Neuroanatomy for Speech-Language Pathology and Audiology 2nd Ed. Matthew H Rouse

Chapter 3. Development of the Nervous System

CHAPTER PREVIEW

How did we get the complex nervous system that we have? This chapter will try to answer this question by exploring the development of the brain from the early weeks of development after fertilization through adolescence to old age. This process is complex, and we will find that when it does not go as planned, the result can be a neurodevelopmental disorder.

IN THIS CHAPTER

In this chapter, we will ...

 Define neuroembryonic terms

 Briefly describe the development of the nervous system

 Describe common birth defects

 Discuss the development of the child's and adolescent's brain

 Survey how the neurological system changes with aging

LEARNING OBJECTIVES

1. The learner will define important neuroembryonic terms.

2. The learner will list and briefly describe the structural development of the nervous system from conception to old age.

3. The learner will list and describe common birth defects.

CHAPTER OUTLINE

 Introduction

 Genes, Chromosomes, and Cells

 Fertilization and the First Weeks of Life

 Structural Development of the Infant Brain

 Dorsal Induction

 Ventral Induction

 Neural Proliferation

 Neuronal Migration

 Cortical Organization and Synapse Formation

 Myelination

 Functional Development of the Infant Brain

 The Development of the Adolescent Brain

 The Brain in Normal Aging

 Conclusion

 Summary of Learning Objectives

 Key Terms

 Draw It to Know It

 Questions for Deeper Reflection

 Case Study

 Suggested Projects

 References

 Introduction

A human being begins as a single fertilized egg and develops into the complex organism we see walking around every day. Usually, this developmental process occurs without error, but about 3% of babies (1 in 33) born in the United States have a birth defect. These defects are the leading cause of death in babies, accounting for about 20% of deaths in infants (Centers for Disease Control and Prevention, 2018). In this chapter, we will survey the neurological development of babies, children, adolescents, and adults and will discuss some common birth defects.

 Genes, Chromosomes, and Cells

Genes reside on chromosomes, and chromosomes reside in the nucleus of a cell. Human somatic cells are diploid, meaning they have pairs of chromosomes. (Somatic comes from the Greek word soma, which means “body”) Overall, there are 23 pairs of chromosomes in humans, 46 individual chromosomes in all. Each person’s unique collection of chromosomes is called a karyotype (FIGURE 3-1). Of these 46 chromosomes, 44 are autosomes (or nonsex chromosomes) and 2 are sex chromosomes, either XX (female) or XY (male). In contrast, sex cells or gametes (either an egg or a sperm) are haploid, meaning they have 23 total chromosomes. A female gamete, or egg, carries only the X sex chromosome, whereas the male gamete, or sperm, can carry either the X or the Y sex chromosome.

Somatic cells divide and duplicate through a process known as mitosis (FIGURE 3-2). In this four-stage process, a mother cell divides and forms two genetically identical daughter cells, each of which has 46 total chromosomes like the mother cell. In comparison, gametes are created through a different process, called meiosis. In this process, cell division occurs twice instead of once like in mitosis. The result of this double division process is four gametes (eggs or sperm); each gamete has 23 total chromosomes. When an egg (23 chromosomes) is fertilized by a sperm (23 chromosomes), a zygote is formed, which is diploid (46 total chromosomes). This zygote will then undergo mitosis and develop into a morula and then into an embryo and finally into a fetus.

FIGURE 3-1 A karyotype is a person's collection of chromosomes. The term also refers to a laboratory technique that produces an image of a person's chromosomes. The karyotype is used to look for abnormal numbers or structures of chromosomes.

FIGURE 3-2 Comparison of mitosis and meiosis.

Errors can occur during mitosis. One possible error is a whole chromosome deletion, known as monosomy. One example of this error is Turner syndrome, in which a female has only one sex chromosome, an X. People with this disorder who survive birth have a small stature and a webbed neck and are unable to reproduce. Sometimes deletions do not involve whole chromosomes, but rather partial chromosome deletion like in cri du chat syndrome. In this condition, children have a weak cat-like cry, small head (microcephaly), high palate, round face, small receding chin (micrognathia), widely spaced eyes, low muscle tone, minor hearing and visual problems, mental retardation, and delayed speech and language. Another possible error in mitosis is the addition of a whole chromosome, which is called trisomy. The most famous example of trisomy is Down syndrome (or trisomy 21), in which the affected person has three copies of chromosome 21 instead of the typical two copies. These children have some level of intellectual disability as well as flat faces, slanted eyes, and growth failure (FIGURE 3-3).

FIGURE 3-3 A girl with Down syndrome.

► Fertilization and the First

Weeks of Life

By the time a child is born, most of his or her neurological development has been completed. This includes the creation of specialized nervous system cells, their migration to their correct location in the nervous system, and their connectivity to each other and other nervous system structures. Events (e.g., maternal alcohol consumption) that may occur while a child is developing in utero may have a profound impact on this neurodevelopmental process (TABLE 3-1).

Pregnancy is often talked about in terms of menstrual or gestational age (GA), which begins at the date of a woman’s last menstrual period. GA is dated this way because it is difficult to discern when fertilization has occurred. GA is conceptualized in terms of trimesters, with the first 12 weeks being the first trimester, weeks 13-28 the second trimester, and weeks 29-40 the third trimester. However, biologically, there are three main phases of this developmental process. The first week is called the germinal stage, the next 7 weeks of pregnancy are the embryonic period, and the final 32 weeks (weeks 9-40) are the fetal period.

The germinal stage begins when a sperm cell penetrates an egg or ovum cell. As the fertilized cell or zygote travels down the fallopian tube over the course of about 5 days, it begins to divide. This process is known as cleavage, and the result is a ball of cells known as a morula. When the morula enters the uterus, it becomes a blastocyst when its cells differentiate into outer and inner cells. The outer cells develop into the support structures for the embryo (placenta, etc.), and the inner cells develop into the embryo. The embryonic stage officially commences once the blastocyst implants into the wall of the uterus. At this point, the inner cells rearrange themselves into a disc from which the embryo forms. Three beginning layers of the embryo can be distinguished in the disc made up of inner cells: the endoderm, mesoderm, and ectoderm (FIGURE3-4). The endoderm will eventually form into the gut, liver, and lungs, and the mesoderm will develop into the skeleton, muscles, kidneys, blood, and heart. The ectoderm, which will be the focus of what follows, turns into the skin and nervous system (Howard Hughes Medical Institute, 2014).

du Plessis (2013) gives a helpful framing to the structural development of the central nervous system. She includes the following six phases: dorsal induction, ventral induction, neural proliferation, neuronal migration, cortical organization and synapse formation, and myelination. These phases do not occur in a strict sequential manner, but rather overlap each other.

TABLE 3-1 Timetable of Major Neurodevelopmental Events

Neurodevelopmental Event Peak Activity (Gestational Age) Example Abnormalities

Dorsal Induction

Neural tube formation

3-4 weeks

Spina bifida, encephaloceles

Caudal eminence development

4-7 weeks

Caudal regression syndromes

Ventral Induction

Prosencephalic development

2-3 months

 

Cleavage

 

Holoprosencephaly

Midline formation

 

Agenesis of the corpus callosum

Neural proliferation

3-4 months

Microcephaly

Neuronal migration

3-5 months

Schizencephaly, lissencephaly

Cortical organization

5 months to years postnatal

Polymicrogyria

Myelination

Birth to years postnatal

Hypomyelination

Cerebellar and Brainstem Development

2 months to postnatal

(Ponto) cerebellar hypoplasia;

Joubert syndrome; Dandy-Walker malformation

Data from: du Plessis, A. J. (2013). Fetal development. In M. L. Batshaw, N. J. Roizen, & G. R. Lotrecchiano (Eds.), Children with disabilities (7th ed., pp. 25-35). Baltimore, MD: Paul H. Brookes Publishing Company.

FIGURE 3-4 Layers of the embryo.

► Structural Development of the Infant Brain

Dorsal Induction (GA: 3-7 Weeks)

Dorsal induction is a neurodevelopmental period in which the neural tube is formed. At around the third week of development, the dorsal ectoderm thickens to form the neural plate. By the fourth week of development, this plate bends and wraps around itself to form a tube (i.e., the neural tube) from which the brain and spinal cord will develop (FIGURE 3-5). The process of forming the neural tube is called neurulation. Both ends of the neural tube are initially open (openings are called neuropores) but close at around 6 weeks’ GA (du Plessis, 2013).

The dorsal induction phase is a critical period of neurological development for the embryo (FIGURE 3-6). During this phase, the embryo is susceptible to what are called neural tube defects (NTDs), which involve failure of the neuropores to close properly. This defect can happen to either the anterior neuropore or posterior neuropore. The three major types of NTDs are encephalocele, anencephaly, and spina bifida.

Failure in anterior neuropore closure can result in encephalocele or anencephaly. Encephalocele is a rare malformation of the skull in which a malformed portion of the brain, usually the occipital lobe, protrudes from the skull in a sac (FIGURE 3-7). Children with this condition typically have hydrocephalus (i.e., excessive fluid in the brain), intellectual disability, craniofacial abnormalities, and motor issues such as ataxia (Liptak, 2013). Treatment involves surgery to remove the sac and place the protruding brain tissue back into the skull. Craniofacial abnormalities will also be corrected, and a shunt may be placed to reduce hydrocephalus. The prognosis for these children varies depending on a number of factors (National Institute of Neurological Disorders and Stroke [NINDS], 2018b). A better prognosis is associated with no hydrocephalus, frontal encephalocele rather than posterior, and minimal brain tissue in the sac (Liptak, 2013).

FIGURE 3-5 Formation of the neural tube.

Anencephaly is a more severe NTD in which neurological development ceases at the brainstem, leaving the infant without cerebral hemispheres and thus without higher cortical functions (FIGURE 3-8). Half of these children are naturally aborted, and the other half die shortly after birth. Anencephaly occurs 2 to 3 times per 1,000 live births. There is no treatment for the condition (Kemp, Burns, & Brown, 2008; Liptak, 2013; NINDS, 2018a).

When an NTD affects the posterior neuropore, the result is one of the more well-known NTDs— spina bifida (SB) (FIGURE 3-9). SB occurs in both severe and less severe forms (FIGURE 3-10). The most severe form is called myelomeningocele, in which the spinal cord, spinal fluid, and meninges protrude from the spine. The infant will have a large cyst on his or her back that is reddish in color. The next type, which is less severe, is meningocele, in which the same cyst is present, but the spinal cord is intact and not wrapped inside the cyst. The final, and mildest, form is occulta, in which vertebrae are malformed. The infant will have a depression in his or her back, often with a tuft of hair on and around it (Kemp, Burns, & Brown 2008; NINDS, 2018g). Children with SB occulta are often asymptomatic, but children with SB myelomeningocele and meningocele may have motor and sensory issues, especially with the lower extremities. They may also have bowel and bladder incontinence (Kemp, Burns, & Brown 2008). Children with SB myelomeningocele sometimes have learning disabilities due to disruptions in neuron migration (Liptak, 2013).

FIGURE 3-6 Embryonic development showing the critical period of development. During the embryonic stage—week 2 through week 8—all the major organ systems are forming. During this critical period of development, the embryo is highly vulnerable.

FIGURE 3-7 Encephalocele.

Courtesy of Centers for Disease Control and Prevention, National Center on Birth Defects and Developmental Disabilities.

FIGURE 3-8 Anencephaly.

Courtesy of Centers for Disease Control and Prevention, National Center on Birth Defects and Developmental Disabilities.

Ventral Induction (GA: 2-3 Months)

Ventral induction is a neurodevelopmental period when the face and brain develop out of the superior end of the neural tube. After the neural tube closes, it will bend ventrally, and the superior end goes on to form the major components of the brain (FIGURE 3-11 ). The first of these components is the prosencephalon (Greek for “front brain”), or the forebrain, which develops into the diencephalon (Greek for “back part of the front”; i.e., thalamic structures) and telencephalon (Greek for “front part of the front”) or cerebral hemispheres. During ventral induction, cleavage of the prosencephalon occurs, resulting in the two cerebral hemispheres, a left one and a right one. In addition, midline formation occurs in what is called the corpus callosum. The corpus callosum is a band of fibers that connects the two cerebral hemispheres and allows them to communicate with each other. Second, the mesencephalon (Greek for “middle”) becomes the midbrain. Third, the rhombencephalon (Greek for “diamond shape”), or hindbrain, develops into the myelencephalon (Greek for “the back of the back”; i.e., the medulla). Fourth, the metencephalon (Greek for “the front of the back”) develops into the pons and cerebellum. A summary of these structures and what nervous system structures they turn into is found in TABLE 3-2.

FIGURE 3-9 Spina bifida.

Courtesy of Centers for Disease Control and Prevention, National Center on Birth Defects and Developmental Disabilities.

FIGURE 3-10 Forms of spina bifida.

Courtesy of Centers for Disease Control and Prevention, National Center on Birth Defects and Developmental Disabilities.

FIGURE3-11 Fetal brain development.

These Greek terms are used by some neuroscientists as an organizational system for the central nervous system, but most of these terms have fallen out of use, except in neurodevelopmental contexts. In organizational systems based on gross or functional anatomy, the only term that is still typically used is diencephalon.

TABLE 3-2 Developmental Divisions and Mature Nervous System Structures

 

Division

Components

Telencephalon

Cerebral cortex, basal ganglia, olfactory bulbs

Diencephalon

Thalamus, hypothalamus, epithalamus, subthalamus

Mesencephalon

Midbrain

Metencephalon

Pons, cerebellum

Myelencephalon

Medulla

Data from: Spence, S. A. (2009). The actor's brain: Exploring the cognitive neuroscience of free will. Oxford, UK: Oxford University Press, p. 157.

One condition involving errors in ventral induction is noteworthy. Holoprosencephaly is a failure in brain cleavage (FIGURE 3-12). The condition is rare, occurring in 1 in every 30,000 births. There are three forms of the disorder. Alobar holoprosencephaly involves no cleavage at all, leaving the infant with no hemispheric development. In other words, the brain is just one mass with no hemispheric divisions or corpus callosum. Children also have craniofacial abnormalities, like cyclopia (having only one eye) or cleft lip. Semilobar holoprosencephaly is a milder form involving some development of the longitudinal fissure that divides the left and right hemispheres. Like the alobar form, the corpus callosum is absent. In lobar holoprosencephaly, the least severe form, the infant’s brain looks nearly normal; however, there are some abnormal connections between the hemispheres and abnormal development of the corpus callosum (Kemp, Burns, & Brown 2008; NINDS, 2018c).

 

FIGURE 3-12 Different degrees of holoprosencephaly.

© University of Florida Department of Pediatrics.

Neural Proliferation (GA: 3-4 Months)

Neurogenesis means the birth of new neurons; this process is at the heart of the neural proliferation stage. Not only neurons proliferate but also glial cells. These cells will eventually form the gray and white matter of the cerebral hemispheres. They are initially born out of the spinal cord and brainstem, but later the whole periventricular area (i.e., the area around the future brain ventricles) is involved in their production. The dorsal part of this area, which will be important for cognition, becomes filled with excitatory neurons. These neurons use the neurotransmitter glutamate; the ventral area develops interneurons (neurons that connect neurons together) that use the inhibiting neurotransmitter gamma-aminobutyric acid (GABA). Interneurons are initially excitatory but later take on an inhibitory role (du Plessis, 2013).

In this stage, if something happens that affects the normal proliferation of nervous system cells, the brain’s mass will be abnormally small because it lacks the correct number of these cells (FIGURE 3-13). This condition is known as microcephaly, and it is most often caused by viruses or alcohol exposure (du Plessis, 2013). The effects of microcephaly vary from child to child. Some have normal intelligence, whereas others have intellectual disability as well as motor and sensory issues. Speech issues are common in those with the more severe form (NINDS, 2018e).

FIGURE3-13 A baby with microcephaly.

© Centers for Disease Control and Prevention.

Neuronal Migration (GA: 3-5 Months)

After the proliferation of nervous system cells, these cells begin to migrate in waves from the inside of the brain where they were produced to the outer layers of the brain. A chemical called reelin signals these cells as to where they should stop in this migration. Eventually, by about a GA of 20 weeks, the migration ends and the six layers of the cerebral cortex are established. During the migratory process, some cells cluster together to form hills in the brain (gyri) while others form valleys (sulci), giving the brain its characteristic bumpy appearance. It is also during this period that the four lobes of the brain develop as well as their specific functions (e.g., occipital lobe and vision).

Two conditions associated with abnormal neuronal migration are schizencephaly (FIGURE 3-14) and lissencephaly (FIGURE 3-15). Schizencephaly is a rare condition characterized by abnormal openings or clefts in the cerebral hemispheres. These clefts are places where neurons failed to migrate. They can be bilateral, affecting both cerebral hemispheres, or unilateral, affecting only one. The issues associated with the condition will be more severe in the bilateral form versus the unilateral form. Possible issues include speech and language problems, developmental delays, and intellectual disability (NINDS, 2018f). Lissencephaly is caused by a lack of reelin, resulting in the brain having a smooth appearance, absent of its characteristic hills and valleys (gyri and sulci) (du Plessis, 2013; Kemp, Burns, & Brown, 2008). Symptoms of this condition include intellectual disability, seizures, and failure to thrive (NINDS, 2018d). Supportive care is the only form of treatment for schizen- cephaly and lissencephaly.

FIGURE3-14 Transverse section of the brain showing schizencephaly. The darkened area (image on the right) illustrates where brain tissue would be missing resulting in a cleft.

© University of Florida Department of Pediatrics

FIGURE3-15 Neuroimaging of a normal brain compared to a lissencephalic brain. The lissencephalic brain is missing the folds of cortical tissue normally seen in the brain.

Courtesy of Dr. Joseph G. Gleeson, The Rockefeller University.

Cortical Organization and Synapse Formation (GA: 5 Months to Years Postnatal)

Once neurons form and migrate to their intended location in the central nervous system, they begin to sprout projections called dendrites and axons. These projections begin to form connections (i.e., synapses) between neurons, leading to the saying, “Neurons that fire together, wire together; those that don’t, won’t.” This process is known as synaptogenesis. Once these connections are made, the neurons begin to communicate with each other. At first there are more connections than are needed. A process called synaptic pruning will take place later and last into the teen years (and perhaps the whole life span), during which these extra connections are eliminated.

One condition associated with errors in cortical organization is polymicrogyria, a condition in which children have too many folds (gyri) in the cerebral hemispheres (Kemp, Burns, & Brown 2008). This can occur in one hemisphere or both or just in one focal hemispheric area. When the condition affects a small part of the brain, the symptoms are mild, with the most common symptom being seizures. The more extensive the polymicrogyria is, the more severe the symptoms are. These symptoms can include epilepsy, developmental delay, intellectual disability, and speech and swallowing problems (National Institutes of Health [NIH], 2009b).

Myelination (GA: Birth to Years Postnatal)

Myelin is a white, fatty substance produced by specialized glial cells called oligodendroglia. This substance coats axons to speed up the transmission of electrical impulses. The myelination process begins at a GA of about 6 months, but only up through the spinal cord and brainstem. The process will continue into the cerebral hemispheres and reach its peak during the first year of postnatal life. This first year of postnatal life is when infants gain greater control of their body and progress from lifting their heads to rolling to crawling and eventually begin to stand and walk. This maturing motor control is due to greater myelination. The myelination process continues into the adult years.

Some children suffer from a recessive genetic disorder called hypomyelination. In this condition, children have a reduced ability to produce myelin. Developmentally, these children are normal up to about 1 year of age, but then development slows. As they continue to age, they experience paresis, muscle atrophy, neuropathy, cataracts, dysarthria, and mild to moderate intellectual disability (NIH, 2009a).

► Functional Development of the Infant Brain

Ultrasound technology has provided a window into prenatal development, allowing detailed observations of fetal behavior over the course of pregnancy. Fetal movements involving flexion and extension of the trunk begin in the first trimester (0-12 weeks) at around 10 to 12 weeks of gestation. Reflexes, such as the startle reflex, begin to be evident as early as 10 weeks. At 12 weeks, the fetus displays isolated movements of the head and limbs. Head movements include head rotation and flexion. Facial behaviors such as eye blinking, mouthing, yawning, tongue protrusion, smiling, grimacing, sucking, swallowing, and hiccupping emerge in the second trimester (13-28 weeks). Head behaviors (e.g., rotation) become more frequent as well as moving the hands to the head, mouth, eye, face, and ear. The frequency of these second trimester movements becomes more numerous in the third trimester (29-40 weeks). At 36 weeks, these movements become more highly coordinated (Du Plessis, 2013; Kurjak et al., 2005).

As can be seen, the structural growth of the nervous system corresponds to the functional developmental of the fetus. Neuron proliferation, migration, and organization lead to greater connections between the brain and the body and thus more coordinated movements of the head, trunk, and limbs.

► The Development of the Adolescent Brain

The beginning of adolescence is marked by the beginning puberty, which typically begins at 10 to 11 years of age in girls and 11 to 12 years in boys. Parents often note this change from childhood to adolescence through a change of behavior. For example, a family friend reported the following regarding her teenage daughter: “She gets mad really easily. I wonder if it’s because she stays up so late and sleeps so long in the morning. The warm, funny, affectionate child I knew seems to be gone, replaced by a moody stranger.” Though this change is shocking for parents, those familiar with neurodevelopment at this age will say that this behavior is typical for adolescence. For the teen in this example, her body as well as her brain are changing, and much of the moody behavior is tied to these changes. The good news for parents is that it will get better as the teen moves through adolescence and enters adulthood.

Adolescence is a period of profound brain development. Previously it was thought that brain development was complete by adolescence, but now we know that this development is not complete until about the age of 25 years. What is the nature of this profound brain development? Synapses are overproduced until just before puberty and then are pruned in adolescence, which increases the responsiveness of neural networks. In addition, gray matter thins as these excess synaptic connections that are not used are eliminated. During this pruning process, the brain is not functioning optimally, and adolescents will typically struggle with tracking multiple thoughts and focusing their attention. Overall, this brain development through synaptic pruning begins in the back of the brain and moves forward to the front of the brain to the prefrontal cortex (FIGURE 2-16). We know that the prefrontal cortex is crucial for three main functions: restraint, organization, and initiative—three functions with which teens struggle. If teens are not relying fully on their prefrontal cortex, then the question is, what are they relying on? The answer would be their emotional processing system (i.e., amygdala), which explains why teens react emotionally and misinterpret emotional cues from others (Giedd, 2004; Powell, 2006).

All of this discussion leads to the conclusion that (1) the adolescent brain is very plastic (i.e., malleable and changeable), and (2) an understanding of adolescent brain development helps to explain much of adolescent behavior. Adolescents rely more on their feelings and impulses rather than logic and planning because the prefrontal cortex has not fully developed. This leads to less-than-ideal planning and judgment and potentially to risky, impulsive behavior. Laurence Steinberg, a professor of psychology, summarizes the teen brain this way: “It’s like turning on the engine of a car without a skilled driver at the wheel” (Wallis & Dell, 2004).

FIGURE3-16 Back to front development of the adolescent brain. Red shows more gray matter, and blue shows less gray matter. Gray matter wanes as the brain matures and neurons are pruned. Areas for basic function mature early, higher executive functions later.

► The Brain in Normal Aging

In normal aging, the brain experiences both structural and chemical changes. Structurally, the brain loses neural circuits and, thus, loses plasticity. In addition, the cortex thins due to a decrease in both gray and white matter. Even neurons show structural change as dendrites thin and decrease in numbers. Chemically, there are decreases in neurotransmitter levels (e.g., glutamate, dopamine, serotonin) and a decrease in the number of receptor sites available for these chemical messengers. Behaviorally, these brain changes can be seen in older, healthy adults as deficits in some memory skills (e.g., working memory), attention, learning, and language (Burda, 2011).

► Conclusion

The development of the nervous system is a complex process. About 3 weeks after fertilization, the neural tube develops. The superior end of the neural tube develops into the face and brain. As the brain develops, neurons proliferate and migrate to their proper spots in the nervous system. Synapses form as the cerebral cortex further organizes itself. Neuron axons are then myelinated, leading to more efficient neural firing, as shown by an infant’s motor development. Synapses continue to be developed during childhood but are significantly pruned back during adolescence. As a person ages, the cerebral cortex thins due to a decrease in both gray and white matter. These changes, along with chemical changes in the brain, lead to the types of cognitive decline we see in normal, healthy aging.

SUMMARY OF LEARNING OBJECTIVES

The following were the main learning objectives of this chapter. The information that should have been learned is below each learning objective.

1. The learner will define important neuroembryonic terms.

• Gestational age (GA): the age of a baby measured against the mother’s last menstrual period

 Germinal stage: when an egg is fertilized by a sperm and becomes a morula

 Morula: an early stage of the embryo when it is a solid ball of cells

 Neural tube: a tube that forms from an embryo’s ectoderm, which will become the nervous system

 Neural tube defect (NTD): a defect in the formation of the neural tube

2. The learner will list and briefly describe the structural development of the nervous system.

 Dorsal induction: Occurs at a GA between 3 and 7 weeks and is when the neural tube is formed.

 Ventral induction: Occurs at a GA between 2 and 3 months and is when the face and brain begin to develop.

 Neural proliferation: Occurs at a GA between 3 and 4 months and is when nervous system cells are created.

 Neuronal migration: Occurs at a GA between 3 and 5 months and is when nervous system cells begin to migrate in waves from the inside of the brain where they were produced to the outer layers of the brain.

 Cortical organization and synapse formation: Occurs at a GA between 4 months and years postnatal and is when neurons sprout projections and make connections.

 Myelination: Occurs between birth and years postnatal and is when axons receive their coating of myelin.

3. The learner will list and describe common birth defects.

 Encephalocele: a neural tube defect in which a malformed portion of the brain protrudes through the skull

 Anencephaly: a neural tube defect in which neurological development ceases with the development of the brainstem, leaving the infant without cerebral hemispheres

 Spina bifida: a neural tube defect that leaves a cyst on an infant’s back, which sometimes has spinal cord fibers in it, leading to possible motor and sensory issues

 Holoprosencephaly: a condition in which the brain fails to cleave, leaving the infant with little to no hemispheric development

 Microcephaly: a failure in neuron proliferation, leaving an infant with a small brain and a small skull

 Schizencephaly: a condition that involves clefts in the cerebral hemispheres

 Lissencephaly: a condition in which the brain does not have its normal convolutions and appears smooth in appearance

 Polymicrogyria: a condition involving insufficient cortical organization, leaving infants with too many gyri in their cerebral hemispheres

 Hypomyelination: a genetic condition in which children do not produce enough myelin, leading to serious motor and sensory issues

KEY TERMS

Anencephaly Dorsal induction Ectoderm Encephalocele Holoprosencephaly Hypomyelination Lissencephaly Microcephaly

Neural plate

Neural tube

Neural tube defects (NTDs)

Neurogenesis

Neuropores

Neurulation

Polymicrogyria

Rhombencephalon

Schizencephaly Spina bifida (SB) Synaptic pruning Synaptogenesis Telencephalon Ventral induction

DRAW IT TO KNOW IT

1. Draw your own flowchart illustrating the processes of mitosis and meiosis.

2. Look at Figure 3-5 and draw the formation of the neural tube.

QUESTIONS FOR DEEPER REFLECTION

1. Compare and contrast the processes of mitosis and meiosis.

2. How are chromosomes different than genes?

3. Explain the six stages of nervous system development.

4. Given the six stages of nervous system development, discuss what disorders can occur in each stage.

CASE STUDY

Michelle is a pregnant mother just about at full term at almost 40 weeks. During a routine obstetrician visit, the physician measured around her belly and remarked, “This baby is small for being 37 weeks.” Michelle responded that she is not 37 weeks pregnant, but rather almost 40 weeks pregnant. The obstetrician looked quickly at the medical chart, realized her error, and stated, “The baby shouldn’t be this small at almost 40 weeks. We need to admit you to the hospital and induce labor.” Labor was induced, and Michael was born weighing just 3 pounds, 7 ounces (1.7 kilograms).

It was observed at birth that Michael was missing fingers on his left hand, displayed webbing between his fingers and toes, and had microcephaly. Later, Michael was diagnosed with Cornelia de Lange syndrome (CdLS), a rare genetic condition caused by a sporadic gene mutation.

1. What is microcephaly?

2. At what stage of development does microcephaly occur?

3. How does microcephaly relate to neurogenesis?

SUGGESTED PROJECTS

1. Pick one of the developmental neurological disorders mentioned in this chapter and write a two- to three-page paper with the following: (a) a description of the disorder, (b) the cause, and (c) long-term effects.

2. Do further research on the adolescent brain and write a two- to three-page paper on your findings. In the paper, reflect on your own teenage years and how some of your behavior during those years might be explained by brain development.

3. Find a senior citizen (someone older than 65 years) and interview him or her about any changes he or she has noticed in cognition and/ or language. Write a summary of the interview in a two-page paper.

REFERENCES

Burda, A. N. (2011). Communication and swallowing changes in healthy aging adults. Burlington, MA: Jones & Bartlett Learning.

Centers for Disease Control and Prevention (CDC). (2018). Birth defects: Data and statistics. Division of Birth Defects and Developmental Disabiliities, National Center on Birth Defects and Developmental Disabiliities. Retrieved from https://www .cdc.gov/ncbddd/birthdefects/data.html

du Plessis, A. J. (2013). Fetal development. In M. L. Batshaw, N. J. Roizen, & G. R. Lotrecchiano (Eds.), Children with disabilities (7th ed., pp. 25-35). Baltimore, MD: Paul H. Brookes Publishing Company.

Giedd, J. N. (2004). Structural magnetic resonance imaging of the adolescent brain. Annals of the New York Academy of Sciences, 1021(1), 77-85.

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