Attention Deficit Hyperactivity Disorder

Attention Deficit/Hyperactivity disorder (ADHD) is one of the most commonly diagnosed behavioral disorder in children and adolescents (Schneider, 2006) which is characterized by symptoms of impaired attention, hyperactivity and impulsive behavior (Polanczyk, 2007).

The clinical features of ADHD were first recognized as early as in 1845 when Heinrich Hoffmann, a German physician identified two boys who had symptoms of deficits in attention and hyperactivity and named them “Johnny Look-in-the Air” and “Fidgety Philip” (Acosta, 2004) and over the years, different clinical presentations of this disorder have been given several names including Encephalitis Lethargica, Minimal Brain Damage (MBD), Minimal Cerebral Palsy, Mild Retardation, Minimal Brain Dysfunction, Atypical Ego Development, Hyperkinesis (“hyperactivity”), and Attention Deficit Disorder (ADD) (Rafalovich, 2001).

However, the diagnostic criteria for ADHD were first delineated in 1980 in DSM III (Acosta, 2004). As discussed above, ADHD is the most commonly diagnosed behavioral disorder amongst children. Different studies have estimated variable rates of prevalence for ADHD ranging on an average from 5-10% globally (Polanczyk, 2007). The American Psychiatric Association (1994) estimated that around 3-5% of children belonging to the school going age group and between 2-4% of the adults suffer from ADHD.

ADHD has been shown to affect males more commonly as compared to females, with the male to female ration approaching 9:1 (APA, 1994). The symptoms of ADHD are diverse and ADHD has been shown to be a “heterogeneous condition” with significant variability being observed in core symptoms amongst children diagnosed with this condition (Amen, 2001 and Newcorn et al. , 2001). The symptoms of ADHD include problems in attention, hyperactivity and difficulty in impulse control. Impairments in attention include poor attention, lack of concentration, forgetfulness, distraction and poor task organization.

Children with ADHD often display hyperactivity with excessive and inappropriate motor activities such as running and being excessively noisy. They also display problems with impulse control and thus often experience difficulties in mingling with others or engaging in group activities. According to both the DSM IV and ICD 10 the above mentioned symptoms should be present in children before the age of seven years and should have been observed in more than one setting (for example at home and in school).

Moreover, the symptoms should persist for more than 6 months for a diagnosis of ADHD to be made (Williams, 1999). For several decades there has been an ongoing debate on the etiology of ADHD with contributions of both nature (genetics) and nurture (environment) and it has been postulated that ADHD is a multifactorial disorder arising from an interplay of both environmental and genetic factors. The ‘nature’ theory of the etiology of ADHD is based on the findings that ADHD is often familial, with higher rates of concordance (varying between 55% to 90%) amongst monozygotic twins (Dopheide, 2001).

Moreover, these findings have been supported by adoption studies which have also proven the role of genetics as opposed to environment in causing the familial clustering observed in ADHD (Morrison, 1971). Spencer et al. in their evaluation of eight studies done on the etiology of ADHD found that approximately 75% of the etiologic contribution to ADHD is genetic (Spencer, 2002). However, the inheritance of ADHD is complex and does not follow the classical Mandelian patterns (Acosta, 2004). There are several biological and physiological abnormalities found in the brains of individuals with ADHD.

It has been proposed that ADHD occurs as a result of a chemical imbalance in the brain resulting from the deficiency of the neurotransmitter, dopamine which also plays a role in the etiology of other neurologic and psychiatric disorders including Depression and Schizophrenia. Various studies have been conducted in order to elucidate the genetic basis of ADHD and several genes have been implicated to play a role in the pathogenesis of ADHD. Amongst these, the most consistent genetic association has been found for the 7-repeat allele of the D4 dopamine receptor gene (DRD4*7) (Spencer, 2002).

It has also been proven that in individuals with ADHD there is an over expression of Dopamine transporters especially dopamine transporter-1 (DAT1) in the presynaptic nerve terminal. This transporter is responsible for the reuptake of dopamine from the synaptic cleft. Moreover, there is a defect in the dopamine receptors (DRD4) on the postsynaptic cell. Both these factors lead to a decreased concentration of dopamine in the brain synapses and hence lead to disorders of attention and impulse control (Dopheide, 2001).

Moreover, studies using SPECT (single photon emission computed tomography) and PET (positron emission tomography) scanning have shown that there is under activity in the caudate nuclei/subcortical striatum, the prefrontal and frontal areas, the limbic system, the posterior periventricular regions, and the corpus callosum of ADHD children (Williams, 1999). However, the temporality of whether these changes precede the onset of attention deficit or follow it is yet to be established.

Other biological findings in ADHD individuals include abnormal thyroid function in up to 5% of the children and association with low birth weight (Williams, 1999). With regard to the ‘Nurture’ theory of ADHD, several environmental factors leading to the development of ADHD have been elucidated. These include an imbalanced diet, food allergies, use of certain antibiotics, and low levels of certain nutrients such as zinc, calcium, magnesium and/or B6 and omega-3 fatty acids (Dopheide, 2001). However, till date none of these factors have been proven to be the primary disorder leading to the development of ADHD in children.

Another important factor which has been implicated in the etiology of ADHD is sleep deprivation and this was validated by a recent study conducted at the University of Louisville School of Medicine showed a reduction in the symptoms of ADHD children in the day following a proper night’s sleep (O’Brien et al. 2003). Early life experiences have also been shown to play a role in ADHD etiology with children who are brought up in institutional settings displaying higher rates of ADHD as compared to those who are not (Williams, 1999).

Similarly, the role of parenting and parenting mental health has also been postulated. It has been shown that offsprings of parents who are more assertive, critical and directive have a higher incidence of hyperactivity. Moreover, chaotic and mentally disturbing home environments including those with family disputes, marital disharmony and hostile parents have also been shown to have an association with ADHD. Parental mental health has also been found to be an important factor with maternal depression having a positive association with ADHD (Williams, 1999).

Although all these factors have been found to be associated with the development of ADHD, it should be kept in mind that these factors do not solely contribute towards the pathology of ADHD. More recently, the psychosocial theory of ADHD has been promulgated whereby in addition to ‘nature’ and ‘nurture’, psychosocial factors have been postulated to play a role in the development of ADHD. However, this is a relatively unexplored arena and further research needs to be undertaken in order to prove an association between psychosocial factors and ADHD.

The management of ADHD is multimodal and includes pharmacotherapy, behavioral interventions and educational interventions (Williams, 1999). In conclusion, ADHD is a common disorder amongst children which can lead to significant social and functional impairment. The etiology of ADHD is diverse and complex and till date no single etiologic factor which exclusively leads to the development of ADHD has been identified, as put by Tranoy: “It is said that children are inattentive because they have ADHD and that they have ADHD because they are inattentive” (Tranoy 2001).

References Acosta, Maria T. , Arcos-Burgos M. and Muenke M. (2004) Attention deficit/hyperactivity disorder (ADHD): Complex phenotype, simple genotype? Genetics In Medicine 6(1): 1-15 Amen, D. G. (2001). Healing ADD: The Breakthrough Program That Allows You to See and Heal the 6 Types of ADD. G. P. Putnam’s Sons: New York. Morrison JR, Stewart MA. A family study of the hyperactive child syndrome. Biol Psychiatry 1971;3:189–195. Newcorn, J. H. , J. M. Halperin, P. S. Jensen, et al.

(2001). Symptom profiles in children with ADHD: Effects of comorbidity and gender. J. Am. Acad. Child Adolesc. Psychiatry 40(2):137-145. O’Brien, L. M. , C. R. Holbrook, C. B. Mervis, et al. (2003). Sleep and neurobehavioral characteristics of 5- to 7-year-old children with parentally reported symptoms of attention-deficit/hyperactivity disorder. Pediatrics 111(3):554-63. Polanczyk G. and Rohde L. (2007) Epidemiology of attention-deficit/hyperactivity disorder across the lifespan.

Current Opinion in Psychiatry 2007, 20:386–392 Rafalovich, A. (2001). The conceptual history of Attention Deficit Hyperactivity Disorder: Idiocy, imbecility, encephalitis and the child deviant, 1877-1929. Deviant Behavior: An Interdisciplinary Journal 22:93-115. Schneider H. and Eisenberg D. (2006). Who Receives a Diagnosis of Attention-Deficit/Hyperactivity Disorder in the United States Elementary School Population? Pediatrics 117;e601-e609

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