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HC2 Flashcards

1
Q

order of development from zygote onwards with timing
>

A

zygote (24 hrs) 1 cell> 2 cells after (30hrs) > 4 cells (40)> 8 cells (60 hours)

> murola (80 hours)

> blastocyst (100 hours)

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2
Q

what happens 14 days after fertilization?

A

the inner mass of the blastocyst develops into structure with 3 layers, namely the;

  • endoderm
  • ectoderm
  • mesoderm
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3
Q

ectoderm forms

A

skin & central nervous system (brain spinal cord)

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4
Q

endoderm forms

A

forms internal organs & digestive system

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5
Q

mesoderm forms

A

forms blood, skeleton, muscles

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6
Q

what is created from the ectoderm?

A

the neural plate> neural groove

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7
Q

what happens after creation of neural plate> neural groove>… and in what week?

A

in the 3rd or 4th week the neural tube is created (process is called neurulation or neural induction)

is the embryonic precursos of the CNS

The neural groove gradually deepens
as the neural folds become elevated, and ultimately the folds meet and coalesce in the
middle line and convert the groove into the closed neural tube

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8
Q

when does the neural tube close in humans?

and what happens after this?

A

in the 4th week of pregnancy (28th day after conception)

after neural tube closure brain starts to develop

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9
Q

what is the center of the neural tube?

and the ectodermal wall

A

neural canal

the rudiment of the CNS

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10
Q

what are closure defects of the neural tube?

A

Anencephaly (closure defect on the head end of the neural tube) – usually fatal> only subcortical areas but not cortex

Spina bifida (incomplete closing of the backbone around the spinal cord (often in
combination with hydrocephalus)

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11
Q

on top of neural tube brain vesicles starts to develop (small brain parts at end of neural tube)

what are the vesicles?

A

telecephalon

diencephalon

mesencephalon

metencephalon

myelencephalon

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12
Q

into what becomes the brain vesicle telencephalon?

A

cortex

this is the biggest brain part in humans (big brain)

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13
Q

what becomes of the brain vesicle diencephalon?

A

thalamus=
Distributes all information to other parts where processing is going further

and hypothalamus=
Motivation and emotion: sexual behavior, aggression, regulates temperature, sleeping, eating, direct contact with pituitary gland

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14
Q

what becomes of the brain vesicle mesencephalon

A

it becomes the midbrain

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15
Q

what becomes of the metencephalon

A

cerebellum (beweging coordinatie) small brains

and pons (connection btwn small brains (cerebellum) and big brains and is part of the brain stem)> sends signals from evenwicht en gehoor to small brains

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16
Q

myelencephalon

A

medulla oblongata

autonomic functions such as sleep, heart-rate

connects higher level of brain to spinal cord

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17
Q

which structures develop in a sort of chronological order but overlapping? in what order

A

spinal cord & brain stem

amygdala, cerebellum, hippocampus

thalamus, basal ganglia

cerebral cortex (posterior=back to front)

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18
Q

what stages do almost all neurons go through?

A

cell proliferation
cell migration
cell differentiation (accents and ganglia characteristics)
selective cell death and synaptic pruning
myelinization

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19
Q

what are the proliferation zones ?

A

1) ventricular zone (all cell types)

2) subventricular zone (esp. front of cortex/ big brain)

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20
Q

what are causes of disorders in cell prolif (2-5 months)

A

genetic

trauma=
infection, fetal alcohol syndrome, radiation, Zika virus

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21
Q

what are the neural effects of disorders in cell proliferation? and what do they mean?

A

microcephaly =
cell division stops prematurely and brain is too small

megalencephaly=
overproduction of cells, production not stopped on time (also partly)

22
Q

what are consequences at functional level of disorders in cell prolif?

A

motor and or intell. impairments

learning problems

epilepsy

23
Q

what is passive migration & where does it occur?

A

occurs in thalamus & brain stem

New cells push out older cells to where the older need to be, older at top layers and new at bottom layers

24
Q

what is active migration and where does it occur?

A

occurs in cortex

follows glial cell while bypassing older neurons, oldest neurons are at the bottom, while newer neurons are at the top (layer 5 e.g.) most superficial layer/position

25
Q

what are causes of disorders in cell migration?

A
  • genetic * toxic substances * viral infection * Intrauterine damage
26
Q

what are neural effects of disorder in cell migration?

A
  • Lissencephaly (smooth cortex, no sulci or gyri) structural problem
  • Schizencephaly (abnormal clefts in cortex, cell layers not clearly defined)
  • Polymicrogyria (multiple small gyri, neurons in abnormal locations)
  • Agenesis (absence) of the corpus callosum (connection between hemispheres I missing)
  • Dysplasia (heterotopia) (abnormal cell layer structure/cells in the wrong place) more subtle
27
Q

what happens during differentiation?

A

-growth of dendrites (geleiden elektirsche impuls door naar cellichaam toe)
en axons (omhuld door myeline geven elektrische impulzen door van het cellichaam af)

formation of synaptic connections (synaptogenesis)

28
Q

overproduction (rise) and death of neurons and synapses

A
  • Apoptosis or programmed cell death happens throughout body
  • Pruning = synapse elimination depending on experience, hormones, and genes
  • Experience:
    – Experience-expectant synapses (sensitive periods) functions do not develop or not-normally
    > visual neurons need to be exposed to light in order to develop that function, if it doesn’t happen within certain period these connections disappear
    – Experience-dependent plasticity (enriched environment) Lots of input which results in large arrange of different connections, more flexibility and thicker cortex
  • ‘Use-it-or-lose-it’ principle Linked to experience things, need to use connections
  • ‘Neurons that fire together will wire together’ – Simultaneous activity of neurons strengthens connection
29
Q

what are causes in disorders in synapse formation and pruning?

and effects

A
  • genetic, * toxic substances, * problems during cell migration and cell differentiation, * stimulus, experiences (?)

-> none bc synapses are felxibles
abnormal brain development

30
Q
  • Disorders related to abnormal apoptosis;
A

– Neurodegenerative disorders (ALS, Arzheimers ) excessive apoptosis
– Autism (depressed or slower rates of apoptosis early on, excessive apoptosis in childhood and adolescence, Wei, 2014) hypothesis

31
Q

Disorders in myelinisation process
effects

A
  • 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)

Difference of neurotypicals and with people ASS in myelination

32
Q

Growth spurts:
* Development is not a linear process
* Several growth spurts can be distinguished (using EEG, brain volume, metabolism)

At what age do they occur?

A

24-25 weeks of gestation (pregnancy)=
completion of neuronal generation

first year of life =
dendritic and synaptic development, myelinisation

7-9 years=
frontal and temporal lobes grow

16-19 years=
myelination is complete except in prefrontal lobe at 17
white matter growth
grey matter reduction

33
Q

plasticity

Kennard principle: ‘Impairments are smaller when lesions occur in infancy than when they take place in adulthood’.

A
  • Based on lesions of the 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. Baby monkeys seem to recover motor functions better than adult monkeys
34
Q

Motor plasticity occurs in children as well (especially after injury before birth when the motor axons are still in development).

Sign of neural reorganisation of motor axons:

A

Mirror movements (evidence) different from mirror neurons: involuntarily moving of other hand when one hand moves, you see this in children before age 3, probably because motor system isn’t entirely mature yet, you have connections that controls both hands instead of one hand separately

Sign that one half of the motor cortex is
probably controlling both hands (i.e., neural reorganization/plasticity). Possibly trough
damage to normal neuronal pathways, there is a reorganization that allows you to have
control of both hands by one hemisphere.

Suppose you get brain damage to left hemisphere: paralyzed in right hand, what if happens in early life, it controls both hands still, so maybe your right hemisphere can take over control (you will get mirror movements tho)

35
Q

Restitution mechanisms:
Diaschisis (von Monakow):

A

Brain areas with connections to the damaged part show temporary disturbance of normal function (due to intracranial pressure, neurotransmitter, disrupted blood flow). Temporarily stop functioning because of connections, then after couple days you see that non damaged areas restart again

36
Q

restitution mechanisms= recover same mechanism:

A
  • 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

*Collateral sprouting: New growth of intact neurons near the damaged tissue that make connections with target neurons to which the damaged neurons originally projected.

  • Denervation supersensitivity: Increased sensitivity for neurotransmitters of target neurons that have lost part of their input through the brain lesion.
37
Q

Substitution mechanisms (keep function due to reorganization):

A

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 brain tissue) – crowding.
Difference between intra-and interhemispheric reorganization, but factors influencing this is
unclear. Equipotentiality is the theory that the brain has the capacity (in the case of injury) to
transfer functional memory from the damaged portion of the brain to other undamaged
portions of the brain.

Behavioral compensation: Functional deficits are compensated using other intact functions
or external devices. For example, use diary in children with memory problems. Verbalization
of complex images when visuospatial functions are disturbed.

38
Q

Is there evidence of reduced cognitive impairment after early
brain injury?
* Language

A

Left hemisphere brain 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:
* 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.

39
Q

what results came out of a recent meta-analysis of lesion studies concerning language development?

A
  • After left hemispherectomy: impairments in all language
    functions (except sentence comprehension) (Nahum & Liegeois,
    2020)
  • After right hemispherectomy (right removal of brain): borderline performance
  • Etiology (cause) matters:
  • Cortical dysplasia: more impairment
  • Left vascular and right Rasmussen’s syndrome: best outcome
40
Q

which hemisphere has a biological advantage?

A

the left regarding the representation of language

41
Q

what happens if language centers in left hemisphere are severely damaged?

A

RH can take over but only to some extent

this plasticity decreases as child develops

42
Q

what happens to intelligence if there is early brain damage? is there a difference btwn R & L h?

A
  • In early original injury (around birth): large
    reduction in IQ (>30 points). No difference between
    right and left hemispherectomy (Liegeois et al.,
    2008).
43
Q

what happens to iq if lesion occurs later in life?

A
  • IQ in general is saved more.
  • Left hemispherectomy: Reduced VIQ
  • Right hemispherectomy: Relatively
    saved/impaired PIQ
44
Q

Aetiology is the greatest predictor of IQ (Pulsifer, 2004):

what happens to IQ when you have Rasmussen syndrome (acquired) or vascular malformations or strokes (acquired)

A

rasmussen en vascular 70s

45
Q

cortical dysplasia (congenital) iq ?

A

30s

46
Q

what are effects of traumatic brain injury at early age?

A

– Cognitive and behavioural problems often more severe after early
injury:

47
Q

what happens to adults vs children age 1-5 with damage in left hemisphere (language)?

A

adults: aphasia

children 1-5: no aphasia but abnormal language and crodwing effect (not fully functional reorganisation)

48
Q

what happens to children vs adults with damage in prefrontal cortex?

A

children: iq and ef impaired

adults: ef impaired but normal iq

49
Q

the development of certain cognitive functions depends on…

A

on the proper functioning
of certain areas of the brain in a certain stage of development (critical periods)

50
Q

recovery continuum model

good recovery and plasticity vs poor recovery and vulnerability

A

– dependent on the interaction between risk and resilience factors
* 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

51
Q

interaction btwn plasticity and vulnerability in injury characteristics and recovery from early brain insult

explain plasticity factors i.e.;

  • severity of lesion
    -nature of lesion
  • age at onset
  • gender
  • psychosocial context
A
  • both small and very large lesions may cause hemispheric reorganisation

*focal lesions, e.g. stroke or tumour

  • greatest in initial 12 months and decreasing through childhood
  • more common in females, especially for left hemisphere
  • High SES, access to rehabilitation, early intervention

dn (4 decks)

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