absence seizure
  • tonic seizure
  • atonic seizure
93
Q

Risk factor for lennox gastaut syndrome

A 
history of infantile spasm
MCS
neurocutaneous disorder (e.g. tuberous sclerosis complex)
CNS infection (meningitis, encephalitis)
hypoxic ischemic injury
no single underlying pathology
94
Q

how is lennox gastaut syndrome characterized?

A

using EEG pattern

  • bursts of fast activity (During slow wave sleep)
  • background EEG is usually slow activity and disorganized

cognitive impairment and behavior impairment

95
Q

Rasmussen syndrome is characterized by

A

progressive unilateral encephalopathy

medically refractory seizures

96
Q

age and presentation of rasmussen syndrome

A

children in 3-14 years
premorbid cognitive and behaviors NORMAL

after seizures begin:

  • loss of cognitive skills related to the side of seizure onset
  • ultimately complete loss of function in the affected hemisphere (HEMIPARESIS!)
97
Q

cause of rasmussen syndrome

A

autoimmune basis

no specific marker

98
Q

treatment for rasmussen syndrome

A

immunotherapy

BEST is surgical intervention (hemispherectomy)

99
Q

NP results IQ in epilepsy

A

low IQ

IQ is a proxy for outcome, disease severity, extent of pathology

100
Q

Risk factor for low IQ in epilepsy

A

age of seizure onset
earlier onset - lower IQ
no progressive decline in IQ in recurrent seizures

101
Q

risk factor for progressive decline in IQ

A

seizure severity
treatment with multiple meds
comorbid LD

102
Q

epilepsy syndromes that have effect on IQ

A

MCD - severe cog impairment and very low IQ

encephalopathic generalized epilepsy (Lennox Gastaut and landau kleffner) has extremely low IQ

103
Q

Attention and epilepsy

A

30-50% have difficulties with attention
ADHD-I more common than other types
ADHD-C related to severity of epilepsy, early onset
affect boys and girls the same way

104
Q

which type of seizure more associated with attention problems?

A

absence seizure
- impaired attention network comprising anterior insulafrontal operculum and medial frontal cortex

nocturnal seizure
- affect attention b/c of sleep patterns

localization-related partial epilepsy
- interictal discharges/transient cognitive impairment

105
Q

how does attention problems in epilepsy differ from adhd?

A

epilepsy kids - more sustained attention difficulties

ADHD kids - more complex and divided attention problems

106
Q

treatment for attention problems in epilepsy

A
  • AED can produce attention problems as side effect
  • not often use stimulants to treat ADHD because of possible increase in seizure in some cases
  • most research suggest AED does NOT lead to more seizure
107
Q

comorbid epilepsy and ADHD brain structures

A 
Decreased gray matter volume in
- sensorimotor
- supplmental motor
- prefrontal
decreased brainstem volumes
frontal cortical and subcortical systems regulating attention
108
Q

processing speed in epilepsy changes due to…

A
  1. side effects of AED
  2. structural or neuroanatomical basis
    - decrease in white matter volume
    - frontal lobe epilepsy
    - interictal epileptiform discharges
109
Q

how does AED work on seizures?

A
  • reduce hyperexcitabilty and neuronal transmission by increasing inhibitory action (of GABA)
  • reduce availability and function of excitatory NT (e.g. glutamate)
110
Q

language in epilepsy

A

common deficit
dependent on onset of seizure
- if onset is during critical language period, it can disrupt important networks involved in language

111
Q

language deficits in epilepsy can be associated with some types of epilepsy

A

frontal and TLE involving dominant hemisphere

- TLE have problems with word finding and semantic knowledge

112
Q

Visuospatial is associated with which types of epilepsy?

A

associated with:

  • primary generalized
  • generalized nonconvulsive epilepsy
  • localization-related epilepsy (non dominant)
113
Q

Visuospatial and epilepsy deficits in?

A 
impaired object recognition
spatial organization
visuomotor integration
visuospatial learning
complex perception
114
Q

crowding effect

A

early onset lesions can lead to reorgnization of language from L to R or become bilateral

preferential neural resources allocated for language development

shifting resources to back up systems in homologous area in contralateral hemisphere

115
Q

learning and memory and TLE

A

lateralized seizure onset
- one temporal lobe is more extensively involved in seizure onset and propogation

more verbal for dominant TLE
nonverbal for nondominant TLE

116
Q

type 1 hippocampal sclerosis and memory

A

impaired (esp list learning)

117
Q

memory outcome following temporal lobectomy is predicted by

A

baseline level of hippocampal function
- WADA testing, memory test performance

low baseline -> decreased risk of exacerbating existing memory impairment
high baseline -> increased risk of decline in memory

118
Q

Intracarotid amobarbital hemispheric suppression =

A

WADA testing

119
Q

gold standard for predicting catastrophic memory loss

A

WADA testing

120
Q

Wada testing is useful for

A

predicting memory loss

predicting common declines associated with TL surgery by analyzing functional adequacy and functional reserve

121
Q

TLE memory declines can also be predicted by

A

fMRI findings of increased activation ipsilateral of seizure focus during memory testing

122
Q

memory problems in other epilepsy syndrome besides TLE

A

CAE - attention problems affecting encoding and sotrage, more VS memory problems
frontal lobe epilepsy - problems with poor organization and strategies for learning and memory

123
Q

predictors of more impaired executive function in epilepsy include

A

early onset
longer duration of seizures
involvement of frontal subcortical systems

124
Q

frontal lobe epilepsy and EF

A 
deficits in planning
mental flexibility
impulse control
motor coordination
less lateralized deficits in FLE
125
Q

Frontal lobe epilepsy characteristics and EF

A

spread rapidly
engage bilateral malformation of cortical development (MCD)
more widespread abnormalities

126
Q

TLE and EF

A

variability in cortical morphometric variations in TLE
extratemporal structures
- frontal and subcortical regions

127
Q

Sensorimotor functions and Epilepsy

A

motor skills deficit (hemiparesis - Rasmussen syndrome)

if epilepsy involves frontal and parietal sensorimotor cortex

128
Q

social cognition and epilepsy

A

ID, ASD

deficits in social cognition

129
Q

social cognition and epilepsy type

A

TLE/FLE

  • social cognition involves frontal cortex (anterior cingulate, temporal lobes, amygdala)
  • other psychosocial factors that affect social cognition and skills
130
Q

emotion and personality and epilepsy

A

mood d/o

  • anxiety, depression (shows differently in diff ages)
  • poor QOL
131
Q

treatment of depression in epilepsy

A

SSRI SNRI

132
Q

PVT SVT

A

20-25% fail PVT

133
Q

atonic seizure problem?

A

high risk for falls

134
Q

psychosocial issue with epilepsy

A

driving restriction
underemployment
reduced independence

135
Q

employment

A

unemployment and underemployment

  • education issues at early age, absences, LD, reduced work choices
  • safety reasons
  • distance
136
Q

driving in epilepsy

A

if history of sustained control, can drive
recurrent seizures despite AED, cannot drive
seizure free and discontinuation of AED, cannot drive during drug withdrawal period

137
Q

focal onset seizures has 2 types

A

aware

impaired awareness

138
Q

focal onset - aware

A

person is awake and aware during a seizure

139
Q

focal onset - impaired awareness

A

person is confused or their awareness is affected in some way during a focal seizure

140
Q

focal motor onset seizures

A

cause a change in muscle activity (jerking of a finger, stiffening of one part of the body, or weakness in specific muscles)

The movements may spread from one area and involve one side of the body or extend to muscles on both sides of the body.

can affect specific muscles or affect speech

141
Q

examples of focal motor seizures

A

automatisms - involuntary, automatic, coordinated, and repetitive movements of the person’s hands, feet, vocal chords, lips and face, or other areas.

atonic - sudden loss in muscle tone
clonic -rhythmic jerking of one limb or one side of body
epileptic spasm - sudden flexion or extension of muscles
hyperkinetic -sudden, large, irregular movements by limbs or one side of the body
myoclonic - brief jerks or muscle contractions, usually in single bursts
tonic - brief increase in muscle tone for the duration of the seizure

142
Q

focal non motor onset seizures

A

changes in any one of the senses.
person remains alert and able to interact
generally last seconds to less than two minutes.

143
Q

examples of focal non motor seizures

A

autonomic -changes in the part of the nervous system that automatically controls bodily functions (heart rate, sensation)
behavior arrest - decrease in amplitude or outright arrest of ongoing motor activity for the duration of the seizure,
cognitive/emotional - Change how people think, feel, or experience things
sensory - affect any of an individual’s five senses

144
Q

Generalized onset has 2 types of seizures

A

motor

nonmotor (absence)

145
Q

Generalized onset motor tonic clonic seizure

A

grand mal seizure

loses consciousness
muscles stiffen
jerking movements

generally last 1 to 3 minutes

146
Q

convulsive status epilepticus

A

1 seizure that lasts > 10 minutes

or 3 seizures without a normal period in between

147
Q

clonic seizures

A

rapidly alternating contraction and relaxation of a muscle (repeated jerking)
movements cannot be stopped by restraining or repositioning the arms or legs

rare occurence

148
Q

tonic seizures

A

causes a sudden stiffness or tension in the muscles of the arms, legs or trunk.
stiffness lasts about 20 seconds
usually happen during sleep.
may fall if standing

149
Q

Generalized onset non motor (absence) seizure

A

“blanking out” or staring into space
usually so brief that they frequently escape notice.

petit mal

150
Q

Generalized non motor seizures has 2 types

A

atypical

typical

151
Q

generalized nonmotor typical seizure

A

a very brief, usually less than 10 second, interruption of ongoing activities.

person staring off into or possibly a brief upward deviation of the eyes

152
Q

generalized nonmotor atypical seizure

A

change in muscle tone
make some kind of movement in addition to staring into space (e.g. blinking, chewing, or hand gestures).
may last up to 20 seconds.

Elsa AACN (35 decks)

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