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Developmental Neuropsychology | Full Lecture Notes | Utrecht University | A+ Study Guide

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Optimized Description for Stuvia University: Utrecht University Course: Developmental Neuropsychology ()

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3. College aantekeningen - Developmental neuropsychology | full lecture notes | utrecht university | a+ study gu...
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DN_Lectures:
Lecture 1: Neurophysiology & Neuroanatomy
-Brain Organisation = Processing + Storage  relevant/NB info is processed simultaneously & stored in different parts of brain
- Regulation: brain controls thoughts/behaviours/emotions (in collaboration w somatic nervous system) + internal body
processes (in collaboration w automatic nervous system)
o E.g. PFC = inhibits impulses, send/receive info via gut-brain axis
o Hypothalamus = regulates stress in collaboration with pituitary & adrenal gland (HPA Axis)
- Integration: brain connects incoming info (sensory input) with already stored info from memory
- Prediction: brain uses prior knowledge to determine future outcomes  does not process all info, only what is not
expected (aka prediction error)  more efficient processing
- Lateralization: two hemispheres have partially different functions  LH = understanding + producing language,
semantic memory  RH: processing social + emotional stimuli, visuo-spatial orientation  LH/RH control opposite
sides of body
- Cooperation & Competition: some brain parts compete and some cooperate  competition = top-down (high>low) vs
bottom-up (low>high)  high = frontal cortex / low = primary projection areas, brainstem, limbic system
- Small vs Large Brain Networks: brain is organized both structurally & functionally into complex networks
-The Nervous System = the Central Nervous System (CNS – brain + spinal cord) + Peripheral Nervous System (PNS – Somatic
Nervous System (SNS) & Automatic Nervous System (ANS)
Peripheral Nervous system:
- 1)Somatic Nervous System: Sensory & Motor neurons  Sensory (afferent)
neurons carry messages from outside to CNS, specialized in transmitting
messages from eyes, ears, & sensory receptors to spinal cord & brain)  Motor
(efferent) neurons carry messages from CNS to skeletal muscles – from brain &
spinal cord to muscles that control voluntary movements
- 2)Autonomic Nervous System: regulates internal environment of body (e.g. respiration/circulation)  senses internal
functions, controls glands and involuntary muscles (heart, blood vessels, stomach)  motivation, emotional behaviour
and stress response  Sympathetic Nervous System + Parasympathetic Nervous System
o 2.1)Sympathetic Nervous System (SNS): physical activation fight-flight response
o 2.2)Parasympathetic Nervous System (PNS): slows body processes and maintains relaxation
Central Nervous System: Spinal Cord + Brain (cranial nerves, brainstem, forebrain)
- 1)Spinal Cord: motor & sensory nerves, organizes reflexes  central pattern
generators (rhythmic movements: walk)
- 1)Brain: divided into 3 parts (forebrain, midbrain, hindbrain)
o 1.1) Hindbrain: vital life  medulla (heart rate + respiration)/ pons
(sleep + arousal)
o Cerebellum: complex/rapid movements, precise timing (motor),
memory & learning
o 1.2) Midbrain: vision, hearing, motor control, sleep, wakefulness,
arousal, temperature regulation
o Tectum = input from eyes/ears  Superior Colliculus (input from optic
nerve) & Inferior Colliculus (input auditory nerve)  integrate info and directs
command to muscles
o Tegmentum= red nucleus (motor coordination), substantia nigra (dopamine, motor-
planning, learning, addiction), ventral tegmental area (complex synaptic network for
homeostasis & reflexes)  largest dopamine-producing area involved in neural reward
system
o 1.3)Forebrain:
o 1.3.1)Hypothalamus: underneath thalamus = motivation & emotion  sexual arousal,
temperature, sleep, eating, pleasure-displeasure, aggression, hormone regulation, contact
with pituitary gland)
o 1.3.2)Thalamus: receives info from sensory organs & distributes to other parts of brain
o Limbic System: coordinates behaviours for motivation & emotion  hippocampus
(storing/recalling/retrieving memories), cingulate cortex (conflict in decision-making, error
detection), amygdala (response to salient stimuli, emotion/fear)
o Basal Ganglia: striatum, caudate nucleus, putamen, globus pallidus  basal nuclei =
learning/controlling voluntary movements (not automatic)
- Cerebral Cortex: 2 hemispheres joined by corpus callosum  4 lobes:
o Lobe1: Frontal = planned motor, planning, thinking, WM, goal-directed behaviour
o Lobe2: Parietal = tactile, somatic sensory info, orienting, associative functions
o Lobe3: Temporal = auditory cortex, perception of social stimuli, language
o Lobe4: Occipital = primary visual cortex

, o Organisation of lobes: Lateral (outside)/medial (within/inside)  Anterior (front)/Posterior (back) Dorsal
(top-back)/Ventral (down/front)
- Brain structure: cerebral cortex = higher cognitive functions  separate brain regions
& their cell structure connect via white matter tracts to allow info exchange
different brain parts have different types of neurons
o gyri/sulci = grooves – sulci enlarge surface of cerebral cortex
o Neurons = 6 layer cell structure
o gray matter = cell bodies + dendrites of neurons  reflect each part of body
(somatotopic map)
o white matter = fatty myelinated axons of neurons
o Role of different brain areas + how they cooperate  global level (brain
networks), local level (brain area function), micro-level (neurophysiology –
neurons that fire)
o Projection Areas = receive info from senses or sends info directly to spinal
cord & muscles
o Association Areas = rest of the brain which does not have signals directly to
muscles/senses
- Brain Tissue: cells in the nervous system: 86 billion neurons + 1000 billion glial cells
o Glial cells: supporting cells, hold neurons in place, manufacture nutrients,
absorb toxins, guide neurons to position
o Neuron cells: cell body (soma) + neural branches (dendrites/axons) + axon terminal (synaptic terminal) +
myelin (white fatty tissue)
o Neural communication: dendrites receive signal from other neurons  elicits electrical impulse in the axon 
travels from dendrite through cell body to axon and exits via axon terminal
o # dendrites & spines determines the # synaptic connections
o Spines = surface of dendrites = small bulbs allowing more connections between other neurons
o Axon terminal: where chemical substance/neurotransmitter is released in the synaptic cleft/space
o Neural communication = electrical/chemical process: neurons generate electricity that create nerve impulses
& release chemicals to allow communication with muscles & glands
o Nerve impulses = action potentials  chemicals = neurotransmitters
o Ions = electrically charged atoms  outside axon = Sodium (NA+) & Chloride (CL-) ions inside axon =
proteins/anions (A-) + Potassium (K+)  Uneven distribution of positive & negative ions inside vs outside cell =
state of polarization (difference = resting-potential)  if stimulated, voltage shifts, leading to depolarization
causing an action potential (neuron fires – from negative to positive change)
o Action potential: channel opens and closes based on depolarization (e.g. chamber of opening/closing doors)
o Resting state = -70mV  stimulation opens NA+ channels >> depolarization >> exceeds threshold >> action
potential >> NA+ will close & K+ will open (refractory period) >> neuron not able to discharge another impulse
o All-or-none law: action potentials only occur when it exceeds a threshold
o Graded potentials: many graded potentials together can elicit action potentials (depolarization which does not
exceed action potential threshold of -50mV (e.g. local anesthetics attach to sodium channels & block flow of
sodium ions into the neuron >> stop pain impulses).
o Neural Activity: 3 Basic Steps: (1) Resting Potential – distribution of positively & negatively charged ions
around axon  (2) Action Potential – stimulation = ions flow into cell membrane channels = electrical charge
 (3) Resting Potential – neuron restores ionic balance.
o Synaptic transmission: neurotransmitters carry messages across synaptic cleft  1. Synthesis >> 2. Storage (in
vesicles) >> 3. Release >> 4. Binding (neurotransmitter to receptor) >> 5. Deactivation (restored into axon)
o Excitatory neurotransmitters = cause post-synaptic neuron sodium channels to open >> depolarize
(graded/action potential)
o Inhibitory neurotransmitters = cause potassium to flow out of neuron or chloride into neuron >> polarization
(increase neurons negative potential – neuron will not fire – maintain state)
o Neurotransmitter types: (a) Acetylcholine (excitatory: muscle movement, memory) (b) Noradrenaline
(excitatory & inhibitory: learning, memory, wakefulness, eating) (c) Serotonin (excitatory & inhibitory: mood,
sleep, eating arousal) (d) Dopamine (excitatory: voluntary movement, emotion, learning, memory,
pleasure/pain) (e) GABA (inhibitory: motor) (f) Endorphin (inhibitory: pain) (g) Glutamate (excitatory)
o Dopamine projection pathways: ventral tegmental midbrain and axons can reach PFC & midbrain
o Serotonin projection pathway: transmitter substances widely distributed across brain, cerebellum, & spinal
cord
Lecture 2: Intro Brain & Plasticity
-Developmental neuropsychology: brain-behaviour relations of immature/developing brain in clinical practice ( 1980s)
-Developmental Cognitive Neuroscience: focus on normal development of cognitive functioning  not same as developmental
neuropsychology (focus on abnormal)

, -Assumptions adult neuropsychology: adult brain = static/organised/less plastic  1:1 relation between structure & function
 symptoms relate to neurological defect (functional localization)
-Assumptions developmental neuropsychology: immature brain = dynamic/spurts in brain related to changes in behavioural,
social and cognitive development symptoms and underlying neurological defect are not clearly related  dependent on
timing of brain damage + social environment  multiple factors: biological, cognitive, social-emotional, developmental &
environmental  later outcome = difficult to predict  address totality
-Anatomical Development:
(1) Zygote = fertilization 2 cells (undifferentiated)
(2) Morula = rapid cell division, cluster cells (undifferentiated)
(3) Blastocyst = differentiation inner cell mass = embryo / outer layer = placenta
14 days after fertilization inner cell mass of blastocyst develops 3 layers
- (3.1) Ectoderm = outer layer (Skin/CNS)
- (2) Mesoderm = middle (skeleton)
- (3) Endoderm = inner (intestines)
Neurulation/Neural Induction forms spinal cord  neural plate created from ectoderm  week 3-
4 = neural tube  Closure Defects: causes = genetic/infection
- anencephaly = fatal closure defect of neural tube  has subcortical structure but no
cortical structure)
- spina bifida = incomplete closing of backbone/spinal cord often combined with HYD
-Brain vesicles: telencephalon (cortex)  diencephalon (thalamus/hypothalamus) 
mesencephalon (midbrain)  metencephalon (cerebellum/pons)  Myelencephalon (medulla
oblongata)
-Development of Nervous System: different structures at different times (but overlapping)  largely develops before birth
(1) spinal chord + brainstem  (2) Amygdala, cerebellum & hippocampus  (3) Thalamus & basal ganglia  (4) Cerebral
cortex (posterior to anterior)
-Histological Development = cellular stages of almost all neurons (also overlapping stages)  all same 5 stages occur for all
cortical areas (some faster than others)  timing varies by brain region:
(1) Cell proliferation = create new neurons  (2) Cell Migration = move to place of function  (3) Cell differentiation & growth
= forming/developing  (4) selective cell death & synaptic pruning  (5) Myelinisation = efficiency
- (1) Proliferation (6-18 weeks): ventricles are hollow filled with CSF  new neurons made inside proliferation zone (e.g.
ventricular zone & subventricular zone)  progenitor cells (precursor cells): AKA Neuroblast and glioblast
o Problems (2-5 months) = causes: genetic/trauma
o neural defects = microencephaly (cell division stops) OR megalencephaly (overproduction cells)  too small/
too large brain
o functional defects = motor/intellectual impairment, learning problems, epilepsy
- (2) Migration move to layer in cortex where cell will function  passive migration = thalamus/brainstem  active
migration = cortex – bypass older neurons
o Problems = causes: genetic/toxicity/infection/intrauterine damage
o neural defects = lissencephaly (smooth cortex, no sulci or gyri)
o Disorders of cell migration (1) Schizencephaly = abnormal cleft in cortex, cell layers not clearly defined  (2)
Polymicrogyria = multiple small gyri, neurons in abnormal locations  (3) Agenesis of Corpus Callosum =
absence  (4) Dysplasia/heterotopia = abnormal cell layer structure/clump in wrong place
o Functional effects: epilepsy, motor/IQ/learning deficits/behavioural problems (severity varies w syndromes)
- (3) Differentiation: cells are at location and then form their function via differentiation  different neurons have
different shapes & varieties (grow dendrites & axons)  form synaptic connections (synaptogenesis)
- (4) Cell Death & Synapse Elimination = brain development  overproduction + death of neurons & synapses
o Apoptosis = programmed cell death (brain & body)
o Pruning = synapse elimination (influenced by genes, experiences, hormones)
o Role of Experience: experience-expectant synapses (sensitive period) = visual system neurons need exposure
to visual input for synapses to survive and become functional (at certain time point)  experience-dependent
plasticity (enriched environment) = not particular period but throughout development - need input from
environment (larger cortex & more connections)
o Neurons that fire together wire together = simultaneous activity of neurons strengthens connections
o Disorders in Synapse formation & Pruning: causes = genetic, toxic, stimulus/experience (?), problems during
migration/differentiation  effect = none (synapses are flexible) OR abnormal development
Disorders of abnormal apoptosis: neurodegenerative disorders (ALS/ Alzheimer’s) – excessive apoptosis & ASD
(hypothesized) – slower in early childhood, excessive in older childhood & adolescence.
- (5) Myelinization = coating of axon fibers increases processing speed & efficient transmitting of info through brain 
different rates in different parts of brain (quicker/earlier for motor/sensory but later/slower for cerebellar and
association areas)
o Disorders of myelinization: causes = genetic, toxic, trauma

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