Children with ADHD and ADHD Symptoms - Essay Example

What Causes ADHD? When your child is diagnosed with any disorder the first questions usually is how did this happen. Parents tend to want to blame themselves or want a way to fix the situation. There are a lot of explanations that have been put forth about causes as well as treatment. It is important to look at the literature, or the research that is available. It appears there are likely multiple factors involved in the cause of ADHD and therefore all these are to be considered in treating the disorder. Research Initially it was thought that brain damage might be a factor that contributes to ADHD; infection, trauma, complications during pregnancy or at the time of delivery or other injuries to the brain are included herein. Several studies show that brain damage is associated with greater attention deficits and hyperactivity (Cruickshank, Eliason, & Merrifield, 1988; ODougherty, Nuechterlein, & Drew, 1984). Moreover, ADHD symptoms occur more often in children with seizure disorders (Hesdorffer et al, 2004, Holdsworth & Whimore, 1974). Such injuries are, however, unlikely to be the cause of ADHD in most of the cases as most cases of child ADHD have no history of brain injuries of this sort. (Rutter, 1983). Re­search also shows that not only do the siblings of children with ADHD who also have ADHD show executive function (i.e. cognitive control) deficits, even those siblings who do not actually mani­fest ADHD appear to have impairments in the same functions, albeit milder. (Seidman, Biederman, Faraone, Weber, & Ouellette, 1997). Based on the responses of children with ADHD to dopamine and norepinephrine, it is suggested that such children may also have neurotransmitter dysfunctions and/or imbalances. Even though research shows that non-disabled children show a positive, though lesser, response to stimulants (Rapoport et al., 1978), evidence from drug responding by itself cannot be used to support a neurochemical abnormality in ADHD. However, some di­rect evidence from studies of cerebral spinal fluid indicates decreased brain dopamine in children with ADHD compared to nondisabled children (Halperin et al., 1997; Raskin, Shaywitz, Shaywitz, Anderson, & Cohen, 1984). However, these findings are not conclusive. Although direct evidence for neurotransmit­ter difficulties being associated with ADHD in children has proven inconclusive, results from animal research and that on typical humans suggests that they may be involved in ADHD. According to research, be­tween 10% to 35% of the immediate family members of children with ADHD are also likely to have the disorder; the risk to siblings of such children to have this disorder is around 32% (Biederman et al. 1992; Biederman, Keenan, & Faraone, 1990). African American families are found to have a higher than expected rate of family aggregation of ADHD, which is quite similar to the rates reported in European American children’s families (Samuel et al., 1997). These higher rates are the same in the families of both girls and boys with ADHD (Faraone et al., 2000; Faraone & Doyle, 2001). Another striking research discovery is that the risk to the offspring of a parent who has ADHD is 57% (Biederman et al., 1995). The genetic factor involved in ADHD is further evident by studies carried out on twins. The evidence is both substantial in scope and striking in the magnitude of the genetic role in this disorder. Early studies demonstrated a greater concordance for symptoms of hyperactivity and inattention between monozygotic (MZ) twins than between dizygotic (DZ) twins (Goodman & Stevenson, 1989; OConnor, Foch, Sherry, & Plomin, 1980; Willerman, 1973). However, studies of very small samples of twins (Heffron et al., 1984) found complete (100%) concordance for MZ twins for hyper-activity, and far less for DZ twins. Many large-scale studies on twins, carried out subsequently, have shown remarkably similar results; this shows that the majority of variance (70-95%) in the attributes of ADHD is due to genetic factors (approx. 80%+ on average). Although it is debatable, these studies show that this genetic contribution may increase as the scores along this trait become more extreme (Coolidge et al., 2000; Gjone et al., 1996; Kuntsi & Stevenson, 2000; Levy et al., 1997; Nadder et al., 2002; Silberg et al., 1996; Thapar et al., 1995; Thapar, Harring­ton, Ross, & McGuffin, 2000; van den Oord, Verhulst, & Boomsma, 1996). Another evidence of the genetic nature of ADHD has been observed by studies of adopted children. Studies showed high rates of hyperactivity in the biological parents of hyperactive children, whereas little or no such trait was found in the adoptive parents of these children Cantwell (1975) and Morrison & Stewart (1973). These studies imply that hyperactive children resemble their biological parents more than their adoptive parents in their level of hyperactivity. Exposure to environmen­tal toxins, and especially lead, is also sometimes construed to be a cause of ADHD. Studies have shown that an elevated body lead burden has a consistent, albeit small, and, statistically, a significant relationship to the symptoms involving ADHD (de la Burde & Choate, 1972; Needleman, Schell, Bellinger, Leviton, & Alfred, 1990). However, some studies do imply that mostly lead-poisoned children do not take on symptoms of ADHD, as it is observed that even when the levels of lead were relatively high, less than 38% of the children are seen to have hyperactive behavior on a teacher rating scale (Needleman et al., 1979). In some individuals, infections may result in autoimmune system antibodies to cross-react with and compromise neural proteins, particularly in the basal ganglia. Peterson et al. (2000) examined 105 individuals having OCD, chronic tic disorder, or OHD, and 37 controls without any disorder antistreptococcal antibody titers in each were measured, as was the integrity of basal ganglia (via MR1). Results indicated ADHD was significantly related to such bodies, even after the effects of OCD and disorders were controlled for, and that those antibodies were related to basal ganglia volume. such findings suggest that some cases of ADHD could arise from or be exacerbated by streptococcal infection. Even if this is so for only a small percentage of cases, this finding is important in further supporting a significant role of "t basal ganglia in the creation of ADHD symptoms. As pregnancy and birth complications can have a negative effect on the brain development of the fetus/newborn, hence researchers in ADHD show a keen interest in them. According to some studies, there is no greater occurrence of such complications in cases involving children with ADHD than those involving nondisabled children (Barkley, DuPaul, & McMurray, 1990). However, according to some studies such increased occurrence has been found; as, for example, Claycomb, Ryan, Miller, and Schnakenberg-Ott (2004) discovered that the mother’s younger age at the time of deliver, her lower educational level, a longer period between onset of labor and birth, and the occurrence of delivery complications accounted for 42% of the variance in ADHD. However, there was no control in the study for maternal ADHD symptoms, as these might have been the cause of the younger age at delivery as well as the lower educational level of the mothers, as if that is the case, it might explain why the children developed ADHD. However, large-scale epidemiological stud­ies have generally not found a strong associa­tion between pre- or perinatal adversity and symptoms of ADHD once other factors are taken into account, such as maternal smoking and alcohol use as well as low SES, all of which may predispose to perinatal adver­sity and hyperactivity (Goodman 8c Stevenson, 1989; Nichols & Chen, 1981; Werner et al., 1968). One psychosocial factor that has received re­cent attention in the popular media is the de­gree of childrens exposure to television. However, there is no research done so far that proves conclusively that television is a cause of ADHD. Problems in parenting or parenting styles can make ADHD better or worse, but they do not cause the disorder. So relax parents; by the end of this lecture you will know some things that will help and you will also come to know that it is not your fault. ADHD is definitely a brain-based disorder and research is in progress to better define the areas and pathways in the brain that are involved. ADHD and Education Along the line of teaching brain processing Dr. Siegfried (2000) has done considerable research using heuristics to train problem solving. The ADHD patient often needs to experience something to learn it. ADHD students often do not grasp a concept by hearing or reading it. They learn better by doing. The educational system, for the most part, teaches verbally and also tests understanding of the information verbally. This asks the ADHD student to use a processing pattern with which he/she is not familiar. Understanding brain processing helps researchers find out how the ADHD functions so cognitive tools can be used to help the individual function successfully. Brain processing has to do with two things, first it is how information coming into the brain is picked up, coded and stored, and second it is how the brain finds that information and uses it together to solve problems (pegservices.cjb.com). Information enters the brain in several ways most of which comes through the five senses. Eyes, ears, nose, mouth and skin provide information about the environment. Each sense is responsible for coding information which the brain then interprets and begins the process of storing that interpretation in memory. The speed of this interpretation and storing process depends on the rate of firing in the neurons of the brain. There can be hundreds of impulses along a single axon per second (Anderson, 2003). There are also patterns to neural activities, which result in cognition. There is a fair amount of evidence suggesting that human knowledge is not localized in any signal neuron but is distributed over the brain in large patterns of neurons (Anderson, 2003). The information picked up by the senses is first registered in the sensory memories but only for a brief period of time. Because our attention is limited, only a few cognitive processes can take place at one time. What actually takes place is that the compiled pattern is decomposed into a set of primitive features, the individual features are recognized and then combined again and the combination feature is recognized to identify the pattern. A set of Gestalt principled determines how to break an overall pattern into features. Combining features in order to recognize a pattern requires attention. The amount of attention decreases with familiarity with the pattern (Anderson, 2003). This method gives the ADHD patient patterns in the form of a heuristic to accomplish a task. Over time the individual learns various pathways of processing, pathways that seem to be missing in the ADHD brain. Peer Relationships Peer relationships is also an area of concern. There are several interventions available and there are several settings for providing these interventions to children, including groups in office clinics, classrooms, small groups at school, and summer camps. All of the programs use methods that include coaching, use of examples, modeling, role-playing, feedback, rewards and consequences, and practice. It is best if these child-directed treatments are used when a parent is participating in parent training and school personnel are conducting an appropriate school intervention (MTA Cooperative Group, 1999). When parent and school interventions are integrated with child-focused treatments, problems in getting along with other children (such as being bossy, not taking turns, and not sharing) that are being targeted in the child’s treatment are also included as target behavior in the home and school programs so that the same behavior is being monitored, prompted and rewarded in all three settings. Children with ADHD have been repeatedly found to experience high rates of peer rejection. They often take the role of a negative social catalysis, fueling conflict interactions among peers (Blackman & Hinshaw, 2002). Social skills training groups are the most common form of treatment, and they typically focus on the systematic teaching of social skills. They are typically conducted at a clinic or in school in a counselor’s office for 1-2 hours on a weekly basis for 6-12 weeks. Social skills groups with children with ADHD are only effective when they are used with parent and school interventions, and rewards and consequences to reduce disruptive and negative behaviors (Bierman, Miller & Stabb, 2006). There are several models for working on peer relationships in the school setting that integrate several of the interventions listed above. They combine skills training with major focus on decreasing negative and disruptive behavior, and are typically conducted by school staff. Some of these programs are used with individual children (for instance, token programs in the classroom or at recess (Pfiffner, 2006) and some are school wide (such as peer mediation programs) (Cunninghan & Cunningham, 2005). Generally, the most effective treatments involve helping children get along better with other children. Programs in which children with ADHD can work on peer problems in classroom or recreational settings are the most effective (Conners, Wells, et al., 2004). One model involves establishing a summer camp for children with ADHD in which child-based management of peer problems and academic difficulties are integrated with parent training (Pelham, Greiner, & Gnagy, 2006). All five forms of peer intervention are incorporated in a 6-8 week program that runs for 6-9 hours on weekdays. Treatment is conducted in groups, recreational activities take up the majority of the day. There is also two hour of academics each day. The knowledge of sports is taught to the children. This is combined with practice in social skills and problem solving, teamwork, decreasing negative behaviors, and developing close friendships. So while there are many parts to the cause there are also many treatments that are helpful. Hopefully knowing more is encouraging and gives you a direction in moving forward with ADHD. References A Cooperative Group. (2005) A 14-month randomized clinical trial of treatment strategies for attention deficit hyperactivity disorder. 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