Psychopharmacology - Research Psychology Essay Paper

Pharmacology of Autism
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Pharmacology of Autism
Autism is defined as a developmental and neurobiological disorder that results in lifetime disability and has these core clinical features that include impairment in social interaction, verbal and non-verbal communication, and repetitive as well as stereotyped patterns of behavior and activities. Autism is also associated with co-existing neuropsychiatric disorders that include seizure disorders, attention deficit hyperactivity disorders, anxiety as well as obsessive-compulsive disorder. Autism is often associated with different problematic behaviors that include self-injurious behaviors (SIB) alongside aggression that is harmful to patients and those around them. In this case, such physical disorder interrupts the normal functioning of the brain that eventually leads to drastic and significant behavior changes (Di Martino et al., 2014).
Etiology of the disorder
The etiology of autism spectrum disorder is widely debated over several years. According to research over the decades, there are suggestions that autism may be a result of genetic or environmental factors. Kern et al (2015), proposes that autism may be caused by a combination of the three factors that include; genetic factors, environmental factors as well as neurological development. The neurological underpinning that associated with autism involves the greater brain volume. In this case, the overgrowth of the early brain alongside related dysfunction provides the strongest evidence within the prefrontal cortex. Some of the overgrowth is identified within the regional gray and white matter that includes the temporary cortex as well as the amygdala. There are specific cognitive deficits that focus on disrupting effective communication as well as developing and maintaining social relationships. Such features are underpinned by the aspect of abnormal inhibitory control of the various motor as well as general cognitive skills alongside the typical face processing. However, there is also a partial explanation of the typical connectivity existing between the frontal lobe as well as the striatum that includes the basal ganglia and at the same time between the temporal cortex and amygdala. The effects are also associated with the regions that involve in social processing such as the fusiform gyrus, insula, and the medial prefrontal cortex. The existing impairments in the brain areas that sub-serves inhibitory control, emotions as well as communication and results into a range of related deficits within interpersonal interaction that entails remembering of problems as well as people identification, lack of sense to perceive social cues and the misunderstanding of non-verbal cues.
The data from Magnetic Resonance Imaging (MRI) shows that 90% of autistic children below the age of five portray a significantly larger brain volume as compared to neuro-typical controls (Di Martino et al., 2014). In this case, the increased brain volume correlates to the accelerated head size that is bigger in circumference. Young children with autism reveal excessive neurons within the prefrontal cortex. These children at the same time exhibit more cortical as well as cerebellar white matter as compared to controls. In the case of autism, there is abnormal pruning of excess neurons that eventually leads to the creation of abnormal white matter connectivity.
The concept of those with autism having social difficulties is associated with the nature of face processing in autism. There are high chances of the impairment of the brain areas involved in controlling the ability to process information from the faces. Individuals with autism have the tendency of neglecting the fusiform face area in the process of responding to faces. In normal circumstances, the neurotypical individuals use fusiform gyrus in the processing of faces as well as the inferior temporal gyrus for objects. This is contrary to autistic people who use the inferior temporal gyrus to combine objects and faces. There is impaired connectivity between the right fusiform gyrus as well as the amygdala (Di Martino et al., 2014).
Genetics
Genetics is considered to play a very important role in the development of autism in children. In this case, genetic researchers reveal that much percentage of the behavioral phenotype of autism relates to inherited genes. According to a review done by Muhle et al (2018), on the genetics associated with autism, the data retrieved from the whole-genome screens revealed the various interactions of close to ten genes within the etiology of autism. In this case, there is a clear revelation that the region that relates speech and language, 7q31-q33, is closely associated with autism. An article in the American Journal of human genetics indicates that chromosome 7 could be “the first widely replicated autism-predisposition gene.” In this case, the gene is responsible for making proteins referred to as Neurexins towards the development of the communication abilities of the brain cells. The other locus anomalies that are frequently associated with a potential cause of autism are located at 15q11-q13. It is notable that there is a higher probability of occurrence of autistic-like symptomology amongst lineage with autism as compared to families with no relations to the condition. Parental induced autism is one of the earlier discovered etiologies for autism. Research reveals that autistic children are born as well to parents that are deficient in the autistic parent personality pattern and also those that are associated with the autistic parent personality pattern. The potential link is also with the individuals that are supposedly pathogenic parents who happen to have normal children.
Different studies reveal that the closest family members are more exposed to contacting autism in comparison to the rest of the population. Further, a strong relationship exists between mothers and children and the same in identical twins. The research on genetic influence shows a general discovery on the high chances and the high number of individuals associated with genes having positive autistic expressions. In this case, the level of combination that exists amongst the different gene variants eventually leads to different signs of autism. Consequently, there is a high risk of autism progression resulting from genetic variances. Notably, hormones play an important role in ensuring the prevalence of autism, and this may entail the effects of estrogens, progesterone, and testosterone alongside others in the responsiveness of the immune system.
Vaccines
The relationship between vaccines and autism in children could be detected in a research that was conducted on children whose first symptoms of autism appeared within the first four weeks of receiving the MMR (measles-mumps-rubella) vaccine. The children involved in the research showed signs and symptoms of gastrointestinal and lymphoid nodular hyperplasia. The research conducted by a British gastroenterologist, Wakefield, postulated the evidential effects of MMR vaccine on the intestinal inflammation, which resulted in the translocation of the non-permeable peptides that leaked to the bloodstream as well as the brain. The result is a profound effect on the development of the child. However, the reports by Immunization Safety Review Committee (ISRC), the Centers for Disease Control and Prevention and Autism Research Agenda demonstrated a lack of relationship on the causative link between autism and the biological vaccines. Therefore, the aspect of MMR being an etiology of autism is not valid. However, the biological effects of fatty acids such as omega-3 and Omega-6 have effects on the retinal and brain development within the first two months of pregnancy. The nigh intake of these components provides a higher risk of autism (Muhle et al., 2018).
Environmental factors
There exist a number of environmental risk factors that are easily identified to influence the pathogenesis of autism through epigenetic effects. These environmental factors are divided into three categories that include prenatal, natal as well as the postnatal risk factors. In this case, each of the categories influences part of the periodic development of the neonates. During prenatal care some of the influencing risk factors include psychological, mental health; economic status affects the health as well as the development of the fetus. Such a set of prenatal risk factors increases the probability of the child developing autism (Karimi et al., 2017). The paternal and maternal age above 34 years has been associated with an increased risk of autism of the child. At the same time, the use of medication by the mother during the prenatal period provides an increased risk to fetus autism. For instance, the use of antiepileptic drugs alongside valproic acid results in the development of valproate syndrome that eventually increases the level of oxidative stress as well as the expression of the gene pattern. This leads to cases of delay in ...