The Role of the Frontal Lobes in Attention - Essay Example

The role of the frontal lobes in Attention –Deficit Hyperactivity Disorder By The role of the frontal lobes in Attention –Deficit Hyperactivity Disorder Introduction Attention-Deficit Hyperactivity Disorder is one of the most widespread diseases afflicting children. The main symptom that allows diagnosing this illness is persistent excessive inattention. Children who suffer ADHD are usually hyperactive and impulsive; consequently their behaviour prevents them from fully fledged social and educational realization. Their educational results are usually very low. (Krain & Castellanos, 2006; Luman, Tripp & Scheres, 2010; Luman, Oosterlaan & Sergeant, 2005; Sonuga-Barke, 2003; Solanto, 2002; Oades, 1998). Some indicators of such behavior are considered to be harmful and destructive for child’s development. ADHD is a widespread disorder that is not studied properly and needs further research. This paper will define how much is already known about this disorder and the ways to cope with it. Neurophysiology of ADHD An essential role in response inhibition regulating is played by prefrontal cortex and basal ganglia. Cerebellum is important for motor coordination and cognitive planning. Physicians usually apply anatomic MRI to check the distinctions in certain brain areas of healthy children and ones with ADHD with the purpose of determination of fundamental neurophysiology of ADHD. In accordance with modern researches and studies the disorder is associated with decreased brain volumes, which are related to age and sex-matched controls and the smaller volume of ADHD children can be explained by genetic or environmental influences. Children with the disorder perform poorly on sustained attention tasks due to the smaller volume of the right superior frontal (Ashtari et al., 2005) and, basically, the smaller brain volumes are connected with greater ADHD symptom severity. These malfunctions result in attention problems and to greater response suppression. There is an improper function of the circuit involving the frontal brain regions, the basal ganglia and the cerebellar hemispheres, which are related features of ADHD symptoms. Literature review Disorder is triggered by the frontal lobes and particularly the prefrontal regions malfunctions, as some scientists claim (Oades, 1998; Boucugnani & Jones, 1989; Shue & Douglas, 1992; Aman, Roberts & Pennington, 1998). In respect to another scope of works in this field it can be claimed that dopamine is involved in reinforcement mechanisms and ADHD is usually connected with different types of the dopamine transporter and receptor genes, as well as with the dysfunction of the midbrain dopamine (Solanto, 2002; Dougherty, Bonab, Spencer, Rauch, Madras & Fischman, 1999; Tripp & Wickens, 2009; Madras, Miller & Fischman, 2005; Swanson et al., 2000). Nevertheless, the concept of ADHD has been restructured and reconsidered in theories of cognitive science and neuroscience. Such deviances as a lack of attention, a bad performance of executive functions, inability to motivate and process information temporarily refer ADHD disease to a disorder of self-regulation, relating it to a behavioral deficit and inability to adapt to a changing environment (Nigg, 2005; Sonuga-Barke, 2003; Toplak, Dockstader & Tannock, 2006; Willcutt, Doyle, Nigg, Faraone & Pennington, 2005). Having considered numerous researches and studies, it is evident that there are different approaches to the etiology of the disease. On basis of some facts it is clear that there is one single deficit in ADHD, which is a lack of dopamine transfer whilst other approaches relate different deficits to cognitive functions breaches. In terms of the neuro-cognitive model the ADHD can be explained as executive dysfunction, which is connected with hypersensitivity. Some other new theories clarify a challenging nature of the syndrome in terms of the frontal lobe theory of ADHD dating back to 1930. This approach explains the referred deficits in ADHD by drawing parallels with similar symptoms between patients with frontal lobe lesions. The frontal lobes integrate the precentral cortex, the prefrontal cortex, the orbitofrontal cortex and the superior mesial regions, which can be found in both the right and left cerebral hemispheres. The precentral cortex is responsible for physical movements control and the dorsolateral part of the frontal lobe is responsible for cognitive planning and executive functioning performance (McHugh, 1995). The verbal and spatial memory is related to the prefrontal cortex while the orbitofrontal cortex is connected with inhibition, control over social behavior and impulse (Kiran, Chaudhury, Kumari & Akhouri, 2011). Therefore, the prefrontal lobes are responsible for attention and coordination and are very important in everyday life of a patient with ADHD. Godefroy, Cabaret & Rousseaux (1994) and McHugh (1995) claims that frontal lobe dysfunction can be explained both in terms of cognitive theory and personality changing theory leading to sociality impacts. A dysfunction in flexibility and planning can be explained by lesions of the dorsolateral part of the frontal lobes while the orbitofrontal region damage leads to a poor impulse control and a reduction of interpersonal sensitivity. Motivation and exploration are performed in the medial region of frontal lobes and lesions of this area can result in apathy and inertness. The frontal lobes dysfunction can be connected with attention deficit or disinterest, or inability to change motor patterns, occurrence of uncoordinated behavior or the inability to make plans in advance because of motivation absence (Godefroy, Cabaret & Rousseaux, 1994). Insensitive personality can be developed in the result of lesions of the dorsolateral part of the prefrontal region; lesions to orbital region of the prefrontal lobe may cause disinhibition and lead to understanding dysfunction of the completed actions (Kiran, Chaudhury, Kumari & Akhouri, 2011). The frontal lobe dysfunction can lead to a suppressed working memory capacity as it involves different brain regions, such as the dorsolateral frontal cortex and the thalamus. ADHD children have many differences in their behavior in comparison with normal children (Boucugnani & Jones, 1989). Very often they experience such problems as lacking of attention, disinhibition, inability to be an organized person and inability to plan. There are many similarities of symptoms between children with ADHD and frontal lobe lesions patients. In recent researches and studies it has been often claimed that the frontal lobe plays a decisive role in inhibition and these patients are unable to mediate responsibility of decision making. These children cannot decide for themselves whether they make right or wrong choice, whether they make the right assessment of their choice etc (Chapter 7—Brief Psychodynamic Therapy). This can be explained by a malfunction of anterior ciangulate cortex and adaptation of a child to the environment is challenged in this case. ADHD children suffer from dysfunction in the frontal lobe and they experience inhibitory and goal-directed behavioral difficulties. In accordance with some studies children with ADHD cannot cope with neuropsychological tasks (Aman, Roberts & Pennington, 1998). These children could not pass such tests as the Tower of Hanoi, the Wisconsin Card Sorting Test and some others. A frontal lobe dysfunction is diagnosed among these children and it means that self-regulation is violated in terms of attention capacity, response analysis, functions of motor control and planning (Valera, Faraone, Murray, Seidman, 2007). There is no doubt that children with ADHD suffer from poor performance and they have many behavioral problems. A dysfunction in the frontal lobe is not the only reason for behavioral dysfunction. A malfunction of visual spatial working memory challenges ability to maintain spatial attention at a certain period of time at a cued location. Carter, Krener, Chaderjian, Northcutt & Wolfe (1995) claim that this ability is dependent on the integrity of catecholaminergic neurotransmission in the contralateral prefrontal cortex. This can lead to violation of ADHD functioning in the frontostriatal catecholamine activity. The Wisconsin Card Sorting Test was rather challenging for children with ADHD. Concerning recent researches and studies, the dysfunction in various components of circuits of different brain regions is determined. There are many problems in the process of cognition and behavioral self-regulation (Ansari, Gouthro, Ahmad& Steele, 1996). Different functions of memory, such as selective and divided attention, planning, care, attention changes, executive control and working memory are developed in terms of the dorsolateral prefrontal cortex and the ventrolateral prefrontal cortex, while social inhibition and impulse control is defined in terms of the orbitofrontal cortex (Drogin, 2007). The primary region, which determines the underlying deficits of ADHD, is the prefrontal cortex of the frontal lobe. Discussion On the one hand it is evident that frontal lobes determine and explain ADHD occurrence, the disorder in these two regions can be a result of numerous reasons and thus psychopathology of ADHD can be considered from many perspectives. Underlining only malfunction of frontal lobe may lead to a neglect of other areas and different functions of brain cannot be considered (Gustafsson, Jacobsson, 2000). Oades (1998) claims: it is difficult to process information and he underlines the importance of methods, which are used in determination of ADHD etiology. Many other functions are not taken into account and it is relevant to consider the amygdala, basal ganglia and the hippocampus functions to determine a model hypothesizing that ADHD is performed by the application of effort and by the consequences for activation and response etiology. The dopamine dysfunction theory is focused on certain models, which underline a deficit in dopamine transmission in the fronto-limbic brain circuit and in the result of this malfunction in the brain ADHD occurs (Solanto, 2002 and Swanson, Flodman, Kennedy, Spence, Moyzis, Schuck, Murias, Moriarity, Barr, Smith, & Posner, 2000). In case of low levels of tonic dopamine, there is a shorter delay between the desired behavior and the reinforcer. In the result of this dysfunction an impulsive behavior occurs (Bijou & Ruíz, 1981). There is a delay of dopmaine transmission in ADHD and children if instantly encouraged and gain rewards, demonstrate a better learning. Tripp & Wickens (2009) in this respect claim that in case there is a direct connection between levels of tonic dopamine and normal responses to actual rewards then ADHD can be compared with a failure of transfer of the dopamine signal and with delayed dopamine responses to reward cues. This can be explained by childrens inability to control and restrain the firing of dopamine cells to an under conditioned stimulus (McFarland, Kolstad, & Briggs, 1995). Sonuga-Barke (2003) pays attention to a dual pathway model, which underlines connection between two independent neural circuits that create different conceptual background and include different psychological processes, which are often connected with attention-deficit hyperactivity disorder. These pathways are the fronto-dorsal striatal circuit, which perform executive functions and the mesolimbic ventral-striatal circuit performing motivational processes (Stewart, Steffler, Lemoine & Leps, 2001). It is necessary for parents and friends to develop appropriate behavioral templates to help children suffering from ADHD: “The give and take between parents and teenager in these sessions is necessary to motivate the teenager to work with the parents in making changes in his or her behavior” (Bijou & Ruíz, 1981). The model considers ADHD as delay aversion and underlines that ADHD children prefer smaller immediate rewards and neglect larger delayed rewards because very often they experience abnormal motivational triggers (Fabiano, Pelham, Gnagy, Burrows-Maclean, Coles, Chacko, 2007). In terms of the executive function theory, children with ADHD suffer from so-called "executive dysfunctional function" (Humanistic Psychology Overview). This type of function refers to a higher order of top-down cognitive processes that make the pursuit of future goals easier. In terms of this model ADHD is associated with the dysregulation of these cognitive factors and children cannot develop and implement their ideas in their lives. Moreover, it is very hard for children to get used to intellectual conditions of a situation (Willcutt, Doyle, Nigg, Faraone & Pennington, 2005). Nigg (2005) claims that ADHD is caused by a malfunction of three neural circuits, such as: the fronto-striatal, the fronto-cerebellar and the prefrontal cortex (Aman, Roberts, Pennington, 1998). The first two pathways are involved in the process of learning. The prefrontal cortex performs the function of the emotional evaluation of a given situation. It is possible to implement BMP or another behavioral modification program: “…even patients with more severe conduct disorders may benefit from such a program [BMP or behavioral modification program] with an extended length of stay. More longitudinal studies using well-defined criteria that measure post-discharge success are needed” (Kazdin 2005, p. 32). There is another pitfall in ADHD, which is disinhibited behavior. It means that a passive behavior can occur in the result of a childs inability to appropriately respond to emotional information. The possibility of punishment is another preventive factor for children to show impaired behavior. They can show different passive features of behavior and they can be easily restrained (Luman, Tripp & Scheres, 2010). Impaired passive avoidance can be associated with the over excessive reaction of sympathetic nervous system to positive triggers (Bush, Valera, Seidman, 2005). The behavioral activation system and the behavioral inhibition system are responsible for behavior. These two systems are independent, but they can trigger extinction behavior. Therefore, children with ADHD can be subjected to the growing influence of the behavioral activation system and they can be easily focused on searching for some rewards. These children are afraid of punishment and that is why their behavior subconsciously discards all possible chances of punishment. Conclusion Attention deficit hyperactivity disorder can occur in the result of numerous causes and mechanisms. It is appropriate to develop some convergent models that are focused on explanations of this disease. It is appropriate to refer to the searching of cognitive science, neurobiology, neuropsychology, developmental psychology, psychophysiology and combination of these and other sciences. In terms of the frontal lobe theory, the frontal and prefrontal cortex is taken into account. Thus, disorder is correlated with the dysfunction in the frontal lobes. This approach is based on research study findings that behavioral symptoms, such as disinhibition, insensivity, impulsivity, inability to provide reasonable behavioral responses or experiences lead to similarities in behaviors of patients with ADHD diagnosis and patients with frontal lobe lesions. It should be noted that this model explains the disorder from one perspective and it is better to focus on various aspects of causal and developmental pathways, which are elaborated to the syndrome (Lindstrøm, 2012). Generally speaking, many theories have not totally demonstrated correlation between family and peer relationship processes and improvement of cognitive deficits in ADHD patients. Further research is focused on multiple ways of dealing with Attention-Deficit Hyperactivity Disorder. References Aman, C. J., Roberts R.J., Pennington B.F. 1998, A neuropsychological examination of the underlying deficit in attention deficit hyperactivity disorder: frontal lobe versus right parietal lobe theories. Developmental Psychology, 34 (5), 956-969. Ansari, A. A., Gouthro, S., Ahmad, K., & Steele, C 1996, Hospital-Based Behavior Modification Program for Adolescents: Evaluation and Predictors of Outcome.Adolescence, 31(122), 469+. 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