‭Chapter 8: Attention-Deficit Hyperactivity Disorders‬ ‭academic, occupational functioning‬‭.

‬
‭ ) The symptoms do not occur exclusively during the course of schizophrenia or another‬
E
‭psychotic disorder &‬‭Not better explained by another mental disorder‬
‭(ADHD)‬
‭Specify‬‭Presentation‬‭:‬
‭8.1 Accompanying Psychological Disorders & Symptoms‬ ‭Combined‬‭(ADHD-C) >‬‭Inattention + Hyperactivity–impulsivity‬‭for past‬
‭6 months.‬
‭DSM-5 Diagnostic Criteria‬ ‭Predominantly inattentive‬‭(ADHD-PI) >‬‭Inattention‬‭but no‬
‭A)‬ P ‭ ersistent inattention‬‭and/or‬‭hyperactivity-impulsivity symptoms that interferes with‬ ‭hyperactivity–impulsivity for past 6 months.‬
‭functioning/development (‬‭6 or more symptoms‬‭for‬‭child‬‭/‭5 ‬ or more‬‭symptoms for‬ ‭Predominantly hyperactive–impulsive‬‭(ADHD-HI) >‬
‭adult‬‭, from each category for‬‭at least 6 months‬‭)‬ ‭Hyperactivity–impulsivit‬‭y but no inattention for the past 6 months.‬
‭1.‬ ‭Inattention‬‭:‬
‭a.‬ ‭Fails to pay close attention to details/makes‬‭careless mistakes‬‭(eg.,‬ ‭Specify if:‬
‭overlooks/misses details‬‭, inaccurate work).‬ ‭In‬‭partial remission‬‭> Full criteria were previously met,‬‭fewer criteria‬
‭b.‬ ‭Difficulty sustaining attention‬ ‭have been met for the past 6 months‬‭& functional impairment still‬
‭c.‬ ‭Does‬‭not seem to listen when spoken to‬‭(even in the absence of any‬ ‭present‬
‭obvious distraction)‬
‭d.‬ ‭Does not follow instructions &‬‭fails to finish assigned tasks‬‭(eg.,‬‭starts‬ ‭Specify current‬‭severity‬‭:‬
‭tasks but quickly loses focus & gets sidetracked‬‭)‬ ‭Mild‬‭: Few symptoms + minor functional impairment‬
‭e.‬ ‭Difficulty organizing materials, tasks & activities (eg.,‬‭difficulty‬ ‭Moderate‬‭: Symptoms + functional impairment between “mild” and‬
‭managing sequential tasks & keeping belongings in order‬‭; messy,‬ ‭“severe”‬
‭disorganized work,‬‭poor time management‬‭& fails to meet deadlines)‬ ‭Severe‬‭: Many symptoms/several severe symptoms + marked‬
‭f.‬ ‭Often‬‭avoids/dislikes/reluctant to engage in tasks that require‬ ‭functional impairment‬
‭sustained mental effort‬
‭g.‬ ‭Often loses things‬‭necessary for tasks/‬‭activities‬ ‭Oppositional Defiant Disorder (ODD), Conduct Disorder (CD) & Antisocial‬
‭h.‬ ‭Easily distracted‬‭by extraneous stimuli (for older adolescents & adults,‬ ‭Personality Disorder (APD)‬
‭may include unrelated thoughts)‬
‭i.‬ ‭Often‬‭forgetful in daily activities‬‭(eg. doing chores, keeping‬ ‭➔‬ ‭50%‬‭of children wt ADHD, mostly boys, get diagnosed for‬‭ODD‬‭by age 7+‬
‭appointments)‬ ‭◆‬ ‭Irritability type: lashing out, short-tempered, tantrums‬
‭2.‬ ‭Hyperactivity & Impulsivity‬‭: 6 or more (for child) OR 5 or more (for adult)‬ ‭◆‬ ‭Defiance type: talking back, argumentativeness‬
‭symptoms for at least 6 months‬ ‭➔‬ ‭30-50%‬‭of children wt ADHD get diagnosed for‬‭CD‬‭(more severe than ODD)‬
‭a.‬ ‭Fidgets‬‭with or taps hands or feet or‬‭squirms‬‭in seat‬ ‭◆‬ ‭Violate societal rules, high risk of trouble wt school & police, get in fights,‬
‭b.‬ ‭Leaves seat in inappropriate situations‬ ‭steal, set fires, destroy property, abuse substances‬
‭c.‬ ‭Runs about/climbs in inappropriate situations‬‭(Feeling‬‭restless‬‭in‬ ‭➔‬ ‭Early onset & ADHD-HI presentation > 10x likelihood of ODD & CD‬
‭adults & adolescents)‬ ‭➔‬ ‭ADHD & ODD/CD co-develop‬‭from childhood to adulthood‬
‭d.‬ ‭Unable to‬‭play/engage in leisure activities‬‭quietly‬ ‭◆‬ ‭Usually ADHD preceded ODD & CD‬
‭e.‬ ‭Often “on the go,” acting as if “driven by a motor” (eg.,‬ ‭◆‬ ‭But ODD & CD in adolescence can lead to later ADHD symptoms‬
‭Unable/Uncomfortable to be still for extended time‬‭)‬ ‭➔‬ ‭Biological vulnerability to ODD/CD in children with ADHD‬‭?‬
‭f.‬ ‭Often‬‭talks excessively‬ ‭◆‬ ‭Persistent & severe ODD & CD outcomes in children with ADHD associated‬
‭g.‬ ‭Blurts out‬‭answers before a question has been completed (eg.,‬ ‭wt‬‭variations in COMT gene‬‭> linked to regulation of neurotransmitters in‬
‭completes people’s sentences; cannot wait for a turn in conversation)‬ ‭brain areas related to ADHD‬
‭h.‬ ‭Difficulty waiting for their turn‬ ‭◆‬ ‭ADHD, ODD & CD also‬‭run together in families: substantial common genetic‬
‭i.‬ ‭Often‬‭interrupts/intrudes‬‭on others‬ ‭contribution‬‭for ADHD, CDD & OD +‬‭possibly shared environment‬‭(parenting‬
‭B) Several inattentive/hyperactive–impulsive symptoms were‬‭present before age 12‬‭.‬ ‭deficits & family adversity)‬
‭C) Several inattentive/hyperactive–impulse symptoms are‬‭present in 2 or more settings‬‭.‬ ‭➔‬ ‭ADHD is‬‭risk factor‬‭for later development of‬‭APD‬
‭D) Clear evidence that the symptoms‬‭interfere with/reduce the quality of: social,‬ ‭◆‬ ‭Pervasive pattern of disregard for & violation of the rights of others‬
‭◆‬ ‭Involvement in multiple illegal behaviours‬
 ‭◆‬ T
‭ ic disorders‬‭may decline by adolescence‬‭& do not significantly affect later‬
‭psychosocial functioning‬
‭Anxiety Disorders‬
➔
‭ ‬2 ‭ 5-50%‬‭of children wt ADHD experience anxiety disorders‬
‭➔‬ ‭Co-occurring anxiety disorder & ADHD compared to Just ADHD‬ ‭8.2 Prevalence & Course‬
‭◆‬ ‭Less aggressive‬‭behaviour‬
‭◆‬ ‭More‬‭social, academic & other‬‭functional impairment‬ ‭General‬
‭◆‬ ‭Poorer quality life & greater‬‭long term impairment‬ ‭➔‬ ‭Increase in diagnosis?‬
‭➔‬ ‭Anxiety problems in children wt ADHD‬‭accounted for by attention problems‬‭not‬ ‭◆‬ ‭Increase in diagnostic practices, growing knowledge‬
‭Hyperactivity-impulsivity problems‬ ‭◆‬ ‭Parental awareness & parental seeking of treatment for their children‬
‭◆‬ ‭Adults identifying ADHD symptoms from their childhood that they now cope‬
‭Mood Disorders‬ ‭with‬
‭➔‬ ‭About 5% of children & adolescents worldwide‬‭are diagnosed wt ADHD‬
‭➔‬ ‭Depresssion & ADHD‬
‭➔‬ ‭Most common referral problem: 50% of children at clinics display ADHD symptoms‬
‭◆‬ ‭20-30%‬‭of children experience‬‭co-occurring ADHD + Depressive & other‬
‭(alone/in combination wt other disorders)‬
‭mood disorders‬
‭➔‬ ‭Assessment: Multiple observers report symptoms, but may not agree‬
‭◆‬ ‭More than 20-30%‬‭of children wt ADHD‬‭develop depressive & mood‬
‭◆‬ ‭behaviours will differ by setting‬
‭disorders by early adulthood‬
‭◆‬ ‭there may be personal emphasis on certain symptoms‬
‭➔‬ ‭Some children wt ADHD experience Disruptive dysregulation mood disorder‬
‭◆‬ ‭Severe emotional & behavioral problems + chronic irritability‬
‭Gender‬
‭➔‬ ‭Suicide risk‬
‭◆‬ ‭Diagnosis of ADHD between 4-6 years old is risk factor‬‭of future depression &‬ ‭➔‬ ‭Boys > Girls‬
‭suicidal behavior‬ ‭◆‬ ‭Ages 6-12: 6-9% > 2-4%‬
‭◆‬ ‭Highest risk when ADHD co-occurs wt depression/conduct problems‬ ‭◆‬ ‭Adolescence: 2.5:1‬
‭➔‬ ‭Family risk of depressive disorders increases risk of ADHD & vice versa‬ ‭◆‬ ‭Adulthood: 1.61:1‬
‭◆‬ ‭So co-ocurring depression isn’t just child wt ADHD becoming hopeless wt‬ ‭◆‬ ‭Differences decrease with age‬
‭their symptoms‬ ‭➔‬ ‭Why?‬
‭➔‬ ‭ADHD vs‬‭Pediatric bipolar mood disorder (BP)‬ ‭◆‬ ‭Under-identification‬‭in girls‬
‭◆‬ ‭Difficult to distinguish ADHD symptoms from BP symptoms‬‭(unregulated high‬ ‭◆‬ ‭DSM-5 criteria was developed & tested on boys‬‭(may not match manifestation‬
‭energy level, poor judgment & over-talkativeness)‬ ‭in girls)‬
‭◆‬ ‭Diagnosis of‬‭childhood BP increases risk for previous/co-ocurring ADHD‬ ‭◆‬ ‭Boys are more likely to be referred due to acting-out behaviours‬‭(overt‬
‭◆‬ ‭ADHD diagnosis prolly not risk factor of BP‬ ‭defiance & aggression)‬
‭➔‬ ‭When girls wt ADHD do show aggression & acting-out behaviours, they get referred‬
‭at younger ages > intolerance of such behaviour from girls?‬
‭Developmental Coordinations & Tic Disorders‬ ‭➔‬ ‭Girls differences‬
‭➔‬ ‭30-50%‬‭of children wt ADHD display‬‭motor coordination difficulties‬ ‭◆‬ ‭Inattentive/disorganized > hyperactive-impulsive‬‭: Sluggish cognitive tempo,‬
‭◆‬ ‭clumsiness, poor performance in sports, poor hand-writing‬ ‭forgetfulness, lethargy, mental confusion, tendency to daydream‬
‭◆‬ ‭Difficulties executing complex motor sequences‬ ‭◆‬ ‭Hyperverbal > hyperactive‬‭motor behaviour‬
‭◆‬ ‭Impaired motor skills in domains of strength, visual motor coordination,‬ ‭◆‬ ‭More anxiety & depression‬
‭adjusting speed & dexterity‬ ‭◆‬ ‭If they do show‬‭more hyperactive-impulsive symptoms > higher risk of‬
‭➔‬ ‭50%‬‭of children wt ADHD may develop‬‭developmental coordination disorder (DCD)‬ ‭●‬ ‭EDs‬‭(binging/purging, body dissatisfaction, etc.)‬
‭◆‬ ‭Marked motor incoordination & delayed in achieving motor milestones‬ ‭●‬ ‭self-harming behaviour & suicidal attempts‬
‭➔‬ ‭20%‬‭of children wt ADHD may have‬‭tic disorders‬ ‭➔‬ ‭Recent studies show‬‭more similarities than differences‬
‭◆‬ ‭sudden, repetitive, nonrhythmic motor movements/sounds (eg. eye blinking,‬ ‭◆‬ ‭Expression & severity of problems‬
‭facial grimacing, throat clearing, and grunting)‬ ‭◆‬ ‭brain abnormalities‬
‭◆‬ ‭Children wt‬‭co-occurring ADHD + tic disorders experience more functional‬ ‭◆‬ ‭Deficits in response inhibition & executive functions‬
‭impairments‬‭than those with ADHD alone‬ ‭◆‬ ‭Response to treatment & outcomes‬
‭Socioeconomic status & Culture‬ ‭◆‬ H ‭ igh level of hyperactive-impulsive behaviours predicts poor adolescent‬
‭outcomes‬
‭➔‬ ‭More ADHD in Low SES groups‬‭> High SES‬
➔
‭ ‬ ‭Most outgrow or learn to cope with ADHD in‬‭Adulthood‬‭, but‬‭some may still‬
‭◆‬ ‭Related to co-occurring conduct problems (linked to family adversity, family‬
‭experience lifelong functional impairment‬
‭conflict, stress)‬
‭◆‬ ‭Better outcomes if‬
‭➔‬ ‭Minority ethnicities equally likely to display ADHD symptoms but less likely to get‬
‭●‬ ‭Less severe symptoms‬
‭diagnosis‬
‭●‬ ‭Receives good care & supervision + wide social support networks‬
‭◆‬ ‭Less access to healthcare‬
‭(parents, family & teachers)‬
‭➔‬ ‭Similar rates of ADHD worldwide but‬‭cultural norms may affect presentation &‬
‭●‬ ‭Access to economic & community resources‬
‭reaction towards symptoms‬
‭◆‬ ‭Presentation in adults‬
‭◆‬ ‭Ex. more value reserved cultures like in Thailand have less rates of ADHD‬
‭●‬ ‭restless, easily bored, constantly seeking novelty & excitement‬
‭than US, but when when there are symptoms, they’re viewed as problematic‬
‭●‬ ‭work difficulties,‬‭motor vehicle violations & accidents,‬‭impaired social‬
‭relation‬
‭Course & Outcomes‬
‭●‬ ‭Depression, low self-concept, substance abuse‬‭& personality disorder‬
‭➔‬ ‭Parent-reported early signs‬‭from‬‭infancy to toddlerhood‬‭(age 2)‬
‭◆‬ ‭Home-based‬‭activity-level‬‭assessments via motion detectors‬
‭◆‬ ‭Difficult temperament‬‭infants (extremely active, unpredictable,‬
‭oversensitive/undersensitive to stimulation, irritable, erratic sleep patterns,‬
‭feeding difficulties)‬ ‭8.3 Theories & Causes‬
‭➔‬ ‭Reliable identification is difficult prior to age 3‬ ‭Genetic‬
‭◆‬ ‭Parental recall bias‬
‭➔‬ ‭ADHD runs in families (‬‭most heritable childhood disorder‬‭)‬
‭◆‬ ‭Difficult temperaments not associated wt ADHD‬
‭◆‬ ‭⅓ biological relatives of children wt ADHD also have ADHD‬
‭➔‬ ‭Reliable early-detection signs in‬‭infancy to toddlerhood‬
‭◆‬ ‭60% risk of having ADHD if parent has ADHD‬
‭◆‬ ‭Negative emotionality‬‭at 6 months (anger/irritability in response to mild‬
‭◆‬ ‭3x higher likelihood of biological parents having ADHD > adoptive parents of‬
‭restraint/non-reward)‬
‭children wt ADHD‬
‭◆‬ ‭Atypical motor development‬
‭◆‬ ‭Average‬‭75% Heritability in twin studies‬‭for hyperactive-impulsive &‬
‭◆‬ ‭Difficulties in sensory processing & perception‬
‭inattention behaviors‬
‭◆‬ ‭Attentional‬‭difficulties‬
‭◆‬ ‭Average‬‭65% concordance rates for identical twins‬‭, 2x that of fraternal twins‬
‭◆‬ ‭Emotion‬‭dysregulation‬
‭➔‬ ‭Large‬‭genetic influence on‬‭the course of‬‭ADHD symptoms from age 8-16‬‭,‬‭separate‬
‭◆‬ ‭Atypical brain development‬‭in regions associated with ADHD symptoms‬
‭from the‬‭genetic influences on baseline ADHD levels at age 8‬
‭➔‬ ‭Increasingly visible‬‭symptoms by‬‭pre-school (age 3-4)‬
‭◆‬ ‭Explains why‬‭some children remit while others persist‬
‭◆‬ ‭Acting without thinking, trouble inhibiting behavior‬
‭➔‬ ‭Genomic risk regions‬‭are usually involved in neurotransmission‬
‭◆‬ ‭dashing from activity to activity‬
‭◆‬ ‭Half play a role in‬‭monoaminergic function‬‭(dopamine & serotonin‬
‭◆‬ ‭reward-seeking behaviours,‬‭can’t resist temptation/delay gratification‬
‭transporters + D4, D5 & 5-HT1B receptors).‬
‭◆‬ ‭easily bored‬‭& strong aversion to routine activities‬
‭◆‬ ‭Half play a role in‬‭different aspects of synaptic transmission‬‭(SNAP25, NOS1,‬
‭◆‬ ‭Non-compliance & oppositional behaviour‬
‭LPHN3 & GIT1)‬
‭◆‬ ‭Disruptive & overtalkative‬‭at school‬
‭➔‬ ‭Genes involved in dopamine regulation‬
‭➔‬ ‭Usual‬‭identification occurs in‬‭elementary school (ages 6-12)‬
‭◆‬ ‭Dopamine‬‭has central role in‬‭psychomotor activity & reward-seeking‬
‭◆‬ ‭Challenging classroom demands for sustained attention & goal-directed‬
‭◆‬ ‭Brain structures implicated in ADHD are rich in dopamine innervation‬
‭persistence‬
‭(dopamine dysregulation in these structures > ADHD)‬
‭◆‬ ‭Outcomes:‬‭low academic productivity, distractibility, poor organization, trouble‬
‭◆‬ ‭Reduced dopaminergic activity > behavioural symptoms of ADHD‬
‭meeting deadlines, following instructions & keeping social commitments‬
‭◆‬ ‭Primary‬‭ADHD medications block‬‭dopamine transporter (DAT1)‬‭that‬
‭◆‬ ‭Hyperactive-impulsive behaviors will continue wt some decline‬
‭reuptakes dopamine into presynaptic neuron to increase its availability in the‬
‭◆‬ ‭Oppositional defiant behaviors‬‭may increase (by age 8-12): aggression,‬
‭synaptic cleft‬
‭defiance, lying‬
‭◆‬ ‭Association of symptoms wt‬‭dopamine receptor genes DRD4‬‭> linked to‬
‭➔‬ ‭ADHD‬‭continues into‬‭Adolescence‬‭for about 50%‬‭of all those diagnosed‬
‭sensation-seeking, responsiveness to medication, executive functions &‬
‭◆‬ ‭Significant‬‭decline in hyperactive-impulsive behaviors‬‭(but still higher than‬
‭attention‬
‭non-ADHD peers)‬
 ‭➔‬ ‭Genes in serotonin system‬ ‭◆‬ ‭sustained attention‬
‭◆‬ ‭Lead to‬‭aversion in reward delay‬ ‭➔‬ ‭Brain regions implicated in ADHD‬
‭➔‬ ‭Epigenetic‬‭influences‬ ‭◆‬ ‭frontostriatal region & its connections with the limbic system, cerebellum,‬
‭◆‬ ‭Abnormal microRNA functioning‬ ‭thalamus & DMN‬
‭◆‬ ‭Variation in DNA methylation‬ ‭➔‬ ‭Brain structure abnormalities‬
‭◆‬ ‭Frontostriatal circuitry‬‭>‬‭Smaller right prefrontal cortex + structural‬
‭Perinatal, Prenatal & Postnatal‬ ‭abnormalities in several basal ganglia regions‬
‭◆‬ ‭Cerebellar-Prefrontal-Striatal Network‬‭> 3-4% s‬‭maller total & right cerebral‬
‭➔‬ ‭Perinatal‬
‭volume & smaller cerebellum‬
‭◆‬ ‭Pregnancy & Birth complications‬
‭●‬ ‭Linked to deficits in learning temporal associations & events & their‬
‭◆‬ ‭Young‬‭Maternal & Paternal age (<20 years)‬
‭consequences‬
‭➔‬ ‭Prenatal‬
‭➔‬ ‭Brain circuitry abnormalities‬
‭◆‬ ‭Maternal acetaminophen use‬
‭◆‬ ‭Thalamic subcircuits‬
‭◆‬ ‭Maternal‬‭exposure to infections‬
‭●‬ ‭Linked to‬‭motor & emotional response regulation‬
‭◆‬ ‭Exposure to‬‭environmental toxins‬
‭◆‬ ‭Default mode network (DMN)‬‭is usually active at rest & shuts off during tasks‬
‭◆‬ ‭Severe stress‬‭during pregnancy‬
‭>‬‭weaker neural connectivity & deficient deactivation during tasks‬
‭◆‬ ‭Maternal substance abuse‬‭(cigarettes, alcohol, drugs)‬
‭◆‬ ‭Faulty connection between Cognitive control network (CCN) & DMN‬
‭●‬ ‭Cigarettes associated wt ADHD for children with genetic risk for ADHD‬
‭●‬ ‭CCN includes several brain regions‬‭involved in executive functions‬
‭& female offspring, but‬‭possibly due to genetics & family environment‬
‭(working memory, inhibitory control, set shifting) & is‬‭active during task‬
‭rather than direct nicotine exposure‬
‭engagement‬
‭●‬ ‭Mothers of children wt ADHD may have higher tendency to use‬
‭●‬ ‭As attention demand increases during task, CCN activation increases,‬
‭substances outside of pregnancy‬
‭DMN activation decreases, but during periods of internally focused‬
‭●‬ ‭Cocaine can‬‭affect brain development‬‭> increased ADHD risk‬
‭thinking, opposite happens‬
‭◆‬ ‭Parental substance abuse >‬‭Chaotic home life‬
‭➔‬ ‭Differences/delays in development of brain regions & circuits‬
‭➔‬ ‭Postnatal‬
‭◆‬ ‭Delay in brain maturation & cortical thickening‬‭, particularly in‬‭prefrontal‬
‭◆‬ ‭Low birth weight‬‭(especially in males)‬
‭regions (regulates self-control)‬
‭◆‬ ‭Malnutrition‬‭during infancy‬
‭●‬ ‭Persistent ADHD symptoms into adulthood > increased cortical‬
‭◆‬ ‭Neonatal jaundice‬
‭thinning in areas of prefrontal cortex‬
‭◆‬ ‭Early neurological insult or trauma (‬‭TBI‬‭, etc.)‬
‭●‬ ‭Remitted symptoms > cortical thickening/minimal thinning‬
‭◆‬ ‭Diseases during infancy‬‭> impacts nervous system development‬
‭◆‬ ‭Earlier maturation of motor cortex‬
‭◆‬ ‭Parental substance abuse‬‭>‬‭Chaotic home life‬
‭●‬ ‭Combined wt delay in prefrontal maturation >‬‭fidgeting, restlessness,‬
‭➔‬ ‭Combination of‬‭Prenatal & perinatal factors + Genetic factors > increase‬
‭hyperactivity‬
‭sensitivity to Postnatal factors‬
‭➔‬ ‭Neurochemical abnormalities‬
‭◆‬ ‭Involvement of neurotransmitters dopamine, norepinephrine, epinephrine &‬
‭Neurobiology‬ ‭serotonin‬
‭➔‬ ‭Children wt ADHD may have‬ ‭◆‬ ‭Selective deficiency in the availability of both dopamine & norepinephrine‬
‭◆‬ ‭diminished arousal/arousability‬ ‭◆‬ ‭Medications focus on increasing dopamine availability, but dopamine‬
‭◆‬ ‭underresponsiveness to stimuli‬ ‭deficiency is‬‭not necessarily a cause‬
‭◆‬ ‭deficits in response inhibition‬
‭◆‬ ‭abnormalities in brain structure, function & connectivity‬ ‭Diet, Allergy & Lead‬
‭➔‬ ‭Neural circuits linked to ADHD involved in‬
‭➔‬ ‭Sugar & Hyperactivity Myth‬
‭◆‬ ‭attentional processes‬
‭◆‬ ‭Numerous studies have shown that sugar is not the cause of hyperactivity‬
‭◆‬ ‭inhibitory control‬
‭◆‬ ‭Nearly half of parents & teacher’s believe sugar causes hyperactivity‬
‭◆‬ ‭executive functions‬
‭●‬ ‭Mothers who believed this were told their children would drink either‬
‭◆‬ ‭Motivation‬
‭sugar or placebo‬
‭◆‬ ‭frustration tolerance‬
‭●‬ ‭But none of the children received sugar‬
‭◆‬ ‭reward anticipation‬
 ‭●‬ M
‭ others who believed their children received sugar rated them as‬ ‭ ‬ ‭dextroamphetamine‬‭(Dexedrine/Dextrostat)‬
◆
‭more hyperactive, were more critical & frequently interacted with them‬ ‭◆‬ ‭amphetamine-dextroamphetamine‬‭(Adderall)‬
‭◆‬ ‭These‬‭beliefs may impact how parents view & report ADHD symptoms & treat‬ ‭◆‬ ‭Methylphenidate‬‭(Ritalin)‬
‭children wt ADHD symptoms‬ ‭➔‬ ‭Mechanism:‬‭alter activity in the frontostriatal brain region brain by affecting‬
➔
‭ ‬ ‭Past belief that food additives caused hyperactivity, leading parents to withhold‬ ‭neurotransmitters (dopamine)‬‭important to this region‬
‭certain foods‬ ‭◆‬ ‭Brain-scan studies suggest that they‬‭may also help normalize structural &‬
‭◆‬ ‭Debunked in the 1990s, but recent studies suggest a potential moderating‬ ‭functional brain abnormalities‬
‭role of genetic factors in how food additives affect behaviour.‬ ‭➔‬ ‭(Short-term) Effect:‬‭Only works in about 80% of children while it is being used‬
‭➔‬ ‭Diet > Current dietary research focuses on‬‭micronutrients‬‭like‬ ‭◆‬ ‭increases‬‭sustained attention, impulse control & persistence‬‭of work effort‬
‭◆‬ ‭essential fatty acids (often lacking in the diet of North American children)‬ ‭◆‬ ‭decreases in task-irrelevant activity + noisy & disruptive behaviors‬
‭◆‬ ‭Zinc & iron > may be‬‭metabolized abnormally‬‭in some children‬ ‭◆‬ ‭may also‬‭improve academic productivity, cooperation & interactions‬
‭➔‬ ‭Most children with ADHD do not have significantly elevated lead levels, but some‬ ‭◆‬ ‭occasionally‬‭improves physical coordination‬‭(eg. handwriting, sports ability)‬
‭studies suggest link between slight lead exposure & ADHD‬‭, particularly when‬ ‭➔‬ ‭Mostly‬‭benign side effects‬‭that can be monitored & eliminated by reducing dosage‬
‭combined with other risk factors‬‭like‬ ‭◆‬ ‭reduced appetite, weight loss, sleep problems‬
‭◆‬ ‭prenatal nicotine exposure‬ ‭◆‬ ‭Addictive if misused‬‭(does not lead to risk of substance abuse & most‬
‭◆‬ ‭genetic variations in‬‭iron metabolism‬ ‭children don’t abuse them)‬
‭➔‬ ‭Limitations‬
‭◆‬ ‭Magnitude & continuity‬‭of the short-term effects of stimulants is‬‭uncertain‬
‭Family‬
‭◆‬ ‭Stimulants are‬‭not a cure‬‭but a short-term stopper on the problem‬
‭➔‬ T ‭ win studies show that family-related psychosocial factors‬‭account only for small‬ ‭◆‬ ‭Need‬‭consistent monitoring to mitigate side effects‬
‭variance‬
‭◆‬ ‭But Family factors‬‭still contribute to symptom severity, associated problems &‬
‭outcomes‬‭despite not being primary cause‬ ‭Parent Management Training (PMT)‬
‭➔‬ ‭Parenting practices‬‭may interact with genetic predispositions‬‭to moderate ADHD risk‬ ‭➔‬ F ‭ ocuses on‬‭teaching effective parenting practices & coping strategies‬‭for‬
‭➔‬ ‭Child temperament x Parenting style‬ ‭parenting a child with ADHD‬
‭◆‬ ‭Overactive child + overstimulating parent = poor fit‬ ‭➔‬ ‭PMT provides skills to‬
‭➔‬ ‭Parent gene x Child gene interaction‬ ‭◆‬ ‭manage oppositional & noncompliant behaviors‬
‭◆‬ ‭Parental ADHD‬‭may lead to‬‭ineffective parenting styles‬‭(Maternal ADHD =‬ ‭◆‬ ‭cope with emotional demands‬‭of raising a child wt ADHD‬
‭less involvement, less positive parenting & more inconsistent discipline)‬ ‭◆‬ ‭contain & prevent problems‬‭from worsening‬
‭◆‬ ‭Mothers with variants in DAT1‬‭are more likely to display‬‭negative & controlling‬ ‭◆‬ ‭Prevent problem from inflicting adverse effects on other family members‬
‭parenting behaviors‬ ‭➔‬ ‭1. Parents are‬‭taught about ADHD‬
‭➔‬ ‭Child-to-Parent Effect‬‭:‬‭Children's ADHD symptoms can influence parents' behaviors‬ ‭◆‬ ‭Info about‬‭its biological basis‬‭>‬‭to alleviate guilt‬‭from parents who may think‬
‭◆‬ ‭Studies show that medicating children with ADHD > decreased symptoms >‬ ‭they caused the problem‬
‭reduced negative & controlling parental behaviors‬ ‭➔‬ ‭2. Parents are‬‭provided wt guiding principles‬
‭➔‬ ‭Family conflic‬‭t may‬‭exacerbate hyperactive-impulsive symptoms‬‭in children at risk for‬ ‭◆‬ ‭using‬‭immediate & consistent consequences‬
‭ADHD‬ ‭◆‬ ‭planning‬‭ahead‬
‭➔‬ ‭Family conflict & parental psychopathology‬‭may be related to early ODD & later‬ ‭◆‬ ‭not personalizing the child's problems‬
‭comorbid ADHD & CD‬‭symptoms‬ ‭◆‬ ‭practicing‬‭forgiveness‬‭.‬
‭◆‬ ‭Children wt ADHD report‬‭observing more interparental conflict‬‭than children‬ ‭➔‬ ‭3. Parents are also‬‭taught behavior management techniques‬‭> how to‬
‭without ADHD >‬‭may exarcebate risk in children wt genetic predisposition‬ ‭◆‬ ‭identify behavior‬‭s to encourage/discourage‬
‭◆‬ ‭use‬‭rewards & sanctions‬
‭◆‬ ‭Praise‬‭their child’s strengths & accomplishments‬
‭8.4 Treatment‬ ‭◆‬ ‭manage disruptive behavior by using‬‭penalties‬‭(eg. loss of privileges,‬
‭time-outs)‬
‭Medication (Stimulants)‬ ‭◆‬ ‭Manage noncompliance in public‬
‭➔‬ S ‭ timulants are the most effective & common treatment for ADHD & its associated‬ ‭➔‬ ‭4. Parents are taught to‬‭implement school-home reward program‬
‭impairments‬ ‭◆‬ ‭teachers evaluate the child's behavior on a‬‭daily report card‬
‭➔‬ ‭Most effective types:‬
 ‭◆‬ C ‭ ard serves as a‬‭means for rewards & punishments‬‭(eg. tokens administered‬ ‭◆‬ p ‭ rovides‬‭continuity to academic work‬‭to ensure that gains made during the‬
‭at home for classroom conduct)‬ ‭school year are not lost‬
➔
‭ ‬ ‭5. Parents are encouraged to‬‭maximise child’s success & minimize failures‬ ‭◆‬ ‭Cost-effective‬
‭◆‬ ‭engage in enjoyable activities‬‭with their child‬ ‭◆‬ ‭Time-effective‬‭: packs 360 hours of treatment into 8 weeks (equivalent to 7‬
‭◆‬ ‭structure situations for success‬‭(eg. breaking down difficult tasks into smaller‬ ‭years of weekly therapy)‬
‭steps & praising completion of each step)‬ ➔
‭ ‬ ‭Coordinated with stimulant medication trials, PMT, social skills training & educational‬
‭◆‬ ‭reduce their arousal levels to respond calml‬‭y‬ ‭interventions‬
‭➔‬ ‭Effectiveness‬ ‭➔‬ ‭Effects: Parent & counsellor-ratings suggest‬
‭◆‬ ‭Stimulants seem to have stronger immediate effect‬ ‭◆‬ ‭overall‬‭improvements in behavior‬
‭◆‬ ‭PMT may produce additional therapeutic benefit by‬ ‭◆‬ ‭Decreases in problem severity‬
‭●‬ ‭treating associated problems‬ ‭◆‬ ‭improvements in social skills & academic‬‭performance.‬
‭●‬ ‭Improving family functioning‬ ‭◆‬ ‭higher levels of‬‭self-efficacy‬
‭●‬ ‭Increasing consumer satisfaction.‬
‭Multimodal Treatment Study of Children with ADHD (MTA Study)‬
‭Educational Intervention‬ ‭➔‬ ‭First large-scale, randomized clinical trial for children with ADHD‬
‭◆‬ ‭Landmark multisite study sponsored by the U.S. National Institute of Mental‬
‭➔‬ I‭ntegrated classroom learning‬‭is preferable over segregation into special education‬
‭Health (NIMH) & the U.S. Department of Education‬
‭classrooms‬
‭◆‬ ‭Aimed to‬
‭➔‬ ‭Focus on‬
‭●‬ ‭compare long-term medication & behavioral treatments‬
‭◆‬ ‭managing inattentive & hyperactive-impulsive behaviors that interfere with‬
‭●‬ ‭assess additional benefits of combined treatments‬
‭learning.‬
‭●‬ ‭evaluate effectiveness of systematic treatments versus routine‬
‭◆‬ ‭Provide a classroom environment that‬‭capitalizes on the child's strength‬‭.‬
‭community care‬
‭➔‬ ‭Techniques for‬‭managing classroom behaviour‬
‭➔‬ ‭Study Design > Children aged 7 ~ 9 with ADHD were randomly assigned to:‬
‭◆‬ ‭setting‬‭realistic goals‬
‭◆‬ ‭Medication management: Received stimulants‬
‭◆‬ ‭Implement mutually agreed-upon‬‭reward systems‬
‭◆‬ ‭Behavioral treatment: Received PMT, teacher/school visits, & intensive‬
‭◆‬ ‭monitoring performance‬
‭summer treatment program‬
‭◆‬ ‭providing‬‭rewards for meeting goals‬
‭◆‬ ‭Combined behavioral treatment & medication‬
‭◆‬ ‭Response-cost procedures‬‭for disruptive behaviours (loss of reward/priviliges‬
‭◆‬ ‭Routine community treatment: Usual community care, often including‬
‭or time-outs)‬
‭stimulants.‬
‭➔‬ ‭Instructional Strategies‬‭to help them focus & remember important points‬
‭➔‬ ‭Findings after 14 months: all groups showed symptom reductions, but‬
‭◆‬ ‭Include‬‭clear expectations‬
‭◆‬ ‭Stimulant medication > behavioral treatment & routine community care‬
‭◆‬ ‭Providing‬‭visual aids‬
‭◆‬ ‭Composite outcome measures‬‭ranked‬‭combined treatment > medication >‬
‭◆‬ ‭Providing‬‭written + oral instructions‬
‭behavior therapy > community treatment‬
‭➔‬ ‭Additional accommodations‬
‭◆‬ ‭Combined treatment increased positive functioning & benefitted non-ADHD‬
‭◆‬ ‭seating arrangements‬‭(seating them nearer teacher’s desk)‬
‭symptoms‬
‭◆‬ ‭designated movement areas‬
‭➔‬ ‭Long-term Follow-up‬
‭◆‬ ‭clearly posted‬‭rules wt visual reminders‬
‭◆‬ ‭Benefits of combined treatment persisted at 24 months but diminished by 36‬
‭◆‬ ‭repeating instructions‬
‭months‬
‭◆‬ ‭providing extra time‬
‭◆‬ ‭Effects of medication & behavioral treatments declined/ceased entirely by 6-8‬
‭➔‬ ‭School-based educational Interventions >‬‭moderate ~ large improvements in‬
‭years‬
‭academic & behavioral functioning‬‭of ADHD students‬
‭◆‬ ‭Low-dose/intensity behavioral treatment (large-group parent training) is more‬
‭cost-effective, with similar if not better outcomes, than low-dose stimulants‬
‭Intensive Interventions (Summer treatment program)‬
‭➔‬ ‭Predictors of Outcomes‬
‭➔‬ t‭reatment is provided in a camplike setting where they engage in classroom &‬ ‭◆‬ ‭Initial clinical presentation & symptom response to treatment‬‭are better‬
‭recreational activities‬ ‭predictors of adolescent outcomes‬‭than the type of treatment‬
‭➔‬ ‭Advantages:‬ ‭◆‬ ‭Behavioral treatments may benefit children with comorbid anxiety & those‬
‭◆‬ ‭maximizes opportunities to build effective peer relations‬‭in normal settings‬ ‭from socially disadvantaged families‬
 ‭➔‬ f‭unctional problems in young adulthood is associated with‬‭persistent ADHD‬‭, which is‬
‭predicted by‬
‭◆‬ ‭Childhood ADHD severity‬
‭◆‬ ‭parental mental health‬
‭◆‬ ‭comorbidity‬

‭Additional Interventions‬
‭➔‬ ‭Family counselling & Support groups‬
‭◆‬ ‭Family stress, conflict & problems may arise with the challenges of raising a‬
‭child wt ADHD‬
‭◆‬ ‭Family members need support to develop new skills, attitudes & responses‬
‭◆‬ ‭Support groups share‬‭information, emotional support, personal experiences,‬
‭referrals to qualified professionals‬‭, etc.‬
‭➔‬ ‭Individual counselling‬
‭◆‬ ‭Children wt ADHD‬‭may attribute their success to uncontrollable factors‬‭due to‬
‭experiences of‬
‭●‬ ‭Being labelled & internalising labels‬
‭●‬ ‭Being punished for their limitations‬
‭●‬ ‭Negative responses from teachers, parents & peers‬
‭◆‬ ‭Addressing these concerns to‬‭alleviate co-ocurring depressive symptoms‬