Developmental Disorders Of Childhood

Front 1

What is a teratogen?

Back 1

agents that can produce CNS defects

Front 2

What 3 types of CNS defects are attributable to teratogens?

Back 2

1. agenesis (failure of organ to develop)
2. dysgenesis (abnormal development of organ)
3. other focal or diffuse effects

Front 3

Nelson gives 5 examples of teratogens. What are they?

Back 3

1. general diseases
2. STDs
3. drugs
4. environmental toxins
5. radiation

Front 4

When is the prenatal brain most vulnerable?

Back 4

weeks 2-8, but continuous vulnerability

Front 5

Impact of teratogens depends on ... (4 items)

Back 5

1. where you are at in terms of brain growth
2. genetic makeup of child/mother
3. quality of intrauterine environment
4. "dosage" and extent of exposure

Front 6

When damage is later in prenatal development, it results in more limited disruption to... (3 items)

Back 6

1. specific cellular layers
2. structures
3. circuitry

Front 7

What aspects of CNS development continue well after birth? (4 specific things)

Back 7

1. cortical cellular migration
2. myelination
3. dendritic arborization
4. synaptogenesis

Front 8

What is one of the most widespread neurotoxins world-wide?

Back 8

inorgan lead

Front 9

At higher levels of inorganic lead exposure, what is there clear evidence of?

Back 9

a negative impact on intellectual functioning

Front 10

Higher maternal blood levels of lead at _____ weeks gestation results in lower ________.

Back 10

28; postnatal intelligence

Front 11

Related to lead exposure, what is the dose-response analysis?

Back 11

most significant impact on intelligence within first few micrograms of blood lead levels

Front 12

What specific cognitive and motor effects are associated with prenatal lead exposure?

Back 12

attentional control, fine-motor speed and dexterity, and visuoconstructive abilities

(which continue to be evident in adolescents)

Front 13

Regarding lead exposure, what do animal studies tell us about implicated structures? (5)

Back 13

1. mesocorticolimbic DA and glutamate brain receptors
---especially nucleus accumbens of basal ganglia
2. frontal cortex
3. hippocampus
4. amygdala
5. cerebellum

Front 14

Nelson lists 11 peri- and post-natal threats. What are they?

Back 14

1. anoxia; 2. medications at L & D; 3. mechanical injury to skull & brain during deliver; 4. low birth weight; 5. traumatic head injury; 6. toxins; 7. radiation; 8. malnutrition; 9. tumors; 10. infections; 11. stroke

Front 15

Resilience is partially related to __________, ____________, and ____________ postnatal environment.

Back 15

responsive, nurturing, stimulating

Front 16

What is plasticity?

Back 16

Enduring changes in neural activity that accompany learning, or recovery of behavioral functioning after brain injury or disease

Front 17

When is plasticity greatest?

Back 17

during development periods when synaptic density is highest (many not yet committed to a function)

Front 18

Plasticity timeframes differ across cortical regions due to different rates of neuromaturation. What are the two windows Nelson lists?

Back 18

1. window smaller for visual cortex (up to 5 years)
2. window longer for prefrontal cortex (late childhood)

Front 19

What are the three concepts associated with the Kennard principle?

Back 19

1. immature brain is more plastic than mature brain
2. greater likelihood of recovery from brain insult if injury occurs earlier rather than later
3. children with focal injury often have milder/less extensive emotional impairments than adults with comparable lesions

Front 20

What evidence is there that the Kennard principle is not a hard and fast rule?

Back 20

some later insults can have more pervasive impact (esp. generalized lesions); may only become apparent as other functions do not develop (e.g., auditory cortex--language)

Front 21

There are significant differences between child and adult brain structures and functions. 3 considerations are esp. important. Name them.

Back 21

1. effects of lesions to immature and mature brains differ significantly
2. disruption of acquisition of abilities (child brain) vs. break down of previously acquired abilities (adult brain)
3. effects of lesions to an adult brain are quite different than those to a child's brain: childhood damage to one region may impact development of other regions

Front 22

What are the differences between child and adult brains regarding lesions to the language area of the L hemisphere?

Back 22

young children rarely show aphasia; early L hemisphere damage usually associated with language abilities at low average range; adults with similar lesions show: high rates of aphasias and a less robust recovery

Front 23

In children, R hemisphere damage is associated with?

Back 23

receptive language deficits

Front 24

In children, L hemisphere temporal damage is associated with?

Back 24

delayed word production but normal comprehension and gestures (OPPOSITE OF ADULTS)

Front 25

R hemisphere damage is associated with visuoconstructive and emotional comprehension and expression deficits. In what developmental state?

Back 25

both children and adults

Front 26

Commitment of brain regions/circuits to language and other abilities with age makes the brain...?

Back 26

less able to reogranize and redistribute functions

Front 27

What two characteristics of brain damage interact to determine immediate or delayed impairment?

Back 27

1. age
2. region of damage

Front 28

List examples of immediate and delayed impairments of cognitive and socioemotional executive functions with early prefrontal damage.

Back 28

social awareness; interpersonal sensitivity; perspective taking; friendship skills; close emotional relationships

Front 29

What is hydrocephalus?

Back 29

excessive accumulation of CSF in the ventricles, with concomitant increase in intracranial pressure and expansion of ventricles (resulting in cerebral tissue comprises and cranium distortion)

Front 30

What is the incidence of hydrocephalus? What are the gender rates?

Back 30

~27 per 100,000 newborns; greater for boys (62%)

Front 31

If untreated, hydrocephalus can lead to?

Back 31

death or severe MR

Front 32

What is spina bifida?

Back 32

incomplete development of the spinal cord or its coverings

Front 33

What is the relationship between hydrocephalus and IVH (intraventricular hemorrhage)?

Back 33

IVH is the most common cause of hydrocephalus peri- and post-natally.

Front 34

What are the two most important aspects of hydrocephalus neuropathogenesis?

Back 34

1. hydocephalus occurs secondary to other other pathologic events/processes
2. it can occur pre-, peri-, or post-natally

Front 35

There are three ways that hydrocephalus is physiologically structured. Name them.

Back 35

1. oversecretion of CSH
2. obstruction of CSF passages
3. impaired absorption of CSF

Front 36

What are the facts about oversecretion of CSF as the physiological explanation of hydrocephalus?

Back 36

its rare; frequently its a secreting tumor of the choroid plexus

Front 37

What are the facts about obstruction of CSF as the physiological explanation of hydrocephalus?

Back 37

its obstructive or non-communicating; aqueduct of Sylvius (of third ventricle) is most commonly the site of obstruction; typically prenatal with ever-expanding impact

Front 38

What are the facts about impaired absorption of CSF as the physiological explanation of hydrocephalus?

Back 38

typically peri- or post-natal insults to a previously normal brain; non-obstructive or communicating HC; (apart from spina bifida) IVH is the most common cause

Front 39

What happens to ventricles in HC?

Back 39

progressively enlarge poster to anterior direction; focal damage at lining of the ventricles

Front 40

what happens to the blood vessels in HC?

Back 40

blood vessels distort

Front 41

What happens to neurons in HC?

Back 41

neurons are injured

Front 42

What happens to neurotransmitters in HC?

Back 42

the concentration of NTs change

Front 43

What happens to white matter in HC?

Back 43

there is extensive damage to the underlying white matter

Front 44

What thins during HC?

Back 44

corpus callosum and cortical mantle

Front 45

What is the common treatment for HC?

Back 45

a shunt draining CSF into the stomach

Front 46

What are the side effects/risks of shunting for HC?

Back 46

increases risk of infection of ventricles, requires lesion to the brain (usually in the R parietal lobe), irritating surrounding brain tissue increases the potential for seizures

Front 47

Three "visuo" based deficits are common with HC, due to damage of three structural areas. List them.

Back 47

1. visuo-perceptial
2. visuospatial
3. visuomotor

1. posterior cortical
2. cerebellum
3. corpus callosum

Front 48

What are the areas of damage related to the poor motor skills seen in individuals with HC?

Back 48

cerebellum; basal ganglia; motor strip; connecting white matter pathways

Front 49

What memory deficits are seen in individuals with HC?

Back 49

poor recall of both verbal and nonverbal content

Front 50

What is "cocktail party syndrome" and how common is it in individuals with HC?

Back 50

fluent but empty speech, with excessive verbiage that lacks clarity, organization, and relevance; 28-41% of cases

Front 51

What achievement/academic deficits are common in individuals in HC?

Back 51

lower: reading comprehension, math computation and problem solving, and writing skills

Front 52

What are the deficit differences in early v. late occurring HC?

Back 52

prenatal obstructive HC = average verbal and language, below average visuospatial and visuomotor

peri- and post-natal insults (e.g. IVH) = comparable verbal and performance abilities but both low average

Front 53

What executive function deficits are seen in HC?

Back 53

deficits in: attentional allocation and control, concept formation, planning, cognitive flexibility, response inhibition, self-regulation

Front 54

The executive functioning deficits seen in HC are not necessarily indicative of frontal cortex damage. The could be?

Back 54

a result from posterior disruption impacting on connections with frontal systems

Front 55

What are the 5 characteristic facial features associated with FAS?

Back 55

1. widely spaced eyes
2. shortened length of eyelids
3. elongated midface
4. flattened nose
5. underdeveloped upper lip

Front 56

Abnormally small head (microcephaly), infantile irritability, seizures, tremors, poor coordination, poor habituation, reduced muscle tone, below average intelligence, inattention, hyperactivity, LDs, and poor behavioral regulation

are CNS deficits related to what developmental disorder?

Back 56

FAS

Front 57

Children exposed to alcohol in utero can still show functional impairments (without facial abnormalities, etc. of FAS). What are the names of these conditions?

Back 57

fetal alcohol effects (FAE) or alcohol-related neurodevelopmental disabilities (ARND)

Front 58

What 4 deficit areas are particularly common in children with FAE or ARND?

Back 58

1. sensory and sensorimotor impairments
2. speech and language delays
3. cognitive and learning weaknesses
4. regulatory deficits (inattention, impulsivity, hyperactivity)

Front 59

What are the incidence facts of alcohol-related developmental disorders?

Back 59

FAS has 1 to 3 in 1000 living births; incidence is higher if include FAE (2-3 times greater); in children of alcoholic mothers incidences range from ~25 per 1000 (FAS) and 90 per 1000 (FAE)

Front 60

What difference does prenatal alcohol exposure period have on deficits?

Back 60

weeks 6-18 (during brain neurogenesis) may result in global cognitive deficits

later exposure may produce more local/circumscribed deficits

Front 61

What do genetic factors have to do with FAS?

Back 61

they have an influence; fraternal twins can have different degrees of effects of in utero alcohol exposure

Front 62

An important, but often neglected, phenotypic-mediating factor of FAS/FAE is ________, for example:

Back 62

postnatal social environment; ex: higher levels of abuse, neglect, inconsistency, stress, etc.

Front 63

Nelson lists 8 neuroanatomic alterations in FAS/FAE. What are they?

Back 63

1. dysgenesis or agenesis of corpus callosum
2. hippocampal damage
3. reduced basal ganglia volume
4. cerebellar anomalies
5. expanded ventricles
6. reduction in white matter
7. reduced brain size (in microcephaly)
8. disruptions of frontal circuitry (why executive dysfunctions)

Front 64

What are the vulnerable multiple cognitive domains associated with FAS?

Back 64

intellect, language, learning and memory, executive functioning impairments

Front 65

What are the primary behavioral difficulties related to?

Back 65

attention deficits and social problems

Front 66

What is a more sensitive marker of prenatal alcohol exposure than global intelligence or facial stigmata?

Back 66

poor attention

Front 67

What is the developmental course of FAS/FAE?

Back 67

infants: low birth weight, poor sleep/feeding/habituation, irritable

age 4: deficits in: motor skills, attention, memory, academics, and reaction time; enuresis and communication dx

elem. school: ADHD sx, behavioral problems

Front 68

By adolescence and adulthood FAS/FAE deficits tend to decline. True or false?

Back 68

both. communication disorders and basic fx problems decline.

cognitive and behavioral deficits persist.

Front 69

There are high rates of ________ and __________ in adults with FAS/FAE.

Back 69

antisocial behaviors; substance abuse

Front 70

What is the best form of treatment for FAS?

Back 70

prevention.