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Prenatal Drug Abuse and It Nuerodevelopmental Effects and Policies and Education

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Discussion- Problems with defining use patterns and the misunderstanding of the public; it is difficult to explain the effects of prenatal drug exposure on the brain. Using research on animal models, scientists are able to correlate the findings with human clinical findings. The scientific research needs to be conveyed to the public in a manner so there is no misinterpretation.

The use of animal models enables scientists to further the research of neurodevelopmental and neurobiological consequences from prenatal exposure to drugs. There are many human and animal variables that must be taken into consideration when creating the ideal animal model. For animals: species, age of the embryo during exposure, length and how often of exposure, drug amount taken at a time, and how the drug was taken. The human mother has to give accurate information of nutritional issues, the length of drug exposure, amount when taken, and any combining of drugs, in order to create clinical profiles and to use the data on the animal model. Knowing the neurodevelopmental timeline of humans and the animals used as models, scientists are able to create exposed animal models during the stages of animal fetus development that best match up with the exposure timing in human pregnancy.

Limited on space, Thompson, Levitt, and Standwood use cocaine, amphetamine and methamphetamine as descriptions for illegal drugs, and nicotine, alcohol, and antidepressant medications for legal. Administration of different drugs vary, cocaine is used more in episodes, whereas nicotine and alcohol have a tendency to be used more regularly. The various drugs and use patterns are important in researching the effects of prenatal drug exposure.

Due to small sample sizing, use of multiple drugs, and lack of information on nutritional issues and psychosocial problems, early reports of prenatal exposure to cocaine, children were thought to be emotionally disruptive, less likely to be socially interactive, and more likely to die from sudden infant death syndrome; introducing the term "crack baby" to describe the prenatally exposed children. It is now proven that prenatal cocaine effects on the brain development vary. Studies do show there are long-term consequences to prenatal cocaine exposure, behavioral dysfunctional are actually mild. Results show that recreational use of cocaine during pregnancy led to the development of Attention Deficit Hyperactivity Disorder (A.D.H.D.). There are also long-term negative effects on the cognitive and attention systems, and increased possibility the child will require to be in special needs programs.

Observations done on an intravenous model of a prenatal cocaine exposed rabbit (resembles the human pharmacokinetic profile), shows the changes in the cortex and the dopamine receptors involved with cognitive functions and attention. Also, the study says the second trimester might be the most vulnerable to cocaine exposure. Other animal models studied shown that prenatal cocaine exposure changes the process of neocortical development that includes cell production and movement.

There is limited research on long-term consequences of prenatal exposure to amphetamines and methamphetamines. Studies have shown that children who were prenatally exposed showed decreased arousal, increased stress, low birth weight, and movement problems. Neurocognitive tests shows prenatally exposed children scored lower on sustained-attention, long-term spatial and verbal memory, and visual motor-integration tests.

Animal tests have shown lower birth weights, smaller and more numerous convolutions in the cerebral cortex, defects in visual development, impaired motor movement, trouble learning, easily startled, and less inhibition. Also, impaired sensory-motor conditions caused from prenatal methamphetamine exposure can be passed down to the next generation offspring.

Nicotine, a proven teratongenic, is usually smoked and can cause decreased birth weight and premature birth, both are factors that can lead to behavioral impairment. Also, smoking increases the risk of sudden infant death syndrome. The variety of tobacco, different amounts of nicotine, and the additional chemicals in tobacco products make it challenging to find the effects nicotine has on the exposed fetus. This factor makes it hard for clinicians to have pregnant women who want to quit smoking use nicotine-replacement therapy (NRT). NRT has none of the additional chemicals that are found in tobacco products, but still have high amounts of nicotine. The transdermal patch may actually be worse for the fetus than if the mother actively smokes. Animal models using the patch showed fetal brain nicotine levels three times higher than the maternal blood levels, because of the continuous release of nicotine from the patch. It has also been shown in animals that prenatal exposure to levels of nicotine equivalent to pregnant women that smokes a moderate-high amount of cigarettes lead to serious neurodevelopmental and neurobehavioral problems.

Prenatal exposure to alcohol causes intellectual disabilities, problems with attention and motor development, and hyperactivity. Defects in the neurodevelopment caused by prenatal alcohol exposure are known as a disorder called Fetal Alcohol Syndrome. Animal models shown birth defects, neurological dysfunction; exposure through the entire gestgational process had huge teratongenic consequences. Prenatal exposure to alcohol may also lead to changes in behavior, cells, and cognition in adulthood.

More studies are being performed now on prenatal exposure to antidepressant medications because of a report that children from mothers who used certain serotonin reuptake inhibitors during pregnancy had higher cardio abnormalities. Health-care professionals face a dilemma with drug treatment for pregnant women with psychiatric illness. They have to decide between the possible neurodevelopmental problems caused from the drug treatment or negative possibilities caused from maternal stress caused by depression or neurochemical imbalances that were not treated.

"Framing" is described as combining partial information into one whole perception of something. For example, the term "crack baby" came from the public's perceptions that pregnant mothers who did cocaine had far worse impact on a fetus because of exposure to an illegal drug. The public lacked the knowledge of maternal stress caused from multiple drugs and malnutrition, and because scientist and the press showed no documentation of biological and behavioral effects. In order to change a frame, we must identify values and explanations that make society goals obvious. The best way is to make simple models of brain development which will show the impact drugs and stressors have on the process. This can show that certain drug policies may

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