Brain Development & Plasticity PDF
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Uploaded by JubilantNeptunium
Simon Fraser University
2023
Banich & Compton
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Summary
This document explains changes in the brain during childhood, focusing on topics like synaptogenesis, synaptic pruning, and myelination. It also covers brain development through adolescence and adulthood, impacting specific scenarios like amputation and blindness.
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Brain Development and Plasticity Chapter 15 Changes in the Brain During Childhood Many processes take place during development: Cell proliferation & migration Development of synap...
Brain Development and Plasticity Chapter 15 Changes in the Brain During Childhood Many processes take place during development: Cell proliferation & migration Development of synapses Myelination Each of these processes has its own time course Development is NOT a linear progression of growth Banich & Compton, Cognitive Neuroscience © Cambridge University Press & Assessment 2023 Changes in the Brain During Childhood Overview of the time frame of human brain development: Initial Synaptogenesis (increase in synapses) Subsequent synaptic pruning (decline in synapses) (Casey et al., 2005) FIGURE 15.1 Banich & Compton, Cognitive Neuroscience © Cambridge University Press & Assessment 2023 Early Development Overview of Neurogenesis FIGURE 15.2 Banich & Compton, Cognitive Neuroscience © Cambridge University Press & Assessment 2023 Early Development 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 Banich & Compton, Cognitive Neuroscience © Cambridge University Press & Assessment 2023 Early Development Overview of Neurogenesis FIGURE 15.2 Banich & Compton, Cognitive Neuroscience © Cambridge University Press & Assessment 2023 Early Development Migration of Nerve Cells: Glial cells provide the scaffolding or “roads” along which nerve cells can migrate to their ultimate destinations. By six months of gestation, most neurons have been produced. FIGURE 15.3 Banich & Compton, Cognitive Neuroscience © Cambridge University Press & Assessment 2023 Synaptogenesis Dramatic increase in the number of neuronal connections (synapses). Dendrites in cortical regions increase greatly, providing greater surface area for synaptic connections. FIGURE 15.4 Banich & Compton, Cognitive Neuroscience © Cambridge University Press & Assessment 2023 Synaptic Blooming and Pruning Synapse proliferation (“blooming”) is followed by the elimination of synapses (“pruning”), reducing the number of neural connections The time course varies across cortical regions: Earliest = sensory and motor regions Latest = frontal cortex (not complete until late adolescence) Synaptic overproduction allows the brain initially to have maximal capacity to respond to the environment Connections that do not receive much stimulation are pruned, allowing brain to be sculpted according to experience Banich & Compton, Cognitive Neuroscience © Cambridge University Press & Assessment 2023 Myelination 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 FIGURE 15.5 (van der Knapp and Valk, 1990) Banich & Compton, Cognitive Neuroscience © Cambridge University Press & Assessment 2023 Result of Synaptic Pruning and Myelination During childhood and teenage years, relative amount of white matter increases and gray matter decreases FIGURE 15.6 Banich & Compton, Cognitive Neuroscience © Cambridge University Press & Assessment 2023 Changes in the Brain During Adolescence Adolescence is a distinct developmental state Dual-Systems Model: Developmental “mismatch” between two systems in adolescence Limbic structures maturing = creates more powerful incentives to seek exciting reward Prefrontal cortex is still immature = multiple consequences related to executive function Likely explains risky behaviors in adolescence (e.g., fast driving, risky substance use) Banich & Compton, Cognitive Neuroscience © Cambridge University Press & Assessment 2023 Dual-Systems Model Evidence: 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 (also called ventral striatum) increases in adolescents when anticipating or receiving a reward Banich & Compton, Cognitive Neuroscience © Cambridge University Press & Assessment 2023 Influence of the Environment on the Developing Brain Experience-expectant systems Develop in response to experiences are common to nearly all members of the species E.g., patterned 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 Banich & Compton, Cognitive Neuroscience © Cambridge University Press & Assessment 2023 Influence of the Environment on the Developing Brain Experience-dependent systems Develop in response to experiences that are not universal, but vary across people based on their unique experiences E.g., musical training early in life, learning to juggle, learning to ride a bike Banich & Compton, Cognitive Neuroscience © Cambridge University Press & Assessment 2023 Environmental Enrichment and Deprivation Many studies of enrichment 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 Banich & Compton, Cognitive Neuroscience © Cambridge University Press & Assessment 2023 Environmental Enrichment and Deprivation 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 placed in foster care before 2 yrs of age showed improvements in intelligence and normalized EEG activity Banich & Compton, Cognitive Neuroscience © Cambridge University Press & Assessment 2023 Bucharest Early Intervention Project Effects of environmental deprivation during critical developmental windows in orphaned Romanian children. (Nelson et al., 2013) FIGURE 15.9 Banich & Compton, Cognitive Neuroscience © Cambridge University Press & Assessment 2023 Developmental Sensitive Periods Sensitive period: organism is particularly sensitive to certain external stimuli during a specific developmental period Examples of sensitive periods in development: Visual system: exposure to visual input in both eyes needed in first months of life to develop normal binocular vision Language: learning a language becomes more difficult in adulthood Banich & Compton, Cognitive Neuroscience © Cambridge University Press & Assessment 2023 Developmental Sensitive Periods Accuracy on a grammar task is highest when exposure to the language occurred at younger ages. FIGURE 15.10 (Hartshorne et al., 2018). Banich & Compton, Cognitive Neuroscience © Cambridge University Press & Assessment 2023 Developmental Disabilities Conditions that typically make their first appearances during childhood Represent a departure from typical developmental path Examples: Intellectual disability Dyslexia Autism Attention-deficit/hyperactivity disorder (ADHD) Banich & Compton, Cognitive Neuroscience © Cambridge University Press & Assessment 2023 Intellectual Disability The four classes of intellectual disability based on severity TABLE 15.2 Banich & Compton, Cognitive Neuroscience © Cambridge University Press & Assessment 2023 Genetic Disorders Some genetic disorders can cause intellectual disability Example: Down syndrome Most common genetically cause of intellectual disability Associated with IQs in the lowest 2% Occurs in about 1 in 700–800 births Caused by trisomy 21 Banich & Compton, Cognitive Neuroscience © Cambridge University Press & Assessment 2023 Down Syndrome Three copies of the 21st chromosome results in Down syndrome FIGURE 15.11 Banich & Compton, Cognitive Neuroscience © Cambridge University Press & Assessment 2023 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. Banich & Compton, Cognitive Neuroscience © Cambridge University Press & Assessment 2023 Fetal Alcohol Spectrum Disorders Intellectual disabilities caused by mother’s alcohol consumption during pregnancy Continuum of severity impacted by exposure: Most severe form is fetal alcohol syndrome (FAS) Banich & Compton, Cognitive Neuroscience © Cambridge University Press & Assessment 2023 Fetal Alcohol Syndrome Symptoms: Hyperactivity, poor impulse control, social/emotional difficulties, difficulties in learning and memory, executive dysfunction Slowed physical growth and abnormalities of the face and cranium Changes in brain structure: 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 Banich & Compton, Cognitive Neuroscience © Cambridge University Press & Assessment 2023 Dyslexia When only one cognitive domain is affected, the condition is referred to as a learning disability. 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 Banich & Compton, Cognitive Neuroscience © Cambridge University Press & Assessment 2023 Dyslexia Characterized by a deficit in phonological understanding: Linking a particular letter to a particular sound, being able to decode words into their constituent phonemes Perceptual mechanisms needed to acquire phonological awareness may be deficient Poor communication between sensory regions and higher- level regions involved in language Banich & Compton, Cognitive Neuroscience © Cambridge University Press & Assessment 2023 Autism Spectrum Disorder Diagnosis involves two 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 development Most diagnoses made around the age of 3 years Behavioral 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 Banich & Compton, Cognitive Neuroscience © Cambridge University Press & Assessment 2023 Brain Development in Autism Cortical thickness in autism: Increased cortical thickness early in development Decreased thickness in later years of development (Varies across brain regions) White-matter development in autism: Increased white matter early in development Later: slower rate of myelination, falling behind peers in white-matter development Banich & Compton, Cognitive Neuroscience © Cambridge University Press & Assessment 2023 Attention-Deficit/Hyperactivity Disorder (ADHD) Compared to the average child of the same age, a child with ADHD is either inattentive, hyperactive/impulsive, or both. The DSM-5 diagnostic criteria require that: Symptoms must be “inconsistent with developmental level” Child must have a clinically significant impairment that interferes with adaptive functioning in more than one setting Banich & Compton, Cognitive Neuroscience © Cambridge University Press & Assessment 2023 Attention-Deficit/Hyperactivity Disorder Many hypotheses: Suppressed frontal lobe activity Dysregulation of Default Mode Network Disruption of attentional filtering by thalamus Disruption of right hemisphere function Underproduction of dopamine ADHD Hypotheses Many hypotheses about the core deficit in ADHD: Suppressed frontal lobe activity deficit in inhibitory control deficit in motivational processes, such as delay aversion Disruption of right hemisphere function Underproduction of dopamine Banich & Compton, Cognitive Neuroscience © Cambridge University Press & Assessment 2023 ADHD and Dopamine Dopamine system is strongly implicated Dopaminergic cells project both to the basal ganglia and prefrontal cortex, regions whose activity is altered in ADHD. Drugs used to treat ADHD influence the dopamine system Dopaminergic cells project to the basal ganglia and prefrontal cortex, regions whose activity is altered in ADHD Genes implicated in ADHD are generally genes that influence dopaminergic neurotransmission Banich & Compton, Cognitive Neuroscience © Cambridge University Press & Assessment 2023 Treatment of ADHD Effects of methylphenidate (Ritalin) on attention (from Rosenberg et al., 2016b) networks Also given behavioral modification strategies FIGURE 15.15 Banich & Compton, Cognitive Neuroscience © Cambridge University Press & Assessment 2023 Prognosis for Specific Learning Disabilities Do children outgrow specific learning disabilities? Some learning disabilities appear to become less severe with age 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 Banich & Compton, Cognitive Neuroscience © Cambridge University Press & Assessment 2023 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. E.g., in the case of an amputation, the map in somatosensory cortex is reorganized; territory previously corresponding to lost part is now responsive to a neighboring part of the body. Banich & Compton, Cognitive Neuroscience © Cambridge University Press & Assessment 2023 Brain Plasticity in Adulthood The somatosensory cortex can reorganize after amputation FIGURE 15.16 Banich & Compton, Cognitive Neuroscience © Cambridge University Press & Assessment 2023 Reorganization of Function “Maps” in sensory cortex are maintained only through continual sensory input When input changes systematically, the map changes Example: phantom sensations in people who lost a limb Some amputees 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 Banich & Compton, Cognitive Neuroscience © Cambridge University Press & Assessment 2023 Reorganization of Function Phantom sensations in an amputee FIGURE 15.17 Banich & Compton, Cognitive Neuroscience © Cambridge University Press & Assessment 2023 Cross-Modal Plasticity Cortex normally dedicated for one purpose can be rededicated to an entirely different purpose. Example: “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 Banich & Compton, Cognitive Neuroscience © Cambridge University Press & Assessment 2023 Types of Damage to the Human Brain FIGURE 15.18 Banich & Compton, Cognitive Neuroscience © Cambridge University Press & Assessment 2023 Dysfunction Following Brain Injury Necrosis: cells begin to die at site of lesion Transneuronal degeneration: cell loss can extend to more distal neurons Edema: swelling which increases pressure within skull (can be life threatening) Dead cells broken down, fluid fills the spaces where cells had been Banich & Compton, Cognitive Neuroscience © Cambridge University Press & Assessment 2023 Neurophysiological Responses to Brain Injury FIGURE 15.19 (Wieloch and Nikolich, 2006) Banich & Compton, Cognitive Neuroscience © Cambridge University Press & Assessment 2023 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 had not previously been connected New synapses form Banich & Compton, Cognitive Neuroscience © Cambridge University Press & Assessment 2023 Recovery of Function Damage to a discrete region of brain tissue 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 may be partly taken over by the parallel region of the opposite hemisphere Banich & Compton, Cognitive Neuroscience © Cambridge University Press & Assessment 2023 Recovery of Function Damage to primary motor cortex (M1) affects primary somatosensory cortex (S1) and premotor cortex (PM), as well as connecting pathways FIGURE 15.20 (Nudo, 2006). Banich & Compton, Cognitive Neuroscience © Cambridge University Press & Assessment 2023 Variables Impacting Recovery of Function Factors that may influence recovery: Degree of recovery from traumatic brain damage varies from person to person Banich & Compton, Cognitive Neuroscience © Cambridge University Press & Assessment 2023 Recovery vs. Compensation True recovery: the original function is restored Compensation: the person learns a work-around, to do task in a new way Window of time for recovery is shorter than for compensation true recovery may be limited to the first few months (due to biological factors) Compensatory rehabilitation strategies can be implemented at any time Banich & Compton, Cognitive Neuroscience © Cambridge University Press & Assessment 2023 Interventions to Promote Recovery Specific training programs physical therapy for motor difficulties following stroke emphasis on repeated use of limb, or speech Stimulation methods (e.g., TMS, tDCS) stimulate damaged hemisphere inhibit contralateral hemisphere to reduce competition Banich & Compton, Cognitive Neuroscience © Cambridge University Press & Assessment 2023 Recovery of Function Kennard principle: The idea that the earlier in life damage is sustained, the better the recovery Damage to young brain does still have 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 Banich & Compton, Cognitive Neuroscience © Cambridge University Press & Assessment 2023 Recovery of Function Kennard principle: The idea that the earlier in life damage is sustained, the better the recovery However, some evidence suggests that early-occurring brain damage may actually produce worse long-term consequences than later-occurring brain damage Sensitive periods of development Consequences of an adult brain are usually obvious, but a childhood-acquired injury may take years to see full consequences Banich & Compton, Cognitive Neuroscience © Cambridge University Press & Assessment 2023 Crowding Hypothesis Children that sustain damage earlier in life typically have better outcomes for recovery However, deficits may emerge later as the child is expected to demonstrate more complex skills Crowding hypothesis: intact areas of the child’s brain must carry out normal functions plus functions that the damaged area would have implemented Banich & Compton, Cognitive Neuroscience © Cambridge University Press & Assessment 2023 Cognitive Changes with Aging “General decline” viewpoint: all abilities decline with age Results of a general reduction in mental resources or a general slowing in processing speed Reality: some abilities decline more with age than others: Decline in “fluid intelligence” but not in “crystallized intelligence” Emotion regulation improves Cognitive functions within frontal and temporal regions show greater decline with age Banich & Compton, Cognitive Neuroscience © Cambridge University Press & Assessment 2023 Cognitive Changes with Aging Age-related changes in fluid and crystallized intelligence FIGURE 15.22 (Salthouse, 2012). Banich & Compton, Cognitive Neuroscience © Cambridge University Press & Assessment 2023 Neural Changes With Aging (Hedden and Gabrieli, 2004) FIGURE 15.23 Changes in brain volume with age for three different brain regions. Banich & Compton, Cognitive Neuroscience © Cambridge University Press & Assessment 2023 Neural Changes With Aging 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 end of lifespan Banich & Compton, Cognitive Neuroscience © Cambridge University Press & Assessment 2023 Neural Changes With Aging Two different trajectories of brain volume over the lifespan FIGURE 15.24 (Douaud et al., 2014). Banich & Compton, Cognitive Neuroscience © Cambridge University Press & Assessment 2023 Slowing the Effects of Aging 1. Aerobic exercise Has multiple benefits Produces a greater proliferation of blood vessels to the brain, resulting in enhanced oxygen supply 2. Remaining intellectually active Mentally stimulating environment produces an elaboration of dendritic trees, allowing more numerous and varied synaptic connections. Banich & Compton, Cognitive Neuroscience © Cambridge University Press & Assessment 2023