Short and Long Term Affects on Fetal and Child Development When Exposed to Cocaine in Utero - Essay Example

Short and Long Term Affects on Fetal and Child Development When Exposed to Cocaine in Utero Case Study: My sister is pregnant and using cocaine regularly. I have explained to her that this is harmful and potentially fatal to her unborn child, but she feels that I am exaggerating. Upon researching the short and long term affects of cocaine to an unborn baby, I have accumulated the following information to provide her with: One of the first things functions that a new baby’s body will perform is self regulation. This is essentially the body’s ability to maintain homeostasis with fluctuating external conditions. An example of a changing external condition is temperature. One of the key survival mechanisms to the human body is the ability to maintain homeostasis (internal body conditions) with varying external conditions. Another aspect of self regulation is heart rate: “Specifically, HR is predictive of later cognitive development and may impact reactivity to external stressors. An elevated resting HR is indicative of a higher level of physiological arousal which impacts both the quality and quantity of infant responsiveness to stimulation” (Schuetze 2006). Clearly, an elevated infant heart rate can be indicative of over-stimulation and a precursor to later cognitive developmental delays. Other aspects of self regulation or homeostasis that are thought to be affected by cocaine use in utero are respiration, blood pressure, sleep patterns, and body temperature. Studies have also indicated that cocaine use by pregnant women reduces blood flow to the placenta and causes fetal vasoconstriction. The placenta is the virtual nutrient source for the fetus. Adequate blood flow to the placenta and overall placental health are critical to fetal health. Cocaine is responsible for inducing the release of certain body chemicals called serotonin and/or epinephrine. The release of these two chemicals has a direct affect on vascular tone and therefore affects the vascular health of the fetus as well as the placental blood flow. Fetuses which develop in utero with a less than healthy placenta experience both short and long term developmental effects as well as defects. If the integrity of the placenta is compromised by the use of cocaine, the resulting lack of blood flow can mean that the fetus is under nourished and under oxygenated. This can result in low birth weight, developmental delays, and even neurological damage. Based on a study conducted at the University of Florida, it can be said that the amount of cocaine used by a pregnant woman has a direct affect on the head circumference of her baby. In cases where babies were born after having been exposed to cocaine in utero, these babies had an altered head circumference and consequently experienced delayed preschool development. This is one example of long term affects experienced by children who are products of mothers who have used cocaine while pregnant. Cocaine is a type of stimulant which interferes with and affects certain neurological pathways: “Cocaine and the amphetamines block the ability of the dopamine (DA) transporter to remove dopamine from the synaptic cleft”(Battaglia et al, 1998). In the brains of individuals who use cocaine, the perfusion of the cerebral cortex is lowered. As a result, multiple biochemical pathways and mechanisms are interfered with, such as that of cortical neurons. For women who are pregnant and use cocaine, this means that not only are their brains being directly affected by the drug, but the brains of their unborn fetuses are also affected. The placenta, as mentioned earlier, acts as a nutrient source to the fetus. In addition, it also acts as a sort of barrier between the bloodstream of the mother and the bloodstream of the fetus. There are, however, certain drugs and chemicals which are able to pass through the placenta from the mother to the fetus. Cocaine is certainly able to pass this barrier and therefore affects not only the mother’s system who is using the cocaine, but also the system of her unborn baby. Frequent administration of cocaine as well as withdrawals from cocaine, can cause what is known as neurotoxicity, cell death, and neurodegeneration. This essentially means that cocaine users can and do suffer from the death of brain cells, loss or degeneration of brain cells, and toxic build up within brain cells. More specifically pertinent to the developing brain of an unborn fetus, cocaine has shown to directly interrupt and alter what is known as 5-HT systems: “During fetal brain development, 5-HT plays a trophic role in regulating the development of 5-HT neurons and the development of target tissues with which these neurons make synaptic contacts. Because drugs that alter fetal 5-HT systems have been shown to alter the development of 5-HT containing pathways, cocaine-induced alterations of fetal 5-HT also would be expected to produce changes in the development of brain 5-HT containing pathways” (Battaglia et al, 1998). During development in utero, brain formation is critical and permanent. In a study conducted at Drexel University, it was discovered that during neurological development in utero, exposure to cocaine can cause dysfunctional signal transductions involving dopamine D1 receptors. As a result, lasting morphological abnormalities in brain structures occurred. On the animals used for these experiments, permanent cognitive damage was noted as well as abnormalities in the ability to process stimuli and attention deficits: “ The long-term cognitive deficits observed in various species are in agreement with recent reports indicating that persistent attentional and other cognitive deficits are evident in cocaine-exposed children as they grow older and are challenged to master more complex cognitive tasks.”( Harvey, 2003). These findings were varied based on frequency and dose of the cocaine that was administered as well as the route of administration. Cocaine has a direct affect on the central nervous system. This is true not only of the individual who is taking the cocaine, but also applies to the central nervous system of the developing fetus within a cocaine user. Cocaine is responsible fro binding not only to dopamine and norepinephrine transporters but also to seratonin transporters. Ultimately this raises the concentration of monoamines within the synaptic cleft. The explanation for the “high” experienced by cocaine users is that norepinephrine transporter is blocked in sympathetic neurons. In addition, the central nervous system is affected by way of the blocking of dopamine transporter. Ultimately, when these mechanisms take place within a developing brain in utero, lasting and irreparable damage can result. Having examined immediate mechanisms that take place when cocaine enters the system of a fetus, it is relatively easy to assume that immediate effects of cocaine are in fact harmful to the developing neurological system. It is more difficult, however, to know the affects of cocaine on a long term basis as the child grows into adolescents. A recent study at Children’s Hospital of Philadelphia examined specifically the long term affects of cocaine on the neurological system: “Evidence from both behavioral and cytoarchitectural studies suggests that intrauterine cocaine exposure results in long-term detriments to the neural system”(Avant et al, 2007). This study was also able to identify brain lesions on neonates whose mothers had used cocaine frequently. Yet another finding of this study was a prevailing theme of attention deficit disorder among individuals whose mothers used cocaine heavily while pregnant. More specific studies have been conducted in order to narrow down exactly how much cocaine can affects fetal and infant development based on dosage and frequency of use. One such study conducted at Columbia University sought to establish whether fetal and infant neurological defects and behavioral issues resulting from prenatal cocaine use were a function of dosage quantity and frequency of use. This study was able to determine that developmental delays detected at six months of age as well as tone abnormality and posture abnormalities were all functions of prenatal cocaine use: “From the neurological perspective, we have identified abnormalities of tone and posture associated with cocaine exposure in a dose-dependent manner, that remained associated with prenatal cocaine exposure in analyses that adjusted for prematurity, birth weight, cigarette smoking and alcohol use during pregnancy”(Chiriboga, 2007). Yet another study conducted at the University of Pittsburgh Medical Center showed affects of prenatal cocaine use to be directly linked to motor development impairment, temperamental characteristics, physical and neurological development. This study is especially unique as it illustrates not only the physiological effects of cocaine on infants but also examines the temperaments and mood swings of effected infants, “Only a few investigators have studied the effects of prenatal cocaine use on infant temperament. Mayes et al reported that 3-month-old infants who were exposed to cocaine prenatally were more fussy and irritable during an information processing task than were non-exposed infants”(Richardson, 2008). Cocaine is also known to affect motor development. A study specific to the affects of cocaine on motor development conducted at Brown Medical School discovered that there is a direct correlation between intrauterine cocaine use and delayed motor skill development appearing within the first two years of growth: “ recent studies conducted on larger samples containing comparison groups appear to find consistent support for motor problems across the first 2 years of life in infants with in utero cocaine exposure”(Miller-Loncar et al, 2004). This study was able to identify coordination difficulties, hyper tonicity and neurobehavioral problems of children between the ages of infancy and two years old, that had been exposed to cocaine in utero. The affects of cocaine are clearly more devastating than simply mild and temporary symptoms or delays. The effects of cocaine introduced within utero are obviously quite detrimental to intrauterine development, all the way through childhood development. Further studies have measured the delays and impairments in speech, hearing, language, and cognitive skills of children as old as 4 years of age who were exposed to cocaine in utero. These studies are not as definitive as to whether cocaine is directly responsible for specific hearing, speech and language impairments, but it can be said that children exposed to cocaine use while in utero are of higher risk to such impairments. Based on all of the empirical evidence from these credible studies conducted by medical and developmental professionals, I would strongly advise my sister to consider the well being of her unborn child and herself. It is clear that cocaine is not only detrimental to her health, but to the health of her child which depends on her for life and sustenance. Clearly, cocaine is a chemical substance which directly affects neurological, behavioral, and physical development of fetuses when consumed by their pregnant mothers. In conclusion, I would admonish my sister strongly for writing my advice off as “exaggeration” when the documented, empirical evidence of the studies discussed have provided credible, scientific proof that cocaine is absolutely unhealthy and dangerous to unborn babies. Lastly, I would encourage my sister to seek the help of trained professionals, in order to safely discontinue the use of cocaine while pregnant. Works Cited: Avant PhD., Brian A. Hurt MD., Hallam. Giannetta BA., Joan. Epstein PhD., Charles. Shera ScD., David M. Rao PhD., Hengyi. Wang PhD., Jiongjiong. Gee PhD., James. “Effects of Heavy in Utero Cocaine Exposure on Adolescent Caudate Morphology” Pediatric Neurology vol. 37 Issue 4 (October 2007) p. 275-279 Battaglia, George. Napier, T. Celeste. “The Effects of Cocaine and Amphetamines on the Brain and Behavior: A Conference Report” Drug and Alcohol Direct vol 52 Issue 1 (Sept 1, 1998) p 41-48. Behnke MD, Marylou. Davis-Eyler PhD., Fonda. Duckworth-Warner PhD, Tamara. Wilson-Garvan PhD, Cynthia. Hou MS, Wei. Wobie MA, Kathleen. “Outcome from a Prospective , Longitudinal Study of Prenatal Cocaine Use: Preschool Development at 3 Years of Age.” Journal of Pediatric Psychology 31(1):41 (2006) p.1-9 Chiriboga, Claudia A. Kuhn, Louis. Wasserman, Gail A. “Prenatal Cocaine Exposure and Dose Related Cocaine Effects on Infant Tone and Behavior” Neurotoxicology and Teratology vol. 29 Issue 3 (May-June, 2007) p. 323-330 Harvey, John A. “Cocaine Effects on the Developing Brain: Current Status” Neuroscience and Biobehavioral Reviews vol. 27 issue 8 (January, 2003) p. 751-764 Miller-Loncar, Cynthia. Lester, Barry M. Seifer, Ronald. Lagasse, Linda L. Bauer, Charles R. Shankaran, Seetha. Bada, Henrietta S. Wright, Linda L. Smeriglio, Vincent L. Bigsbey, Rosemarie. Liu, Jing. “Predictors of Motor Development in Children Prenatally Exposed to Cocaine” Neurotoxicology and Teratology vol 27 Issue 2 (March - April, 2005) 213 - 220 Richardson, Gale A. Goldschmidt, Lidush. Wilford, Jennifer. “The Effects of Prenatal Cocaine Use on Infant Development” Neurotoxicology and Teratology vol. 30 Issue 2 (2008) p. 96-106 Schuetze PhD., Pamela. Eiden PhD., Rina. “The Association Between Maternal Cocaine Use During Pregnancy and Physiological Regulation in 4 to 8 Week Old Infants: An Examination of Possible Mediators and Moderators” Journal of Pediatric Psychology 31 (1): 15. (2006) 1-12. Wesson-Cone, Barbara. “Prenatal Alcohol and Cocaine Exposure: Influences on Cognition, Speech, Language and Hearing” Journal of Communication Disorders vol 38 Issue 4 (July-August, 2005) p. 279-302 Read More