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Download SHIP conference July 31 2012 Linda Grossman M.D. Anna Maria Wilms Floet M.D.
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SHIP conference July 31 2012 Linda Grossman M.D. Anna Maria Wilms Floet M.D. Disclosures Presenters have: No conflict of interest No commercial affiliations Off label use of medication(s) may be discussed Goals and objectives (1) Offer an overview of what is new in the guidelines regarding assessment and treatment of ADHD Discuss the rationale for these changes based on new insights in etiology, and research Goals and objectives (2) Discuss the impact of these guidelines on treatments (non-medical and medical) Description of new medications used in treatment of ADHD Describe information about co-occurring problems and long term outcomes and their implications for individuals with ADHD Historical Perspective Descriptions go back to Greek and Victorian times Medical concerns began in 1910’s following severe influenza epidemic – post encephalitic survivors often had overactivity, inattentiveness and learning problems Minimal brain damage Minimal brain dysfunction (1960s) Hyperactivity and attention separated from learning problems in late 60’s-early 70’s Current thoughts on the Disorder Syndrome based: relies on observable signs and symptoms Symptoms in 2 separate domains: impulsivity/hyperactivity and inattention Does not involve deficits in sensory, perceptual, short- or long term memory although function in these areas worsens 2nd to attention problems Current thoughts on the Disorder Brain based disorder Disorder of response inhibition Response selection and response inhibition thought as 2 sides of the same coin Disorder of attention allocation ADHD etiologies ADHD is a heterogeneous behavioral disorder with multiple possible etiologies: no single causative cause o o o o o Inherited Genetic Neuro-anatomical/neurochemical CNS insults Environmental factors Behavioral Genetics Genetic influences account for about 75 % of the variance on average (range 60-90 %): polygenic The remaining variance appears to be due to non- shared environmental influences (with little evidence for shared environmental influences) Certain genetic conditions (Tourette’s disorder, neurofibromatosis-I) show higher prevalence of ADHD Neuroanatomical: MRI and Functional MRI Results Research findings Decrease in size and/or activity of key parts of brain Right frontal region (alerting and executive fx) Anterior cingulate gyrus (executive function) Left dorsolateral area (verbal working memory) Basal ganglia (caudate and globus pallidus) and cerebellum (inferior posterior lobe and lobes VIII-X of vermis) – all with regard to movement and activity Problems with research Lack of controls Some kids medicated and some not Differences by age, gender Lack of replication by others - ? validity ADHD: neuro-imaging Delayed cortical maturation: Neurochemistry Dysregulation of neurotransmitters Stimulants act on neurotransmission pathway of catecholamines ( block re-uptake of dopamine and norepinephrine) Candidate gene studies are Dopamine genes DAT1: dopamine transporter DRD4: dopamine receptor D4 Noradrenergic /adrenergic Drug metabolizing genes ?? CNS insults Infection Trauma Prenatal toxins: Tobacco Alcohol Postnatal toxins: Lead Environmental factors No consistent research findings regarding food allergies, too much screen time, poor parenting, poor home life, poor school as causing ADHD, though may exacerbate symptoms and impairment Correlations/Potential Causes Pediatrics 2011; 128:4 772-774 Conclusion Currently imaging and genetic analysis are not helpful on a clinical basis because of the wide variety of size and function of the brain in children with/without ADHD and the small numbers that have identified gene abnormalities ADHD – Diagnosis under DSM-IV 6 of 9 inattentive items and/or 6 of 9 hyperactive/impulsive items Note: items were selected by committee decision – not via scientific process DSM-IV Hyperactivity-Impulsivity At least 6 of: Hyperactivity Impulsivity Squirms and fidgets Can’t stay seated Runs/climbs excessively Blurts out answers Can’t wait turn Intrudes/interrupts others Can’t play/work quietly “On the go”/”Driven by a motor” Talks excessively DSM IV Inattention At least 6 of: Inattention Careless, fails to attend to details Difficulty sustaining attention in activity Doesn’t seem to listen No follow through on instruction, fails to finish Avoids/dislikes tasks requiring sustained mental effort Loses things Easily distracted by extraneous stimuli Forgetful in daily activities ADHD - Other Requirements Symptoms for at least 6 months Some symptoms before age 7 yrs. Impairment in 2 or more settings Significant impairment in social, academic, or occupational functioning R/o PDD, schizophrenia, mood disorder, anxiety disorder, or personality disorder 3 Types Under DSM-IV Attention Deficit Hyperactivity Disorder, Predominantly Inattentive Type Attention Deficit Hyperactivity Disorder, Predominantly Hyperactive-Impulsive Type Attention Deficit Hyperactivity Disorder, Combined Diagnostic Process History - of vital importance, need information from more than one source Physical exam to rule out a variety of medical and non-medical possibilities with similar symptoms to look for contraindications to certain medical interventions Laboratory tests - rarely useful except when need to rule out another condition NICHQ Vanderbilt Assessment Scales (Vanderbilt ADHD Rating Scales) Based on DSM-IV scales Includes items for ODD, CD, anxiety and depression Subscales: Inattention, Hyperactivity/impulsivity, Oppositional Defiant/Conduct Disorder, Anxiety/Depression • Impairments in School function: Academic Performance, Behavioral Performance, Home: Relationship with parents, siblings, performance in organized activities ADHD 2011 guidelines Replace 2 previously published guidelines (2000: diagnosis, 2001: management) Expanded age range (now includes preschoolers) Expanded scope: behavioral interventions if not full criteria met, though problems identified (DSM-PC) Pediatrics 2011;128;1007 ADHD 2011 guidelines Treatment recommendations vary by age: o Preschool-aged children (4–5 years of age) o Elementary school–aged children (6–11 years of age) o Adolescents (12–18 years of age) DSM-5 1980 1987 1994 2000 New insights : DSM-5 Age of onset of impairing symptoms increased from by age 7 to by age 12 Change subtypes to current presentations Add 4th presentation: restrictive inattentive* * criterion A1 is met(inattention) but no more than 2 symptoms from criterion A2 (hyperactive-impulsive) over the last 6 months) New insights : DSM-5 Change examples in the items to accommodate a lifespan relevance of each symptom and to improve clarity Remove PDD from exclusion criteria Information from 2 different informants (parents and teachers for children, 3rd party/significant other for adults) www.dsm5.org ADHD as a chronic condition 60-85% continue to meet criteria as teen Adult prevalence varies Core symptoms differ from childhood o Impaired peer relations o Injuries/health problems o Poor job performance o Legal encounters Van Cleave and Leslie. 2008 Pliszka et al. 2007 Impairment or success: to be determined!