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College (Knowledge Clips) aantekeningen Developmental Neuropsychology (500880-M-6) £9.44
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Lecture notes

College (Knowledge Clips) aantekeningen Developmental Neuropsychology (500880-M-6)

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  • Module
  • Developmental Neuropsychology (500880M6)
  • Institution
  • Tilburg University (UVT)

A summary of the knowledge clips (lectures) in the course Developmental Neuropsychology of the master's study 'Clinical Neuropsychology'

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Document information

  • July 19, 2024
  • 54
  • 2023/2024
  • Lecture notes
  • Marion van den heuvel
  • All classes

Subjects

  • knowledge clips
  • college
  • lecture
  • clinical neuropsychology
  • cognitive neuropsychology
  • developmental neuropsychology

Written for

  • Tilburg University (UVT)
  • Unknown
  • Developmental Neuropsychology (500880M6)
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DEVELOPMENTAL NEUROPSYCHOLOGY



Neuroimaging
CAT/CT scan – Computerized Axial Tomography
Structural neuroimaging. Involves taking a series of X-ray images of multiple locations
of the head, images are combined to construct an image of the brain. Low resolution but
can visualize major structural problems (e.g. a tumor).

MRI – Magnetic Resonance Imaging
Structural neuroimaging. Applying a combo of magnetic fields and radiofrequency
energy waves of the brain, hydrogen atoms respond to these by emitting energy. The
MRI machine receives this energy and can tell from which brain part this came from. A
computer uses this info to reconstruct a brain image. Better resolution than CAT scan.

PET scan – Positron Emission Tomography
Functioning neuroimaging. Patient is injected with a radioactive substance that emits
positrons. The positrons collide with tissue and emit gamma rays. The gamma rays are
detected by the PET scanner. The PET scan detects the movement of blood throughout
the brain. Blood flow to a brain area increases when the area is active. So, the PET scan
shows which brain areas are most active while the patient is lying in the scanner.

fMRI – Functional Magnetic Resonance Imaging
Functional neuroimaging. Focuses on the different responses of oxygenated and
unoxygenated blood make to magnetic field and radiofrequency energy. It uses blood-
oxygen-level-dependent (BOLD) contrast to identify changes in blood flow in the brain.
So, it identifies which brain areas are most active. It shows activity along with high resolution
structural image.



Week 1 – Pregnancy and Birth
Preterm Birth & Cerebral Palsy

1.1 Early Brain Development
Early brain development
1. In hierarchical order: brainstem & cerebellar → posterior → anterior
2. Additive and regressive:
 Additive → many processes increase over time (e.g. myelination)
 Regressive → other processes have inverse development with an initial
overproduction and then selective reduction (e.g. synaptogenesis followed by
synaptic pruning)
3. In growth spurts: most processes are not linear and happen in growth spurts that
often lead to overproduction (and later pruning). Are these growth spurts sensitive or
critical periods?

,DEVELOPMENTAL NEUROPSYCHOLOGY


Rapid brain growth: fetus
 Critical stages of brain development (brain growth and connectional specificity) occur
during pregnancy.
 Primitive forms of neuronal networks can already be found in the fetal brain
(structure)
 At birth all anatomical structures are present


Prenatal period
Structural formation with a series of processes – neurulation, proliferation (neurons intended
to form the cerebral cortex are generated from gestational weeks 6-18), migration,
dendritization, synaptogenesis, differentiation and apoptosis. There is a linear decrease in
cortical thickness between 8 and 20 years of age, and volumetric studies showed increases in
frontal gray matter in pre-adolescence followed by a decrease during adolescence.
→ Damage mostly impacts the structure of the brain (morphology)
! Book: myelination happens after birth, but new research found that myelination already
starts in the 3rd trimester




Postnatal period
 Growth spurt in dendrites (image). Number of neurons stays
the same, dendrites increase in length and amount
 Synaptogenesis (more dendrites = more connections)
 Myelination increases processing speed
→ Damage mostly impacts the function of the brain

Influences on brain development
 Prenatal factors: Maternal stress and age, maternal health (e.g., history of infection,
rubella, cytomegalovirus, AIDS, herpes), nutrition (diet, malnutrition), maternal drug
and alcohol addiction (smoking, alcohol, marijuana, cocaine, heroin), and
environmental toxins (lead, radiation, trauma)
 Postnatal factors: birth complications, nutrition, environmental toxins (lead,
radiation), cerebral infection, environment (trauma, like neglect and abuse)
Environment may be a critical modifiable risk factor for these children and families.

,DEVELOPMENTAL NEUROPSYCHOLOGY


Early disruptions in brain development
 Injury → direct or too few nutrients/oxygen
 Maternal (mental) health → severe depression/anxiety, infection, sickness
 Environmental → exposure to toxins (e.g. lead, radiation), smoking or drug use
 Genetic disorders (e.g. down syndrome)


Rapid growth: strength or vulnerability?
 Plasticity (strength) → immature brains are extremely plastic and are able to recover
better after brain injury than adults (clinical observation). Kennard Principle → “if
you’re going to have brain damage, have it early.” This is the description of relative
plasticity and recovery of function after early brain damage, following research that
showed greater improvements in children than adults.
o Plasticity → the young brain is less differentiated and more capable of
transferring functions from damaged tissue to healthy tissue (theory of
recovery of function)
o Equipotential → functional specialization: the view that all brian regions are
equally able to take responsibility for any function (contrast: innate
specialization → every region has a specific function).
 Vulnerability → as a result of dramatic developmental processes the brain may be
extremely sensitive to environmental influences early in life.
o Critical periods → time window during which external influences have a
significant effect. Brain damage within this window may be more detrimental.
Correspond to growth spurts.
o Functional plasticity may only be restricted to certain sensitive periods


 The recovery continuum model
→ combination of both theories. a continuum approach fits better, where several risk
and resilience factors (age, injury, region) interact to determine
long-term outcome:
 Injury → nature (diffuse/focal) and severity
(mild/severe)
 Cognitive skill → simple or complex
 Developmental phase of child → age at insult and age at
assessment
 Environment → distal and proximal factors, access to interventions and
social support.
 Pre-injury characteristics of child
Impact of these factors is not linear (e.g. larger lesions does not mean worse outcome
bc of hemispheric transfer; earlier lesion does not mean worse outcome bc of critical
periods).

 Non-verbal learning disability (NVLD)

, DEVELOPMENTAL NEUROPSYCHOLOGY


→ NVLD explains cognitive and behavioral implications of early cerebral
dysfunction from brain insult, attributed to white matter deficiencies. NVLD occurs
when white matter development is disrupted during critical periods.
 Dennis Developmental stage at insult and cognitive outcome
→ Focus on age/developmental stage at time of insult and progression in cognitive
skills with time since insult. Three levels of skill development: (1) emerging, (2)
developing, and (3) established. Three crucial age-related variables: (1) age at lesion,
(2) age at testing, (3) time since injury.
Early brain insults cause few problems early post-injury, but children may ‘grow into’
deficits. Dennis implies that the full impact of childhood brain injury is not clear until
full brain maturation in adulthood.

 The Cognitive Reserve Model
→ why kids with brain injuries have different
challenges.
 Brain Reserve Capacity (BRC) → how much
healthy tissue? Measured by quantifying
variables, e.g. insult severity, brain volume,
structural connectivity, and neurological
sequelae such as epilepsy. When BRC is
depleted below threshold, functional deficits
emerge, e.g. physical, cognitive and socio-
emotional symptoms.
 Cognitive Reserve Capacity (CRC) → includes internal factors like preinjury
and post-injury cognition and behavior (IQ), and external factors like SES and
family.

The more BRC and CRC (functional plasticity) the better the outcome. In
addition to the mediating role of reserve capacity, moderating factors for
functional outcome are proposed:
 Age and time variables: early brain insult diminishes reserve to a greater
extent than later insult, restricting the capacity to support recovery and
development.
(1) Age at lesion → determines the nature of cognitive dysfunction (e.g. early
lesion disrupts language development, later lesion disrupts specific high-level
language)
(2) Age at testing → healthy children vary in cognitive skills.
(3) Time since injury → cognitive skills differ at different stages of recovery
 Lesion location and functional network involvement – involvement of
different brain structures and networks determine functional plasticity and
outcome.
The influence of these moderating factors is not constant over time. The more time
elapsed since injury, the less the effect of brain insult characteristics and the greater
the effect of environmental variables on cognitive functioning.

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