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Lecture 8

Psychology 46-322 Lecture 8: Lectures 8-10 on ADHD

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University of Windsor

Lecture 8,9 on ADHD History of ADHD  Pro-pharmacy movement  new disorder  George Still in 1902 o British o Impair volitions and marked inability to concentrate and sustain control  1770 (German Text)  described ADHD as mental disorder influent by parenting  Equine Encephalitis  aka sleeping sickness in 1917/8  sickness in winter time; looked like the flu, but actually a brain inflection (much like the movie Awakenings) o Many died from this; those who did not die left in veggie states o Had impulse control, attention problem and hyper activity o First time to identify symptoms to diagnosis like ADHD o George Still  biological problem  Bradley  drugs to treat ADHD 1930s-1950s  Brain inflection to cause them to have ADHD  Could not find damage in the brain DSM2  Hyperconnesis (hyperconnectic) to describe ADHD DSM 3  Split off subtypes; now have ADD with hyperactivity, without hyperactivity, resistual type DSM 3R  Changed the ADHD label  Now have ADD undifferentiated, ADHD DSM 4  Now only have ADHD, inattentive type, hyperactive impulsive type, ADHD combined type, ADHD NOS (not otherwise specified)  No such thing as ADD anymore DSM 5  ADHD and flow cognitive tempo SLIDE 6  5-10 times more common in boys than girls  7% of childhood meets diagnostic criteria  More common type is inattentive type of ADHD  There must be some evolutionary for ADHD  Comes from: o People who are more adventurous are more likely to move those emigrations o ADHD in africa, europe, and north/south america Etiology of ADHD  ADHD is a disorder that is not caused by one single thing; there are many risk factors  Is more common than other child psychopathologies  Neural substrates  what parts of the brain is different between those who have ADHD and those who don’t  Family members who do not have ADHD have these neural differences in the brain as well  Prefrontal cortex is different with people who have ADHD o it is smaller, slightly to the left, less connected to the rest of the brain  Differences in Cerebellum  sense of timing o People with ADHD, it is slight smaller, more symmetrical in size (left and right are same size) o Subcortical differences  Callosum  narrower, particularly at the front  Neurotransmitters differences o Lower levels of dopamine  Genetic risk factors o Inheritability  Higher than for any other disorders (70-80%); higher than Alzheimer, type-1 diabetics o 4 particular genes/chromsomes that inherit ADHD  GRD, DRD4, DRD2, DAT1 o First two are dopamine o Third is dopamine transport structures o Everyone has GRD, DRD4  the focus is how the genes look in those who have ADHD and those who don’t o Those who have ADHD are more likely to have less common alleles of these particular genes; family members are just as likely to have these even though they don’t develop ADHD  Prenatal influences o Problem for research: cannot randomly assigned o Research suggests babies born with low birth weight are more likely to have ADHD (whether mother was smoking) o Prenatal use of alcohol and tobacco; easier to trigger disorder when the child carries the alleles of ADHD o Birth injury  Other factors o Diet  often blamed for ADHD  sugar intake (research shows sugar does not increase levels of activity)  Food dye and artificial flavour  Food allergies  possibly responsible for ADHD  but research do not find it to be a big influence o Lead exposure  particular at very high levels predict ADHD or significant affect on behaviours  Might be a risk factor but not common o **National children study  collect data from 100,000 children throughout their lives (funded study for 100 years)  Focused on environmental toxics that affect ADHD and other childhood problems  Psychosocial factors  they increase or decrease the likelihood of ADHD according to other risk factors Family adversity affect the likelihood of ADHD Parenting, parent psychopathology  Omega 3,6,9 like flax oil and fish oil decrease the likelihood when they are taken during pregnancy or first 5 years of life  They improve functioning and behaviours, not ADHD Theories about ADHD  Delay aversion  people with ADHD will go out of their way to make sure they get their rewards, regardless of how big/small the reward is; they cannot wait Incentive has to be more meaning; kids with ADHD do not want incentives with little values This model explains a lot of risk factors  Sergeant  Dutch  working memory and arousal problems Because the person is not as aroused and alert, they don’t get the memory practice that they need Brain stems are not as active in people with ADHD Arousal active is low in these individuals, they are not aware of things around them  Executive dysfunction  difficulty in staying organized Problem is in the prefrontal cortex, problem is not attention but intention, as in intended to do this the right way Individuals with ADHD don’t have enough self-regulation They can increase self-regulation but comes at a cause  Subcortical neural dysfunction  Halpelin  takes first two theories People don’t have enough arousal but the prefrontal cortex picks up the slack as brain matures and fix things Their level of arousal is testable  Transactional model  alleles of genes at risk, which lead to neural differences; but mostly the environmental influences that increase or decrease the level of functioning, but does not cause ADHD  No evidence shows ADHD explicit positive effects to other aspects of life Not that people won't succeed but it won't be ADHD that causes the success   Medications to treat ADHD is not necessarily dangerous  not anesthetic (increases dopamine level)  Figuring out what each individual needs to adjust the education system; but not preparing the individual how to function in the society  This video implies that kids with ADHD are simply creative; empirical data suggests that this is false Developmental Course  Early childhood o kids who are going to develop ADHD are more active o Research shows that vast majority of toddlers and pre-schoolers have ADHD; are at their maximum hyperactivity thus, hard to tell if they have ADHD or not o Tend to have comorbid behaviour problems but not always o Tend to hit their motor milestones later and failing to hit them o They are happily noisy o Only half of the kids will meet the criteria prior to age 6  School-age o Age 7 and above  ADHD symptoms occurs o Highest of ADHD are at ages 7-9; second highest is ages 10-14 o Comorbidity  Learning disabilities, peer problems o ODD might appear in many kids at this age; very likely to develop conduct disorder  Adolescence/adulthood o 40-80% are fully diagnosed with ADHD; those are not diagnosed still continue to have symptoms (based on 5 longitudal studies) o People with ADHD in childhood continue to have ADHD in adulthood  Symptoms persist into adulthood have different outcomes o Less likely to finish their education o More likely to have appointment problems, relationship problems (ex. divorces), teen pregnancy, drug problems, sexual risk-taking o Less likely to recall their symptoms in childhood o However, data suggests that mid to late 40s  memory problems, struggles wi
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