This document contains a summary of all the lectures given during the course Developmental Neuropsychology at the Utrecht University in the year . Lecture 4 is not included, as this was a lecture about an assignment. Lecture 8 is also not included, as this lecture was cancelled.
Lecture 1: Introdu...
- Developmental neuropsychology = study of brain-beahaviour relationships with the context of an
immature but rapidly developing brain and implementation of knowledge gained into clinical practice.
- Other terms: child neuropsychology, paediatric neuropsychology.
- Focuses on normal (development of) cognitive functioning, but uses info from deviant functioning and
development as nature’s experiments, which can shed light on neural basis of normal cognition.
Assumptions:
- Adult neuropsychology = brain is static, tightly organized, less plastic. One-to-one relationship between
structure and function. Symptoms (= function impairment) can be related to underlying neurological defect
(= localization).
- Developmental neuropsychology = brain is dynamic. Changes in brain development are closely related to
changes in behavioural, social and cognitive development. Symptoms and the underlying neurological
defect are not clearly related.
Example: same brain damage can lead to different symptoms in childhood. Reverse also true.
Brain development = dynamic process. Many factors are involved: biologic, cognitive, social-emotional,
developmental and environmental. Later outcome difficult to predict and need to address the totality of
the child.
Development of CNS.
Anatomical development.
1. Zygote.
2. Morula = clump of 16 – 36 cells, undifferentiated. After rapid division of cells.
3. Blastocyst. Some differentiation between cells: outer ring of cells and inside the inner cell mass. Outer ring
will become placenta and inner will become embryo.
4. 14 days after division: inner cell mass develops into structure with three layers:
Endoderm = becomes intestines.
Mesoderm = becomes vescular system and skeleton.
Ectoderm = becomes skin and central nervous system (CNS).
5. Top of ectoderm folds neural groove/ neural plate.
Top closes around this neural groove neural tube (3rd/ 4th week) CNS.
Closure defects.
- Anencephaly = closure defect on the head end of the neural tube. This is fatal.
- Spina bifada = incomplete closing of the backbone around the spinal cord. Often in combination with
hydrocephalus.
- Development of different structures at different times, but overlapping:
- Spinal cord & brainstem amygdala, cerebellum, hippocampus thalamus, basal ganglia cerebral
cortex (posterior to anterior).
,Histological development.
Various stages: cell proliferation, cell migration, cell differentiation and growth, selective cell death and
synaptic pruning, myelinisation.
Proliferation.
- Week 6 – 18.
- About 250.000 new cells a minute.
- Hollow in middle where ventricles come from ventricular zone where neurons are made and cell
division occurs.
- Proliferation zones:
1. Ventricular zone (all cell types).
2. Subventricular zone (especially in front of the cortex).
- Two different types of cells are made:
1. Neuroblast neurons.
2. Glioblast glial cell = more supportive role.
Problems during cellular development.
- 2 – 5 months.
- Causes: genetic, trauma (infection, fetal alcohol syndrome, radiation, Zika virus).
- Neural effects: microcephaly (cell division stops prematurely) and megalencephaly (overproduction of
cells).
- Functional effects: motor and/ or intellectual impairments, learning problems, epilepsy.
Migration.
1. Passive migration (thalamus, brain stem) = new cells push older cells to outer layers. Older cells can find at
surface of structure.
2. Active migration (cortex) = glial cells that guide these neurons to location where they ultimately start
functioning. Follow glial cell to place where they have to be.
Subcortical structures: oldest neurons end up in deepest layers of cortex and new neurons more in superficial
layers.
Disorders in cell migration.
- Causes: genetic, toxic substances, viral infection, intrauterine damage.
- Neural effects:
Lissencephaly = smooth cortex, no sulci or gyri. Surface of cortex is smaller.
Schizencephaly = abnormal clefts in cortex, cell layers not clearly defined
Polymicrogyria = multiple small gyri, neurons in abnormal locations.
Agnesis of the corpus callosum.
Dysplasia/ heterotopia = abnormal cell layer structure/ cells in the wrong place.
- Functional effects: epilepsy, motor and/ or intellectual impairments, learning problems, behavioural
problems, severity varies within and between syndromes.
Differentiation.
= growth of dendrites and axons, formation of synaptic connections (synaptogenesis).
Very different types of neurons.
Cell death and synapse elimination.
- Brain development is characterised by overproduction (rise) and death (fall) of neurons and synapsis.
- Apoptosis = programmed cell death.
- Pruning = synapse elimination depending on experience, hormones and genes.
- Experience. Experience-expectant synapses (sensitive periods) and experience-dependent synapses
(enriched environment).
,- Use-it-or-lose-it principle = if you don’t use it, you loose it.
- Neurons that fire together, wire together = simultaneous activity of neurons strengthens connection.
- During adulthood, less connections, at age 6 more connections.
Problems during cellular development.
- Disorders in synapse formation and pruning.
Causes: genetic, toxic substances, problems during cell migration and cell differentiation, stimulus,
experiences.
Effects: none (synapses are flexible), abnormal brain development.
- Disorders related to abnormal apoptosis.
Down syndrome (excessive apoptosis).
Autism (depressed or slower rates of apoptosis early on, excessive apoptosis in childhood and
adolescence).
Myelinisation.
- Fibres that allow to connect to other neurons. Speed that up by putting myelin sheet around these axons
signals jump from one node to other node speeds transmission up.
- Final part of development.
- Occurs at different ages. Fibres connecting different brain areas, up to adulthood.
- DTI: fetal brain.
In adolescence, you see a lot of development of myelinisation of fibres.
Disorders in myelinisation process.
- Causes: genetic, toxic substances, trauma.
- Effects: neurological, cognitive and behavioural disorders.
- Especially vulnerable during first 8 months after birth (but depends on part of brain).
Histological development.
- Goes through same stages for all cortical areas.
- However, time of each stage varies by area of the brain.
- Earlier for sensory and motor areas. Later for association areas and PFC.
Functional development.
Growth spurts.
- Development is not a linear process.
- Several growth spurts can be distinguished: 24-25 weeks of gestation, first year of life, 7-9 years, 16-19
years.
Sensitive or critical periods:
- When brain circuits are maximally sensitive to acquiring certain kinds of info.
- Necessary for making essential interconnections.
- Both positive (learning) and negative (abuse).
- Clear for sensory and motor systems.
- Less clear for higher order functions (language?).
Effects of early brain damage on development.
- The effects of brain damage for sensory-motor and cognitive functioning differ between children and
adults.
- Two contradictory ideas: effects are less severe (plasticity) or effects are more severe (early vulnerability).
, Plasticity.
Kennard principle:
- Impairments are smaller when lesions occur in infancy than when they take place in adulthood.
- Based on lesions of motor cortex of apes.
- Motor impairments smallest when created in the first 6 months.
- While this study does have methodical limitations, motor recovery seems to be greater after early brain
injury.
Possible mechanisms:
- Regrowth of motor fibres after damage to these fibres (regeneration).
- Formation of new fibres after cortical lesions.
- Retention of axons that disappear in normal development.
- Reduced degeneration of non-damaged areas.
Reorganization/ recovery also occurs in humans.
Mirror movements = children are not able to inhibit movement with two hands, when they are asked to do it
with one hand. Disappears during development. In some people, continues to be there enhanced motor
skills.
signal of neural reorganisation of motor axons.
Restitution mechanisms:
- Diaschisis = brain areas with connections to damaged part show temporary disturbance of normal function
(due to intracranial pressure, NT, disrupted blood flow).
- Collateral sprouting = new growth of intact neurons near damaged tissue that make connections with
target neurons to which the damaged neurons originally projected.
- Denervation supersensitivity = increased sensitivity for NT of target neurons that have lost part of their
input through brain lesion.
- Regeneration of damaged neurons = occurs, but how functional is it? Especially in peripheral nervous
system.
Substitution mechanisms:
- Anatomical reorganisation.
Other brain areas take over function: consistent with equipotentiality principle. More ‘free’ brain tissue in
children, so greater recovery, but also sometimes at expense of other functions, crowding.
Difference between intra- and interhemispheric organization, but factors influencing this are unclear.
- Behavioural compensation.
Functional deficits are compensated by use of other intact functions or external devices.
For example: diary use in children with memory problems or verbalisation of complex images when
visuospatial functions are disturbed.
Evidence of reduced cognitive impairment after early brain injury?
Yes, language, spatial perception, intelligence.
Language.
- Left hemi brain damage in children rarely results in aphasic syndromes observed in adults.
- Equipotentiality. At birth, both sides of brain suited for language function, but left side becomes more
important later. Evidence from lesion studies.
- Innate specialisation. Language is innate function, which is always represented in special cortical areas.
Evidence from developmental studies.
- Lesion studies:
Hemispherectomy = surgical removal of one half of brain. Operation performed to treat severe epilepsy
that cannot be controlled with medication. Procedure performed only on patients where original brain
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