lecture 1 & 2 Flashcards
- (87 cards)
1
Q
Anencephaly
A
(closure defect on the head end of the neural tube). Fatal
2
Q
Spinabifida
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in complete closing of the backbone around the spinal cord). Often in combination with hydrocephalus
3
Q
Telencephalon
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cortex
4
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diencephalon
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thalamus and hypothalamus
5
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mesencephalon
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midbrain
6
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metencephalon
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cerebellum and pons
7
Q
myelencephalon
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medulla oblongota
8
Q
Proliferation zones:
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- Ventricular zone (all cell types)
- Subventricular zone (especially front of the cortex)
9
Q
Progenitor cells
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– Neuroblast -> Neuron
– Glioblast -> Glial cell
10
Q
- Neural effects cell proliferation:
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– Microcephaly (cell division stops prematurely)
– Megalencephaly (overproduction of cells)
11
Q
Passive migration
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thalamus, brain stem
12
Q
Active migration
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cortex
13
Q
- Disorders in cell migration causes
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genetic,
toxic substances, viral infection, Intrauterine damage (harm injury in womb)
14
Q
Disorders in cell migration due to neural effects neural effect: lissencephaly
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smooth cortex, no sulci or gyri
15
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Disorder in cell migration neural effect: Schizencephaly
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abnormal clefts in cortex, cell layers not clearly defined
16
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Disorder in cell migration neural effect:
Polymicrogyria
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multiple small gyri, neurons in abnormal locations
17
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Disorder in cell migration neural effect: Agenesis (absence)…
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of the corpus callosum
18
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Disorder in cell migration neural effect: Dysplasia (heterotopia)
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abnormal cell layer structure/cells in the wrong place
19
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Disorders in cell migration/Functional effects:
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- Epilepsy
- Motor and/or intellectual impairments, learning problems
- Behavioural problems
- Severity varies within and between syndromes.
20
Q
Differentiation
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– Growth of dendrites and axons
– Formation of synaptic connections (synaptogenesis)
21
Q
Cell death and synapse elimination/overproduction (rise)
and death (fall) of neurons and synapses
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- Apoptosis or programmed cell death
- Pruning = synapse elimination depending on experience, hormones, and genes
- Experience:
– Experience-expectant synapses (sensitive periods)
– Experience-dependent plasticity (enriched environment) - ‘Use-it-or-lose-it’ principle
- ‘Neurons that fire together will wire together’
– Simultaneous activity of neurons strengthens connection
22
Q
Disorders in synapse formation and pruning;
A
Causes:
* genetic,
* toxic substances,
* problems during cell migration and cell differentiation,
* stimulus, experiences (?)
– Effects:
* None (synapses are flexible),
* abnormal brain development
23
Q
Disorders related to abnormal apoptosis;
A
– Neurodegenerativedisorders(ALS,Alzheimer)
– Autism(depressedorslowerratesofapoptosisearlyon,excessive apoptosis in childhood and adolescence, Wei, 2014)
24
Q
Diffusion Tensor Imaging (DTI)
A
type of MRI (Magnetic Resonance Imaging) technique that measures the diffusion of water molecules in the brain, primarily in white matter. It is particularly useful for studying fiber tracts
25
Disorders in myelinisation process
Causes:
* e.g. genetic, toxic substances, trauma
– Effects:
* neurological, cognitive (information processing) and behavioural disorders (autism?)
* Later in life: Multiple sclerosis
Especially vulnerable during first 8 months after birth (but depends on part of brain)
26
Histological development = refers to the process by which the cells in the body, particularly in the brain, develop and differentiate
- goes through the same stages for all cortical areas.
- However, the time of each stage varies by area of the brain.
- Earlier for sensory and motor areas. Later for association areas and prefrontal cortex.
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growth spurts
* Development is not a linear process
* Several growth spurts can be distinguished (using EEG, brain volume, metabolism)
– 24-25 weeks of gestation (completion of neuronal generation)
– First year of life (dendritic and synaptic development, myelinisation) – 7-9 years
– 16-19 years
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sensitive or critical periods:
* Whenbraincircuitsaremaximallysensitivetoacquiringcertainkinds of information
* Necessaryformakingessentialinterconnections
* Bothpositive(learning)andnegative(abuse)
* Clearforsensoryandmotorsystems.
* Lessclearforhigherorderfunctions
– Language ?
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Summary
* The maturation process is no simple, linear process.
* Rather, there is more a gradual fine-tuning of the nervous system, characterised initially by neural growth, followed by specification and, finally, connections within and between different functional systems until optimal efficiency has been achieved.
* This process is very complex and very specifically timed. Each disruption can lead to deviation from the normal development line and final result.
30
The effects of braindamage on sensory-motor and cognitive functioning...
differ between children and adults.
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The effects are less severe:
plasticity
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The effects are more severe:
early vulnerability
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Kennard principle:
‘Impairments are smaller when lesions occur in infancy than when they take place in adulthood’.
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Mirror movements
Sign of neural reorganisation of motor axons
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recovery process plasticity: Restitution mechanisms
- Diaschisis (von Monakow): Brain areas with connections to the damaged part show temporary disturbance of normal function (due to intracranial pressure, neurotransmitter, disrupted blood flow).
* Regrowth of motor fibres after damage to these fibres (regeneration),
especially in peripheral nervous system.
* Formation of new fibres after cortical lesions.
* Retention of axons that disappear in normal development.
* Reduced degeneration of non-damaged areas
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Restitution mechanisms
*Collateral sprouting:
New growth of intact neurons near the damaged tissue that make connections with target neurons to which the damaged neurons originally projected.
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Restitution mechanisms * Denervation supersensitivity:
Increased sensitivity for neurotransmitters of target neurons that have lost part of their input through the brain lesion.
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Substitution mechanisms: Anatomical reorganization:
* * *
*
Other brain areas take over function: Consistent with the equipotentiality principle.
More 'free' brain tissue in children, so greater recovery, but also sometimes at the expense of other functions (so how 'free' was the brain tissue), crowding
Difference between intra-and interhemispheric reorganization, but factors influencing this are unclear.
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Substitution mechanisms :
* Behavioural compensation.
* Functional deficits are compensated by the use of other intact functions or external devices.
* For example, use diary in children with memory problems.
* Verbalisation of complex images when visuospatial functions are disturbed.
40
language, left hemispere damage in children....
- rarely results in the aphasic syndromes observed in adults.
- Equipotentiality: At birth, both sides of the brain are suited for language function, but the left side becomes more important later.
Evidence comes from lesion studies.
- Innate specialisation: Language is an innate function, which is always represented in special cortical areas.
Evidence comes from developmental studies.
Lesion studies:
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Lesion studies:
* Hemispherectomy
surgical removal (or disconnection) of one half of the brain.
*This operation is performed to treat severe epilepsy that cannot be controlled with medication.
* The procedure is performed exclusively on patients where the original brain injury occurred as a child.
42
Alex/Language: Sturge-Weber syndrome..
development disorder accompanied by calcification of the gyri, port-wine stain on the face, epilepsy and hemiparesis)
3.5-4 years no mental development * Left hemispherectomy was performed when 8.5 years old.
* Anti-convulsant medication stopped at 9 years.
* After that, he learnt to speak
* After five years, his linguistic development was at the level of children aged 8-10
So: clearly articulated, well structured speech can be learnt by children aged 9 and who have only a right hemisphere
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language production in hemispherectomy..
Involvement of Broca’s area (left) and right hemisphere equivalent
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After left hemispherectomy:
impairments in all language functions (except sentence comprehension)
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After right hemispherectomy:
borderline performance
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cause brain damage matters/Cortical Dysplasia:
more impairment/abnormal development of the brain's cortical layers
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Left vascular and right Rasmussen’s syndrome:
best outcome
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The left hemisphere probably has a biological advantage regarding the representation of language, but....
but if the language centres are severely damaged, the right hemisphere can take over this function to some extent. P decreased during development
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The earlier the damage occurs, the more ..... the effects
serious
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aphasia
Adults with damage in the left hemisphere
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Adults with damage in the left hemisphere --> damage in children between 1 and 5 years -->
no aphasia. However: language not normal and crowding effect (see hemispherectomy)
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Prefrontal cortex:
- Adults: executive functions impaired, but normal IQ
– Children: EF and IQ impaired
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Recovery continuum model (Anderson et al. 2011)
* Nature and severity of the insult
* Developmental stage of the child
* Pre-injury child characteristics, e.g. cognitive skills
* Environmental context (distal and proximal), access to interventions and social supports
54
Attention is important for (acquiring) many different other cognitive skills:
(memory, executive function, perception)
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Exogenous attention:
triggered by external stimuli (reflexive).
* Develops earlier (in infancy)
* Involves ventral attention network
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Endogenous attention:
Internal (voluntary) * Develops later in childhood
* Depends on dorsal attention network
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Attentional Control: The ability to manage and shift attention based on goals. 3 kinds are:
Divided Attention: Managing multiple tasks simultaneously.
– Little evidence for this before the
age of 9 years
– Linked to anterior cingulate and prefrontal cortex
Inhibition: Suppressing irrelevant or unwanted impulses and behaviors.
Self-regulation and Monitoring: Controlling emotions and behaviors, and keeping track of progress towards goals.
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Selective Attention:
Ability to focus on one particular
task/stimulus, filtering out irrelevant information.
* Disengagement, shifting, engagement, inhibition of return and anticipatory eye movements
* 7-10 months can already focus (Lawson & Ruff, 2004)
* Further growth spurts at: – 3-6 years of age
– 8-10 years
– Around 15 years
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Vigilance:
Ability to maintain attention over time * Emerges gradually during infancy and early childhood * Accelerated development 8-11 years old
* Only gradual improvements during adolescence
60
arousal
Mainly brainstem structures: Reticular formation and medial thalamus.
61
Stroop Color-Word Task:
Measures: Selective attention and inhibition.
Test: Identify the color of the word, not the word itself.
62
Bourdon-Vos Test:
Measures: Focused and sustained attention.
Test: Cross out groups of 4 dots among many scattered dots. Used for children (6-17 years).
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Trail Making Task:
Version A: Focused attention (connect numbered circles in order).
Version B: Divided attention (alternate between numbers and letters). Measures attention and cognitive flexibility.
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Test of every day attention for children:
* 6-16 years
* Nine subtests
* Assessing:
– Selective attention – Sustained attention – Attention control
– Response inhibition
* Dutch and Australian norms available
65
memory duration
- Sensory register
- Milliseconds to seconds
– Short-term memory
* Several minutes, capacity about 7 items
– Working memory
* Manipulation of material
– Long-term memory
* Hours, days, months, years, capacity > 7 items
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Gradual increase in memory span..
* 3-4 items: 3 years old
* 5-6 items: 9 years old
* 7 or more: early adolescence
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Development influenced by
– Repetition speed
– Development of strategies: Chunking
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Implicit memory:
develops earlier than explicit memory: basal ganglia and brainstem relatively well developed at birth.
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The Delayed Non-Match to Sample (DNMS) task is a memory test used to assess working memory and recognition memory in animals, including monkeys.
In this task:
An animal is shown a sample object.
After a delay, two objects are presented: one is the same as the sample (the "match"), and the other is a new object (the "non-match").
The animal is required to choose the non-matching object.
Hippocampal lesions ....
impair the ability to correctly perform this task, demonstrating the hippocampus's role in memory processes, especially in recognizing and distinguishing between objects over a short delay.
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explicit memory
The hippocampus and medial temporal lobe are less developed at birth
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Long-term memory
– Pre-explicit:
hippocampus
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LTM, Explicit:
hippocampus + medial temporal cortex
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* Development of the prefrontal lobe takes even longer:
– Is involved in the organisation of memory and retrieval strategies (metacognition).
* Recognitiondevelopsearlierthanrecall.
* Sourcememory(rememberingwhereyoulearntsomething)develops only later (from 4 years onwards)
74
Jon's Case
– Premature birth (26 weeks)
– Impaired episodic memory
– Impaired spatial memory
– Normal semantic memory
– Normal intelligence
– Verbal functions also normal
– Recognition better than recollection
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Developmental amnesia
– Memory disorder resulting from abnormal neural development or damage before birth.
– Usually no laterality effects.
– Different aspects of memory can be impaired in different
combinations.
– Selective, therefore the other cognitive functions often develop normally.
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conslusion developmental amnesia:
there is no fixed relationship between episodic memory and the development of cognitive functions, implying that the development of episodic memory and semantic memory can vary. In some cases, episodic memory may develop before semantic memory, but this relationship is not fixed and can differ in individual cases, especially in conditions like developmental amnesia.
77
Acquired memory disorders occur due to damage or changes to the brain after birth. Causes include:
Traumatic brain injury: Physical damage to the brain from an accident or blow.
Anoxia: Lack of oxygen to the brain, which can damage memory systems.
Epilepsy: Seizures can disrupt brain function, affecting memory.
Tumor: Brain tumors can impair memory by damaging tissue.
Neurosurgery: Surgical procedures on the brain can result in unintended memory deficits.
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Assessment of memory functions in children
- Rey auditory verbal learning test
- Kaufman ABC-II (3-18 years old) --> Movements of the hand, spatial memory, recognizing faces
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Development of executive functions depends on the development of..
of prefrontal lobe
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* Object permanence
– ‘A not B’ task
– Not in babies under 7 months
– Coincides with growth spurt in prefrontal cortex
– Two aspects:
* Short-term memory
* Inhibition of previous response
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Growth spurts in prefrontal myelinisation:
– 0-2 years
– 7-9 years
– 16-19 years
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Executive functions
Components
* Attentional control
* Cognitive flexibility
* Goalsetting
* Information processing
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Executive functions
Normal development (Smidts & Anderson, 2002) * Attentional control
– Development begins in babies and goes quickly during the first years of life.
– Growth spurt around 15 years old
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Executive functions Normal development
* Cognitive flexibility, information processing and goal setting
– Develops later, usually between 7-9 years, and is relatively mature when the child is 12 years old.
* Followed by
– Integration with executive control
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Executive functions tests
– Wisconsin card sorting (6.5-89 years)
– Trail making (B) (as from 12
years)
– Tower of London (7-15 years, 16-80 years)
- Inhibition
- BADS-C
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BRIEF-2 (Behavior Rating Inventory of Executive Function) (Huizinga & Smidts, 2020)
* Questionnaire (58-59 items) completed by parents/teacher or child (12-18 years old)
* From 5-18 years.
* Eight factors 1) inhibition,
2) Understanding own behaviour, 3) Flexibility,
4) Emotion regulation,
5) Initiation,
6) Working memory,
7) Planning and sorting
8) Task behaviour
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In adults after prefrontal lesions problems with:
* Planning
* Flexibility of behaviour
* Regulation
* Self-reflection
* Taking decisions
* Temporal organisation
