Attention-Deficit Hyperactivity DisorderADHD StatisticsPsychiatric ComorbidityADHD: EtiologyPowerPoint PresentationADHD: Adult Common Comorbid DiagnosisRisk Factors for ADHDHistory of ADHDWhat is ADHD?Executive Functions“Focus” and Executive FunctioningDevelopment of Brain Structures that Support EFContinuing Brain Development in Late Childhood and AdolescenceEF: Development & DemandsHow can EF become impaired?Diagnosing ADHD: DSM-IVSlide 17Slide 18Problems of DiagnosisADHD and the BrainADHD and the Brain IIWhat causes ADHD?Dopamine in the BrainGenetic Linkages to ADHDDRD4TreatmentStimulantsMethylphenidateEffects of MPHSide EffectsProbable Mechanism of Action of Methylphenidate Wilens and Spencer. Handbook of Substance Abuse: Neurobehavioral Pharmacology. 1998;501-513.NeurotransmittersMRI in Adults with ADHDSlide 34Slide 35The Mechanisms of Action of Amphetamine Wilens and Spencer. Handbook of Substance Abuse: Neurobehavioral Pharmacology. 1998;501-513.Dopamine Neurotransmission Relative to ADHDNorepinephrine Neurotransmission Relative to ADHDCatecholaminergic Neurotransmission Relative to ADHDSlide 40Atomoxetine HClOutcomeAttention-Deficit Hyperactivity DisorderADHD Statistics3-5% of all U.S. school-age children are estimated to have this disorder.5-10% of the entire U.S. populationMales are 3 to 6 times more likely to have ADHD than are females.At least 50% of ADHD sufferers have another diagnosable mental disorder.Psychiatric ComorbidityAnxiety(34%)Non-comorbid(55%)CD(8 – 20%)4%2%7%MD(20 to 30%)7%23%ADHD: EtiologyADHD is a heterogeneous behavioral disorder with multiple possible etiologiesADHDNeuroanatomicNeuroanatomicNeurochemicalNeurochemicalCNS CNS insultsinsultsGenetic Genetic originsoriginsEnvironmental Environmental factorsfactors“It’s a guy thing.”ADHD: Adult Common Comorbid DiagnosisFemaleMaleRisk Factors for ADHDGirlsBoysHistory of ADHDMid-1800s: Minimal Brain DamageMid 1900s: Minimal Brain Dysfunction1960s: Hyperkinesia1980: Attention-Deficit DisorderWith or Without Hyperactivity1987: Attention Deficit Hyperactivity Disorder1994-present: ADHD Primarily InattentivePrimarily HyperactiveCombined TypeWhat is ADHD?“The unifying abstraction that currently best encompasses the faculties principally affected in ADHD has been termed executive function (EF), which is an evolving concept…there is now impressive empirical support for its importance in ADHD” –Castellanos FX. (1999) The psychobiology of attention-deficit/hyperactivity disorder. In HC Quay, AE Hogan (Eds), Handbook of Disruptive Behavior (pp. 179-198). Kluwer AcademicExecutive FunctionsWide range of central control processes of the brainConnect, prioritize and integrate cognitive functions – moment by momentLike a conductor of a symphony orchestra“Focus” and Executive FunctioningIntention symptoms in the DSM-IV –Do not mean•Unable to focus…as in holding the camera still to take a photo of an unmoving object–Do mean•Unable to focus…as in focusing on the task of driving a car.Development of Brain Structures that Support EFStructures and functions that support EF are not fully developed at birthNeural networks underlying EF control begin at 2-4 years of age, but don’t fully develop until the 20’s.Development of EF capacities continues into early adulthood.Continuing Brain Development in Late Childhood and Adolescence6-15 years of age: extreme growth (80%) occurs at the collosal isthmus that supports associative relay, while considerable synaptic pruning occursBrain myelination increases 100% during the teenage yearsDopamine (DA), norepinephrine (NE) and Serotonin (5-HT) transmitter systems in the brain continue to develop into one’s 20’sEF: Development & DemandsEF capacity develops through childhood/teens to adulthood – it is not totally present in early childhood.Environmental demands for EF increase with ageEF impairments are frequently unnoticeable by age 7How can EF become impaired?Developmentally (eg, ADHD etc.)Trauma (eg, TBI)Disease (eg, Alheimer’s)In trauma & disease, the patient usually has adequate EF, then loses it.In ADHD, EF has not developed adequately.Diagnosing ADHD: DSM-IV Inattentiveness:Has a minimum of 6 symptoms regularly for the past six months.Symptoms are present at abnormal levels for stage of developmentLacks attention to detail; makes careless mistakeshas difficulty sustaining attentiondoesn’t seem to listenfails to follow through/fails to finish projectshas difficulty organizing tasksavoids tasks requiring mental effortoften loses items necessary for completing a taskeasily distracted is forgetful in daily activitiesDiagnosing ADHD: DSM-IVHyperactivity/ Impulsivity:Fidgets or squirms excessivelyleaves seat when inappropriateruns about/climbs extensively when inappropriatehas difficulty playing quietlyoften “on the go” or “driven by a motor”talks excessivelyblurts out answers before question is finishedcannot await turninterrupts or intrudes on othersHas a minimum of 6 symptoms regularly for the past six months.Symptoms are present at abnormal levels for stage of developmentDiagnosing ADHD: DSM-IVAdditional Criteria:Symptoms causing impairment present before age 7Impairment from symptoms occurs in two or more settingsClear evidence of significant impairment (social, academic, etc.)Symptoms not better accounted for by another mental disorderProblems of DiagnosisSubjectivity of CriteriaInconsistent evaluations--presence of symptoms usually given by teacher or parentStudy by Szatmari et al (1989) showed that the number of diagnosed cases of ADHD decreased 80% when observations of parent, teacher and physician were used rather than just one sourceSymptoms in females more subtle---leads to underdiagnosisADHD and the BrainDiminished arousal of the Nervous SystemDecreased blood flow to prefrontal cortex and pathways connecting to limbic system (caudate nucleus and striatum)PET scan shows decreased glucose metabolism throughout brainComparison of normal brain (left) and brain of ADHD patient.ADHD and the Brain IISimilarities of ADHD symptoms to those from injuries and lesions of frontal lobe and prefrontal cortexMRIs of ADHD patients show:Smaller anterior right frontal lobeabnormal development in the frontal and striatal regionsSignificantly smaller splenium of corpus callosumdecreased communication and processing of information between hemispheresSmaller caudate
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