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Developmental Neuropsychology Full Exam Chapter Notes () - Utrecht University

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201800818 (201800818)

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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...

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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

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