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Summary Child Neuropsychology
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Case 1: brain development and brain damageWhich processes can be distinguished in prenatal brain development?
1. Gastrulation (2nd-3rd week): embryo transitions from a single cell layer (blastula)
into a three-layered structure (gastrula) consisting of:
o Ectoderm (outer layer) -> nervous system + skin
o Mesoderm (middle) -> muscles, bones, blood vessels, somites, etc.
o Endoderm (inner layer) -> internal organs
2. Neurulation (end of 4th week): thickened area of ectoderm, neural plate, forms
along the embryo's dorsal midline. A groove appears in the neural plate, folds in
on itself, and closes to form the neural tube, which becomes CNS.
o The neural plate has 3 layers -> form different components of the NS:
Neural progenitor cells -> nervous system
Part of the ectoderm flanking the neural plate -> epidermal skin cells and other
external structures
o Neuroepithelial cells (stem cells) located along the midline of the upper layer of the 3-
layer disc receive molecular signals from other cells/adjacent tissues -> induce them to
differentiate into neural progenitor cells.
o These cells line the inside wall of the neural tube and establish what will
become the zones that will give rise to neurons and neural support cells.
Neural differentiation of ectodermal cells into one of these cell types =
neural induction
o Since the neural tube gives rise to the CNS, mutations at this stage can lead to fatal
deformities or lifelong disabilities.
Emergence of early structure
The anterior part of the neural tube expands and forms 3 primary brain vesicles (forebrain, midbrain, hindbrain), which align
along the rostral-caudal axis of the embryo, establishing the primary organization of the CNS. A fluid-filled central chamber
forms, connecting the telencephalon to the spinal cord's central canal, which will become the ventricular system.
Intrinsic + extrinsic molecular signals drive lineage divergence of neural progenitor cells. Morphogens (vary in concentration
across the brain) direct cell migration of neural progenitor cells and influence gene expression, affecting cell fate + function.
Process of neuronal proliferation and migration
Most neural progenitor cells are produced in the ventricular zone (center of the brain),
inside the neural tube, and migrate radially to the developing neocortex.
First, the neurons don’t travel far and migrate by extending a basal process,
which attaches to the outer boundary between gray matter and CSF; at this
stage, this is the outer surface of the developing brain.
o The nucleus of the cell then moves from the ventricular zone to where
the basal process is on the outer surface, remaining attached to the
outer surface -> forms foundation in the embryonic cortex for
additional cells to migrate towards and attach themselves to.
o As migration distances increase, radial glial cells act as guides. These extend a basal process to the brain's
surface, while their nucleus remains in the ventricular zone, forming a scaffold that other progenitor cells use to
migrate outward. Radial glial cells are also progenitors themselves.
This migration creates the laminar/layered structure of the neocortex. Earlier migrating neurons form the deeper layers, while
later waves bypass previous neurons to form more superficial layers -> inside-out cortical development pattern. Molecular
signaling directs each new wave to its appropriate layer.
Neuronal differentiation and death
In addition to having a vertical, laminar organization, the cortex is organized into discrete functional areas distinguished by the
types of neurons, their connections, and their functions During neurogenesis, signaling determines where neurons go (e.g.
motor/visual/auditory areas), setting the stage for subsequent developmental changes that will eventually give rise to
,functionally distinct cortical regions. However, neuron specialization remains flexible and depends on developmental events and
sensory input.
Evolution involves overproduction of neurons, axons, and synapses, followed by cell death and synaptic pruning. About
half of prenatal neurons undergo apoptosis before birth, a regulated process influenced by various factors that either
trigger or prevent the cell death cascade.
What changes occur during postnatal brain development?
Human brain development continues after birth, even though neuron production and migration are mostly completed. Glial
progenitor proliferation, migration, differentiation, and maturation extend through childhood
Early cortical expansion and changes in gray and white matter
Total brain volume increases through early childhood and approaches adult levels by middle childhood. However, there continue
to be microstructural changes.
Brain volume stabilizes between ages 5-30, with gray matter volume decreasing and white matter volume increasing
during this time. However, some research shows a slight increase in brain volume through adolescence, followed by
stabilization or slight decline.
o Differences across studies arise from individual variability in development, sample composition, timing, and
other factors which can affect estimates of gray and white matter volumes.
Gray matter thinning
During childhood rapid synaptic proliferation is followed by gradual synapse elimination (=synaptic pruning), which fine-tunes
brain circuits for greater efficiency. Gray matter volume increases over the first few years of life, due to an increased number of
neurons and synapses, then decreases throughout childhood and adolescence, likely due to synaptic pruning and myelination
The timing of these process varies across brain regions -> could help explain the development of different cognitive skills
at different times and could be relevant for the timing of brain plasticity in different neural systems.
Instead of a gray matter volume increase from age 4, one study found a decrease with more pronounced changes in
higher-level cognition areas (prefrontal + parietal cortices) than in sensory regions (visual + auditory cortices).
White matter changes, especially myelination of long-range fiber tracts, also play a role in cortical thinning. Myelination
increases during childhood and adolescence, shifting the gray/white matter boundary, and contributing to cortical thinning in the
ventral temporal cortex. Myelination improves communication between distant brain regions.
White matter microstructural changes
Major white matter pathways in the brain include projection fibers (connecting cortical-subcortical regions), commissural fibers
(connecting homologous regions in the left and right hemispheres) and association fibers (connecting cortical regions within a
hemisphere). These are in place by the 3rd trimester, but microstructural changes continue into adolescence, with different tracts
maturing at different rates -> white matter development is heterogeneous
Fractional anisotropy (FA) = index derived from DTI describing the directionality of diffusion of water molecules through tissue ->
higher FA values indicate stronger white matter pathways
Increased FA during development is associated with improved anatomical support for communication between distant
brain regions -> there is an overall increase in FA throughout childhood, particularly in the corpus callosum and inferior
longitudinal fasciculus, (connects the occipital and temporal lobes), with more protracted changes for the inferior
longitudinal fasciculus than the corpus callosum.
o For the inferior longitudinal fasciculus and other association fiber tracts, a substantial proportion of
individuals continued to show increased FA throughout their twenties
Explanations for increased FA include myelination, which thickens axons and restricts water diffusion and denser axon
packing of larger diameters, leading to more efficient neural signaling.
o Increased FA is often linked to white matter integrity and neural communication efficiency.
White matter volume + tract coherence increase during childhood and adolescence contributing to brain network reconfiguration
Reorganization of functional brain architecture
Reorganization of functional brain architecture is explored through functional connectivity analyses, which measure the
strength of synchronization in brain activity between regions (BOLD activitiy)
, There are age-related differences in resting-state functional connectivity, with sensory and motor networks (visual,
auditory, and somatomotor) well-defined from infancy, while higher-order cognitive networks develop more gradually
throughout childhood and adolescence.
As brain networks develop, they become more specialized, with increased within-network connectivity improving
efficiency in neural processing. At the same time, between-network connections may either weaken or strengthen,
reflecting a balance between network segregation (specialization) and integration (coordination).
While the overall brain structure is complete at birth, brain growth and subtle changes continue through childhood. Overall, both
pre- and postnatal brain development is characterized by growth followed by regression (apoptosis and synaptic pruning).
How does development relate to learning, and which 3 main types of brain plasticity can be distinguished?
Development = the changes that an individual undergoes over time, often involving learning, which is the acquisition of
knowledge or a skill through instruction and/or practice.
The relationship between development and learning varies, with some seeing learning as part of development, while
others consider them distinct phenomena that can be distinguished by three dimensions:
o Magnitude of plasticity: development as large-scale, learning as smaller changes and different construction
o The amount of input/effort required to change systems: more required for learning once systems are in place.
o Timescale of change: development takes years, learning occurs over hours or days
In this way of thinking, development and learning are on a continuum according to dimensions like magnitude of
change, effort involved, and the timescale of change. A related, but more neurally grounded, way of thinking about this
development-learning continuum is in terms of the degree to which they involve different types of brain plasticity
Three types of brain plasticity/brain development:
1. Experience-independent = a process of change that unfolds similarly regardless of the individual’s environment or
experiences -> early fetal brain development follows a genetically controlled sequence of molecular and cellular events.
o Is only seen in the early fetal development, as gestation progresses, and the sensory organs mature
2. Experience-expectant = development triggered by specific stimuli within critical periods, such as sights and sounds that
a developing organism is likely to encounter. It does require a critical period -> all-or-nothing change that depends on
exposure to a specific stimulus during a narrow window in development.
o This form of plasticity is still under tight genetic control and follows a precise temporal sequence across
individuals of a species, but it requires a little push to initiate it.
3. Experience-dependent = brain changes shaped by an individual's unique environment, like their home or school.
o This form is highly idiosyncratic: it is part of what makes you you.
o Involves prolonged/repeated exposure and does not require input during a critical period.
o It is more prominent in infancy and early childhood than in adulthood -> some refer
to the period of maximal potential for experience-dependent brain plasticity as a
sensitive period rather than a critical period.
Development involves mostly experience-expectant plasticity, occurring mainly in
infancy, while learning relies on experience-dependent plasticity, which continues
throughout life.
What is the underlying mechanisms of brain plasticity? (critical/sensitive period, long-term potentiation, cellular
changes, expansion-renormalization model)
Neuron doctrine = idea that the nervous system is made up of independent cells (neurons) that serve as the fundamental unit of
communication and that are densely interconnected.
Dendritic spines and LTP
Specific experiences elicit changes in dendritic spines; changes are observed in parts of the brain that encode the experience. The
stabilization of new spines after learning depends on the presence of a specific protein -> essential for long-term potentiation
(LTP) = the strengthening of synapses through repeated stimulation, where a presynaptic neuron (cell A) increases the likelihood
of firing a postsynaptic neuron (cell B)
A synapse gets weaker if the two neurons' activity patterns are decoupled = long-term depression (LTD).
Hebbian plasticity describes how neurons that fire together strengthen their connections, while neurons that fire out of
sync weaken them, a process known as long-term depression (LTD).
, Exposure to enriched environments enhances brain development -> animal studies where rats raised in stimulating environments
had better spatial learning and developed thicker visual cortices with fewer but larger neurons, more dendrites and glial cells,
and longer dendrites.
Extent of changes depends on the level + age of environmental exposure = experience-dependent brain development
Critical Period for Plasticity
Experience-expectant plasticity = certain brain systems, especially sensory systems, require specific environmental inputs during
a critical period for proper development -> exposure to visual and auditory stimuli during this window is essential for normal
development of the visual and auditory cortices.
Visual system: primary visual cortex (V1) contains ocular dominance columns = groups of neurons that respond to input
from either the left or right eye. These columns are initially formed by molecular cues that guide axons to different sites
in the cortex and spontaneous brain activity, which is experience-independent (does not require visual input). However,
their maintenance depends on visual input from both eyes during infancy (experience-expectant) and it requires both
eyes to receive visual stimulation in infancy.
o Monocular Deprivation Experiment: if one eye is deprived of input during the critical period neurons in V1 stop
responding to that eye, and its corresponding ocular dominance columns shrink.
Expansion of columns from the non-deprived eye takes over the territory in V1 due to the lack of
competition from the deprived eye -> results in a permanent imbalance if deprivation occurs during
the critical period (before 3 months of age).
Mechanism: thalamic neurons transmit visual signals to V1. Neurons from both eyes normally compete for input to V1.
o In monocular deprivation, thalamic neurons associated with the deprived eye fire less, weakening their
synapses with cortical neurons in V1 (LDP), while neurons from the
spared eye strengthen their connections (LTP) -> result: a permanent
expansion of columns related to the spared eye if deprivation
happens during the critical period.
During the critical period for plasticity, healthy competition between inputs from both
eyes is crucial for maintaining the balance of ocular dominance columns. Monocular
deprivation during this time leads to irreversible changes, favoring the spared eye's
dominance in V1.
Types of structural brain changes
There are ten classes of brain changes at the cellular level:
Some of them involve neurons:
o Axon sprouting = a presynaptic neuron forms connections with more
neurons
o Increased dendritic branching/aborization = postsynaptic neurons grow
more dendrites, leading to synaptogenesis (new synapse formation).
If extensive enough, either of these types of changes could be
detected as changes in cortical gray matter in a structural MRI scan.
o Neurogenesis = the formation of new neurons (mostly occurs during infancy)
Changes at the neuronal level cannot be directly observed with MRI,
o Myelination of previously unmyelinated axons, as well as myelin remodeling
-> changes in the amount of myelin wrapped around an axon
If dramatic enough, these changes can be detected as changes in
white matter volume as measured via structural MRI, or as changes
in white matter microstructure, as measured with DWI
Non-neural forms of experience-dependent plasticity:
o Increase in the number and/or size of glial cells -> astrocytes regulate levels
of neural activity as well as synapse formation and elimination
Such changes could perhaps account for, or contribute to, gray
matter changes observed with structural MRI
Astrocytes also promote angiogenesis = formation of new blood
vessels when neural tissue becomes more active -> increases in
blood flow could help account for experience-dependent changes in
activation observed via fMRI.
Experience-dependent plasticity
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