ASSIGNMENT: FETAL DEVELOPMENT

ASSIGNMENT: FETAL DEVELOPMENT ASSIGNMENT: FETAL DEVELOPMENT Assignment: Environmental and Genetic Impact on Fetal Development Both environmental and genetic influences impact fetal development. Some substances (e.g., folic acid, hormones, etc.) have the biggest influence at sensitive periods during gestation. Early in gestation, when neurological development is at its peak, folic acid is most important. Hormones, such as androgen and estrogen, are necessary for external genital differentiation between 9 and 12 weeks of gestation. Prenatal alcohol exposure, however, can impact fetal growth at any time during gestation. On the other hand, environmental influences such as maternal genetics, nutrition, health, and immunization can have a positive impact on fetal development, mitigating the impact of substances and other negative influences. In addition to environmental influences, you must also consider the impact of genetic influences. Genes determine not only an individual’s physical features at birth—they also contribute to hormonal processes throughout the lifespan. The interaction of environmental influences and genetic influences impacts the development of a fetus. Permalink: https://nursingpaperessays.com/ assignment-fetal-development / ? For this Discussion, you will examine environmental and genetic influences on fetal development. To prepare for this Discussion Assignment: Fetal Development: · Select one genetic influence and one environmental influence on fetal development and think about how these influences might impact each other. By Day 4 of this Assignment: Fetal Development Post a brief description of the genetic influence and the environmental influence you selected. Then, explain how the environmental influence might positively or negatively affect the development of a fetus with the genetic influence you selected. Be specific and provide examples. Use your Learning Resources to support your post. Use proper APA format and citations. Berk, L. E. (2014). Development through the lifespan (6th ed.). Upper Saddle River, NJ: Pearson Education. Chapter 2, “Genetic and Environmental Foundations” (pp. 44–77) Chapter 3, “Prenatal Development, Birth, and the Newborn Baby” (pp. 78–117) Charness, M. E., Riley, E. P., & Sowell, E. R. (2016). Drinking during pregnancy and the developing brain: Is any amount safe? Trends in Cognitive Sciences, 20 (2), 80–82. doi:10.1016/j.tics.2015.09.011 Note: You will access this article from the Walden Library databases. Entringer, S., Buss, C., & Wadhwa, P. D. (2015). Prenatal stress, development, health and disease risk: A psychobiological perspective—2015 Curt Richter Award Paper. Psychoneuroendocrinology, 62 , 366–375. doi:10.1016/j.psyneuen.2015.08.019 Note: You will access this article from the Walden Library databases. Tzouma, V., Grepstad, M., Grimaccia, F., & Kanavos, P. (2015). Clinical, ethical, and socioeconomic considerations for prescription drug use during pregnancy in women suffering from chronic diseases. Therapeutic Innovation & Regulatory Science, 49 (6), 947–956. doi:10.1177/2168479015589820 Note: You will access this article from the Walden Library databases. Grace, T., Bulsara, M., Robinson, M., & Hands, B. (2015). The impact of maternal gestational stress on motor development in late childhood and adolescence: A longitudinal study. Child Development, 87 (1), 211–220. The Impact of Maternal Gestational Stress on Motor Development in Late Childhood and Adolescence: A Longitudinal Study by Grace, T., Bulsara, M., Robinson, M., & Hands, B., in Child Development, 2015/October. Copyright 2015 by John Wiley & Sons-Journals. Reprinted by permission of John Wiley & Sons-Journals via the Copyright Clearance Center. Retrieved from https://www.researchgate.net/profile/Tegan_Grace/publication/282873739_The_Impact_of_Maternal_Gestational_Stress_on_Motor_Development_in_Late_Childhood_and_Adolescence_A_Longitudinal_Study/links/56244b7d08ae70315b5db881.pdf March of Dimes Foundation. (2016). Retrieved from http://www.marchofdimes.org Centers for Disease Control and Prevention. (2016). Birth defects. Retrieved from http://www.cdc.gov/ncbddd/birthdefects/index.html Prenatal Development Assignment Case Study Paper Prenatal Development Assignment Case Study Paper PRENATAL DEVELOPMENT STEP 1: TED Talk and Reflection Watch the following Ted Talk on the visualization of prenatal development: Answer the following 2 questions: 1. Describe two things you found interesting and/or surprising. 2. What do you want to learn more about prenatal development? STEP 2: 1. Choose ONE article from the list below. Prenatal Development Assignment Case Study Paper High-Stress Pregnancies Slow Childhood Development, Study Warns http://time.com/3757864/air-pollution-babies/ http://www.cnn.com/2016/08/19/health/pregnancy-adhd-unhealthy-diet/index.html http://www.cnn.com/2017/01/02/health/parental-obesity-child-development/index.html Answer the following 2 questions: 1. Identify the article you chose from above. Why did you choose that specific article? What made you interested in that subject? Prenatal Development Assignment Case Study Paper 2. Summarize the article. Be thorough. Explain the article as if you were telling someone who had not read it. STEP 3: TED Talk and Reflection Watch the following Ted Talk on what we learn before we are born: Prenatal Development Assignment Case Study Paper Answer the following 2 questions: 1. Describe some of the studies that Annie Murphy Paul discusses. What do they tell us about learning in the womb? 2. What did you learn and/or find interesting about this TED Talk? Prenatal Development Assignment Case Study Paper Prenatal Development and Infancy Research Paper – Essay This sample Prenatal Development and Infancy Research Paper is published for educational and informational purposes only. If you need help writing your assignment, please use our research paper writing service and buy a paper on any topic at affordable price. Also check our tips on how to write a research paper, see the lists of psychology research paper topics, and browse research paper examples. Birth, of course, does not mark the beginning of human development; rather, development begins at conception. Although much of prenatal development occurs within the physical domain, developments in the cognitive and psychosocial domains also emerge at this time. Moreover, although these developments are driven by genetic and maturational forces, experiential factors also play an influential role during this period. Within this research-paper, we address some major areas of prenatal development: sensory experience, neurobehavioral functioning, and teratogenic risks. Postnatally, the period of life known as infancy traditionally consists of the first two years following birth, and it is during this period that often dramatic and rapid developments take place in all domains. Some of the most important of these phenomena, including brain development, visual and auditory perception, cognitive development, temperament, and attachment, are reviewed in the remainder of this chapter. While discussion of the selected topics provides a glimpse into the array of developments occurring during gestation and infancy, they are necessarily limited in their overview of the vast number of changes and issues that have been studied during these earliest phases of life. The reader is thus strongly encouraged to review additional sources for a discussion of subjects such as fetal programming, prematurity, language, and social cognition that are also germane to prenatal and/or infant development. Sensory Development Even though sensory development begins long before birth, it is inherently difficult to observe the responses expressed by the fetus. Early fetal chemosensory experience has been examined largely in animals, whereas most studies with human fetuses have investigated auditory responsiveness in the second half of gestation. Our primary sources for knowledge about sensory development in human fetuses derive from studies of prematurely born infants and research using sophisticated noninvasive techniques. For example, magnetic fields generated by active neurons in fetal brain tissue can be detected and used to examine a fetus’s response to auditory stimulation (Huotilainen, Kujala, & Hotakainen, 2005; Zappasodi, Tecchio, & Pizzella, 2001). Generally speaking, the senses become functional sequentially between 8 and 26 weeks, with touch developing first, then taste and smell, hearing, and finally vision. Touch Sensitivity to touch or pressure begins early in gestation and develops in a cephalocaudal direction (Field, 1990). By about 8 weeks of gestation, the fetus responds to touch on the area around the lips by moving. By 12 weeks, the fetus responds with a grasping movement when fingers are touched. During early gestation, the fetus typically responds by moving away from the source of stimulation. Later in gestation, the fetus tends to move toward the stimulation. For example, touch stimulation on the cheek of a fetus can elicit rooting-like responses, which later help the infant locate the source for nursing. Overall, the sensory abilities to detect touch, along with body motion, appear to be the most developed at birth (Field, 1990). Taste and Smell Scientists conclude that fetuses have gustatory and olfactory detection. However, with the exception of the taste for sweet, there has been no direct evidence for fetal chemo-sensory preferences. Flavors and odors from the mother’s diet do pass into the fetus’s amniotic fluid and bloodstream. Thus, the sensation of taste and smell can occur through the fetus’s nose, mouth, and bloodstream. When the fetus engages in breathing movements (beginning at about 10 weeks of gestation), amniotic fluid not only is swallowed but also passes through the nose after the plugs blocking the nostrils dissolve (James, Pillai, & Smoleniec, 1995; Schaal, Orgeur, & Rognon, 1995). Additionally, through blood circulation to the nose and mouth, the fetus has the opportunity to experience different smells and tastes (Schaal, 2005). Following birth, neonatal detection of a variety of odors and flavors is evident, with preferences emerging quickly (e.g., mother’s scent). Hearing The fetus’s auditory system develops gradually starting at around 6 weeks of gestation, and by 28 weeks it is sufficiently well developed to enable the fetus to reliably respond to sounds, typically with startle responses and increased heart rate (Lecanuet, Granier-Deferre, & Busnel, 1995). Within the uterine environment, the fetus is regularly exposed to its mother’s voice, gastrointestinal sounds, and heartbeat. During the last trimester, a fetus also appears to hear external sounds that pass through the uterine walls (Fernald, 2004). Vision At about 8 weeks of gestation, the lens, eyelids, and muscles controlling eye movement begin to develop. By 15 weeks, the integration of the optic nerve in each eye is complete. By 28 weeks, the development of the visual cortex in the brain resembles that in the adult. Although the fetus can open and blink its eyes for some time, it receives relatively little visual input before birth because of in utero darkness. However, if the fetus is born prematurely at this time, it can already detect changes in brightness (i.e., light and dark; Slater, 2004). Because the neural structure of the eyes and pathways to the brain are still immature, vision appears to be the least sophisticated of the senses and continues to develop substantially after birth. Neurobehavioral Development and Functioning The identification of fetal activity patterns and their underlying neural mechanisms is critical not only for understanding the beginnings of human behavior, but also for monitoring the fetus’s healthy development in the functioning of peripheral and central nervous systems. Most knowledge about neurobehavioral development in the fetus has been generated by real-time ultrasound and Doppler-based electronic fetal monitors (DiPietro, 2005). Four aspects of fetal functioning are typically involved in a multidimensional neurobehavioral assessment: motor activity, heart rate, behavioral state (e.g., from active to inactive), and responsivity to stimulation (DiPietro, 2005). Motor Activity Movements first appear between 7 and 16 weeks of gestation. The development of fetal movements shows an increase in repertoire. Movements include both large generalized movements (e.g., startle, stretch, rotation, and breathing) and movements of specific body parts (e.g., head, eyes, fingers, jaw opening, yawn, and hand-face contact). Initially, movements tend to appear scattered in a random fashion, but gradually the occurrences of movements are more coordinated and clustered together into bursts, and finally into longer periods of fluctuating activity (Robinson & Kleven, 2005). Although there are individual differences in the quantity of movements among fetuses, they occur less frequently but with more vigor during the second half of gestation (DiPietro, Hodgson, & Costigan, 1996). Increasingly longer periods of inactivity are common as fetuses mature. Thus, motor inhibition is believed to also be a significant marker for neurological development. Fetal Heart Rate The heart rate in healthy fetuses is almost twice that of adults, fluctuating between 120 and 160 beats per minute. Cycles of increased and decreased variability in baseline heart rate can be observed throughout the day. Whereas spontaneous accelerations indicate responsiveness in the sympathetic nervous system, general trends in the rate and variability of fetal cardiac activity reflect the maturation of the nervous system. Overall, heart rate shows a pattern of decrease in rate and increase in variability during the prenatal period. However, decelerations after 28 weeks tend to be markers of pathology. Contrary to some common beliefs, fetuses’ heart rates are not in synchrony with their mothers’ heart rates. In a quiet and resting condition, a mother’s heart rate does not influence fetal heart rate, or vice versa (DiPietro et al., 2006). Furthermore, the presence of heart rate acceleration coupled with fetal movements is viewed as a sign of fetal well-being. Increases in the coordinated coupling between the two different systems indicate the integration of the central nervous system. Behavioral States Behavioral states are relatively stable periods characterized by coordinated patterns in the fetus’s eye and motor movements as well as heart rate activity. Beginning at about 28 weeks, the fetus begins to show rest-activity cycles. Four fully developed behavioral states can be detected at around 36 weeks: quiet sleep, active sleep, quiet awake, and active awake (de Vries & Hopkins, 2005). The quiet sleep state features the absence of eye movements and a stable heart rate within a narrow range. The active sleep state is characterized by eye movements, a wider range of heart rate oscillation, and periodic stretches and gross body movements. The state of quiet awake is characterized by the absence of gross body movements, a stable heart rate with a wide range of oscillation, and the absence of heart rate acceleration. The active awake state features the presence of eye movements and continuous, vigorous activities with unstable and large accelerations in heart rate. Compared to neonates, fetuses take a longer time to complete a state change and make fewer transitions between quiet and active sleep states. Because behavioral states are believed to reflect neural functioning, and therefore fetal health, observations of fetal states can be used to discriminate abnormalities in pregnancy and growth retardation. Responsivity Fetuses respond to stimulation originating outside of the uterus. Compared to airborne sound stimuli, fetuses respond to vibro-acoustic stimuli (comparable to an electric toothbrush) with greater heart rate accelerations and more body movements. In response to repeated presentation of stimuli, a pattern of decreased response (i.e., habituation) reflects healthy fetuses’ capacity for self-regulation and information processing. Conclusion Fetal neurobehavioral development is predictable. Overall, it goes through a transition of rapid changes with decreased heart rate, increased heart rate variability, and increased movement-heart rate coupling between 28 and 32 weeks of gestation, after which the development levels off and a stable pattern is established ( DiPietro, 2005). Because similar patterns of coupling and/or disassociation (e.g., between fetal movement and heart rate) are found among fetuses, it is assumed that these fundamental properties of neurobehavioral development prior to birth are universal (DiPietro et al., 2006). Future research will need to explore the underlying mechanisms and experiential factors that may facilitate or impede fetal development and functioning. Teratogens Traditionally, teratology is the study of physical damage in the embryo or fetus caused by prenatal exposure to foreign substances. More recent teratology focuses on the impact to the developing central nervous system and its manifested behavioral consequences (Fried, 2002). The most common teratogenic risk factors linked to children’s negative outcomes have been prenatal exposure to maternal use of tobacco, alcohol, or cocaine. According to the Substance Abuse and Mental Health Services Administration (2005), approximately 18 percent of pregnant women in the United States reported smoking cigarettes, 9.8 percent reported drinking alcohol, and 4 percent reported using at least one illegal drug in the previous month. Tobacco Cigarette smoking is known to directly deliver chemical toxins to the fetus through the mother’s bloodstream, and thus may influence the developing brain and cause neurophysiological deficits. Prenatal exposure to maternal smoking is associated with an array of problematic physical and behavioral outcomes in both perinatal and postnatal periods such as reduced fetal growth, disruptive fetal heart rate regulation, preterm delivery, perinatal mortality, and suboptimal neonatal neurobehavioral functioning (e.g., increased tremors and startling and increased distractibility; Zeskind & Gringras, 2006). The negative effects of prenatal smoking often persist into childhood and adolescence. For example, longitudinal studies found that offspring of mothers who smoked during pregnancy show an increased risk for exhibiting oppositional behavior, criminal offending behavior, and smoking behavior (Buka, Shenassa, & Niaura, 2003; Gibson, Piquero, & Tibbetts, 2000; Montreaux, Blacker, & Biederman, 2006). Even when mothers did not smoke cigarettes during pregnancy but were exposed to environmental tobacco smoke (i.e., secondhand smoke), adverse perinatal effects have been demonstrated. Schuetze and Eiden (2006b) found that infants of both mothers who were exposed to secondhand smoke and mothers who smoked cigarettes had a significantly increased baseline heart rate and decreased heart rate variability compared to infants of mothers who had no exposure to cigarette smoke; these outcomes suggest a compromised nervous system. Moreover, this same study documented a dosage effect of prenatal direct and indirect exposure to cigarette smoking on compromised neonatal neurophysiological functioning. Alcohol In 2002, over 50 percent of women in their childbearing years drank alcohol without using birth control, and thus potentially were at risk for pregnancy complicated by teratogenic exposure (Centers for Disease Control and Prevention, 2004). The detrimental effects of prenatal alcohol exposure range along a continuum, downward from fetal alcohol syndrome, the most severe result of exposure, to alcohol-related birth defects, alcohol-related neurodevelopmental disorders, and, finally, specific cognitive and psychosocial deficits. Because impairments are not limited to the most severe form of exposure, even low levels of maternal alcohol use during pregnancy may cause potential harm. Prenatal alcohol exposure is linked to a host of cognitive deficits, including mental delays and problems in attention, memory, learning, problem solving, planning of actions, and state regulation (e.g., Howell, Lynch, Platzman, Smith, & Coles, 2006). Emerging evidence shows that these problems begin as early as infancy and often persist into adulthood (O’Connor & Paley, 2006). Researchers have hypothesized that central nervous system abnormalities caused by prenatal exposure to alcohol result in attentional difficulties, which in turn impact higher-order cognitive processes and subsequently compromise functioning. In addition to cognitive deficits, prenatal alcohol exposure is found to be associated with psychosocial problems, including hyperactivity, aggressive behavior, depression, poor interpersonal skills, and psychiatric disorders (O’Connor & Paley, 2006). Cocaine Much of the recent research on the effects of prenatal drug exposure has focused on cocaine. Evidence suggests that detrimental effects of prenatal cocaine exposure are modest but consistent on neurobehavioral functioning, physiological regulation, motor development, frustration reactivity, attention and arousal regulation, and language (Beeghly et al., 2006; Bendersky, Bennett, & Lewis, 2006; Dennis, Bendersky, Ramsay, & Lewis, 2006; Schuetze & Eiden, 2006a). Research also has suggested a dosage effect of prenatal cocaine exposure on particular outcomes. Infants who had higher levels of exposure to cocaine showed smaller birth head size, more compromised physiological regulation, and more negative engagement with their mothers than did infants with less prenatal exposure (Behnke et al., 2006; Schuetze & Eiden, 2006a; Tronick et al., 2005: Prenatal Development Assignment Case Study Paper). Follow-Up Risk Prenatal exposure to maternal smoking, alcohol, and/or cocaine use is related to some common long-term neurobehavioral and cognitive outcomes, including attention deficit and hyperactivity disorder, decreased cognitive functioning, and deficits in learning (Huizink & Mulder, 2006). The teratogenic insult of prenatal exposure on long-term impact is usually compounded by developmental risks associated with being reared by a substance-abusing parent. Oftentimes, maternal substance use or abuse is a marker of social and psychological problems in the childrearing environment. In other words, in addition to direct effects of maternal prenatal use of tobacco, alcohol, and/or cocaine on the fetus, adverse outcomes may be due to indirect effects mediated through other, related risk factors such as the mothers’ low socioeconomic background, single parenthood, high stress levels, low social support, and deficits in parenting behaviors. For example, Schuetze, Eiden, and Dombkowski (2006) demonstrated that compared to women who did not smoke cigarettes during the prenatal period, women who smoked during pregnancy were insensitive and less affectionate to their newborn infants. This linkage can be further explained by high levels of anxiety and hostility in mothers who smoke cigarettes during pregnancy (Schuetze et al., 2006). Similarly, Tronick and colleagues (2005) reported that, compared to control dyads, levels of dyadic engagement were lower and more negative for infants and their mothers who used cocaine during pregnancy. This suggests that any impact of teratogenic risk of prenatal exposure to cocaine on offspring may be exacerbated by the poor quality of interaction between child and parent. The above evidence indicates that a simple explanation of teratogenic risk on subsequent problematic behavior may not be sufficient. More sophisticated research approaches are required to examine the complex relations between prenatal substance exposure and various environmental risk factors. Future research regarding teratogenic effects on child development should focus not only on the type, timing, and amount of substance exposure during pregnancy, but also on the joint contribution with multiple risk factors in the childrearing environment (Bendersky et al., 2006; Mayes, 2002). Moreover, researchers have reported that boys and girls may be differently affected by prenatal substance exposure. For example, compared to female neonates, male newborns’ autonomic regulation is more vulnerable to the negative effect of maternal smoking and secondhand smoke exposure (Schuetze & Eiden, 2006b). Prenatal cocaine exposure appears to have a stronger impact on language development in preschool-age girls (Beeghly et al., 2006), whereas it has a significant influence on boys’ frustration reactivity and aggressive behavior (Bendersky et al., 2006; Dennis et al., 2006). Thus, the effect of child characteristics such as sex and temperament in altering the relations between teratogenic risk factors and child outcomes should be considered. Finally, despite the existence of adverse effects, not all children are negatively impacted by prenatal substance exposure. Some resilient children are able to adapt positively and experience healthy development. In addition to understanding the risk of prenatal exposure to teratogens and their direct and indirect effects on child outcomes, investigating the protective factors in buffering against the risks also deserves research attention (Dennis et al., 2006). Infancy Brain Development Formation and Growth of the Brain Brain development begins remarkably early during the prenatal period and involves multiple processes and stages. During the second half of the first month of gestation, the brain begins to form from a neural plate through a process called neural induction. The neural plate then transforms into a tube shape through a process termed neurulation. One end of the neural tube develops into the brain and the other becomes the spinal cord. Problems in neural tube development lead to anatomical abnormalities in the brain and/or spinal cord (Couperus & Nelson, 2006). Once this basic structure of the brain is established, the next stage of development is the production of neurons (i.e., cells that transmit information). The brain houses billions of neurons. The process of proliferation begins in the neural tube at five weeks of gestation, reaches its peak at three to four months of gestation, and is largely complete by the end of the second trimester. At the peak, it is estimated that several hundred thousand new cells are generated each minute. The new cells transform from uncommitted cells to differentiated neurons when they travel to their final location in specific regions of the brain. This process of migration begins at six weeks gestation and continues through four to five months after birth (Nelson, de Haan, & Thomas, 2006). Once a neuron has migrated into its final location, the cell further differentiates and develops. Each neuron consists of a cell body and two ends—axons and dendrites. The primary function of neurons is to process and communicate information. Axons send out information, while dendrites pick up information from other cells. Whereas the proliferation and migration of neuronal cells occur primarily during the prenatal period, the production and growth of axons and dendrites begin at 15 weeks of gestation and continue after birth. The dendrites in some regions of the brain continue to develop throughout the first two years after birth. Despite massive growth and rapid differentiation, neurons also are eliminated through a normal process of apoptosis (i.e., programmed cell death). It is estimated that 40 percent to 60 percent of all neurons may die naturally during embryonic or fetal development (Buss, Sun, & Oppenheim, 2006; Couperus & Nelson, 2006; Nelson et al., 2006). The establishment of connections within the brain occurs when axons and dendrites come together to form synapses so that information can be transmitted between neurons. A healthy, functional brain is one with a vast array of connections. The first synapses can be observed by 23 weeks of gestation, with the peak of production (i.e., synaptogenesis) at the end of the first year after birth; production continues until adolescence (Kagan & Herschkowitz, 2005; Nelson et al., 2006). It is estimated that 40 percent more synapses than the final number found in adults are produced (Nelson et al., 2006). Thus, the process of synaptic pruning also takes place to eliminate excessive production in synapses. The occurrence of synaptic pruning appears to vary by brain regions, with some reaching adult numbers of synapses by two years after birth while others do not do so until late adolescence. It is believed that the level of communication among neurons determines the pruning. Active synapses are strengthened, whereas inactive synapses are pruned. The pruning process can occur either quantitatively (i.e., overall reduction in number) or qualitatively (i.e., elimination of incorrect or abnormal connections; Nelson et al., 2006). The last process of brain development is myelination. Myelin is a fatty substance that surrounds and insulates axons to increase the speed and efficiency in transmitting signals. It first appears during the last trimester of the prenatal period. In some brain regions, this process continues until young adulthood or middle age (Kagan & Herschkowitz, 2005; Nelson et al., 2006). Plasticity of the Brain Within a period of seven months, a small group of cells transforms into a complete form of the adult brain, with six layers of cortex. The old belief was that brain development is based on a predetermined genetic process unfolding according to a fixed sequence and timing. New data suggests that even the early stages of brain formation are not determined by genetic factors alone; environmental factors also play an important part in the process. Soon after the anatomical structures are formed and connections are made, the brain begins to interact with itself and the environment. The ability for the brain to adapt to the change in itself and/or the environment is referred to as plasticity. Overall, during the prenatal period, neural connectivity is changed by internal spontaneous activity. After birth, there is a shift to the effect of external environmental inputs. Disease, metabolic disturbances, malnutrition, and trauma can produce maladaptive changes in the brain, whereas practice and learning can lead to adaptive functional changes in the brain. Furthermore, changes in one neural system can also influence the organization of another in the brain. For example, visual cortex areas in individuals who are born blind can be activated by Braille reading (a method of reading text through touch). Although many neural networks have a preferred connectivity pattern, this connectivity is not ixed because experience can alter the innate pattern. In response to exposure to certain experiences, the resultant changes in the brain may serve to maintain, reorganize, or even lose the initial pattern of connectivity. The newly reorganized brain can then serve as a foundation to facilitate the effect of subsequent experience, which can result in further neural changes. Such effects are referred to as cascading influences. For example, the prenatal experience of listening to speech leads to a preference for the rhythmical properties in native language, which further results in an ability to segment words from continuous speech (Werker & Tees, 2005). Evidence of functional brain reorganization also can be found in infants who are deprived of sensory input. For example, profoundly deaf children who received their cochlear implant (a surgically implanted electronic device that directly stimulates the functioning auditory nerves inside the cochlea with electrical impulses) before age two improved their performance of speech recognition and production more than those who had implantation after age four or five (Geers, 2006; Nicholas & Geers, 2006; Rubinstein, 2002). Clinical evidence for the loss of neural connections in infancy is also available. For example, repeated infections in the middle ear (i.e., otitis media) during infancy, which interfere with sound transmission due to fluid in the ear, can reduce experiential input and lead to deficits in phonetic categorization and difficulties in reading and spelling (see Werker & Tees, 2005). The evidence of plasticity in brain development has implications for early intervention. With the aid of devices such as cochlear implants, maintenance and reorganization of the neural structures is