The Brain on ADHD. Ms. Komas. Introduction to Healthcare Careers
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1 The Brain on ADHD Ms. Komas Introduction to Healthcare Careers Ms. Komas Period 9/2/2016
2 Komas 1 HOOK: Attention Deficit Hyperactivity Disorder (ADHD) plagues between 5% and 7% of children and less than 5% of adults. Of those people, a significant portion BIG IDEA/SEE CONCLUSION! are discriminated against in the world of academia for using medication to treat their ADHD; they are often times seen as having an advantage over other students, because ADHD patients are prescribed stimulants at therapeutic doses, due to the disorder being perceived as fake. It doesn t help that the medical world has debated for decades over whether or not ADHD can actually be confirmed by scientific empirical evidence, rather than by subjective symptoms expressed by patients. THESIS: Recently, however, neuroimaging has been able to prove that people with ADHD have whole brain structural differences, compared to their neurotypical counterparts, causing brain chemistry differences as well. This has lead to several important advances in not only the understanding of how people with ADHD function and process external stimuli, but also how to chemically balance the brain with medication to lessen the symptoms of ADHD. ( In English: Medical machines have recently allowed us to be able to see differences in what a normal brain looks like compared to the brain of someone with ADHD, and confirm that ADHD exists. This has lead to doctors being able to understand how people with ADHD function, how they process the world around them, and how to use medications to help lessen symptoms of ADHD) Connecting your thesis to your body paragraph topic and conclusion sentences. Recently, however, neuroimaging has been able to prove that people with ADHD have whole brain structural differences, compared to their neurotypical counterparts, causing brain chemistry differences as well. This has led to several important advances in not only the understanding of
3 Komas 2 how people with ADHD function and process external stimuli, but also how to chemically balance the brain with medication to lessen the symptoms of ADHD. History of ADHD (Body Paragraph #1) TOPIC SENTENCE: Historically, ADHD was not even considered a disease until recently. In the 1960 s and 70 s the diagnosis of ADHD focused on symptoms of hyperactivity, inattention, lack of focus, behavioral defiance, and academic struggles in conjunction with learning delays. The primary focus was originally only on male children, due to female children not typically exhibiting hyperactive or defiant behavioral symptoms. By 1980, Attention Deficit Disorder (ADD) had appeared in the DSM, and brought more understanding to the concept that ADHD patients did not have to present as hyperactive in order to be diagnosed with the focus and attention disability. This was especially important for female children, and lead to the beginning of female children being diagnosed in addition to male children. Most recently it has been stated that patients with ADHD do not have to have a learning disability in conjunction with having ADHD. CLOSING SENTENCE: Opening the diagnostic criteria allowed symptomatic people, who had been previously been dismissed or misdiagnosed due to being innately intelligent, to finally be treated for ADHD with medication. Types of ADHD (Body Paragraph #2) TOPIC SENTENCE: There are currently three known types of ADHD and all types manifest with a variety of symptoms depending on the individual. The lack of a clear cut way to determine whether a patient has ADHD based on symptoms alone makes the diagnosis incredibly difficult for health care providers. This is especially true due to the incredibly high comorbidity rate of ADHD with other neurological disorders, such as anxiety, depression, and frontal lobe epilepsy. The only unanimous criteria for all three types is that for a diagnosis to be
4 Komas 3 as accurate as possible, the patient needs to have had symptoms of ADHD persisting for the past six months, and be maladaptive and incongruent with the typical development expected of that person. Additionally, a diagnosis is only given if symptoms were present before the patient was seven years old, the symptoms occurred in more than one setting, and the outcome of the symptoms caused significant issues with social and school functioning. Symptoms of ADHD-Primarily Inattentive (PI) vary. Most patients are disorganized, have a lack of ability to focus for a developmentally appropriate amount of time, and have a hard time paying attention to details. Patients are often unable to keep up with school work due to being disorganized and losing paperwork, as well as are observed zoning out during school lectures or activities. Patients also have having trouble staying on topic while talking, are not adequate listeners, and have trouble following social rules and cues regarding conversation and interrupting. Most neurotypical individuals are able to have a conversation that flows from topic A to B, and on to topic C, fluidly without much difficulty, while people with ADHD- PI seemingly process information as they speak causing them to jump from topic A to D, then back to C, ultimately concluding with topic B. Other common symptoms include being forgetful, being easily distracted, general mental and physical fatigue, and sometimes having a lack of impulse and emotional control. ADHD Hyperactive (H) patients often present with all of the core symptoms of ADHD- PI and additionally restlessness, inability to sit in one place for an extended period of time, more severe behavioral disorders such as Oppositional Defiance Disorder (ODD), and an overall feeling as though the patient is a running motor that refuses to turn off. The final form of ADHD is referred to ADHD Combination (C). ADHD-C presents with symptoms of both ADHD-PI and ADHD-H, whether the symptoms exist in the patient at the same time, different symptoms
5 Komas 4 occur at different times of the day, or the patient has a few symptoms matching each category. CONCLUDING SENTENCE: Overall, all three types of ADHD change the way a person affected by it processes external stimuli and alters how they view and interpret the world as a whole. Biology of ADHD (body paragraph 3) Pathophysiology and Etiology of ADHD TOPIC SENTENCE The renaming of ADHD, to include an emphasis on the different subtypes, has led to a broad range of neurocognitive and neurobiological hypotheses regarding the etiology (origin) and pathophysiology (How the disease manifests) of ADHD (This relates to the thesis because it s a general statement that introduces elaboration of what causes ADHD, the structural differences in the brain, and the chemical differences in the brains of people with ADHD vs neurotypical brains). Current theories emphasize the central role of attentional and executive dysfunctions in children, as well as affective components involving emotional control and motivation. Evidence supports multiple genetic and environmental factors during early development to create neurobiological susceptibility in developing ADHD. Genetic Factors. Evidence of twin, family, and adoption studies has supported a strong genetic contribution and suggests heritability ranging from 60-90%. Genes regulating neurotransmitter systems have been implicated in ADHD, and an increased rate of large, rare, chromosomal deletions and duplications have been reported in individuals with ADHD. It is theorized that parents with established neurogenic disorders (such as Turner Syndrome, Williams Syndrome, and Prader-Willy syndrome) are at a higher risk of passing ADHD to their offspring due to the effects of their genetic abnormalities affecting the neural circuits in their offspring.
6 Komas 5 Environmental Factors. Pre-, peri- and postnatal environmental factors play a significant role in the pathogenesis of ADHD. Prenatal exposure to alcohol is known to induce brain structural abnormalities in the cerebellum, increasing the risk of a child to become hyperactive, disruptive, and impulsive. Maternal smoking is known to cause a 2.7% higher risk for a child to develop ADHD and hyperactivity due to the effect of smoking on nicotinic receptors that regulate the activity of dopamine. Low birth weight can also be a contributing factor towards the development of ADHD as well as various other pregnancy and birth complications. Post natal factors such as an imbalance of omega-3 and omega-6 intake, as well as iron deficiency, can be linked to development of ADHD as well. The Brain on ADHD TOPIC SENTENCE #2 to introduce a new topic under the same general idea which is structural/chemical differences between ADHD brains and non ADHD brains. In ADHD patients, reductions in size have been seen in the total cerebral volume, the prefrontal cortex, the basal ganglia, the corpus callosum, and in the cerebellum. In studies of cortical development in children with ADHD, the maturation of the grey matter peaks in the prefrontal cortex regions were delayed 3 years compared to healthy controls. This is said to cause delays in cognitive processes such as problem solving, planning, cognitive flexibility, sustained attention, and working memory. Neuroimaging has also confirmed that reduced white matter volume is common in brains of people with ADHD. The lessening of white matter volume is typical in the inferior parietal, occipito-parietal, inferior frontal, and inferior temporal cortexes for people with ADHD; the white matter that is found in those areas of the brain is commonly dysfunctional or hypoactive. There are also developmental changes in the cortical white matter pathways in the prefrontal regions, and the pathways surrounding the basal ganglia and cerebellum, reflecting a
7 Komas 6 decrease in the amount of myelinated axons. This causes people with ADHD to have decreased speed of neuronal communication. Evidence is also currently supports the involvement of the frontostriatal circuts to be a large contributor to the pathophysiology of ADHD. The frontostriatal circuits are neural pathways that connect the frontal lobe regions with the basal ganglia, which regulates motor, cognitive, and behavioral functions within the brain. Studies have suggested that motor control difficulties and delays, reported by 50% of people with ADHD, may be due to structural and functional abnormalities in the basal ganglia and cerebellum. Commonly this appears as sensory motor coordination issues, such as poor handwriting, clumsiness, and marked delays in achieving motor milestones. Chemically, the brain of a person with ADHD differs from a neurotypical brain as well. Studies have shown that in people with ADHD, methylphenidate hydrochloride (MPH) blocks dopamine active transporters, causing extracellular dopamine levels to increase in proportion to the level of the blockade and the rate of dopamine being released. This is said be a contributing factor of why external stimulus is more distracting and noticeable to people with ADHD. CONCLUDING SENTENCE: Given these points, there is clear evidence of the existence of ADHD due to documented structural and chemical brain differences, caused by genetic and environmental factors, in the brains of people with ADHD. Concluding Thoughts RESTATING THE THESIS: The existence of ADHD is thoroughly documented by evidence depicting differences in brain structure and chemistry. There is also a clear correlation of people experiencing symptoms of ADHD having chemical and structural differences in the brain compared to neurotypical controls. BIG IDEA THAT CONNECTS TO SOCIETY: Due to
8 Komas 7 this, ADHD should be able to be treated as any other medical condition: without stigmatization and without stimulant medication usage being considered cheating or an unfair advantage in the academic world.
9 Komas 8 References Cite your references here in MLA format!
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