Neuro + Clinical🧠

Question 1

Heritability

Answer 1

Estimate of how much variance of characteristic in population is due to differences in heredity
Varies between 1 and 0
Twice the difference between the correlations for identical - non identical A2= 2(rMZ-rDZ)

Question 2

Twin studies

Answer 2

50% attributed to genetics for Big 5 similarities
Control for genetic effects through variance- covariance decomposition (biometric modelling)
Monozygotic- If trait heritable completely, twins would score the same as each other, if reared together environment would explain
Dizygotic- If large difference between monozygotic, likely to be genetic

Question 3

VACE heritability

Answer 3

V- Variance of trait
A- Genetic influence of trait (making siblings similar)
C-Common (shared environment)
E- Non shared environment (making siblings different)

MZ- A2+C2
DZ 1/2 A2+C2

Question 4

Heritability and environment’s importance

Answer 4

High heritability does not imply environment doesn’t alter the trait
Can have 100% heritability but environment may not express the characteristic
Environment can affect heritability throughout age

Question 5

Multiplier effect

Answer 5

If genetic or prenatal influences produce small increase in trait, this magnifies over time to become a larger effect

Question 6

Tobacco use heritability

Answer 6

65%- Much less population smokes but genes haven’t changed, heritability may be same but incidence dropped due to known health risks
Different heritable components e.g. gratification
Social change, anti-social peers (sharing environment increases heritability estimate)

Question 7

Assumption about sample comparisons for twin studies and issues with this

Answer 7

Assume equal environments for sample comparisons
BUT
-Mono twins treated more similarly, more time together with more similar environments
-Adoptive parents higher SES, more marital stability and mental health than biological parents

Question 8

Traits explained by genetics or shared environment

Answer 8

Personality, mental disorders
Shared environment explains adolescent substance abuse
Genetic effects increase with time

Question 9

Keywords-

Allele, heterozygous, homozygous

Answer 9

Allele- variant of gene
Heterozygous- different form of alleles Bb
Homozygous - same form of allele BB
Use Punit square

Question 10

Mendel

Answer 10

Dichotomous traits (occur in one form or another, never in combination)
Pea plants green and yellow parents gave no yellow offspring but 3:1 green to yellow 2nd gen pea plants
Assigned letters to represent genotypes (G dominant to g)

Question 11

DNA

Answer 11

Nucleotide bases- two strands are complementary A+T and C+G

Question 12

DNA structure unwinding

Answer 12

Bases find new bases, make more complementary strands
Mitosis- DNA replicates, cell divides, cell multiplication
Meiosis- DNA replication and recombination, cell divides twice, one chromosome in gamete

Question 13

DNA making proteins

Answer 13

DNA unwinds, makes single strand of messenger RNA (complements unwound DNA)
RNA U base replaces T so A+U and C+G
DNA transcribed to mRNA which translates to proteins

Question 14

DNA proteins

Answer 14

Bases in 3s
tRNA brings amino acid to ribosome
Ribosome incorporates amino acids to grow protein chain
mRNA translated
Particular gene will encode particular protein which may have different properties

Question 15

Gene for Tryptophan Hydroxylase (serotonin) mutant form

Answer 15

Rare mutant form of Tryptophan Hydroxylase gene that doesn’t make serotonin as well
In vitro cells with this gene make 80% less serotonin

Question 16

Zhang mutant form of Tryptophan Hydroxylase study

Answer 16

Of 9/87 depressed patients had mutant form
3/219 control had mutant form (did have anxiety, mental health issues etc)
HOWEVER still very rare and many who were depressed did not have it
Difficult to replicate study

Question 17

Gene for serotonin transporter (5-HTT) short allele

evaluate

Answer 17

Short allele gene= more depression and anxiety

Short allele not always linked to depression and psychological measures may be inaccurate or link may
not exist SO use brain scan:

Question 18

5-HTT short allele brain scan

and negative

Answer 18

Judge angry and afraid faces
Shorter gene= more active amygdala, may overrespond to negative emotion, risk factor for depression
BUT could be environmental
Depressed patients 84% stress previous year vs 32% control

Question 19

Diathesis model and Capsi

Answer 19

Effect when genetic risk factor and environment interact

1037 subjects- genotype non significant on own and no difference in number of stressful events. Interaction of 2 short forms of 5-HTT short allele= HIGHER DEPRESSION

Question 20

Comorbidity

Answer 20

Shared genetic effects for wide range of conditions Traits may have many genetic elements e.g. smoking with impulsivity, addiction etc

Question 21

Difficulty diagnosing childhood and adolescent psychological problems

Answer 21

May lack language capacity to articulate difficulties
Cultural norms
May be just childhood
Some issues not diagnosed in children
Symptoms may be confused with physical ones
Comorbidities, quick developmental trajectories

Question 22

Issues with not treating conditions in children

Answer 22

Worsens, difficult to solve later
Interfere with other areas e.g. education
Delayed coping strategies

Question 23

Incidence for childhood disorders

Answer 23

Around 20% 5-10 and 11-16years

Question 24

Externalising and internalising disorders

Answer 24

Externalising-disorders based on outward directed behaviour problems such as aggressiveness, hyperactivity

Internalising- inward and withdrawn behaviours such as depression and anxiety

Question 25

Separation anxiety

Answer 25

Specific to childhood, separated from those they feel attached to Ongoing and unnecessary fear about harm coming to attached figure, fear of being left alone

Question 26

OCD

Answer 26

Obsessions and compulsions causing relief, behaviour believed to prevent catastrophising, affects other functions Can get compulsions without obsessions

Question 27

GAD

Answer 27

Similar to adult, chronic worrying about problems and threats, pathological worrying across domains 4-7yrs worry about separation from parents, fear of imaginary creatures 11-13yrs worry about social threats 1% but some US studies show 11%

Question 28

Phobias

Answer 28

Normal-appear and disappear quickly e.g. spiders | Social phobia- begins as fear of strangers

Question 29

Anxiety

Answer 29

``` Moderate heritability (54%) More environmental influence when younger Traumatic events, modelling and exposure to info causes anxiety ``` Children anxious after being exposed to scary info about a spider

Question 30

Anxiety and overprotective parenting style

Answer 30

Not allowed to explore or has hostile parenting style Difficult to determine since children share genetics with parents Small genetic tendency affects how interacts with environment (multiplier effect)

Question 31

Depression

Answer 31

Difficult to recognise in young children Clingy, low mood, refuse school, exaggerated fears, somatic complaints e.g. headaches Range of heritability, in younger children abuse or neglect are risk factors Increased risk if parents have depression (less care and may not respond to child’s emotions, less activities)

Question 32

AST-D

Answer 32

To diagnose depression Neutral statements which could be interpreted more negatively Children of depressed parents score more pessimistically

Question 33

Drug treatments for childhood disorders

Answer 33

Drug treatments similar to adults : | ADHD Ritalin, depression SSRIs, anxiety benzodiazepines

Question 34

Issues with drug treatments Mouse anxiety drug test

Answer 34

SSRIs increase motivation to act on thoughts e.g. suicide but fewer side effects compared to older medicines Affects developing brain, long term changes Does not provide coping strategies or treat social and language impairments Prozac trial child mice were less nervous (walked around less)

Question 35

Family interventions for childhood disorders

Answer 35

Systematic family therapy-communication, structure, organisation Parent management training-not rewarding antisocial behaviours Functional family therapy-strengthens relationships CBT-work through problems, not much empirical evidence Play therapy- difficult to get clinical evidence

Question 36

Callous and unemotional traits (CU)

Answer 36

Disregard for others, lack of empathy, deficient affect | Distinct problems in emotional and behavioural regulation, less sensitive to punishment

Question 37

Behavioural problems definition

Answer 37

Challenging behaviour outside the norm for age and level of development Limited social opportunities may increase behaviour for attention ADHD most common disorder for children and adolescents

Question 38

Autism

Answer 38

Repetitive interests, rituals abnormal social approach Difficulties developing relationships Normal development followed by regression at 2-3years

Question 39

Disruptive behaviour disorder types

Answer 39

Conduct disorder (CD) Oppositional defiant disorder (ODD)fight against authority figures (if do not meet full criteria for CD) Formally known as externalising disorders, most common behavioural problems in preschool and school children

Question 40

Conduct disorder

Answer 40

Older child in a pattern of violating others and being aggressive. Children often grow out of it Long term chronic impulses, disregard for authority, brings issues to adulthood, brushes with the law Adapt better if identified sooner Diagnostic criteria based on behavioural symptoms but doesn’t inform about underlying cognitive or emotional processes Difficult to differentiate between ADHD, ODD

Question 41

CD later issues in adulthood

Answer 41

Physical and mental health disorders, substance abuse, arrest and criminal charges, unemployment, homelessness relationship and parenting issues

Question 42

CD incidence and heritability

Answer 42

1.2% incidence 5-74% heritability but extensive studies say 40% CD is heterogenous (displayed differently in different people) 32,000 symptom profiles could get a diagnosis May not have valid diagnostic criteria, huge variation Underlying construct may not exist

Question 43

Environmental and dispositional risks for CD

Answer 43

Around 50% of variance is environmental Maternal- smoking, alcohol, drug use, stress Birth- complications, parental psychopathy, malnutrition Family- harsh and inconsistent discipline, maltreatment, parent-child conflict, low SES Extra familial- community violence, association with violent peers

Question 44

Genetic factors CD

Answer 44

Automatic, neurocognitive, social information processing, temperament, personality traits Candidate gene based approaches used small sample sizes

Question 45

Gene-environment correlations CD

Answer 45

Passive- genetic predisposition and also exposed to it in the environment Active-actively seek out environment that suits genetic predisposition Evocative- predisposition evokes responses from environment

Question 46

Finding specific genes for CD

Answer 46

Genome wide association (GWAS) Observational study of genome wide set of genetic variants in individuals to see if variants are associated with a trait Focus on single nucleotide polymorphisms (allele) Compare DNA of participants with phenotype for a particular trait or disease. If one variant is more frequent in people with the disease suggests region at risk of condition

Question 47

Gene not understood found for conduct disorder

Answer 47

RB FOX-1 Upper DNA molecule differs from the lower molecule by single base pair

Question 48

MAO and CD

Answer 48

``` Enzyme that breaks down monoamine neurotransmitters Faulty gene (low MAO) so more monoamines in the synapse Leads to more CD behaviour ``` When combined with severe maltreatment=very high CD risk

Question 49

Neurocognitive aspects of CD

Answer 49

Less sensitive to punishment although some studies indicate overly sensitive Overly sensitive to reward Different verbal IQ , WM, executive function, emotion regulation May take more risks but threat and reward system confused Less cortisol activity to stress

Question 50

Brain regions CD

Answer 50

Frontal region- executive function, also involved in rewards Striatum- reinforcement/learning, decisions Amygdala-emotion, empathy, threat response. More activated with low MAOA genotype

Question 51

CD cognitive hostile attributional bias

Answer 51

Interpret cues as hostile | Frontal cortex more activated with low MAOA genotype

Question 52

Managing CD without comorbidity

Answer 52

Psychosocial intervention, social learning theory + skills training if adolescent Pharmacological therapies of poor response to psychological intervention. Ritalin, antipsychotics Boot camps etc are likely to prolong symptoms, should tailor to specific details If has limited prosocial emotions- add parental warmth, child empathy

Question 53

Managing CD with comorbidity

Answer 53

Internalising, externalising symptoms and developmental disorder comorbidities = Psychotherapy and or medication (initially stimulants for ADHD then risperidone for impulsive aggressive behaviour and hyperactivity)

Question 54

3 presentations of ADHD

Answer 54

ADHD inattentive presentation-poor attention and listening, difficultly organising ADHD predominantly hyperactive/impulsive presentation-figit and unable to sit still Combined presentation

Question 55

ADHD symptoms DSM5

Answer 55

Hyperactivity, impulsivity and attentional problems Interferes with functioning or development Often difficulty sustaining attention in tasks (inattentive type) Often fidgets, taps, squirms (hyperactive type) Reduce academic, occupational functioning Several symptoms to be present before age 12 manifest in more than one context, called hyperkinetic disorders in ICD10

Question 56

Incidence of ADHD

Answer 56

5% children/adolescents have diagnosis Boys to girls 3:1 (difference may be real or have differences in diagnosis) Symptoms continue to adulthood, 8-43% cases may be adult version of disorder. Hyperactivity reduces but inattention may remain

Question 57

Treatment for ADHD

Answer 57

5years+ drugs | Ritalin, amphetamine, methylphenidate (often drugs which are abused)

Question 58

Timeline of ADHD treatments 1902

Answer 58

1902- George Frederick Still 20 children with defect of moral control without impaired intellect or physical disease 3 symptoms: Immediate gratification to self, little regard for others Figity Abnormal incapacity for attention

Question 59

Timeline of ADHD treatments 1917-28 and 1940-1950

Answer 59

1917-28 Encephalitis epidemic: surviving children were irritable, hyperactive, antisocial Clinicians linked ADHD with brain damage 1940-1950s Children with brain damage showed post encephalitic behaviour. Clinicians diagnosed brain damage on behaviour purely

Question 60

Timeline of ADHD treatments 1960s

Answer 60

No necessary relationships between brain damage and symptoms Replaces term with minimal brain dysfunction Term became considered too broad, had to focus on specific symptoms (hyperactivity)

Question 61

Timeline of ADHD treatments 1968

Answer 61

DSM2 ‘hyperkinetic reaction of childhood’ Defined what was most important to define disorder Hyperactivity was not in many brain disorder cases

Question 62

Timeline of ADHD treatments 1970-1980s

Answer 62

Realised attentional problems were as significant as hyperactivity DSM3 ‘Attention Deficit Disorder’ with or without hyperactivity Hyperactivity no longer essential for diagnosis 1987 Develop 3 subtypes of ADHD, separated out again

Question 63

Timeline of ADHD treatments 1994

Answer 63

Clinical trail found 3 subtypes seen in DSM 4 and DSM 5 up to 2013

Question 64

Impact of ADHD: poorer educational achievement

Answer 64

4 Scotland wide NHS databases matched with school records ADHD children were 6.5% more likely to have sub-GCSES compared to control Girls worse than boys

Question 65

Impact of ADHD: occupational attainment was poorer

Answer 65

Adults diagnosed at 6-12 years Were less likely to be employed (85%), lower job responsibility and lower median salary

Question 66

Impact of ADHD: peer relation issues

Answer 66

ADHD children more rejected by peers compared to same sex classmates

Question 67

Impact of ADHD: health impacts

Answer 67

ADHD children 1.6% more likely to have an accident that requires medical treatment

Question 68

Impact of ADHD: mental health impacts

Answer 68

Children 6-17 years high comorbidity for depression, anxiety also ASD and Tourette’s Adults previously diagnosed with ADHD more likely to become drug dependent Drugs control the symptoms when given as a child and reduce adult chance of addition

Question 69

2 classical theories of ADHD

Answer 69

``` Frontal cortex (brain damage, structural, functional) Dopamine (reuptake, reward) ```

Question 70

Classical theories of ADHD: frontal cortex Brain damage

Answer 70

Symptoms of ADHD similar to changes following frontal cortex damage (see Phineas Gage) Impulsivity found in ADHD and frontal cortex damage (Iowa Gambling Task) fail to realise they will win with smaller gain advantageous card DELAY AVERSION

Question 71

Classical theories of ADHD: frontal cortex DELAY AVERSION

Answer 71

Delay aversion led to Barkley’s behavioural disinhibition theory of ADHD: poor inhibition as central deficiency of ADHD, accounts for attentional and kinetic symptoms Localised in frontal cortex

Question 72

Classical theories of ADHD: frontal cortex Structural (MRI)

Answer 72

Frontal lobe grey matter volume is lower in ADHD vs control

Question 73

Classical theories of ADHD: frontal cortex Functional (PET)

Answer 73

Tracer in bloodstream, radionucelotide produces positron when nucleus broken apart, produces two gamma photons when meets electrons which are picked up by scanner ADHD teens had different rates of glucose metabolism in anterior and posterior frontal regions. Less activity vs control

Question 74

Classical theories of ADHD: dopamine levels

Answer 74

Drugs used to treat ADHD increases dopamine levels Microdialysis- small, semi permanent probe inserted to brain, fluid put through, chemicals in the extra cellular fluid diffuse across membrane and are collected. Analysed with chromatography Rats- greater dopamine levels in striatum after D-amphetamine

Question 75

Classical theories of ADHD: dopamine reuptake

Answer 75

ADHD associated with increase in dopamine reuptake SPECT-Gamma rays Large radioactive signal means high amount of transporters ADHD has more dopamine transporter, takes up more transmitter May be issues with dopamine system

Question 76

Classical theories of ADHD: dopamine, reward system

Answer 76

Release of dopamine when presented with food or engages in sex (rat) School children had to release a response key when stimulus lit up Experimenter either praises faster than last time (continuous reinforcement) or every other time (partial reinforcement) or random (non contingent) Children with ADHD more affected by non contingent reward, longer time to react as wanted the reward now (delay aversion)

Question 77

ADHD and psychiatric disorders

Answer 77

Genetic architecture of ADHD is similar to neuropsychiatric disorders DNA sequence variants are associated but only when thousands of SNPs (single nucleotide polymorphisms) are combined into duplications (copy number variants)

Question 78

What do ADHD treatments focus on relief from

Answer 78

Relief from core somatic symptoms such as inattention, overactivity