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BMB Test 3 > B7.047 Neurodevelopmental Disorders > Flashcards

B7.047 Neurodevelopmental Disorders Flashcards

1
Q

classes of neurodevelopmental disorders

A
  1. affecting cognition
    - intellectual disability (mental retardation)
    - autism (socialization disability)
  2. affecting motor function
    - cerebral palsy
  3. disease acquired in childhood
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2
Q

characterize encephalopathies acquired during childhood

A

lesion: brain
manifestations: vary
etiologies: anything that can damage the brain during childhood

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3
Q

definition of intellectual disability

A 
intelligence substantially below average
important limitations in adaptive function
-difficulty coping with life demands
onset before age 18
IQ < 70 (2.5% of population)
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4
Q

description of IQ

A

average = 100
standard deviation = 15
< 70 is 2 SDs below normal

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5
Q

severity of intellectual disability

A

borderline: IQ 70 to 84
mild: IQ 50 to 69
- often not noticed until school
- reading and writing typical of a child aged 9-12
- often become independent
moderate: IQ 35 to 49
- delayed speech development
- usually require lifelong partial support
severe: IQ 20 to 34 or profound: IQ <20
- usually require lifelong support

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6
Q

cause of intellectual disability

A 
unknown in 33%
common causes:
genetic
-downs (trisomy 21)
-fragile x (boys > girls)
-rett syndrome (girls)
malnutrition
toxin exposure: lead
neonatal injury
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7
Q

definition of autism

A

impaired socialization detected before age 3
-impaired social interaction
-impaired communication (verbal and non verbal)
-restricted interests with stereotyped behaviors
more than half with associated intellectual disability

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8
Q

autism spectrum disorder

A

included people with more mild forms that may have been detected after age 3

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9
Q

lifelong nature of autism

A

not progressive
special educational programs can lead to improvements with age
most with life-long difficulty in social situations
preferences for routine and restricted behavior patterns

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10
Q

epidemiology of autism

A

prevalence: 1%
increasing: may be due to changing definition, improved recognition, or a true epidemic
males > females
-overall 4:1
-within subset without intellectual disability (aspergers) 8:1

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11
Q

theory of mind

A

humans understand mental state of others

explain and predict behaviors of others

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12
Q

lack of mutual attention

A

faces preferred over objects

abnormal gaze in social situations (don’t focus on eyes like people without autism)

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13
Q

presentation of autism

A 
parents first to notice
by definition, changes before age 3
early socialization normal
-gaze to faces
-social smile
-vocalization to others
early manifestations 12-18 months
-baby does not turn when called by name
-does not attend to person or object of other people's attention
more severe = earlier signs
aspergers often not diagnosed until school age
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14
Q

where is the pathology in autism

A 
no specific pathological change
functional imaging defects:
-orbitofrontal cortex
-anterior cingulate cortex
-amygdala
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15
Q

cause of autism

A 
NOT a simple environmental exposure
strong genetic component
-10-15% have known genetic disease
-monozygotic twins: 60-91% concordance
-dizygotic twins: 10-30% concordance
-polygenetic inheritance
-many likely x-linked
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16
Q

characterize cerebral palsy

A

encephalopathy (brain lesion)
acquired early (before age 3)
manifested by disorder of movement or posture

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17
Q

static nature of CP

A

brain lesion does not progress

clinical manifestations can progress as child and nervous system mature

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18
Q

prevalence of CP

A

2-2.5 per 1000 birth worldwide

10,000 babies born in US per year

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19
Q

classification of CP

A 
based on motor manifestations
spastic (UMN)
ataxic (cerebellar)
dyskinetic (basal ganglia)
hypotonic
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20
Q

symptoms of spastic CP

A

most common
spasticity
hyperreflexia
upgoing toes

21
Q

symptoms of dyskinetic CP

A

rigidity
abnormal involuntary movements: choreoathetosis
difficulty with voluntary motor control

22
Q

patterns of spastic CP

A

spastic diplegia (legs only, most common)
spastic hemiplegia
spastic quadriplegia

23
Q

symptoms of ataxic CP

A

least common
severe appendicular and gait ataxia
vermian system defect

24
Q

signs of CP in general

A 
symptoms range from mild to severe
lack of muscle coordination
exaggerated reflexes (spasms)
one foot or leg dragging
difficulty swallowing, speaking
difficulty with precise movements
25
Q

findings associated with CP

A

30-50% have intellectual disability
communication may be impaired
expression of intellectual capacity may be difficult
15-60% have epilepsy

26
Q

etiology of CP

A 
any prenatal, perinatal, or postnatal event affecting the brain
multiple risk factors:
-preterm birth
-multiple gestation
-male sex
-low apgar
-intrauterine infection
-birth asphyxia
27
Q

clinical manifestations of early brain injury (non genetic)

A

because brain is not fully functional at time of insult, the sequelae become obvious only with time
hypotonia (floppy baby)

28
Q

major events in brain development

A

primary neurulation- weeks 3-4 of gestation
prosencephalic development- months 2-3 of gestation
neuronal proliferation- months 3-4 of gestation
neuronal migration- months 3-5 of gestation
organization- month 5 to years postnatal
myelination- birth to years postnatal

29
Q

what is the germinal matrix

A

area of developing brain located in the subependyma of the ventricular walls

30
Q

function of germinal matrix

A

at 8-28 weeks gestation, the matrix produces neurons and glial cells, which migrate to populate the cerebral cortex
-neurons earlier, glial cells later

31
Q

involution of germinal matrix

A

begins late in second trimester

nearly complete by 32 weeks gestation

32
Q

structure of germinal matrix

A

metabolically active with a rich supply of blood via a thin, fragile capillary network
premature babies at risk of bleeding since germinal matrix is still present at birth

33
Q

pathogenesis of germinal matrix hemorrhage

A
  • poor autoregulation of blood flow and blood pressure
  • thin microvasculature is susceptible to rupture
  • fluctuations in blood pressure injure vessels leading to hemorrhage
34
Q

result of germinal matrix hemorrhage

A

hypo-perfusion and hypoxia can lead to infarction

hemorrhage can occur in infarcted regions after reperfusion as well

35
Q

discuss the vulnerability of premature infants to germinal matrix hemorrhage

A

most cases occur in first week of life for these infants (65%)
approximately 50% in first day of life
high risk: neonates born at <32 weeks’ gestation and with birth weights less than 1500 g
unusual after 34 weeks gestation (germinal matrix is gone)

36
Q

selective vulnerability of brain to hypoxia

A

brain is most oxygen dependent organ

within minutes of oxygen deprivation, permanent damage results

37
Q

mechanisms of ischemic injury of brain

A

pure hypoxia
pure hypo-perfusion
mixed

38
Q

what is a watershed zone

A

last area where blood perfuses

if a circulation problem occurs, these zones don’t get enough oxygen and typically suffer first

39
Q

watershed zones of the brain preterm

A

periventricular region

-watershed between penetrating arterial vessels from the cortex and vessels arising from deep ventricular margins

40
Q

watershed zones of the brain after term

A

area between ACA and MCA

area between PCA and MCA

41
Q

periventricular leukomalacia (PVL)

A

second most common CNS complication in preterm infants

caused by ischemia in the preterm watershed territory

42
Q

regions most commonly affected in perinatal vascular insult

A

optic radiations
trigone of corpus callosum
frontal periventricular region

43
Q

regions affected by PVL

A

corticospinal tract
sensory association fibers
visual tract
auditory tract

44
Q

effects of ischemia on oligodendroglia

A

myelination is impaired

45
Q

selective vulnerability of fibers to the leg to periventricular pathology

A

leg portion of the cortices (based on homunculus) is closest to the periventricular region, thus most susceptible to issues there

46
Q

spastic diplegia in premature infants

A

may result from parenchymal-intraventricular hemorrhage or periventricular leukomalacia
no risk factors identified in term infants

47
Q

vascular injuries after term

A

most often in the distribution of the middle cerebral artery, resulting in a spastic hemiplegic CP
also susceptible to hypo-perfusion, which targets watershed areas of the cortex resulting in spastic quadriplegic CP

48
Q

pure hypoxia vulnerability of brain

A

BP is ok, but lung function not
areas a risk:
1. cerebral cortex: intellectual disability
-layer 3 (laminar necrosis)
-mesial temporal lobe (hippocampus)
2. basal ganglia (globus pallidus): dyskinetic CP
3. purkinje cells of the cerebellum: ataxic CP

49
Q

kernicterus

A

bilirubin induced neuro dysfunction
primarily premature infants with very high bilirubin
uncommon
can lead to dyskinetic CP

BMB Test 3 (21 decks)

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