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| Frage | Antworten |
| childhood disorder | disorders that show themselves early in life early in life and persist through as person grows older |
| 3 consequences of inadequate social skills | 1. not learning communication from peers 2. social distance 3. disruption of communication leading to reduced intelligence |
| ADHD - attention deficit/ hyperactive disorder | pattern of inattention, hyperactive, implusive, disruption of social rela., fidgety, impatient, frequent unfinished tasks |
| two types of symptoms for ADHD | one or both can be present to be diagnosed as ADHD 1. inattention 2. hyperactivity/ impulsivity |
| 5 Consequences of ADHD | 1. poor academic performance 2. dangerous and risky bhav 3. social rejection 4. low-self esteem 5. negative feedback from authority figures |
| 6 ADHD STATS | 1. 6% of school-aged children 2. 4:1 male:female ratio 3. onset, IDing around 3-4 years 4. very active, mischievous, slow toilet trainers, oppositional 5. 68% have difficulty into adulthood 6. increase driving recklessness |
| oppositional defiant disorder - ODD high comorbid w/ ADHD | a pattern of negative, defiant, hostile bhav, refusing to obey, angry, argumentative |
| conduct disorder | childhood precursor to ASPD, risk for ADHD comes from boys not girls |
| 4 Genetic Causes of ADHD | 1. high genetic influence in families w/ high psychopathology 2. multiple Gene influence 3. associate w/ DOPA, NE, SERO, GABA 4. DOPA D4-Receptor, DAT1 DOPA transporter gene, DOPA D5-R |
| DAT1 DOPA transporter | Ritalin - methylpenidate works on inhibiting this gene and increasing DOPA in brain |
| 4 Researchers are linking brain deficits w/ | 1. working memory functions 2. attention system 3. impulsivity 4. cognitive processes |
| 4 gene-environment interaction ADHD | 1. mutation of DAT1 gene 2. more likely if mothers smoked during pregnancy 3. low SES 4. parental martial instability & discord |
| 2 Brain deficits w/ ADHD | 1. no damage 2. 3 areas are smaller: frontal cortex (outer portion), basal ganglia, cerebellar vermis (part of cerebellum) occurring early in development |
| food additives in ADHD | an increase in preservative, food colourings increase hyperactivity |
| 3 social causes ADHD | 1. negative responses from parents, teachers, peers 2. increase depression 3. negative self-image |
| 4 Biological Treatment for ADHD | 1. stimulant meds: Mehylphenidat (Ritalin, Metadate, Concerta), D-amphetamine (Dexedrine, Dextrostat), pemoline (Cylert) 70% of cases reduce hyperactivity 2. psychostimulant: Adderall 3. antidepressant: (bupropion, imipramine) 4. clonidine- high blood pressure |
| 2 problems w/ stimulant use | 1. abuse of meds creating elation, reduce fatigue 2. long term side effects are unknown: over prescribed - insomnia, irritability, appetite suppression and no gains to social skills, academics |
| 3 Psychosocial inventions ADHD | 1. set goals for time remained seated 2. reinforcement programs 3. family training |
| learning disorders | in reading, math, written expression, characterized by performance is below IQ, age, education |
| reading disorder | significant discrepancy b/w persons reading achievement and what is expected of age, cannot be cause by hearing or sight problems: dyslexia |
| mathematics disorder | significant discrepancy b/w persons math achievement and what is expected of age |
| disorder of writing expression | significant discrepancy b/w persons writing achievement and what is expected of age |
| 6 learning disorders STATS | 1. 5-10% of pop 2. more than half of canadian students classified as having learning disability 3. reading: 5-15% 4. math: 6% 5. 32% of LDs drop out of school 6. employment rate 60-70% |
| verbal communication disorders | stuttering, expressive language, selective mutism, tic disorders: presence in early can lead to problems later on |
| 4 Causes of LDs | 1. parents and siblings increased likelihood 2. twins - 100% chance of same diagnoses 3. reading D: genes on chromosomes 2,3,6,15, 18 4. phonological processing- dyslexia |
| 8 Treatment for LDs | 1. intelligence and achievement tests point towards specific problems 2. Ritalin 3. solve underlying problem 4. improve cognitive skills through listening/ instruction 5. targeting bhav skills needed to compensate 6. language treatment excerises 7. strategies training 8. phonological skills training |
| pervasive developmental disorders | experience problems w/ lanuage, socialization, and cognition, are not minor but significant: autistic disorder, Asperger's disorder, Rett's disorder, childhood disintegrative disorder |
| Autistic disorder | childhoood sidorder w/ significant impairment in social interactions, communication, and restricted by bhav, interest, activities |
| 3 major characteristics | 1. social impairment 2. communication impairment 3. restricted bhav, interest, activities |
| 2 social impairment | 1. do not develop social relationship and lack of joint attention, eye tracking shows following nonsocial aspects of scene 2. lack of theory of mind- ability to appreciate other |
| 3 communication impairment | 1. 50% acquire useful speech 2. echolalia use 3. lack of spontanous pretend play |
| 2 restricted interest, bhav, activities | 1. maintenance of sameness: change in room 2. stereotyped & ritualistic Bhav: obsession, severe tantrum if ritual is interrupted |
| 6 STATS | 1. autism 1/500 births 2. prevalence of autism spectrum disroders: 1/110 births 3. females higher IQ under 35 4. higher IQ in males 5. have associated problems b4 36 months 6. 45-60% of ppl w/ autism have average or above average IQs |
| 5 biological Causes of Autism | 1. congential rubella (german measles) 2. hypsarrhythmia (brain wave abnormality in infants) 3. tuberous sclerosis (degenerative disease from benign tumour-like nodules) 4. cytomegalovirus -herpes virus infection 5. difficult pregnancy/ labour |
| 3 Genetic Causes of Autism | 1. 5-10% risk in families have another child 2. 50/200Xs risk in general pop 3. oxytocin - involved in bond for social memory |
| 4 Neurobiological Causes of Autism | 1. amygdala: increased fear/ anxiety use cortisol damage area = fewer neurons 2. 30-70% clumsy, poor posture/ gait: reduced cerebellum size 3. oxytocin: giving improves memory and ability to process emotion info 4. mercury in childhood vaccine - thimerosal |
| 3 Psychological Social Causes | 1. tradition: cold aloof mother 2. lack of self-awareness --- actually slow developmental progression 3. deficient socialization |
| 4 psychosocial treatment | 1. self-harm reduction 2. reducing tantrum 3. encourage ego development 4. skill building |
| 4 communication treatment | 1. teach languages: cant or wont imitate 2. shaping & discrimination training: taught to imitate, reinforced child to make sounds 3. can learn labels, plurals, sentences after imitate 4. Picture exchange communication system PECS, exchange picture for single item |
| socialization treatment | bhev procedures, have not found a way to teach social skills |
| timing and setting of treatment | 40hrs a week, inclusion helps autistic childs to play w/ peers |
| 3 biological treatment | 1. no cure 2. major tranquilizers 3. SSRIs |
| 4 integrative treatment | 1. bhav approach 2. Meds 3. parental support 4. skill development |
| intellectual disability | evidence in childhood significantly below average intellectual and adaptive functioning |
| 3 intellectual disability | 1. depending on level of impairments changes abilities 2. degree of independence 3. language and communication is most obvious |
| 3 groups of Int D | 1. sub average intellectual functioning =- IQ 70 or below: 2-3% of pop 2. concurrent deficits or impairments in adaptive functioning: difficulty in two of these- communication, self-care, home living, use of community resources, self-direction, work, leisure, health, academic skills and safety 3. age of onset: evident b4 age of 18 years |
| 3 IntD IQ classification system | 1. mild: 50-70 2. moderate: 35-50 3. severe: 20-35 |
| AAIDD definition of IntD level of support or assistance needed | intermittent, limited, extensive, pervasive |
| 3 categories education system negative expectation, stigmatizing | 1. educable intellectual disability: 50-75 IQ - learn basis academic skils 2. trainable intellectual disability: 30-50 IQ - rudimentary vocational skills 3. severe intellectual disability 30 below |
| 3 STATS IntD | 1. 90% fall in mild category 2. 70 babies born a week w/ intellectual disabilities 3. 1.6:1 male female ratio |
| 4 causes InD | 1. environmental deprivation, abuse, neglect 2. prenatal: drugs/ disease, fetal alcohol syndrome, lack of oxygen, malnutrition 3. Perinatal: diff. during labour and delivery 4. Postnatal: infections, head injury |
| 5 Biological IntD Causes | 1. 300 genes influence IntD 2. single gene disorders 3. dominant gene: tuberous sclerosis 4. recessive gene: phenlketonuria/ PKU (inability to breakdown chemicals in foods) 5. X-linked gene: Lesch-Nyhan syndrome |
| 3 Chromosomal Influence | 1. Down Syndrome: extra 21st chromosome stick together, past age of 40 have Alzheimers, 1/800 births 2. Amniocentesis: removing same sample of fluid around fetus to see if Down S. 3. Fragile X syndrome: mutation of top of chromosome, affects mostly males, hyperactivity, short attention span, gaze avoidance, speech repetition |
| cultural-familial IntD | ppl w/ these characteristics are thought to have gonitive impairments result from combination of psychosocial and biological influences: neglect, abuse, social deprivation (results slower paced, lectual disability) |
| 7 Treatment of IntD | 1. improve areas of learning disabilities 2. bhav innovation, task analysis, reinforcement 3. communication training 4. augmentative communication strategies 5. alternatives to punishment to reduce self harm, aggression and abuse 6. support 7. what and where of learning |
| 6 prevention of developmental disorders | 1. eugenics 2. intensive preschool program 3. medical and nutritional support 4. improve amygdala performance in fragile X disorder 5. gene therapy 6. advances biomedical technology |
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