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50 Cards in this Set
- Front
- Back
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α Anatomic Development
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o Beginning as a hollow tube, the brain develops steadily through temporally distinct stages to its final anatomic & functional state of well-delineated cellular layers & regions
o The development of the central nervous system, brain, & spinal cord is orderly & systematic, generally unfolding from head (cephalic) to tail (caudal), form near (proximal) to far (distal), & from inferior (subcortical) to dorsal (cortical). o The earliest stage of brain development, neurogenesis, involves the proliferation of neurons of the neural tube & the migration of these cells to predetermine locations o Subsequent stages include the growth of axons & dendrites |
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When does the central nervous system (CNS) & peripheral nervous system (PNS) develop from the midline ectoderm layer of the fertilized egg?
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approx. 18 days after conception,
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α Neurogenesis & Cellular Migration
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1) CNS & PNS develop
2) o Ectodermal tissue (neural plate) rises, & subsequently folds & fuses to form the neural tube surrounding a fluid-filled cavity 3) Precursor and Progenitor Cells create the neurons & glia of the brain 4) o The open ends of the neural tube close at approximately the 25th day of gestation, with the anterior end subsequently giving rise to the brain, & the posterior end forming the spinal cord 5) neurulation 6) Corticogenesis 7) cortical neurons reachtheir designated locations at 18 weeks 8) o Disruption in the migratory process can cause significant & extensive damage to the developing brain |
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precursor/progenitor cells
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cells lining the wall of the neural tube
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neurulation
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process of forming & closing the neural tube
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corticogenesis
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The development of the cortex
begins in the 6th embryonic week |
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α Axon & Dendrite Development
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o little extensions called spines begin to extend out from the dendrites
o The dendrites & dendritic spines create synapses for gathering information to be sent to the neuron o The most intensive period of dendritic growth occurs from birth - approx. 18 months o The development of the dendrites & spines is highly sensitive to the effects of environmental stimulation |
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α Synaptogenesis
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o Paralleling the growth of the axons & dendrites of the brain is the formation of synapses, that is synaptogenesis
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α Myelination
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o As cellular migration near completion, glial cells begin to encircle the axons, providing a protective white, insular sheath called myelin.
o The significant increase in brain weight in the postnatal years is primarily a function of the brain’s increased Myelination |
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Pruning
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o Subsequent development eliminates. large numbers of neurons, w/ the process often beginning at the sites of the dendritic spines
o a purposeful sculpting of the brain o primarily a postnatal process, eliminating 40% of the brain’s cortical neurons during childhood o The remaining neurons are eliminated during adolescence, & possibly into early adulthood |
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α Regional Development
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o As previously noted, the anterior, cranial end of the neural tube expands to form the brain, & the posterior end evolves to form the spinal cord.
o 3 vesicles (dilations or expansions) develop at the anterior end o These vesicles subsequently form the forebrain (prosencephalon), midbrain (mesencephalon), & hindbrain (rhombencephalon) |
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α Lobular & Convolutional Development
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o In the initial stages of prenatal development the brain surface is smooth, lack both gyri & sulci.
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α Ventricular Development
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o As the CNS matures, the cavities within the cerebral vesicles of the neural tube subsequently form the ventricular system & the central canal of the spinal cord
o CSF is produced in the ventricles, cushions the brain & spinal cord w/in the skull & vertebral column, & removes waste products from the brain o Excessive accumulation of CSF in the ventricular system during pre- or postnatal development can lead to extensive damage to the brain |
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hydrocephalus
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expansion of the cranium
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α Postnatal Development
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o During the last 3 mths of prenatal life & the 1st 2 yrs of postnatal development, the brain changes very rapidly
o Final adult weight of approx 1,300 to 1,500 grams o By age 2 the brain has achieved 3/4 of its eventual adult weight o In addition, the cortical surface area of the hemisphere doubles, reaching adult dimensions by age 2 |
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Language
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o emerges in 1-2 yrs of life & coincides w/ development of the anterior region of the braino
During the next 9 mths, growth in the speech & orofacial areas of the rt hemisphere exceeds that of the lft hemisphere o This growth pattern is consistent w/ the early emergence of non-verbal expressive language (for example, gestures), in contrast with later developing verbal language |
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Broca's area development
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o Btw 12-15 mths, dendritic growth of the lft Broca’s area exceeds that of the rt
o expanded development of the lft Broca’s area correlates w/ the onset of spoken language o By 6 years the dendritic complexity of the lft & rt Broca’s areas has significantly exceeded that of the motor areas o The lft Broca’s area now resembles that of the adult, suggesting that speech has lateralized |
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α Neurocognitive Development
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o The development of cognition, or knowing, involves the unfolding of biologically determined brain structures & functions in interaction with environmental forces
o The maturation of the cortical regions is characterized by abrupt changes of electrical activity in specific brain regions |
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executive function
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higher-order regulatory & integrative processes are involved
o Included in this grouping are planning, mental flexibility, attentional allocation, working memory, & inhibitory control o Disruption of executive functions results in significant cognitive, emotional, & social impairment o The maturation of executive functions is crucial to psychological adaptation & adjustment across the life span o (Levin et al., 1991) suggest that basic executive functions develop early in life & follow a protracted, multistep trajectory to maturity in adulthood |
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frontal lobe
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o For over a century, controversy, confusion, & speculation have existed over the function(s) of the frontal lobes
o Fortunately, a consensus is emerging on the role of the frontal lobes as serving supervisory or control functions |
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Goldman-Rakic
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o Important advances in understanding the development of executive functions are due to the remarkable investigations of Goldman-Rakic (1987) & Diamond (1991)
o Goldman-Rakic studied the relationship of prefrontal development to the emergence of the cognitive operation of object permanence, that is, the capacity to store in memory a representation of an object, for the purpose of guiding future behavior, that is removed from view |
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Case studies in children
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o Case studies of children who sustained damage to the frontal cortex provide further insight into frontal lobe development & the regulation of emotional & social behavior
o Children demonstrate impairments in emotional regulation & interpersonal relations, regardless of the age at which the damage occurred |
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o Phenylketonuria (PKU),
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a genetic metabolic disorder can be inherited or result from alterations of cellular material, as evident in Turner’s syndrome
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α Vulnerability & Plasticity of the Developing Brain
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o The brain may fail to develop structurally & functionally as a consequence of genetic anomalies & environmental insults
o Environmental causes relate to damaging agents (such as alcohol) that preclude, alter, or halt natural brain development o The prenatal brain appears most vulnerable to structural damage during the 3rd through 8th weeks of development, a period that correlates with the rapid proliferation & migration of cells o Further, a wide range of potential dangers threaten postnatal development. o Traumatic head injury, toxins, radiation, malnutrition, tumors, infections, & stroke can all cause significant injury to the developing brain |
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Teratogens
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o are agents that, if introduced or present during certain periods of prenatal development, can produce central nervous system defects
o Examples of potential Teratogens are general disease (such as rubella, influenza, & mumps), sexually transmitted diseases (such as syphilis, AIDS, & genital herpes), drugs (such as alcohol, barbiturates, & vaccines), environmental toxins (such as mercury, carbon monoxide, lead, & PCBs), & radiation (such as from x rays & exposure to radioactive materials) |
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agenesis/dysgenesis
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o the failure of an organ to develop
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plasticity
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enduring changes in neural activity that accompany learning or the recovery of behavioral functioning after brain injury or disease.
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Kennard Principle
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suggested that the immature brain was more plastic than the mature brain
o That is, the earlier the damage, the more pervasive & disruptive the developing function o The effect that a lesion has on the developing brain varies with regard to the age of insult. o Lesions occurring before age 1, including prenatal development, typically correlate with more global & lasting impairment than later injuries |
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α Child & Adult Brain: Structural & Functional Differences
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o An important realization is that the child’s brain differs in many significant ways from the adult brain.
o The adult brain is anatomically, physiologically, & functionally mature, whereas that of the child is still developing o With the achievement of brain maturity comes greater stability & predictability of behavior o In comparison, the cognitive & behavioral functions of the developing brain can vary dramatically |
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α Child & Adult Brain: Structural & Functional Differences Part 2
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o This variability depends on the current developmental stage & on the nature & quality of the child’s social-psychological-physical environment
o With lesions of the mature brain, assessing the degree of functional loss & potential for recovery often involves examining the adult’s premorbid history o The impact of adult injury is generally apparent soon after the lesion occurs, whereas the effects of injury to the immature brain are less straightforward |
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α Specific Developmental Disorders
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o In this section we review several groups of developmental disorders that frequently come to the attention of neuropsychologists
o These include abnormalities of anatomic development, genetic & chromosomal disorders, & acquired cerebral insults & diseases |
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α Abnormalities of Anatomic Development
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o Extensiveness & severity of damage to the developing brain tends to reduce life expectancy of children with anatomic brain malformations.
o Surviving children show a high rate of mental retardation, speech & language delays, learning disabilities, motor impairments, physical anomalies, & epilepsy. o Children with severe & global neuropsychological deficits often require lifelong supervision & assistance |
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Hydrocephalus
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o can occur during any developmental period & seriously damages the developing brain, disrupting both subcortical & cortical functions
results from an excessive accumulation of cerebrospinal fluid (CSF) in the brain’s ventricles o The increased volume of CSP produces a concomitant increase in intracranial pressure & expansion of the ventricles o As the ventricles expand, cerebral tissue is compromised & the cranium distorts. |
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what can occur if hydrocephalus isn't treated?
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mental retardationo
If unchecked, HC can have a devastating impact on the developing brain & skull |
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intraventricular hemorrhage (IVH)
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o In contrast, the most common cause of perinatal & postnatal HC that occurs in premature infants
o Increasing pressure extensively damages underlying white matter of the braino As CSF volume increases, & the ventricles progressively enlarge, brain anatomy & function are disturbed |
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α Turner’s Syndrome
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o In 1938, Turner presented a syndrome characterized by a failure to develop secondary sexual characteristics, short stature, webbed neck, & cubitus valgus (an increased carrying angle at the elbow)
o This disorder was subsequently named Turner’s syndrome (TS) o The factors accounting for these difficulties are unclear, but the small stature & sexual limitations of the individual with TS likely contributes to social difficulties & negative emotionality |
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How is HC commonly treated?
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o Most children with symptoms of HC receive a shunt.
o This medical procedure drains excessive CSF away from the ventricular system into the stomach o Before the widespread use of the shunt, only a quarter of untreated HC children survived to adulthood, & many survivors were profoundly retarded o The prognosis for HC children was dire before the development of shunting o However, the advent of shunting markedly increased the number of children who both survived & escape the significant destruction of their cognitive functioning |
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o Ultrasonography
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a procedure that uses sound waves to image internal structures, has enabled medical personnel to identify HC in utero by measuring the ventricular expansion that precedes the later developing enlargement of the cranium
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What is the cause of TS?
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o TS is the result of an anomaly of the female sex chromosome
o The XX chromosome defines the developing embryo as female o In TS, the second X is either missing or otherwise abnormal in formation or location |
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What are the results of TS?
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o The intellectual functioning of children with TS is generally within the low=average to average range
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What are the signs of TS?
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o The majority of children with TS are diagnosed before school age
o During the preschool years, children with TS are described as immature, overactive, distractible & having difficulties sustaining attention o Children affected with TS tend to be compliant, unassertive, & conforming in their interactions with caretakers & peers o In light of these factors, it is not surprising that teenagers with TS are at risk for developing anxiety, insecurity, & depression |
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How is TS diagnosed?
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o Measure (blood assays) of gonadotroins assist in diagnosing the disorder
o In the female, gonadotrophins are hormones that stimulate the functions of the ovaries |
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How is TS treated
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o It is essential that adolescents with TS receive estrogen therapy due to their gonadal dysgenesis
o Further, the short stature associated with TS often requires growth hormone therapy |
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α Acquired Disorders
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o The number of agents, events, & processes that can potentially injure the prenatal & postnatal brain is staggering
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α Fetal Alcohol Syndrome
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o Children with FAS frequently exhibit intrauterine growth retardation; characteristic facial features of widely spaced eyes, shortened length of eyelids, elongated midface, flattened nose, & underdeveloped upper lip; & deficits associated with central nervous system involvement
o Central nervous system deficits include microcephaly (abnormally small head), infantile irritability, seizures, tremors, poor coordination, poor habituation (difficulty in tuning out repeating stimuli), & reduced muscle tone; below-average intelligence, inattention, hyperactivity, learning disabilities, & poor behavioral regulation commonly characterized children with FAS |
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o What causes FAS?
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o The children of mothers who consumed relatively low levels of alcohol (social drinking) did not exhibit either physical or structural stigmata, but experienced behavioral disturbances, social maladjustment, & cognitive deficits that extended into adolescence
o Thus, significant neuropsychological deficits can appear in children who are exposed prenatally to excessive alcohol use, even though they may appear physically normal o The risk to the developing fetus seems much greater in alcoholic mothers who chronically abuse alcohol or “binge” (multiple drinks consumed in a relatively short period of time) during pregnancy o Also, alcohol consumption seems to do greater damage during the early months of pregnancy, but there may be no period in pregnancy when the developing child is completely risk free |
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FAS research
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o Fraternal twin studies suggest that genetic factors may play a role in determining the vulnerability of the embryo or fetus to FAS
o Further, a comprehensive neuropsychological evaluation is needed to identify & interpret the cognitive, behavioral, & adaptive dysfunctional that characterizes the child |
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o Prevention
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o It goes without saying that the best form of treatment for an acquired disorder is prevention
o Eliminating or significantly reducing alcohol consumption during pregnancy markedly decreases or reduces the risk of FAS for the unborn child |
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Effects of FAS
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o Children with FAS exhibit a broad spectrum of neuropsychological deficits
o In addition to mental retardation, common FAS deficits are evident in attention, response inhibition, complex problem solving, spatial & object memory, language skills, verbal learning & memory, speed of information processing, consistency of task performance, cognitive flexibility, planning, & academic performance o FAS children who are mentally retarded generally require specialized educational services either within the public schools or in a residential setting, depending on the severity of retardation & particular learning needs of the child o The array of deficits that accompanying FAS often exceeds what might be predicted based on intelligence, suggesting that limited cognitive ability alone cannot explain these impairments |
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o FAS in adolescence/adulthood
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o Of considerable concern are reports that teenagers with FAS tend to manifest high rates of antisocial behaviors & substance abuse
o Unfortunately, the multiple cognitive, behavioral, & adaptive deficits of FAS appear to continue into adulthood |
