College aantekeningen

Developmental Neuropsychology Full Exam Chapter Notes () - Utrecht University

0 keer verkocht

Vak
201800818 (201800818)

Instelling
Universiteit Utrecht (UU)

In-depth exam summaries covering all topics related to the Developmental Neuropsychology Module. Including: Dimensions of Theory & Practice; Cerebral Development; Cognitive Development; Recovery from early brain insult – plasticity / early vulnerability; ADHD & AUTISM, Specific Language Impairmen...

[Meer zien]

Voorbeeld 4 van de 49 pagina's

Bekijk voorbeeld

Geupload op 27 februari 2024
Aantal pagina's 49
Geschreven in 2023/2024
Type College aantekeningen
Docent(en) C.d.
Bevat Alle colleges

plasticity
nature nurture
adhd
autism
cerebral development
cognitive development
early brain insult
early vulnerability
sli
dld
child intervention
child assessment
develop
specific language impairment

€8,99

Ook beschikbaar in voordeelbundel v.a. €20,39

In winkelwagen

Opslaan

100% tevredenheidsgarantie
Direct beschikbaar na je betaling
Lees online óf als PDF
Geen vaste maandelijkse kosten

Ook beschikbaar in voordeelbundel (1)

Neuropsychology Exam Notes (Utrecht University) Package Deal

€ 26,97 € 20,39 3 items

1. College aantekeningen - Exam summaries for advanced neuropsychology - utrecht university
2. College aantekeningen - Cognitive neuropsychiatry full exam notes - utrecht university
3. College aantekeningen - Developmental neuropsychology full exam chapter notes (201800818) - utrecht universi...
Meer zien

Developmental Neuropsychology Chapter Notes:
Chapter 1: Dimensions of Theory & Practice
-Child neuropsychology = brain-behaviour relationships in dynamic context
-Brain insult in childhood = rapidly evolving system  alteration of normal developmental processes at neurological & cognitive
level  advantages & disadvantages  emore flexible & capable of transferring functions = minimal loss of function OR less
able to support efficient attention, memory and learning skills = greater gap between peers
-Address totality of the child (physical, cognitive, psychosocial experiences) = interact to influence recovery  dynamic path of
maturation potential of disruption at various stages
-Dimensions of child neuropsychology = foundations from adult models (cerebral localization and integrated brain systems) 
= static, mature, unable to accommodate dynamic early cerebral pathology (insufficient)
-Developmental neurology + cognitive psychology map expected changes in child CNS  growth spurts in CNS + increments in
cognitive abilities
-Neuro-dimension: CNS in early gestation ongoing development in infancy & childhood
- Prenatal: Structural formation (basic hardware)  interruptions = structural abnormalities (dysplasia, spina bifida,
dandy-walker syndrome, AgCC)
- Postnatal development: elaboration of CNS (connectivity)  continues into adolescence (incl. dendritic arborization,
myelination, biochemical changes)  greatest maturation in anterior cerebral areas (hierarchically: posterior/anterior)
 step-wise model of development rather than gradual progression (early infancy, 7-10 yrs, early adolescence)
- CNS injury/insult = infection, environmental factors (malnutrition, sensory deprivation, toxins)
- Dose-response relationship: severe cerebral pathology = greater neuropsychological impairment
- Acquired Disorders = generalized (TBI, HYD, infection, metabolic disorder)/ Focal disorders (e.g. tumor, stroke = rare)
- Specific impairments (aphasias/apraxias) less common in kids  generalized disturbances of information processing
(attention, memory, psychomotor skills, EFs) more common
- Discrepancy in recovery between adults & children  long-term recovery patterns differ in favor of more mature brain
- Plasticity = damage to immature brain = less significant disability than equivalent insults in adults
- Increased Vulnerability = little advantage for immature CNS
- Transfer of function = cognitive functions subsumed by damaged brain tissue have capacity to transfer to healthy tissue
 influenced by timing (pre/post natal) and nature (focal/generalized) of insult
- Prenatal CNS damage may not result in functional transfer but skills may be maintained ineffectually by damaged tissue
 developmental delays
- Transfer of skills = crowding leading to generalized depression of neuropsychological functions
- Childhood CNS insult may not be static but may interrupt ongoing maturation in a variety of ways detrimental to long-
term outcomes.
- electrophysiological and radiological techniques  measure rate & localization of development over time  map
cerebral activation in young children + directly describe brain correlates  formulate developmental theories 
minimize removal of functional tissue  EEGs/ERPs measure temporal aspects of cerebral function  EEG = epilepsy +
sleep  ERP = sensory / information processing
-Cognitive dimension: early models of cognitive development focus on Piagetian theory  hierarchical/stage-like process 
preset series of developmental stages (some variation in timing)  quality and level of thinking are key characteristics to
change and progress Increase symbolic thought & ability to deal with complex information
- Premotor (birth-2yrs) simple motor & sensory activities, little abstract thought  gradual object permanence (WM)
- 2 yrs = symbolic thought (language, communication, imagery)  higher level = limited  unidimensional & egocentric
- Operational thought (7yrs) reasoning/problem-solving  multiple dimensions, mental transformations, emerge EFs
- Formal operations: fully established in early adolescence
- Transitions evident on standard neuropsychological measures  timing of growth spurts in myelination, metabolic and
electrical activity are roughly consistent with cognitive progressions
- Theory of generalized progression of cognitive skills through childhood  different rates and progressions in specific
domains (motor vs language)  development of individual cognitive modalities is not independent
- Rather domain-specific development occurs in cooperation with similar maturation in other systems – (WM & IP)
- multidimensional relation between memory, processing speed, and EFs are jointly responsible for age-related progress.
- Neuropsychological impairment measured against age-appropriate expectations  plot development of cognitive skills
through childhood, identify deviations from expected patterns, formulate diagnosis + treatment  normative data
- Adult tests for evaluating developing cognitive skills is problematic  do not necessarily measure the same skills
children may achieve similar end points using different brain networks or perform poorly due to cognitive deficits
- Interpretation of test performance as indicative of impairments in higher-order skills is problematic in kids  poor
performance may reflect expected developmental progress or impairment of lower-order skills or age-appropriate
immaturity of higher order skills.
- Cognitive developmental theory posits that EFs may be developing in infancy but not measurable until late childhood 
cannot reliably identifying deficits until later when they should be present and accessible
- 12 might show deficits when impairments have emerged at the time of developmental expectations (leading to
functional dependence)  child may grow into their cognitive deficits as the brain matures (does not necessarily reflect
a deterioration in cognitive skills) – may be a consequence of early cerebral insult.

,-Psychosocial Dimension: social system, family unit, quality of environment, access to resources, appropriate context for
learning, & acceptance of disability  influence of parental & family adjustment
- Social skills develop in stages  infancy largely dependent on family (support & structure)  learn behaviours and
rules  outside world (school) = independence  egocentricity <, cooperate, rational judgments  adolescence =
independence, identity & broader context
- Biological characteristics of child, immediate home environment, and broader social setting influence social
development (no single factor can be understood in isolation)  dynamic interplay of child and environment
- CNS insult  child may interact different with environment  influence individual & family level  early onset CNS
disorder = problems acquiring social knowledge, social rules due to low IQ, stigma, limited interaction  less social
support = more problematic social interactions = social withdrawal
- adolescence = aware of severity of residual deficits & functional impairments  restricts participation  extra pressure
= academic and social expectations  increasing social problems
- 2 distinct aetiologies that influence outcomes for CNS kids: (1) direct effects of injury (2) psychosocial factors  interact
to produce increased behaviour disturbance
-Neurological correlates: psychiatric disorders 5x more likely in brain damaged kids than in kids with physical disorders 
epilepsy is additional risk  contribution of brain dysfunction to behavior and psychosocial functioning
- Behavioural presentation: impulsive, hyperactive, aggressive, lack insight, depressed, anxious  depend on region
- More severe = emotional & behavioural disturbance
- Right lesions and Anterior lesions = behavioural dysfunction  Right Anterior damage = generalized emotional and
behavioural difficulties
- Anxiety and depression = all kids regardless of injury site (psychological factor from hospitalization, separation)
- Aggressive, hyperactive, impulse, perceive emotions = Right Anterior pathology (link to brain)
- Psychosocial correlates: after insult = acceptance, adjustment, and possible disability  anxiety related to illness, miss
school = reduced experiences and confidence  Residual impairments restrict interaction & cause social stigma
- Family experience anxiety, separation, difficulties coping, trauma
- Unidimensional approach to psychosocial factors: identify low SES, multiple family stressors, previous psychological
disturbance, low maternal education  poorer long-term outcomes
- Family cohesion, supportive social networks  better outcomes
- Double-hazard hypothesis: brain insults > consequences in kids from low SES  others suggest kids with low SES are
already compromised, biological risks make less of a difference to recovery and outcome
- mTBI = more pre-injury problems  severe TBI = psychiatric disturbance after injury
- Mariages fail  family isolation  risk factors may change over time since onset of disorder
- Early outcome predicted by disease severity & long-term outcome linked to psychosocial factors
- Too simplistic to treat biological and social issues linearly  relative impact of these factors best conducted using a
multidimensional approach  longitudinal research
-Theoretical framework for child neuropsychology: adult neuropsychology models influence on developmental approach 
assumed fundamental principles also applied
- Functional systems = cognitive abilities are not dependent on a single isolated cerebral location but subsumed by
integrated systems, with damage to any component having repercussions
- Developmental specific principles:
- (1) detection & localization of brain lesions is irrelevant to child neuropsychology (insult my result in anomalous
cerebral organisation so that ongoing development may be inconsistent with localization of function from adult models
- (2) Functional implications of assessment data  identify patterns of deficit, severity & underlying components
- (3) Emphasize cognitive strengths & weaknesses in relation to environment  generalized across lifespan  develop
rehabilitation for educational and social skills
- (4) relate test results to day-to-day performance
-Developmental Neurology: plasticity & critical periods –
- Kennard Principle: if you’re going to have brain damage, have it early  relatively good recovery after early insult  
findings in follow-up of kids with hemispherectomy
- Theory of recovery of function: child’s brain is less differentiated than adult and more capable of transferring functions
from damaged tissue to healthy tissue
- Critical periods = time window when external influences have a significant effect  insult will have different
consequences at different times throughout development  brain insult early in life may be more detrimental to later
injury because some aspects of development are critically dependent on the integrity of a particular cerebral structure
at certain stages  cognitive skills subsumed by those regions can be irreversibly impaired  may be some functional
plasticity but may be quite restricted and not related linearly
- Prenatally lesions or insults in first year of life may be particularly severe
- Environmental deprivation or enrichment models = developing cells are dependent on the type of stimulation available
(sensitive period)  appropriate experience must occur for visual system to develop  deprivation during non-critical
periods does not lead to irreversible consequences.
- Rapid language development (2-5 yrs)  critical period = language shift from one hemisphere to the other with
minimal consequences
- Children isolated from language from birth acquire language best if intervention occurs in preschool or < 10 yrs

,-Neuropsychological theories: unified developmental neuropsychological model
(1) the spectrum of neurobehavioral ability & disability
(2) the progressive development & interaction of 3 principle axes in brain: Left/Right, Up/Down, anterior/posterior 
incorporates interactions among biological cognitive and psychosocial factors.
- Theory of non-verbal learning disabilities (Rourke; 1987) = syndrome for neuropsychological impairments during
perinatal period or infancy  changing cerebral development with specific cognitive profiles  social and cognitive
characteristics and relevance across disorders  timing of insult is NB!
- Dennis’s Heuristic of cognitive development and change with time : age/developmental stage at time of insult and
progression in cognitive skills with time since insult  increased vulnerability of the immature CNS (earlier disruption =
fewer established cognitive skills = greater impact)
- Non-verbal learning disability (NVLD) (Rourke; 1980s) = consistent pattern of neurobehavioral deficits in kids with early,
generalized cerebral dysfunction  central characteristics: (1) bilateral tactile-perceptual deficits (more impaired on L
side of body) (2) impaired visual recognition & discrimination and visuospatial organisation (3) bilateral psychomotor
coordination (more impaired on L) (4)difficulties managing novel information
- If deficits not global  NVLD have intact skills in auditory/verbal domain: (1) simple motor skills (2) auditory perception
(3) rote learning (4) selective / sustained attention of auditory-verbal stimuli (5) basic expressive/receptive language (6)
word reading & spelling
- Secondary & tertiary deficits: reduced exploratory behaviour, poor visual attention & memory, difficulty complex/novel
information & higher order (concept formation, strategy, hypothesis testing, self-monitoring), subtle language
- writing difficulties, poor concept formation, problem solving, socioemotional problems, difficult adapting to social
situations, poor social perception & judgement, interactions, emotional disturbances, internalizing
- Impairment in essential skills for learning  Exploratory behaviour restricted due to deficits in visual, psychomotor and
tactile abilities  impact new learning / understanding (cause-effect relation)  limits exposure & experience 
difficulties with novel/complex non-verbal situations in flexible way  rely on routine  isolation
- Underlying neurology: WM hypothesis (Goldberg & Costa, 1981)  progressive LH lateralization of function throughout
lifespan  degree of WM damage, nature of lesion, developmental stage at time of insult = NB for determining
symptom severity  NB = intact WM function for normal development
- WM develops through childhood  axonal myelination begins prenatally and continues into adolescence  prolonged
developmental period of white matter = vulnerable to disruption (TBI, HYD, cranial irradiation)
- White matter = axons connecting grey matter of cerebral cortex with other centers of the brain and spinal cord 
myelin = bulk of this cerebral WM and progressively coats the axons  insulates and facilitates transmission
- 3 principle classes of cerebral white matter
- (1) commissural fibers (join RH/LH = corpus collossum, anterior, posterior, and habenuclar & hippocampal commissure)
- (2) association fibers (interconnect cortical regions within each hemisphere – arcuate fasciculus)
- (3) projection fibers (link cortical and subcortical regions)
- RH WM is NB for development & maintenance of functions (intermodal integration)
- LH WM is NB for development but not necessarily maintenance
- RH (functional integrity) – LH function is encapsulated and can be maintained in absence of RH input  severe insult to
RH = sufficient to produce NVLD
- Unclear from the model at which developmental stages insult to CNS lead to NVLD  immaturity of anterior regions
- Myelination continues = vulnerable to insult  primary deficit in IP and attention and tertiary executive dysfunction
- Different axes may be differentially important at certain stages  L/R axis may be most important in early 
cortical/subcortical and anterior/posterior axes NB later  < 5 = slower IP but not poorer executive skills than those
with injury later in childhood  earliest lesions affect all axes = global deficits  later lesions = more specific impact
- Very early insults = accumulation of deficits reflecting dysfunction on all 3 cerebral axes resulting in typically generalized
nature of early syndromes.
- Older children = more differentiated, reflecting intact early development with deficiencies relating to the remaining
immature structures.
-Implications of developmental stage: Dennis (Heuristic) language development (extended): aphasia is not standard because
language development may be incomplete resultant impairments viewed in context of age-appropriate language expectations
- 3 age-related variables:
- (1) age at lesion: different effects on language at different developmental stages
- (2) age at testing: vary in ability to perform cognitive tasks (expectations)
- (3) age of lesion (time since insult): time since injury may be relative deterioration in age-related performance or
detour/deviation in pattern of normal behaviour, stress changes, developing skills emerge at delayed rate
- Lesions in infancy appear to cause relatively few immediate problems with ongoing development young children grow
into or fail to acquire- expected skills
- Dennis divides skill development into (1) emerging: early acquisition, not yet functional  (2) developing – capacity is
partially but not fully functional  (3) established – abilities are fully matured
- When brain injury occurs in context of an emerging skill, onset of skill may become delayed  rate of acquisition lags
due to detour strategy  leading to shortfall in final level of skill competence
- When brain injury occurs in established skills  less vulnerable  rare in children  control of skill may be deficient =
temporary loss of function  younger = fewer established skills = opposite to plasticity = greater impact

, - Validation Dennis’s theory is problematic  employs chronological age, no operationalization of core concepts
Chapter 2: Cerebral Development
-Development of CNS follows precise/genetically predetermined stages  complex & overlapping process
-CNS development parallels cognitive progressive stages  understanding sequence of events occurring in CNS timing may
enhance current knowledge & nature of recovery
-Interplay between predetermined factors and environmental influences  during initial stages of development = continuous
dialogue between biological and environmental influences despite hard-wired genetically determined processes
-Brain development: cerebral development is ongoing through gestation & childhood  fastest rate prenatally (rapid cell
division)
- Structural morphology matures by birth but growth continues until adulthood
- Post-natal increase in brain weight (differentiation, growth and maturation of existing neurons, elaboration of dendrites
and synapses, and ongoing myelination)  Qualitatively distinct stages of CNS development
- prenatal development: structural formation of CNS (largely genetic)  interruptions via genetic mechanisms,
intrauterine trauma or infection  morphology = abnormal even at macroscopic level
- postnatal development: elaboration of CNS: dendritic arborization, myelination, synaptogenesis  (largely genetic) 
more susceptible to neuronal activity and environment  brain damage less impact on gross brain morphology but
may interfere with ongoing interconnection and functional systems
- Early gestation: CNS = day 40  recognizable at 100 days  multiple developmental mechanisms – not a simple linear
progression  phenomena occur simultaneously with different timings and under different models
- Immature CNS has 2 main developmental processes:
- (1) simple additive development = ongoing accumulation & growth  myelination in stages  continuous increase in
formation & elaboration of dendritic connections
- (2) different style of development = periods of regression with initial overproduction followed by elimination of
redundant elements  number of neurons generated in excess than required for mature CNS  redundant ones die
off  similar process for synapses (increase rapidly in early childhood, exceed adult levels, then decrease to adult
levels)  regressive processes not detrimental but represent fine-tuning to ensure efficient & direct transmission
- (3) macro-level changes: accumulation of growth processes in growth spurts during pre/postnatal development with
anterior regions last to mature  24-25 weeks (completion of neuronal generation), year 1 (dendritic and synaptic
development + myelination), 7-9 yrs & 16-19 yrs  disruption during growth spurt may be detrimental to ongoing
development causing cessation of ongoing processes
- Critical/sensitive periods = aspects of behaviour function experience major progression  if unduly influenced, then
milestone may never occur (irreversible effects on maturation)
- Critical period = Window of opportunity for skills to be consolidated  establish interconnections
- Sequence of brain development  hierarchical progression of CNS  cerebellar/brain stem, then posterior areas, lastly
anterior regions  progresses in spurts
- Not all CNS development conforms to hierarchical model  e.g. synaptogenesis appears simultaneous in multiple areas
and layers, neurotransmitter receptors throughout brain mature at same time
- CNS development is complex with range of mechanisms occurring in sequence AND simultaneously  trauma can
result in irreversible change to final outcomes  impact of gross trauma is more clearcut while more subtle
interruptions affect schedules and can be difficult to predict
-Influences on brain development: brain development fairly genetically fixed but factors can interfere leading to abnormal
developmental consequences  common causes: biological agents = genetic factors and intrauterine trauma (infections,
toxins, injury)  lead to major structural malformations and cerebral reorganization (effect structure & function) 
environmental agents = influence maternal nutrition = alcohol, drug addiction, stress
- Postnatal development: biological risks of infection, external trauma, toxins, environmental deprivation
- TBI during preschool = more severe and persistent intellectual disability that injury in older kids
- Psychosocial factors: mother-child relation, stimulation, social support, resources  biological vulnerability
-Prenatal CNS Development (Structural): earliest stage: dorsal & ventral induction  fertilized cell = rapid cell division 
cluster of cells  embryonic disc  3 layers = organic systems  nervous system emerges via neurulation, outer
layer/ectoderm of embryonic disc folds in on itself and forms tube (2nd week of gestation)  neural plate becomes visible
(thickened area)  neural groove  flanked by two edges (neural folds)  folds deepen and fuse creating hollow cylinder
(neural tube) – week 4  disruptions in early stages = serious structural anomalies: myelomeningocele (incomplete closure of
spinal chord), anencephaly (incomplete closure of neural tube), Arnold-Chiari Malformation (structural abnormality with HYD)
- Neural tube develops along 3 different dimensions – length, circumference, & radius  length is NB for major
structural aspects (forebrain, midbrain, spinal cord)
- cell proliferation in neural tube = vesicles emerge in anterior portion  vesicles = recognizable mature CNS features 
telencephalon = cortex, diencephalon = thalamus/hypothalamus, mesencephalon = midbrain, metencephalon = pons &
cerebellum, myelencephalon = medulla oblongata  remaining areas of neural tube = spinal cord
- structures grow with more divisions  basic subdivisions  disruption = failure to form structural divisions 
holoprosencephaly = failure to form 2 cerebral hemispheres  craniosynostosis encephaly = incomplete fusion of skull
- Circumference dimension = differentiation between sensory and motor systems  dorsal = sensory cortex, ventral =
motor cortex

Dit zijn jouw voordelen als je samenvattingen koopt bij Stuvia:

Bewezen kwaliteit door reviews

Studenten hebben al meer dan 850.000 samenvattingen beoordeeld. Zo weet jij zeker dat je de beste keuze maakt!

In een paar klikken geregeld

Geen gedoe — betaal gewoon eenmalig met iDeal, creditcard of je Stuvia-tegoed en je bent klaar. Geen abonnement nodig.

Direct to-the-point

Studenten maken samenvattingen voor studenten. Dat betekent: actuele inhoud waar jij écht wat aan hebt. Geen overbodige details!

Veelgestelde vragen

Wat krijg ik als ik dit document koop?

Je krijgt een PDF, die direct beschikbaar is na je aankoop. Het gekochte document is altijd, overal en oneindig toegankelijk via je profiel.

Tevredenheidsgarantie: hoe werkt dat?

Onze tevredenheidsgarantie zorgt ervoor dat je altijd een studiedocument vindt dat goed bij je past. Je vult een formulier in en onze klantenservice regelt de rest.