Attention Deficit Hyperactive Disorder

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7 July 2016

PSYC 4213 Physiological Psychology and Neuroscience

Dr. Carol Armstrong

(ADHD) is a neural disorderaffecting mostly children and can be carried to adulthood. ADHDsymptoms include persistent inattention, which entails increaseddistractibility and reduced attention span hyperactivity andincreased impulsivity with reduced inhibitions (Kalat, 2015). ADHDhas a very high prevalence in young people accounting for about 6% ofchildren (based on DSM-IV criteria). Around 40-50% of childrendiagnosed with ADHD carry the symptoms in adulthood. 2-3% of adultshave the disorder.

The negative symptoms of ADHD are worrisome and affect children’sperformance and growth patterns (Kalat, 2015). Many studies have beenmade on this disorder and various treatment schedules have beenrecommended to counter the symptoms. It is paramount that moreresearch be made to enable early diagnosis and timely treatment ofthe symptoms before they get worse. This paper will look into thegenetic predisposition of ADHD, brain parts affected prevalenceaccording to age, gender and ethnicity and the effects of ADHD onboth physical and developmental patterns as well as current treatmentschedules.


In many twin studies, ADHD has been correlated with geneticinheritance from the parents. In 75% of cases, children of patientswith ADHD have about 4 times likelihood of having the disorder(Gizer, Ficks &amp Waldman, 2009). Many gene studies have markedvarious genes associated with ADHD. Most of these genes are based ontheir involvement in dopamine neurotransmission especially in thebasal ganglia which regulates dopamine activity in these regions(Gizer, Ficks &amp Waldman, 2009). Inheritance of the polymorphismsand mutations in these genes accounts for the disease process andsymptoms seen in ADHD.

DAT1 gene has been marked as a major candidate for ADHD geneticinheritance and many twin studies on DAT1 polymorphism has positivelyproved the association with ADHD development (Gizer, Ficks &ampWaldman, 2009). DAT1 is a dopamine transporter gene on chromosome 5which codes for carrier protein for reuptake of dopamine fromsynaptic clefts to presynaptic neurons. Many current treatments forinstance, methylphenidate block these proteins thereby increasingdopamine levels in the synaptic clefts for neurotransmission. Anothermajor gene associated with ADHD is dopamine D4 receptor gene (DRD4)on chromosome 11 (Gizer, Ficks &amp Waldman, 2009). DRD4 is aG-protein coupled receptor which inhibits adenylyl cyclase therefore,increasing available dopamine levels. DRD4 is chiefly expressed infrontal lobe regions of the cortex, the brain regions involved in theetiology of this disorder. Orbitofrontal cortex andanteriorcingulatein particular, have high expression of these receptors(Gizer, Ficks &amp Waldman, 2009).

The other major gene that have been associated with the disorderinclude Dopamine D2 receptor gene (DRD2) which code for D2 receptorsexpressed in many brain parts thought to be involved in ADHD such asbasal ganglia and prefrontal cortex (Gizer, Ficks &amp Waldman,2009). It plays an important role in reward pathways ofneurotransmission. Dopamine D5 receptor gene (DRD5) is also involvedin the disorder and is well expressed in the hippocampus and relatedstructures (Gizer, Ficks &amp Waldman, 2009). Dopamine D3 receptorgene (DRD3) involved in incentive based learning is also mapped withADHD. It is highly expressed in substantia nigra and nucleusaccumbens parts of basal ganglia. Catechol-O-methyl-transferase(COMT) gene is associated with ADHD in that it plays a key role inregulating dopamine levels in the brain (Gizer, Ficks &amp Waldman,2009). Dopamine beta hydroxylase (DBH) gene involved in theconversion of dopamine to norepinephrine is indicated in ADHD sinceboth neurotransmitters are involved in the disorder (Gizer, Ficks &ampWaldman, 2009).

Other dopaminergic genes involved in the disorder includeNorepinephrine transporter gene (SLC6A2) and Monoamine oxidase A(MAOA) genes (Gizer, Ficks &amp Waldman, 2009). Other genesassociated with ADHD involve serotonin and adrenergic pathways andinclude SERT, ADRA2A and GRIN2A, TPH2, BDNF HTR1B, and SNAP25(Gizer, Ficks &amp Waldman, 2009). In heritance of all the mutationsin such genes from the parents distort the normal mechanism ofneurotransmission in dopamine, serotonin and adrenergic pathwaysthereby, bringing the effects and symptoms of ADHD.

Age, Gender, and Ethnicity

ADHD presents before the age of 7 years and varies from one person toanother. The patients presents with abnormal developmental milestonesfrom the other children presenting with delayed motor and speechdevelopment, hyperactivity and inattention. ADHD affect more malesthan females (Kessler et al., 2006). Non-Hispanic white have a higherprevalence of ADHD as compared to Hispanics and African Americansblacks. This is probably related to genetic predisposition in thispopulation.

Affected Areas of the Brain

ADHD affects the parts of the brain involved in Dopamine,Norepinephrine and Serotonin neurotransmission. The basal ganglia andits parts is a chief part of the brain that is affected in ADHD(Konrad &amp Eickhoff, 2010).Prefrontal lobe of the cortex is alsoinvolved. These areas show reduced brain volume in patients with ADHDas compared to those without the disorder. Certain pathways are alsoinvolved such as prefrontal-striatal-cerebellar as well asprefrontal-striatal-thalamic pathways (Konrad &amp Eickhoff, 2010).

Prefrontal cortex is involved in execution functions (cognitive andbehavior control) which include cognitive processes such as attentioncontrol working memory flexibility in cognition inhibitorycontrol problem solving reasoning and planning (Konrad &ampEickhoff, 2010). Any mutations in the dopaminergic and noradrenergicpathways to prefrontal cortex result into the symptoms ofinattention, hyperactivity and impulsiveness seen in ADHD. Thepatients also have problems with handwriting and speech development.Their short or working memory is impaired and cannot remember learnedthings easily. Language and motor development is also compromised.

Basal ganglion is involved in reward perception, motivation,reinforcement, stimulus response learning and motor function (Konrad&amp Eickhoff, 2010). Basal ganglia include the striatum, nucleusaccumbens and hippocampus and parts of the thalamus. Blunted pathwaysfrom the basal ganglia correlate with the symptoms seen in ADHD suchas de-motivation, blunted memory, learning difficulties, bluntedspeech development and poor motor development.

Physical Appearance

Children with ADHD have many physical changes from birth. They arealways restless. They have sleep disorders and stay awake most of thetime (Kalat, 2015). They have soft signs like problems with fingertapping, always fidgeting and have impaired fine motor skills. Theyoften talk excessively with no apparent meaning to the conversation.

Developmental Delays

Patients with ADHD have many cognitive and behavioral problems basedon the disturbances in the dopaminergic and noradrenergic pathways tothe prefrontal cortex and basal ganglia. The patients also haveproblems with handwriting and speech development (Kalat, 2015). Theirshort or working memory is impaired and cannot remember learnedthings easily. Language and motor development is also compromised.

Current Suggested Treatment

The current treatment schedules are both medical and cognitivetherapies. The commonly used medical treatments are psycho-stimulantswhich include Methylphenidate, Amphetamine and Dextrpamphetamine(Kliegman et al., 2011).These drugs work to increase the level ofdopamine in the brain. Other medical regimens include TricyclicAntidepressants like Imipramine and Desipramine noradrenergicreuptake inhibitor like Atomoxetine and alpha agonist like Clonidine(Kliegman et al., 2011).

Medical treatment alone is not recommended and cognitive therapiesare indicated too. Some of the therapies indicated include cognitivebehavioral therapy psycho-educational input family therapy andschool based interventions (Kliegman et al., 2011). These therapiesare particularly important for patients with mild symptoms of ADHD.


Gizer, I. R., Ficks, C., &amp Waldman, I. D. (2009). Candidate genestudies of ADHD: a meta-analytic review. Human genetics, 126(1), 51-90

Kalat, J. W. (2015). Biological psychology. Scarborough:Nelson Education.

Kessler, R. C., Adler, L., Barkley, R., Biederman, J., Conners, C.K., Demler, O., &amp Spencer, T. (2006). The prevalence andcorrelates of adult ADHD in the United States: results from theNational Comorbidity Survey Replication. American Journal ofPsychiatry, 163(4), 716-723

Kliegman, R. M., Sarnat, H. B., Behrman, R. E., Jenson, H. B., &ampStanton, B. F. (2011). Nelson textbook of pediatrics.Amsterdam: ElsevierPublishing Company

Konrad, K., &amp Eickhoff, S. B. (2010). Is the ADHD brain wireddifferently? A review on structural and functional connectivity inattention deficit hyperactivity disorder. Human brain mapping, 31(6), 904-916