Brain Developement and Plasticity Flashcards
What changes occur in the brain during childhood?
- Cell proliferation and migration
- Development of synapses
- Myelination
Not a linear process of growth
(Figure in slide 3)
Synapse development
1.— Initial synaptogenesis (increase in synpases)
2.— Subsequent synaptic pruning (decline in synapses)
(see table in slide 3)
Neurogenesis
Starts in ventricles
Progenitor cells divide and create daughter cells
— divided cells either become progenitor cells or migrate
Eventually becomes the fetal brain
————-
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
Neurogenesis
— Generation of new nerve cells occurring in the area right around the ventricle
Migration of Nerve Cells
Relies on glial cells
— provide “roads” or “scaffolding” for migration
— After 6 months, most neurons have been produced
Synaptogenesis
After birth, dramatic increase in synapses
Dendrites increase greatly early in life, allowing greater surface area for connections
Synaptic Blooming and Pruning
Blooming: Proliferation
Pruning: follows, process of reducing neural connections
Time course varies across cortical regions
—- Earliest: sensory and motor regions
—- Next: Parietal and Temporal association cortex
—- Latest: frontal cortex (not complete until late adolescence
Blooming allows the brain to have maximal capacity to respond to the environment
Connections that do not recieve much stimulation are pruned
Myelination
– Longer process
– Varies by region of nervous system
– Myelination of basic sensory and motor system: within 1st year of birth
– Myelination of integrative systems occurs later
What is the result of synaptic pruning and myelination?
Relative amount of white matter increases, grey matter decreases (slide 11)
What changes occur in the brain during adolescence?
uses a Dual-Systems Model
Developmental mismatch between two systems in adolescence
1. Limbic structures maturing: more incentive to seek reward
2. Prefrontal cortex still immature: multiple consequences related to executive function
… Limbic structures maturing, prefrontal is not yet developed = risky adolescent behaviour
Dual-Systems model evidence
> When no reward is involved, adolescents show adult-like logical reasoning skills
Strong emotional incentives = riskier choices
Activity in the nucleus accumbens (AKA ventral striatum) increases when adolescents when anticipating or recieving a reward.
Experience-expectant systems
Influence of the environment of the developing brain
– Develops in response to experience common to most members of the species
– Neural systems develop normally when the expected input is received, but is seriously affected when that is absent
– like learning to speak
Experience-dependent systems
– Develops in response to experiences that are not universal, but vary based on unique experiences
– like riding a bike
Influence of environment on the devleoping brain
Environmental Enrichment vs. Deprivation
Enriched environments positively influence synaptic connectivity in early development and adulthood
Changes persist when the animals are later removed from the enriched setting (slide 16 experiment on rats)
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 foster family
Those in the foster care before age 2 showed improvements in intelligence and normalized EEG activity
Sensitive Periods in Development
Organism is particularly sensitive to certain external stimuli during a specific developmental period
EG:
– Visual system: exposure needed in the first months of life
– Language: becomes more difficult in adulthood
Developmental Disabilities
- Intellectual disability
- Dyslexia
- Autism
- ADHD
Typically make their appearances during childhood
Represent a departure from the difficult developmental path
Intellectual disability-Mild
IQ Level: 55-70
%: 85
Typical presentation:
– develops normally during preschool but do not acquire academic abilities above the 6th grade level
– As adults, can be self-supporting, and live independently with community and support
Intellectual Disability-Moderate
IQ Level: 35-55
%: 10
Typical Presentation:
– Can acquire communication skills during early childhood
– As adults, need some supervision for living and work, but can take care of themselves in those contexts
Intellectual disability (severe)
Intellectual disability (profound)
Genetic Disorders
Can cause intellectual disabilities
Example: Down Syndrome
Down Syndrome
Most common genetically cause of intellectual disability
Associated with IQs in the lowest 2%
1 in 700-800 births
Caused by trisomy 21 (3 copies of the 21st chromosome)
Down Syndrome Symptoms
—- Characterized by a specific morphology of body and face
—- Slower rate of cognitive development than peers
—- Characterized by reduced gray-matter volume due to reductions in cortical surface area
—- In middle age, many people with Down syndrome begin to exhibit symptoms similar to those of Alzheimer’s disease.
Fetal Alcohol Spectrum Disorders
> > Intellectual disorders caused bt alcohol consumption during pregnacy
Most severe form: fetal alcohol syndrome
Fetal Alcohol Syndrome Symptoms
Fetal Alcohol Syndrome brain structure
Learning Disability
Occurs when only one cognitive domain is affected
Dyslexia
— AKA Specific Reading Disability
— Specific inability to read at an age-appropriate level
— Characterized by a deficit in phonological understanding (linking a letter to a sound, decoding words to their phonemes)
— Perceptual mechanisms needed to acquire phonological awareness may be deficient
— Poor communication between sensory regions and higher-level regions involved in language
— learn based on whole words, not letters
Autism Spectrum Disorder
2 main characteristics:
1. Impairment in social interaction across a range of contexts
2. Restrictive or repetitive activities or interests
Symptoms must be present in early dev.
— Most diagnoses made around age 3
— Behavioural signs often evident later
Many potential causes
Potential causes of ASD
- Genetics
- Infectious diseases
- Birth injuries
- Metabolic diseases
- Environmental factors
Brain Development in autism
Cortical thickness:
—- increased in early development
—- decreased in later years of development
White-matter development:
— increased in early development
— slower rate of myelination later, falling behind peers
ADHD
DSM-5 Criteria
— Symptoms must be “inconsistent with developmental level” (kind of subjective)
— Child must have a clinically significant impairment that interferes with adaptive functioning in more than one setting
Compared to the average child of the same age, a child with ADHD is inattentive, hyperactive/ impulsive, or both
ADHD and Dopamine
Dopamine system is strongly implicated
Dopaminergic cells project to basal ganglia and prefrontal cortex, regions whose activity is altered in ADHD
— Drugs used to treat ADHD influence influence dopamine system
— Dopamineric cells project to basal ganglia and prefrontal cortex (activity is altered in ADHD)
— Genes implicated in ADHD are generally genes that influence dopaminergic neurotransmission
Hypotheses for ADHD causes
- Suppressed frontal lobe activity*
»_space;> deficit in inhibitory control
»_space;> deficit in motivational processes, luke delay aversion (unwillingness to wait for rewards) - Dysregulation of Default Mode Network
- Disruption of attentional filtering by thalamus
- Disruption of right hemisphere function*
- Underproduction of dopamine*
ADHD Treatment
Medication often influences dopamine systems
Methylphenidate (Ritalin)
—- slows rate of reuptake
Also given behavioural modification strategies
Prognosis for Specific Learning Disabilities
(Do children outgrow specific learning disabilities?)
Do children outgrow specific learning disabilities?
»> some symptoms decrease in severity, others may manifest in different forms and manner
»> Disabilities persist but effective compensation mechanisms develop
Brain Plasticity in Adulthood
– Changes in experience in adulthood can lead to changes in the representation of information in the brain
— training can strengthen cortical representations
Loss of input of a certain kind can cause representations to wither away (somatosensory cortex in amputations)
Reorganization of function
- Maps in sensory cortex are maintained through continual sensory input
— input changes, map changes - Examples: Phantom limb sensations
Cross-Modal Plasticity
Cortex normally dedicated for one purpose can be rededicated to entirely different purposes
EG: blind from birth (visual cortex now activated by tactile stimulation, some auditory and verbal stuff)
Dysfunction following brain injury
– Necrosis: cells begin to die at the site of lesion
– Transneuronal degeneration: cell loss can extend to more distal neurons
– Edema: swelling which increases pressure within skull (can b life threatening)
Dead cells break down, fluid fills spaces where there were cells
Cellular-level changes that aid recovery
Generation of new cells: Neurogenesis, Gilogenesis
Angiogenesis: new blood vessels grow and reestablish blood supply to damaged region
Axonal sprouting connection regions that had not previously been connected, forming new synapses
Recovery of Function
Damage affects: cells in the immediate area, surrounding tissue, distant brain tissue
If the damaged area within the M1 is relatively large, there may not be enough intact tissue to support recovery of function. In that case, the function is taken over by the parallel region of the opposite hemisphere
Factors that may influence brain damage recovery:
- Severity of insult
- Number of insults
- Spacing of insults
- Age at time of insults
- Premorbid cognitive status
- Extent to which function can be taken over by another
- Overall brain integrity
- Individual differences in brain function
- Motivation
- Emotional factors
- Extent and quality of rehabilitation
Recovery vs. Compensation
Recover: original function is restored
Compensation: person learns a work-around, to do a task in a new way
Window of recovery is shorter than for compensation
Interventions to promote recovery
- Specific training programs
— physical therapy
— emphasis on use of repeated limb/ speech - Stimulation methods (TMS, tDCS)
— stimulates damaged hemisphere
— inhibits contralateral hemisphere to reduce competition
Kennard Principle
The earlier the damage is sustained, the better the recovery
Consequences of damage to the young brain
— 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
___
Early-occurring brain damage can produce potentially worse long-term consequences
— Especially during sensitive periods of development
— consequences on a young brain may take years to see fully
Crowding Hypothesis
Intact areas of the child’s brain must carry out normal functions + functions that the damaged area would have implemented
No initial deficits: Deficits may emerge later as the child is expected to demonstrate more complex skills
Cognitive changes with aging
General decline: all abilities decline with age
— Reality:
> Decline in “fluid intelligence” but not in “crystallized intelligence”
> Emotion regulation improves
> Cognitive functions within frontal and temporal regions show greater decline with age
Neural changes with aging
— different brain regions show different changes in brain volume
»> less decline in sensory cortexes
Some show general decline, some are curvilinear (last in, first out)
To slow the effects of aging:
- Aerobic exercise
» multiple benefits
» greater proliferation of blood vessels to the brain - Remaining intellectually active
»> mentally stimulating environments
