A developmental perspective to attention-deficit hyperactivity disorder (ADHD) in children

Diagnoses and treatment of attention deficit hyperactive disorder in children. Biological susceptibility of the disorder. Twin and adoption studies. Psychosocial adversity, its developmental course. The significant effect of environment on the syndrome.

Рубрика Психология
Вид статья
Язык английский
Дата добавления 19.11.2020
Размер файла 26,1 K

Отправить свою хорошую работу в базу знаний просто. Используйте форму, расположенную ниже

Студенты, аспиранты, молодые ученые, использующие базу знаний в своей учебе и работе, будут вам очень благодарны.

Размещено на http://www.allbest.ru/

A DEVELOPMENTAL PERSPECTIVE TO ATTENTION-DEFICIT HYPERACTIVITY DISORDER (ADHD) IN CHILDREN

Olusegun Emmanuel

University of Botswana, Botswana

Abstract. The debate about diagnoses and treatment of attention deficit hyperactive disorder (ADHD) in children continue to range on between the developmental and biological perspectives. While there is increasing evidence that support the biological susceptibility of the disorder, a number of researches also emphasized the significant effect of environment on the syndrome. This study used developmental perspectives to evaluate and bring together various bio-psychosocial factors that impact on children diagnosed with ADHD. The study explored and integrated the existing and advancing study on ADHD to a more refined pattern that embraced developmental perspectives. The study also discussed how the linkage in childhood ADHD fits within the developmental psychopathology perspective. The study revealed that ADHD as a developmental disorder is influenced by prenatal, biological and psychosocial environmental risk factors, and suggested that better understanding of genomic susceptibilities, family environment and parental characteristics would transform the pathway for development of ADHD in children

Keywords: attention deficit hyperactive disorder, developmental perspectives, childhood disorder, genetic factors, environmental factors

Афолабі Олусегун Еммануель. Віковий підхід до гіперактивного розладу та дефіциту уваги (ГРДУ) у дітей

Анотація. Сьогодні тривають суперечки щодо діагностики та лікування гіперактивного розладу з дефіцитом уваги (ГРДУ) у дітей. У статті проаналізовано дві позиції, що намагаються пояснити цей неврологічно-поведінковий розлад розвитку. Одну з них пов'язують із процесом розвитку дитини, а іншу з біологічними осбливостями. У той час як з'являється дедалі більше доказів на користь біологічних витоків розладу, багато дослідників також підкреслюють істотний вплив середовища на цей синдром. Дослідження спирається на вікові позиції з метою оцінки та інтегрування різних біопсихосоціальних чинників впливу на дітей з ГРДУ. Вивчення враховує традиційні та нові погляди на ГРДУ для побудови вікової моделі. Висвітлено питання про зв'язок ГРДУ та віковою психопатологією дітей. Установлено, що ГРДУ як віковий розлад перебуває під впливом передродових, біологічних та психосоціальних чинників ризику середовища. Автор уважає, що глибше розуміння генетичних схильностей, характеристик сім'ї та батьків здатне внести зміни до перебігу ГРДУ у дітей.

Ключові слова: гіперактивний розлад з дефіцитом уваги, вікові підходи, дитячий розлад, генетичні чинники, чинники середовища

Introduction

attention deficit disorder children

Attention-Deficit/Hyperactivity Disorder (ADHD) is a severe childhood disorder that affects many facets of human being, particularly young children populace (American Psychiatric Association, 2000) and has been a subject of intensive research for decades (Barkley, 2006). While studies over the years demonstrated the advancement made on ADHD, the intense interest on the disorder continue to produce a number of empirical data on etiological factors, complex genetic and the neurobiological variables that underline it, particularly, the developmental causes and treatments that are relevant for diagnosing the disorder in children. For example, studies like molecular and behaviour have long offered considerable suggestions to support the significant effect of genetic factor on ADHD. (e.g., Kuntsi, & Stevenson, 2000; Sunohara et al., 2000). Additionally, a quite number of models were proposed to address the syndrome, particularly on children's cognitive deficiency (e.g., Berger & Posner, 2000; Sergeant, 2000). However, contrary to the progress reports on bio-cognitive development, the theory on social and relational features of the syndrome remains stagnant, as general consensus showed multiple casual pathways, with environmental factors primarily labelled as ameliorating the symptom in children (Sonuga-Barke, Auerback, Campbell, Daley & Thompson, 2005).

Although research on family of children with ADHD continue to be acknowledged, (e.g., Sonuga-Barke, Auerback, Campbell, Daley & Thompson, 2005), the debates about children diagnosed of ADHD, particularly, its occurrence and origin continues to range on. More disturbing is the fact that developmental conceptualizations of the syndrome in children and adolescence have been neglected. Specifically, the clinical and social effects of the symptom have been waned, to say the least downplayed in most literature. This made it hard for practitioners and families of children diagnosed with ADHD to cope with its challenges, and projected the problems and discriminations experienced by families and children with ADHD an important issue for consideration. Therefore, much is desire on influence of the gene-environment interactions on socio-cognitive development of children diagnosed of ADHD.

Methods and objectives

This study provides a brief overview on the social and clinical factors associated with children diagnosed with ADHD, and uses developmental perspectives to evaluate and bring together various bio-psychosocial factors that impact on their development (e.g., Rutter & Sroufe, 2000). To achieve these objectives, this study examines and integrates the existing and advancing study on the ADHD to a more refined pattern that embraced developmental perspectives. Also, the study organized into sections, the clinical and social factors related to childhood ADHD and explained how these factors influenced children's development. Finally, the study discussed how linkage in childhood ADHD fits within a developmental psychopathology perspective and makes recommendations for future research.

Scientific status of attention deficiency hyperactive

ADHD is multidimensional disorder that exacts a significant effect on individual and society. This disorder has negative impact on families, as well as academic and vocational outcomes of vulnerable children (Biederman et al 2004). As the most generally diagnosed neurobehavioral illness in children, the disorder is mostly treated with stimulant and non-stimulant drugs (United States, 2003, & 2007; Pastor, & Reuben, 2008). Even though the exact causes of the ADHD are still unknown, past and present research confirmed the significant effect of genetic and environmental factors on the disorder (Nigg, Nikolas, & Burt, 2010, Thapar, Langley, & Asherson P, 2007). Besides, research on ADHD emphasised more on the period of birth by establishing a strong correlation between period of birth and children psychological and behavioural disorders (Tochigi, Okazaki & Kato, 2004), This is in contrast with several other disorders where a reliable seasonal form is yet to be established. (Atladottir, Pamer , & Schendel, 2007; Hauschild, Mouridsen, & Nielsen, 2005).

As an unsatisfactory umbrella term, ADHD is applied to children with broadly differing temperaments and functional problems in school, home, and social settings. This group of children shared certain core features, such as limited sustained attention span, poor impulse control, and motor over activity. They also developed abnormal syndromes, such as severe development, distraction and thoughtlessness that cause severe impairment in their learning (Hauschild, 2005). Research on ADHD also showed a strong genetic orientation on the disorder. For example, the inattentiveness aspect of the disorder is documented as fantasizing, distractibility, and associated with problems, such as lack of concentration on specific task for a lengthy period, while the hyperactivity element of the syndrome is pronounced as fidgeting, unnecessary talking, and restiveness (Faraone, Perlis, Doyle, Smoller, Goralnick & Holmgren, 2005). The signs of ADHD are also predisposed to accidents, strain interpersonal relationships, disruptions and improper conduct. However, apart from its association with clinically oriented disorder in children, ADHD also linked to characteristics in adulthood, such as drugs and alcohol misuse; socio-cognitive disorders; disruptive conduct and delinquency (Thapar, Langley, O'Donovan, 2006).

Despite the above illustrations and evidences, the developments of ADHD remain debatable, as the causes of the symptom pointed toward multidimensional perspectives and linked to children and adults mental health, (Thapar et al, 2006). This further shows the effect of genetic factors on its development. It also shows that its relations with ecological risk variables are complex. Based on this foregoing, there is a need to ponder on the evolving nature of the symptom and the differences in the phenotypic indicator, particularly, the influence of ecological factors on childhood ADHD (Thapar et al, 2006).

Diagnosis consideration of ADHD

Research in the last 60 years has witnessed the use of several terminologies for attention deficit- hype reactivity disorder (ADHD). Some of this terminology includes: hyperkinetic impulse disorder, minimal brain dysfunction, hyperactivity, attention deficit disorder. However, the core characteristics of the disorder are inattention, impulsivity, and hyperactivity and affects about 4 % of all children.

Besides, the signs of the syndrome are more noticeable in young people and vary between 3 to 11% or more (Berger, 2011, Childress & Berry, 2012). However, despite its occtrrence in yotng children, the origin of the disorder is yet to be identified. This difference in expression revealed the diverse conceptions of the primary symptoms and its asstmed ftndamental pathophysiology.

Literature on ADHD revealed that the prospect of finding a diagnostic indicator for the disorder is not achievable. This is dte in part, to the nature and complexity of the syndrome (Batmeister, & Hawkins, 2001, Zimmer, 2009). However, research identified three subtypes of ADHD and each of this subtypes were differs on symptomatology. For example, for a child to be diagnosed of ADHD, and labelled with particular subtypes, he/she must display 6 symptoms for a period of 6 months. Although achieving such diagnostic criteria is difficult, this method is used as a bench mark for diagnosing the disorder in children. Children diagnosed with ADHD also showed some degree of functional impairment in multiple settings (Berger, 2011, APA, 2013). However, due to the parallel characteristics of the disorder, the comorbidities, such as anxiety disorders and ODD, influenced its sub-type in children.

While the criteria listed in DSM-V for ADHD is more or less broader over DSM-IV-TR, the issue of sex differences in children hyperactive disorder continue to range on (Berger, 2011, APA, 2000). For instance, male child are 3 times potential of having ADHD and display hyperactive behaviour or combination of it, than female child, (Childress, & Berry, 2012). Also, females are more expected to display predominantly absent-minded subtype and suffer from mental impairment and eating disorders (Trent, & Davies, 2012). Further, there is higher sense of aggressiveness and abuse of law among male than female diagnosed of ADHD (Trent, & Davies, 2012). On the basis of this assumption, it is imperative for professionals working with children diagnosed of hyperactive disorder to be consciously aware of its sexual and developmental variances. This would prevent over-or under diagnosed of the disorder in children. Furthermore, there should be proper analysis and assessment of parents and teachers reports, so as not to mislabel the underline disorders (Dopheide, 2005, Rader, McCauley, & Callen, 2009).

Etiological model of ADHD

While it was established that the main aetiology of ADHD is unknown (Sonuga-Barke & Halperin, 2010), it is important to understand its aetiology and other associated disorders that relates with the syndrome. This would help clinicians to identify the interactions between the genetic and environmental factors and how they increase vulnerability in young children. The process would also offers a way out for the heterogeneity of the disorder in a meaningful manner, as research showed lack of systematic incorporation of the findings across multiple levels of analysis (e.g., Coghill, Nigg, Rothenberger, Sonuga-Barke, & Tannock, 2005; Sonuga-Barke & Halperin, 2010). Therefore, etiological models on ADHD emphasised the impacts of genetic and environment factors; their correlations and interactions; influence on brain composition and function, and the mediating role on the symptom expression, As a result of these challenges, more investigation is needed to create a clear relationships between supposed fundamental genetic and neural processes, and the behavioural manifestations of the disorder. This would increase and encouraged new and effective treatments (biological and nonbiological), and offered necessary information on the framework that supports the management of ADHD particularly, in hypothesising, diagnostic of boundaries and current arrangement of the illness.

In addition, the hypotheses for reducing brain function in children diagnosed of ADHD were grounded on several observations that reduced the volume of gray and white matter in the brain. This causes shortfalls in cognitive processing, responsiveness, motor planning, speed of processing responses, and other related behaviour in the disorder (Cortese, 2012). Though, prefrontal cortex (PFC), caudate, and cerebellum were the primary source of shortfalls in children diagnosed of hyperactive disorder, this was formed by different neurons that together, regulate attention, thoughts, emotions, behaviour, and negative actions in children (Arnsten, & Pliszka, 2011, Kesner, & Churchwell, 2011). Poor development of PFC11 reduced the activity of the PFC, caudate, or cerebellum (Arnsten, & Pliszka, 2011). The system activity between the regions is “subtle to the neurochemical environs,” (Arnsten, & Pliszka, 2011) and sustained by the combination of neurotransmitters (NTs), dopamine (DA), norepinephrine (NE) and multiple receptors (Arnsten, 2007, Robbins, 2003).

Etiological model also identified aggressiveness, impairment and other related problems, (i.e., antisocial conduct) as the key goals of the symptom in children. Though, medication was identified as a way of reducing hyperactive disorder in children, its long-term supports for the broader outcomes of ADHD are yet to be established. These underscore the importance of identifying the geneticenvironment factors that caused the negativity and impairment in children with ADHD, and provide answer to the growth of active risk decline tactics in the longterm management of the disorder. Based on this aforementioned, it is imperative for research to focus on understanding the genetic and environmental risk factors that associated with ADHD, as well as the clinical characteristic that projected the outcomes of the disorder in children. This would target resources and monitor children at risk of adverse concerns.

The need for a new model on ADHD

A decade of scientific study on ADHD has highlighted the need for a new theory that explains the syndrome; as ADHD is confirmed as a disorder particularly, in respects to its basic nature. Most research on the ADHD is more or less investigative and descriptive, with exception of two. First, Quay's (1988a, 1988b, 1996) used the neuropsychological model of anxiety developed by Gray's (1982) to describe the source of the poor inhibition manifested in ADHD. This model relates thoughtlessness to under-functioning of the brain's behavioural inhibition system. Also, it explained that children with hyperactive disorder are highly subtle to the signs of conditioned punishment, and less sensitive to passive avoidance models (Quay, 1988b). The second model failed in its attempt to set tp a concept similar to the one established in Quay-Gray theory. The model makes a comprehensive theory construction that offers coalescing explanation on various mental shortfalls that are related to children diagnosed with attention/hyperactive disorder.

The developmental approach

The desire for a theory that embraced the clinical and social aspects of attention/hyperactive disorder has prompted the need for developmental approach to the ADHD. Although a comprehensive neuropsychological model of ADHD has yet to be proposed, other models of psychopathologies was previously recommended (Gray, Feldon,Rawlins, Hemsley, & Smith, 1991). Developmental approach entails the correlation between the etiological heterogeneity, high level of comorbidity, and biological and psychosocial/family of ADHD (Cummings, Davies, & Campbell, 2000 ; Sonuga- Barke & Halperin, 2010 ). These interactions underscore the need to posit a multiple developmental pathways to treatment of children diagnosed of ADHD (Sonuga-Barke et al., 2005 ; Sonuga-Barke & Halperin, 2010 ), and were mediated by a variety of within child and family contextual factors that associates with either the diminution or exacerbation of the symptoms over time.

For example, dynamic developmental psychopathology approach offers an explanation on how attention/hyperactive disorder evolved, and how the interactions between multiple risk and protective factors impact on children development (Rutter&Sroufe, 2000). The model proposed that, children in the course of their development were influenced by biological risk factors, with a relatively lesser impact from the ecological factors. The model also highlighted that, across children and across time, there are variables that influence the development of attention/hyperactive disorder. The theory predicts that though, precise symptom of ADHD at a particular time in life varies, they are influenced by factors that have positive or negative effects on the symptom development. Further, the theory explained that, individual differences in dopamine functioning have significant impact on motor functions and children learning. This produced behaviours, such as attention problems, hyperactivity, and impulsiveness that associated with ADHD, and predicted an increase in children's behavioral variability. Overall, dynamic developmental theory proffer better explanation on how person predispositions interacted with the above mentioned conditions and relatively created behavioral, emotional, and cognitive effects that balanced the behavioral patterns of children with ADHD. Thus, a child's characteristics coupled with the family situation exerted collaborating influence on ADHD and offered unique opportunity for analysing the disorder symptomatology.

Psychosocial adversity and its developmental course

Though, many studies have proposed significant evidence for the existence of psychosocial problems in children with hyperactive disorder, such evidences predicts the socio-cognitive and emotional development, rather than precise predictors of the disorder. Therefore, it remains uncertain whether experience of violence in infancy is a risk factor for ADHD, as there was no theoretical basis for observing this possible relationship. For example, exposure to violence in a household may act through psychosocial adversity and lead to permanent brain change that occurs as a result of prolonged exposure of the developing brain to steroid hormones (Yehuda, 2000).

However, Rutter et al (1975) reported that the combination of environmental factors (i.e., severe marital discord, low social class, paternal criminality, maternal mental disorder), rather than existence of a single factor, promote psychopathology in children. This argument was supported by a lot of scholars, such as Campbell (2000); Faraone and Biederman (1998); Rutter and Sroufe (2000); and Taylor (1999) where they established that genes- environment multiple interactions are linked to attention/ hyperactive disorder in children. Similar findings by Biederman et al (1995b,) corroborated earlier work by Rutter and his colleagues to establish that negative family-environment significantly influenced children with ADHD. In addition, the finding established that, exposure to parental psychopathology (particularly maternal) is more pertinent to families of children with ADHD than the control families (Biederman et al 1995b).

Interestingly, while some studies in the field of developmental approach established that children are born with a genetic predisposition that relates to hyperactive disorder (e.g., Faraone, Perlis, Doyle, Smoller, Goralnick, Holmgren, 2005), others maintained that heredities are rarely the sole reason for the development of attention/ hyperactive disorder, as MZ concordance rates is not near 100% (Faraone & Biederman, 2000; Kuntsi & Stevenson, 2000). Besides, some scholars maintained that 50% of children with hyperactive disorder do not display the biological anomaly associated with congenital factors (Swanson, et al., 1998). Therefore, in situation where biological predisposition is strongly established, family characteristics was viewed as reflection of the indicator and consequence of the disorder in children.

Furthermore, the categorization of relative contributions of shared versus non- shared hereditary and ecological menaces within the families of children diagnosed of ADHD is important for proper analysis of the disorder. For example, in a situation where there is a problem in a family, which is due to the disorder, or shared genetic susceptibilities, the family environments must be related to the child characteristics. On the other hand, when family breakdown is linked to the child empathy, the constancy of the disorder became aggravated. In this case, the family environment is associated with attention/hyperactive disorder not as a main cause, but as a factor that increased and influenced its development. However, children with ADHD develops relatively little tendency to the disorder, as confusing and uncaring family setting increase their behaviours (e.g., Carlson, Jacobvitz, & Sroufe, 1995). This means that, the degree of intellectual and physical stimulation that children received in their immediate environment impacted on their brain development and behavior (Halperin & Healey, 2011). Therefore, responsive and sensitive parenting promotes child self-regulation skills and parental difficulties that harmonize parents' activities with child's desires for development of disinhibited behaviour (e.g., Carlson, Jacobvitz, & Sroufe, 1995). So, when the family and child characteristics work in tandem, child`s temperament antecedents of inattentiveness and impulsivity that create or exacerbate parents' problems are moderated.

Genetic contributions to ADHD and developmental course

ADHD is not a genetic disorder in a clear sense, but can be categorised as a genetic factor that was shaped by developmental pathways. (Thapar, O'Donovan, & Owen, 2005). While past and present research continues to highlights the importance of genetic factors on ADHD (Faraone & Doyle 2001; Faraone & Tsuang 1995), attempts to recognize its source of using a candidate gene method to detect common hereditary variant have been less successful (Neale et al., 2010). Thus, genetic explanations of ADHD are determined by data, such as family and twin studies that shows ADHD as a familial and highly hereditary. This heritability was estimated to be in average of 76 % (Faraone et al., 2005). While it was established that attention/hyperactive disorder is a family oriented symptom, the first-degree families of affected persons displayed higher rates of the disorder (relative risk 4 -5). In addition, it was confirmed that the threats of the disorder are higher in families of those with history of hyperactive disorder (Faraone et al., 2005). This finding highlighted the significant agreement between early studies of children diagnosed with hyperactivity syndrome (Morrison and Stewart 1971) and successive studies that uses DSM-III and DSM-III-R definitions of ADHD (Biederman, Faraone, Keenan, Knee, & Tsuang, 1990).

A meta-analysis study conducted by Faraone et al., ( 2005 ) revealed a small but significant impacts for a number of assumed functional variants in genes controlling brain neurochemistry particularly, in the dopamine system (e.g., D4 and the dopamine transporter (DAT1) The common variants in genes of other neuromodulator systems (i.e., serotonin and norepinephrine) was also related with genes that control the general brain function and growth (e.g., Brophy, Hawi, Kirley, Fitzgerald, & Gill, 2002, Oades et al., 2008 ).

Furthermore, the analysis of comorbid psychiatric disorders supported the inherent heterogeneity of the ADHD in children. This established a significant degree of ADHD among families of adults with ADHD (Biederman et al 1995a). For example, the independent samples of children with DSM-III attention-deficit disorder and DSM-III-R ADHD are related to familial susceptibilities (Biederman et al., 1990; 1991b; 1992), while attention/hyperactive disorder and bipolar conditions was established as a separate familial subtype of ADHD in children (Faraone, Biederman, & Monuteaux , 2001a). Attention/ hyperactive disorder were also found to be familially free from anxiety disorders and learning disabilities (Faraone et al 1993). Based on this foregoing, we can conclude that stratification by behaviour and bipolar disorders divides the life of children diagnosed of ADHD into more familial related subgroups, and that major depressive disorder is a generic expression of different subtypes of ADHD in children. Therefore, persistent attention/hyperactive disorder are a useful phenotype for molecular genetic studies (Faraone et al 2001). However, despite the inaccessible findings in literature, individual gene relationships account for modest variation in ADHD expression in children (Faraone et al., 2005; Neale et al., 2010).

Twin and adoption studies

Due to the genetic nature of ADHD, twin's studies are consistently used to establish the heritability, or the level at which genetic characteristics influence attention/hyperactive disorder (Hudziak, Rudiger, Neale, Heath, & Todd, 2000; Kuntsi and Stevenson 2001; Martin, Scourfield, & McGuffin, 2002). The studies also offered a reliable evidence to support that, hereditary factors add to the aetiology of ADHD i.e., (60-91%) (Thapar et al, 2005b). Twin studies also confirmed that inherited factors are the main source of continuousness of attention/ hyperactive disorder particularly, the relationship between the disorder and disruptive behaviour (Thapar et al, 2006). The studies revealed that inherited factors impacted on ADHD and its developmental progression. Research on twins and adoption studies also established extra risk factors that do not have any significant influence on the origin of ADHD, but contributed to its clinical developmental outcomes. However, this notion was condemned because children genetic factor are chosen with a priori notion of genetic involvement in the syndrome, while in neuropsychiatric illnesses, the pathophysiology is typically unidentified.

Biological adversity

Research suggested that some biologic factors, such as lead contamination, food additives/diet, cigarette and alcohol exposure, to mention a few, contributed to the development of attention/hyperactive disorder in children. Though, Feingold Diet for ADHD was promoted by the media and acknowledged by most parents as a contributing factor, scientific enquiry showed that the idea is ineffectual, as addictiveness to food cannot cause attention/hyperactive disorder (Conners 1980). Research also argued that exposure to lead pollution causes restlessness, hyperactivity, distractibility, and lower intellectual ability in children diagnosed with hyperactive disorder. This idea was opposed by other studies, as it was established that lead account for only few of the majority of ADHD issues in children. This means that exposure to high lead environment does not necessary lead to hyperactive disorder in children. Further, research identified complications during pregnancy and delivery (i.e., maternal age, poor maternal health, and duration of labour) to mention a few as influenced development of ADHD in children (Sprich-Buckminster, Biederman, Milberger, Faraone, & Krifcher, 1993). They also confirmed that maternal smoking is related to the pathophysiology of ADHD that caused disruption to nicotinic receptors and changed dopaminergic activity.

Gene-environment interaction and ADHD

Though, studies on children with ADHD revealed a significant relationship between heredity and attention/hyperactive disorder, there are quite a number of environmental factors that connected with ADHD symptoms. Two of these factors have been systematically analysed and reported as a contributing factors for development of ADHD. These are: exposure to maternal smoking in pregnancy (Langley, Rice, & van den Bree, 2005) and low birth weight/prematurity (Bhutta, Cleves. & Casey, 2002). However, not all the vulnerable children that are exposed to environmental severity developed attention hyperactive disorder. The effects of gene-environment interaction on ADHD occurs when genes responds to environmental adversity. This is documented as important features of attention/hyperactive disorder in children.

However, only few works have probed the influence of G6E on development of children hyperactive disorder. For instance, a recent research on the issue established strong link between a DAT1 haplotype (combination of risk alleles) and attention/hyperactive disorder when mother is alcoholic during pregnancy (Brookes, Mill, & Guindalini, 2006), while others studies reported the DAT1 risk allele earlier found to be related with attention/hyperactive disorder as associated with hyperactive-impulsive symptoms found in children exposed to maternal smoking during pregnancy (Kahn, Khoury, & Nichols, 2003). Further, studies that focus on childhood behavioural disorder symptoms reported that children who carried the COMT gene risk variant are more vulnerable to the negative effects of lower birth weight (Thapar et al, 2005a). While all these findings require replication, the indication so far showed that, some genetic factors influenced children sensitivity to ecological adversity and the developmental sequence of attention/hyperactive disorder. Discussion

This systematic review used developmental perspectives to address the clinical and social factors associated with children diagnosed of ADHD. Specifically, it demonstrates that gene- environment interactions are important factors in the development of attention/ hyperactive disorder in children. By focusing on developmental perspective, the paper provided considerable evidence to support the influence of bio-psychosocial factors on behaviour of children diagnosed with attention/hyperactive disorder. Therefore, the present study supported the growing body of research that emphasised the use of developmental perspective as opposed to clinical treatment of children with attention/hyperactive disorder. The study also charted a developmental framework as bases for conceptualizing the effect of gene - environment interaction on children with ADHD, and reviewed the consequences and limitations of existing studies on the symptom by exemplifying the areas where untimely deductions have been obtained and where further effort is desirable.

Also the study established that parent-child interactions and gene-environment interaction impacted on the development of children with attention/hyperactive disorder. This means that, the stressful demanding and intrusive nature of children diagnosed with attention/hyperactive disorder evoked negative reactions from other family members and disrupted family relationships (Langley et al, 2005). The review of literature in this present study also revealed that children with attention/hyperactive disorder influenced their parent's behaviour and adjustment, and that parent's behaviour also impacted on development of children diagnosed with the disorder (Brookes et al, 2006). This further confirmed family characteristics and histories as the cause of attention/hyperactive disorder in children, as parent behaviour was linked to children conduct problems (Thapar et al, 2006).

Overall, there is a general concession of continuum association between genetic and environmental factors in children diagnosed with ADHD, as family factors were mentioned as the most influential variable that promote attention/hyperactive disorder in children. Though, the number of unsupportive or inconclusive studies actually limits these conclusions, this present review motivated research and hastens full informed conclusions about the clinical and social factors associated with children diagnosed of ADHD. Therefore, the dynamism of social and biological variables in children diagnosed with attention/hyperactive disorder is not only influenced by environmental factors, but also by common genetic characteristics of the parent and the child (Biederman,Faraone, et al., 1995).

Conclusions and recommendations

Although attention deficit hyperactive disorder is a predominant neurobehavioral illness in children, the symptom is characterised by factors such as hereditary, ecological, and biologic aetiologies that begin from conception to adulthood. Although its aetiology remains indeterminate, the developing evidence on the symptom documented its strong neurobiological and hereditary foundations and emphasised the phenotypic difficulty of disorder on children development. Therefore, there is a need to understand how genomic susceptibilities, family environment, parental characteristics, and children's experiences interrelate and modify its developmental pathway in children; as such efforts would prospectively enlighten and proffers intervention strategy that support its diagnose. Based on these assumptions, the following recommendations are suggested:

1. Effort should be directed toward understanding the mechanisms that underlie the associations between parental maladjustment and development of ADHD in children.

2. Future research should focus on developmental progression of attention/hyperactive disorder in children and underlie observed associations of family characteristics on the disorder.

3. Future research should focus on addressing the gaps and the great inconsistencies in the area of families characteristic and childhood attention/hyperactive disorder, because such inconsistencies remain unclear.

4. Future research should regularly embrace multiple informants and impartial assessments on childhood attention/hyperactive disorder, so that more confidence can be placed on the associations that are revealed.

5. Lastly, future research should be directed toward development of better focus theoretical models that focus on family influences and childhood attention/ hyperactive disorder, as most of the existing theory on the topic were focused on either the biological contributions of families or the contributions of family environment.

References

1. American Psychiatric Association.(2000). Diagnostic and StatisticalManual of Mental Disorders. 4th ed. Washington, DC: American Psychiatric Association.

2. American Psychiatric Association.(2013). Diagnostic and StatisticalManual of Mental Disorders.5th ed. Washington, DC: American Psychiatric Association.

3. Arnsten, A.F, (2007). Catecholamine and second messenger influenceson prefrontal cortical networks of “representational knowledge”:a rational bridge between genetics and the symptoms of mental illness. Cerebral Cortex, 17, i6-i15.

4. Arnsten, A.F, & Pliszka, S.R. (2011). Catecholamine influences on prefrontalcortical function: relevance to treatment of attentiondeficit/hyperactivity disorder and related disorders. Pharmacology, Biochemistry and Behavior, 99, 211-216.

5. Atladottir H.O, Parner E.T, & Schendel D. (2007). Variation in incidence of neurodevelopmental disorders with season of birth. Epidemiology, 18, 240-245.

6. Barkley, R. A. (2006). Attention deficit/hyperactivity disorder: A handbook for diagnosis and treatment (3rd ed.). New York: Guilford

7. Baumeister A.A, Hawkins M.F (2001). Incoherence of neuroimaging studies of attention deficit/ hyperactivity disorder. Clinical Neuropharmacology, 24, 2-10.

8. Berger I. (2011). Diagnosis of attention deficit hyperactivity disorder: much ado about something. Israeli Medical Association Journal, 13, 571-574.

9. Berger, A., Posner, M. I. (2000). Pathologies of brain attentionalnetworks. Neuroscience andBiobehavioral Reviews, 24, 3-5.

10. Biederman J, Faraone S.V, Keenan K, Knee D, &Tsuang M.T (1990): Familygenetic and psychosocial risk factors in DSM-III attention deficit disorder. Journal of American Academy of Child and Adolescent Psychiatry, 29, 526 -533.

11. Biederman J, Faraone SV, Keenan K, Tsuang MT (1991b): Evidence of familialassociation between attention deficit disorder and major affective disorders. Archives of General Psychiatry, 48, 633-642.

12. Biederman, J, Faraone, S.V, Keenan K, Benjamin, J, Krifcher, B. &Moore C. et al (1992). Further evidence for family-genetic risk factors in attention deficit hyperactivity disorder. Patterns of comorbidity in probands and relativesin psychiatrically and pediatrically referred samples. Archives of General Psychiatry, 49, 728 -738.

13. Biederman, J., Milberger, S., Faraone, S. V., Kiely, K., Guite, J.,Mick, E., Ablon, S.,

14. Warburton, R., & Reed, E. (1995). Family environment risk factors for attention deficit hyperactivity disorder: A test of Rutter's indicators of adversity. Archives of General Psychiatry, 52, 464-470.

15. Biederman, J., Faraone, S.V., Mick, E., Spencer,T.,Wilens,T., Kiely,K., Guite, J., Ablon, J. S., Reed, E., & Warburton, R. (1995). High risk for attention deficit hyperactivity disorder among children of parents with childhood onset of the disorder: A pilot study. Journal of American Psychiatry, 152, 431-435.

16. Biederman J, Faraone S.V, Monuteaux M, Spencer T, Wilens T, Bober M, et al (2004). Gender effects of attention deficit hyperactivity disorder inadults, revisited. Biological Psychiatry, 55, 692-700.

17. Brookes, K.,Mill, J.,&Guindalini,C., et al (2006). Acommon haplotype of the dopamine transporter geneassociated with attention-deficit/hyperactivity disorderand interacting withmaternal use of alcohol duringpregnancy. Archives of General Psychiatry, 63, 74-81.

18. Brophy, K., Hawi, Z., Kirley, A., Fitzgerald, M., & Gill, M. (2002). Synaptosomal- associated protein 25 (SNAP-25) and attention deficit hyperactivity disorder (ADHD): Evidence of linkage and association in the Irish population. Molecular Psychiatry, 7,913917

19. Campbell, S. B. (2000). Attention-Deficit/Hyperactivity Disorder: A developmental view. In: Handbook of Developmental Psychopathology. (pp. 383-401). A. J. Sameroff, M. Lewis, & S. Miller (Eds.). New York: Kluwer Academic/Plenum.

20. Carlson, E. A., Jacobvitz, D., & Sroufe, L. A. (1995). A developmental investigation of inattentiveness and hyperactivity. Child Development, 66, 37-54.

21. Childress, A.C, Berry, S.A (2012). Pharmacotherapy of attention-deficit hyperactivity disorder in adolescents. Drugs, 72, 309-325.

22. Cortese, S (2012). The neurobiology and genetics of attention-deficit/hyperactivity disorder (ADHD): what every clinician shouldknow. European Journal of Paediatric Neurology, 16, 422-433.

23. Dopheide, J.A (2005). ASHP therapeutic position statement on theappropriate use of medications in the treatment of attention deficit/hyperactivity disorder in paediatric patients. American Journal of Health System Pharmacy, 62, 1502- 1509.

24. Coghill, D., Nigg, J., Rothenberger, A., Sonuga-Barke, E., & Tannock, R. (2005). Wither causal models in the neuroscience of ADHD? Developmental Science, 8, 105-114.

25. Cummings, E. M., Davies, P., & Campbell, S. B. (2000). Developmental Psychopathology and Family Process: Research, Theory, and Clinical Implications. New York: Guilford.

26. Faraone, S. V., Perlis, R. H., Doyle, A. E., Smoller, J. W., Goralnick, J. J., Holmgren, M. A., et al. (2005). Molecular genetics of attention-defi cit/hyperactivity disorder. Biological Psychiatry, 57 , 1313-1323.

27. Faraone, S, Biederman, J, Krifcher Lehman, B, Keenan, K, Norman, D, Seidman, L. et al. (1993). Evidence for the independent familial transmission of attentiondeficit hyperactivity disorder and learning disabilities: Results froma family genetic study. American Journal of Psychiatry, 150, 891- 895.

28. Faraone, S. V, Tsuang, M. T. (1995). Methods in psychiatric genetics. In: Textbook in Psychiatric Epidemiology, Tohen, M, Tsuang, M., Zahner, G. (Eds). (pp. 81-134). New York: John Wiley& Sons.

29. Faraone, S. V. & Biederman, J. (1998). Neurobiology of attentiondeficit hyperactivity disorder. Biological Psychiatry, 44, 951-958.

30. Faraone S.V, Biederman J, &MonuteauxM.C. (2001a). Attention deficit hyperactivity disorder with bipolar disorder in girls: Further evidence for a familial subtype? Journal of Affect Disorders, 64, 19 -26.

31. Faraone S.V, Doyle A.E (2001): The nature and heritability of attention

deficit/hyperactivity disorder. Child and Adolescent Psychiatric Clinics of North America, 10, 299 -316, viii-ix.

32. Faraone, S.V., & Biederman, J. (2000). Nature, nuture, and attentiondeficit hyperactivity disorder. Developmental Review, 20, 568-581.

33. Faraone S.V, Perlis R.H, Doyle A.E, Smoller J.W, Goralnick J, &Holmgren M.A, et al. (2005). Molecular genetics of attention deficit hyperactivity disorder. Biological Psychiatry, 57, 1313-1323.

34. Gray, J. A., Feldon, J., Rawlins, J. N. P., Hemsley, D. R., & Smith, A. D. (1991) The neuropsychology of schizophrenia. Behavioral and Brain Sciences, 14, 1-84.

35. Gray, J. A. (1982). The neumpsychology of anxiety. New York: Oxford University Press.

36. Halperin, J. M., & Healey, D. M. (2011). The infl uences of environmental enrichment, cognitive enhancement,and physical exercise on brain development: Can we alter the developmental trajectory of ADHD? Neuroscience and Biobehavioral Reviews, 35,621634.

37. Hauschild K.M, Mouridsen S.E, & Nielsen S. (2005). Season of birth inDanish children with language disorder born in the 1958-1976 period. Neuropsychobiology; 51, 93-99.

38. Hudziak J.J, Rudiger L.P, Neale M.C, Heath A.C, & Todd R.D (2000). A twin study of inattentive,aggressive, and anxious/depressed behaviors. Journal of the American Academy of Child and Adolescent Psychiatry, 39, 469 -476.

39. Kahn, R. S., Khoury, J. & Nichols,W.C., et al (2003). Role of dopamine transporter genotype and maternal prenatal smoking in childhood hyperactive-impulsive,inattentive, and oppositional behaviors. Journal of Pediatrics, 143, 104-110.

40. Kesner R.P, & Churchwell J.C (2011). An analysis of rat prefrontal cortexin mediating executive function. Neurobiology of Learning and Memory, 96, 417-431.

41. Kuntsi, J.,& Stevenson, J. (2000). Hyperactivity in children:Afocuson genetic research and psychological theories. Clinical Child and Family Psychology Review, 3, 1-24.

42. Langley, K., Rice, F., & van den Bree, M. B., et al (2005). Maternal smoking during pregnancy as an environmental risk factor for attention deficit hyperactivity disorder behaviour. A Review. MinervaPediatrica, 57, 359-371.

43. Manshadi M, Lippmann S, O'Daniel R, & Blackman A (1983): Alcohol abuse and attention deficit disorder. Journal of Clinical Psychiatry, 44, 379 -380

44. Martin N, Scourfield J, McGuffin P (2002).Observer effects and heritability ofchildhood attention-deficit hyperactivity disorder symptoms. British Journal of Psychiatry, 80, 260 - 265.

45. Neale, B. M., Medland, S. E., Ripke, S., Asherson, P., Franke, B., Lesch, K. P., et al. (2010). Meta-analysis of genome-wide association studies of attention-defi cit/ hyperactivity disorder. Journal of the American Academy of Child and Adolescent Psychiatry, 49 , 884-897.

46. Nigg J, Nikolas M, & Burt S. A(2010). Measured gene-by-environment interaction in relation to attention-deficit/hyperactivity disorder. Journal of the American Academy of Child and Adolescent Psychiatry, 49, 863-73.

47. Oades, R. D., Lasky-Su, J., Christiansen, H., Faraone, S.V., Sonuga-Barke, E. J.,

48. Banaschewski, T., et al. (2008). The influence of serotonin- and other genes onimpulsive behavioral aggression and cognitive impulsivity in children with attentiondeficit/hyperactivity. A Developmental Perspective on ADHD disorder (ADHD): Findings from a family-based association test (FBAT) analysis. Behavioral and Brain Functions, 4, 4-48.

49. Pastor P. N & Reuben C.A. (2008). Diagnosed attention deficit hyperactivity disorder and learning disability: United States, 2004-2006. Vital Health Statistics, 10, 1-14.

50. Quay, H. C. (1988a). Attention deficit disorder and the behavioral inhibitionsystem: The relevance of the neuropsychological theory of Jeffrey A. Gray. In: Attention deficit disorder: Criteria, cognition, intervention (pp. 117-126). L. M. Bloomingdale & J. Sergeant (Eds.). NewYork: Pergamon.

51. Quay, H. C. (1988b). The behavioral reward and inhibition systems inchildhood behavior disorder. In: Attentiondeficit disorder W; New research in treatment, psychopharnmcology, and attention (pp. 176-186). L. M. Bloomingdale (Ed.). NA: Pergamon.

52. Quay, H. C. (1996, January). Gray'sbehavioral inhibition in ADHD:An update. Paper presented at the annual meeting of the InternationalSociety for Research in Child and Adolescent Psychopathology, Los Angeles, CA.

53. Rader, R, McCauley L,& Callen, E.C. (2009). Current strategies in thediagnosis and treatment of childhood attention-deficit/hyperactivity disorder. American Family Physician, 79, 657-665.

54. Robbins, T. W. (2003). Dopamine and cognition. Currpin Neurol,16, (2), S1-S2.

55. Rutter, M, Cox, A, Tupling, C, Berger, M, &Yule, W. (1975). Attainment and adjustment in two geographical areas. 1--The prevalence of psychiatric disorders. British Journal of Psychiatry, 126, 493-509.

56. Rutter, M., &Sroufe, L. A. (2000). Developmental psychopathology: Concepts and challenges. Development and Psychopathology, 12, 265-296.

57. Sergeant, J. (2000). The cognitive-energetic model: An empiricalapproach to attention- deficit hyperactivity disorder. NeuroscienceandBiobehavioralReviews, 24, 7-12.

58. Sherman D, McGue M, &Iacono W (1997). Twin concordance for attention deficit hyperactivity disorder: A comparison of teachers' and mothers'reports. American Journal of Psychiatry, 154, 532-535.

59. Sonuga-Barke, E. J., Auerbach, J., Campbell, S. B., Daley, D., & Thompson, M. (2005). Preschool varieties of hyperactive and dysregulated behaviour: Multiple pathways between risk and disorder. Developmental Science, 8,141-150.

60. Sonuga-Barke, E. J., Bitsakou, P., & Thompson, M. (2010). Beyond the dual pathway model: Evidence for the dissociation of timing, inhibitory, and delayrelated impairments in attention-defi cit/hyperactivity disorder. Journal of the American Academy of Child and Adolescent Psychiatry, 49,345-355.

61. Sonuga-Barke, E. J., & Halperin, J. (2010). Developmental phenotypes and causal pathways in attention deficit/hyperactivity disorder: Potential targets for early intervention? Journal of Child Psychology and Psychiatry, 51, 368-398.

62. Sprich-Buckminster S, Biederman J, Milberger S, Faraone S, &Krifcher LehmanB (1993): Are perinatal complications relevant to the manifestation ofADD? Issues of comorbidity and familiality. Journal of American Academy of Child and Adolescent Psychiatry, 32, 1032-1037

63. Swanson, J. M., Sunohara, G. A., Kennedy, J. L., Regino,R., Fineberg, E.,Wigal, T., Lerner, M.,Williams, L., LaHoste,G. J.,&Wigal, S. (1998). Association of the dopamine receptorD4 (DRD4) gene with a refined phenotype of attention deficithyperactivity disorder (ADHD): A family-based approach.Molecular Psychiatry, 3, 38-41.

64. Taylor, E. (1999). Developmental neuropsychopathology of attentiondeficit and

65. impulsiveness. Development and Psychopathology, 11, 607-628.

66. Thapar, A.,O'Donovan,M., &Owen,M. J. (2005b). The genetics of attention deficit hyperactivity disorder. Human Molecular Genetics, 14, 275-282.

...

Подобные документы

  • The study of harm to children from watching American cartoons. Problem of imitating negative or mindless characters from cartoons. Leading role of American cartoon industry in the animation history. First steps in the progress of a child’s development.

    эссе [16,3 K], добавлен 11.04.2013

  • The problem of evaluation, self-assessment of personality as a psychological category. Factors of formation evaluation and self-esteem of children of primary school age. An experimental study of characteristics evaluation and self-esteem of junior pupils.

    курсовая работа [28,6 K], добавлен 19.05.2011

  • Research of negative influence of computer games with the elements of violence and aggression on psychical development of children and teenagers. Reasons of choice of computer games young people in place of walk and intercourse in the real society.

    доклад [15,3 K], добавлен 10.06.2014

  • Studies by Fischer and his colleagues and Dawson (2006) have investigated development in a wide range of domains, including understanding of social interaction concepts such as "nice" and "mean", skills in mathematics, and understanding "leadership".

    реферат [20,2 K], добавлен 22.12.2009

  • The characteristic features of the two forms of eating disorders: anorexia nervosa and bulimia. Description body dysmorphic disorder syndrome as a teenager painful experiences of his "physical disability." Methods of treatment and prevention of disease.

    курсовая работа [17,9 K], добавлен 31.03.2013

  • The children's theatre, puppet shows and an important role in the ideological and aesthetic education of children, appreciation of literature's classical heritage. The thematic plan of the theatre. The Moscow Central Children's Theatre's repertoire.

    контрольная работа [12,1 K], добавлен 18.07.2009

  • Russian press for the young reader as opposed to the "adult" started with a magazine. History of child Journalism Beginning of a new era in the Children's journalism. Authors of children's creative destiny "Chizh", "Hedgehog" - to the brightest example.

    реферат [11,6 K], добавлен 28.02.2009

  • Tweens and teens problems. Beating children will be a crime. High-tech and children. Modern family problems and generation gap. Internet as dangerous drugs of present tense. New anti-drugs campaign for young people. Suicide among the teenagers.

    реферат [31,5 K], добавлен 22.02.2011

  • The Communicative Approach. Children’s ability to grasp meaning. Children’s creative use of limited language resources. Children’s instinct for play and fun. Lessons preparation in junior forms. The role of imagination. General steps a lesson preparation.

    курсовая работа [8,2 M], добавлен 02.01.2012

  • Establishing in single customs territory of the Customs Union uniform mandatory requirements for the use and implementation of products intended for children and adolescents, to ensure the free movement of products intended for children and adolescents.

    презентация [10,6 M], добавлен 26.10.2021

  • The word "family" is connected with warm relations between members. Family relations. Both the husband and the wife create their future together. Children should love and respect the parents. A family role in children's formation of individuality.

    топик [11,2 K], добавлен 04.02.2009

  • Instability, disorder, harm, discomfort to the ecosystem. Pollution control environmental management. Pollution generated by human activities. Some of the major causes of the pollution. Deforestation due to urbanization in various parts of the world.

    реферат [290,9 K], добавлен 22.11.2012

  • Features of training of younger schoolboys and preschool children. Kognitivnoe development of preschool children. Features of teaching of English language at lessons with use of games. The principal views of games used at lessons of a foreign language.

    курсовая работа [683,5 K], добавлен 06.03.2012

  • Irony, as a widely used figure of speech, received considerable attention from linguists. The ways of joining words and the semantic correlation of words and phrases. Classification of irony and general distinctions between metaphor, metonymy and irony.

    реферат [20,5 K], добавлен 05.02.2011

  • Problems of child's psychological development. "Hot-Cold" games (for children till 7 years old). Intellectual Eye Measurer. Definitions and classification. Assessment. Computer, teacher's version. Mathematics. Statistics (for training of banking workers).

    реферат [46,3 K], добавлен 19.09.2015

  • The pathological process Acute Respiratory Distress Syndrome (ARDS). Specific challenges in mechanical ventilation of patients with ARDS. Causes of ARDS, and differential diagnosis. Treatment strategies and evidence behind them. Most common causes ARDS.

    презентация [2,6 M], добавлен 21.05.2015

  • Methods of foreign language teaching. The grammar-translation method. The direct, audio-lingual method, the silent way and the communicative approach. Teaching English to children in an EFL setting. Teaching vocabulary to children. Textbook analysis.

    курсовая работа [142,6 K], добавлен 09.12.2012

  • Mathematical learning for young children. Patterns and perspectives of teaching mathematics in primary school. The purposes and content of modern mathematical education in primary school. The methods of child’s acquaintance with geometric shapes.

    реферат [35,9 K], добавлен 02.04.2009

  • The events in the novel "To Kill a Mockingbird". The opposition between children’s and adults. "The Secret Diary of Adrian Mole" as the picture of the world from the point of view of a teenager. Examples of Adrian’s relations with adults in the novel.

    реферат [13,5 K], добавлен 16.05.2016

  • The Description of the UK climate and factors which influence the climate of Britain. The description of seasons and weather in different months and its description in classical literature and children’s books. The theme of the weather in everyday speech.

    курсовая работа [4,7 M], добавлен 18.04.2011

Работы в архивах красиво оформлены согласно требованиям ВУЗов и содержат рисунки, диаграммы, формулы и т.д.
PPT, PPTX и PDF-файлы представлены только в архивах.
Рекомендуем скачать работу.