brain development and plasticity Flashcards
what brain processes happen during development
cell proliferation and migration
development of synapses
myelination
each process has their own time course (some happen at birth, others through adolescence)
neurulation
formation of the hollow tube that becomes the CNS
with time, the tube folds,turns and expands to become the fetal brain
the hole inside the tube becomes the ventricles
around the 7th week of gestation, nerve cells and glia near inside tube divide, proliferate and begin to migrate outward
neurogenesis
generation of new nerve cells occurring in the area right around the ventricle
migration of nerve cells
happens during early development
glial cells provide the scaffolding or “roads” along which nerve cells can migrate to their ultimate destinations
- cells that migrate often travel along radial glia
by six months of gestation, most neurons have been produced
synaptogenesis
dramatic increase in the number of neuronal connections (synapses)
one of the largest changes after birth
dendrites in the cortical regions increase greatly, providing greater SA for synaptic connections
occurs rapidly (increase more than 10 fold during the first year of life)
regional differences across brain regions
- occurs most rapid in primary sensory and motor area (functionally needed before learning more complex things) then the prefrontal cortex
synaptic pruning
reducing the number of neural connections
happens because cells do not receive the “survival factor” signals from other neighbouring cells. The ones not getting enough stimulation wither
this allows the brain to fine tune and specialize in specific environments. allows it to be sculpted according to experience
earliest in sensory and cortical regions
latest in frontal cortex (not complete until late adolescence)
synaptic overproduction
allows the brain initially to have maximal capacity to respond to the environment
myelination
glial cells provide myelin sheath
which matter increases and grey matter
a longer process that varies by region of the nervous system
myelination of basic sensory and motor systems: within 1st year after birth
myelination of integrative systems occurs later
medulla and spinal cord and myelinated early on in life - support basic functions
myelination in childhood and teenage years
relative amount of white matter increases and gray matter decreases
brain volume generally larger in boys for both grey and white matter
dual systems model
when no reward is involved, adolescents show adult-like logical reasoning skills
when strong emotional incentives are present, adolescents make riskier choices
activity in the nucleus accumbens (ventral striatum) increases in adolescents when anticipating of receiving a reward. Combination of this and the still developing prefrontal cortex leads to riskier behaviours. decreases in adulthood b/c prefrontal cortex matures and has better control over the limbic system.
experience-expectant systems
develop in response to experiences are common to nearly all members of that species
ie/ patterened light, presence of caregiver, exposure to language
neural systems develop normally when the expected input is received, but are seriously affected when the expected experience is absent
experience-dependent systems
develop in response to experiences that are not universal, but vary across people based on their unique experiences
ie/ musical training early life, learning to juggle, learning to ride a bike
we are likely to develop different motor and musical skills
environmental enrichment and deprivation
many studies have been conducted in other species
control condition: rat alone in a small plastic cage
enriched condition: large area with varied spatial arrangement, toys and social interaction with other rats
enriched environments positively influence synaptic connectivity in early development and adulthood
changes persist even when the animals are later removed from the enriched setting
bucharest early intervention project
orphaned children in state care randomly chosen to receive
1. continued care in state run orphanage (little social or intellectual stimulation)
2. placement with a highly trained family
those placed in foster car before two years of age showed improvements in intelligence and normalized EEG activity
effects of environmental deprivation during critical developmental windows in orphaned Romanian children
sensitive periods
organism is particularly sensitive to certain external stimuli during a specific developmental period
(though certain effects can influence over a lifetime)
- allows for locking in influence
visual system: exposure to visual input in both eyes needed in first months of life to develop normal binocular vision
language: learning a new language becomes more difficult in adulthood
deprivation of social contract during this time can effect development
developmental disabilities
conditions that typically make their first appearances during childhood
represents a departure from normal developmental path
lots of unknown causes
intellectual disability
mental retardation
can be caused by genetic disorders, infections, toxins and oxygen deprivation
classified based on severity
genetic disorders
some genetic disorders can cause intellectual disability
ie/ down syndrome
down syndrome
most common genetic cause of intellectual disability
severve disability
associated with IQs in the lowest 2 percent
occurs in 1 in 700-800 births
caused by trisomy 21 (three copies of 21st chromosome results in down syndrome)
characterized by morphology of face and body (aids early diagnosis)
deficits in language and verbal memory - sometimes better functioning in visuospatial and social tasks
trisomy 21
a condition where the 21st pair of chromosomes contain 3 chromosomes instead of 2
fetal alcohol spectrum disorder
intellectual disabilities cause by mother’s alcohol consumption during pregnancy
continuum of severity impacted by exposure, this is most sever
symptoms of fetal alcohol syndrome
hyperactivity, poor impulse control, social/emotional difficulties, difficulties learning and memory, executive dysfunction
slowed physical growth and abnormalities of the face and cranium
changes in brain structure for fetal alcohol syndrome
reductions in gray matter volume throughout the brain
altered trajectory of white matter development throughout childhood and adolescence, especially connections between the frontal lobes with other brain regions
learning disability
when only one cognitive domain is affected
dyslexia
sometimes referred to as a specific reading disability
a specific inability to learn to read at an age-appropriate level, despite adequate opportunity, training and intelligence
characterized by a deficit in phonological understanding: linking a particular letter to a particular sound, being able to decode words into their constituent phonemes (misreading house for hose)
perceptual mechanisms needed to acquire phonological awareness may be deficient
poor communication between sensory regions and higher level regions involved in language
autism spectrum disorder
diagnosis involves two main characteristics:
1. impairment in social interations across a range of contexts (non-verbal communication, reciprocity, developmental of social relationships)
- restrictive or repetitive activities or interests (inc.motor actions)
symptoms must be present in early development
- most diagnoses made around the age of three
- behavioural signs are often evident earlier
many potential causes: genetics, infectious diseases, birth injuries, metabolic diseases, and environmental factors
no evidence that vaccines cause or contribute to autism
enlarged overall brain volume
cortical thickness in brain
increased cortical thickness early in development
decreased thickness in later years of development
varies across brain regions
white matter development in autisim
increased white matter early in development
later: slower rate of myelination, falling behind peers in white-matter development
attention-deficit/ hyperactivity disorder (ADHD)
8-10 percent of children in U.S
boys more commonly diagnosed
compared to the average child of the same age, a child with ADHD is either inattentive, hyperactive/impulsive or both (compared to the average child at that age)
symptoms must be “inconsistent with developmental level”
child must have a clinically significant impairment that interferes with adaptive functioning in more than one setting
many hyptheses of ADHD
suppressed frontal lobe activity
- deficit in inhibitory control - inability to inhibit inappropriate responses assess using stop signal task
- deficit in motivational processes, such as delay adversion
dysregulation of default mode network
disruption of attentional filtering by thalamus
disruption of right hemisphere function
underproduction of dopamine - unwillingness to wait for rewards
ADHD and dopamine
dopamine system is strongly implicated
dopaminergic cells project both to basal ganglia and prefrontal cortex, regions, regions whose activity is altered by ADHD
- drugs used to treat ADHD influence the dopamine system
- genes implicated in ADHD are generally genes that influence dopaminergic neurotransmission
treatment of ADHD
effects of methylphenidate (Ritalin) on attention networks
also given behavioural modification strategies
do children outgrow specific learning disabilities
some learning disabilities appear to become less severe with age (maturation hypothesis)
however, difficulties may manifest in a different form and manner as an individual matures
disabilities persist, but effective compensation mechanisms are developed
people with learning disabilities have successful personal and professional lives, often by emphasizing other cognitive strengths and/or utilizing compensation mechanisms
brain plasticity in adulthood
brain is not fixed in adulthood - brains can respond to environmental input
increased experience can change brains representation of info
training can increase cortical representations
loss of input of a certain kind can cause representations to wither away
brain maps are not set in stone - maintained through continual input
new neurons generated just not at the rate of the perinatal period
plasticity in amputation
the map in somatosensory cortex is reorganized; territory previously corresponding to lost part is now responsive to a neighbouring part of the body
somatosensory cortex can reorganize after amputation
amputee continue to feel sensations in their limbs even though they know it is missing
reorganization of function
“maps” in sensory cortex are maintained only though continual sensory input
- when input changes systemically, the map changes
some people continue to perceive sensations that can be distracting and painful
phantom limb sensations may occur when cells used to code for the lost limb are now being stimulated by new input from a different body location
cross model plasticity
cortex normally dedicated for one purpose can be rededicated to an entirely different purpose
ie. visual cortex in people blind from birth
no visual input - but is activated by braille reading, other tactile stimulation, and some auditory and verbal tasks
indicates that the visual cortex can reorganize to respond to nonvisual information in congenitally blind people
- reorganizes “visual” info for other functions
necrosis
cells begin to die at site of lesions
affects nurons and glia that insulate neurons
transneuronal degeration
cells loss can extend to more distal neurons
if cells do not recieve optimal stimulations and chemical factors
can occur across more than one synapse
edema
swelling which increase pressure within skull (can be life threatening)
cellular level changes that aid recovery
generation of new cells: neurogenesis and gliogenesis
angiogenesis: new blood vessels grow and reestablish blood supply to damaged region
axonal sprouting connecting regions that has not previously been connected
- new synapses
what doees damage to a discrete region of the brain region affects
cells in that immediate area, surrounding tissue and more distant brain tissue
when the damaged area within the primary motor cortex is relatively large, there may not be enough intact tissue in that hemisphere to support recovery of function. in such a case, function maybe partly taken over by the parallel region of the opposite hemisphere
damage to primary motor cortex (M1)
affect primary somatosensory cortex (S1) and motor cortex (PM), as well as connecting pathways
true recovery
the original function is restored
may be limited to the first few months
compensation
the person learns a work-around, to do a task in a new way
strategies can be implemented at any time
specific training programs
promotes recovery
physical therapy for motor difficulties following stroke
emphasis n repeated use of limb or speech
stimulation methods
promotes recovery
TMS tDCS
stimulate damaged hemisphere
inhibit contralateral hemisphere to reduce competition
kennard principal
not as many consquences in children
the idea that the earlier in life damage is sustained, the better the recovery
damaged to you brain still has consequences:
early left-hemisphere damage: no aphasia, but still deficits in phonology, syntax, and linguistic semantics
early right-hemisphere damage: difficulties in spatial cognition, analogous to those of right-hemisphere-damaged adult
some evidence say early-occurring brain damafe may actually produce worse long term consequences than later occuring damage
- sensitive during development
- consequences of an adult brain are usually obvious, but a childhood-acquired injury may take years to see full recovery
crowding hypothesis
intact areas of the child’s brain must carry out normal functions plus functions that the damaged area would have implemented
cognitive changes with aging
general decline
- all abilities decline with age
- results show a general reduction in mental resources or a general slowing in processing speed
reality: some abilities decline more with age than others:
- decline with fluid intelligence but not crystallized intelligences
-emotional regulation improves
- cognitive functions within frontal and temporal regions shows greater decline with afge
a lot of older people remember what happened early on in life
neural changes with aging
changes in brain volume
different brain regions show different trajectories of growth and decline over the lifespan
some show general decline in volume over lifespan
some show curvilinear pattern
last in first out: last to develop in childhood, soonest to decline at the end of the lifespan
slow the effects of aging
can never completely
aerobic exercise:
- multiple benefits
- produces a greater proliferation of blood vessels to brain, resulting in enhanced oxygen supply
remaining intellectually active
- mentally stimulating environment produces an elaboration of dendritic trees, allowing more numerous and varied synaptic connections
- will continue to work if you continue to use it
- use if or lose it
