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Emotional Disorders - Coggle Diagram
Emotional Disorders
Externalising Disorders
- Maladaptive emotions and cognitions manifested in outer behaviour. Often antisocial and cause harm to others. Disruptive, impulse control and conduct disorders.
Prevalence in Development
- Onset at any age, intermittent explosive disorder, substance misuse, pyromania/kleptomania.
- In adulthood, antisocial personality disorder, but required conduct disorder in childhood
Conduct Disorder
- Antisocial behaviour in young people, include (DSM-5) aggression to people/animals, destruction of property, theft, truancy (skipping school, going missing for some time).
- 3+ symptoms past 12 months with at least 1 in past 6 months.
- Clinician will also look at severity or impact on daily function (e.g., with relationships), age of onset, and limited prosocial emotions (callous-unemotional) specifiers.
- ODD more common in children under 11 years, CD in those over 11
Prevalence
- NICE (2013)
- one most common reason referral to CAMHS
- prevalence 5% 5-16 y/os, strange though as onset seemingly at 11
- more prevalence in males (2:1), children low SES
- very common (up to 40%) in kids looked after, abused or child protection list.
- Blair et al. (2014) 46% boys 36% girls CD have at least 1 other condition. Up to 40% met ADHD criteria, 50% will be diagnosed with ASPD when adults. Anxiety, depression, substance misuse, poor literacy and other learning difficulties common
- Huge social and financial costs (Erskine et al., 2014)
Heterogeneity
- Highly heterogeneous, with overt (fighting) and covert (stealing) behaviours. Trajectory and stability behaviours over time variable. Early vs. adolescent onset variable too.
Trajectories
- Dual Taxonomy (Moffitt, 1993) life course persistent onset will be in childhood, and will have lower cognitive ability. Adolescence-limited onset often specific, linked to aggression, and will go away after the end of adolescence
Genetics
- 40-50% heritability
- Possible 2 separate genetic factors (Kendler et al., 2013) rule breaking and overt aggression
- Hyde et al. (2019) adoption cohort 561 families, history severe antisocial behaviour biological mothers. 27 months old. Despite limited/no contact with offspring, biological mother antisocial behaviour predicted early CU behaviours. High adoptive mother positive reinforcement buffered the effects of heritable risk CU
Environment
Fairchild et al. (2019)
- evocative - individual's heritable behaviour elicits particular environmental response
- Negative treatment child behaviour evokes from parents and other authority figures (such as hard punishment), risk developing CD increased
- active - genetic predispositions lead them to seek particular environments
- For example, choose to associate with antisocial peers and/or seek highly stimulating but dangerous environments. Owing to effect child's genes on friendship choices, risk CD increased
- passive - type environment provided to child correlates with inherited genotype.
- Environment correlation occurs when children inherit genetic variants that also contribute to the environment that the parents create. e.g. genes that increase risk of psychopathology and increase probability parent will maltreat their child. Parents may transmit a genetic liability for CD to child and provide abusive rearing environment reflecting parents' genetic liability
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Neurobiology
- Meta-analysis brain structure children and adults CP. Robust reductions in grey matter volume in left amygdala, bilateral insula, ventral PFC/OFC, superior temporal gyrus (Rogers et al., 2015)
- Brain function in meta-analysis 29 studies task activation found reduced activation in areas related to hot EF. (bilateral amygdala, bilateral insula, right striatum, left medial/superior frontal gyrus, left precuneus) (Nordermeer et al., 2016). Strong evidence abnormalities in amygdala specific CD, correlating with symptoms.
- Review fMRI studies youth conduct problems: empathy, acute threat response, reinforcement-based decision-making, response inhibition associated with symptoms sets seen in individuals CP. (Blair et al., 2018)
- reduced amygdala response to distress underpins high CU traits
- increased amygdala threat responses likely underpin reactive aggression and anxiety
- forms of decision-making dysfunction underpin substance abuse and antisociality
- reduced response control associated with impulsiveness in some youth CD/ODD
Cognition
- Emotional Recognition (Fairchild et al., 2009) 6 emotion face task 5s, ps had to select label from 6 options. Male ps, approx n=80. Relative to controls:
- Early onset CD far less success recognising anger, disgust, happiness.
- Adolescence-onset recognition fear impaired
- Those high psychopathic traits (beh conflict social norms, disregard rights others, inability distinguish right and wrong, difficult showing remorse/empathy, tendency lie, manipulating/hurting others) impaired fear, sadness, surprise recognition relative to those low psychopathic traits. Perhaps do not realise someone is sad, so lack of empathy as result
- These link to neural basis e.g., amygdala deficient activation in adolescents fearful expression processing high levels psychopathic traits and disruptive behaviour disorders (Marsh et al., 2008)
- Decision-making (Fanti et al., 2016) 85ps stoplight task, traffic light type thing where green you can respond, red must stop. Yellow you could choose to speak or stop. Get money if finish response requirement before red light. High CD many more risks than low CD group. Perhaps not developing decision-making skills in childhood
Callous and Unemotional (CU) Traits
- Frick & Viding (2009) increasing evidence subtypes based on levels CU traits, lack of guilt and empathy, and unemotional and uncaring aspects.
- Those with absence of traits have strong relationship between childhood CU traits and adult psychopathy.
- High CD/high CU more likely early onset CD resistant to intervention
- Low CD/CU more likely adolescent onset and/or limited
Internalising Disorders
- Maladaptive emotions and cognitions manifesting in a child's inner psychological environment. Anxiety and Depressive Disorders
Neurobiology
- High degree overlap between mental health disorders, with specific findings for internalising vs. externalising in amygdala and hippocampus (Goodkind et al., 2015).
- Mega-analysis grey matter SAD 174 patients. Larger GM in right putamen (within dorsal striatum) in SAD, no related alterations in amygdala-hippocampal, PFC or parietal regions. The increase in right putamen correlated positively with the severity of self-reported social anxiety symptoms Bas-Hoogendam et al. (2017)
- Right dorsal striatum grey matter in social anxiety increased activation even when controlling for MDD, but not large variability in this Bas-Hoogendam et al. (2017)
- Across internalising disorders, reduced activation in PFC, insula, inferior parietal lobule and putamen. Increased activation left amygdala, dorsal anterior cingulate cortex, right thalamus. (Janiri et al., 2019)
Cognition
- Walter (2016) genetic, environmental and neurobiological factors affect information processing factors (e.g., attention, threat-safety cue discrimination, memory, and appraisal biases), which can cause the symptoms and disorders
- Lau & Waters (2016) research review consider how youth with and without anxiety/depression vary in regards to attention to social-affective stimuli, discriminate between treat and safety cues, and retain memories of negative events and appraise ambiguous info. Difficulties in threat-safety cue discrimination characterised anxiety, differences in retrieval negative and over-general memories in depression.
- Larger differences in attentiona; bias to threat between clinically anxiours and non clinical children with increasing age (Vasey et al., 1995) BUT not consistent for phobias (Martin et al., 1992)
Environment
- Anxiety and depression share risks of physical, sexual or emotional abuse, neglect, adverse life events (e.g., separation from parents), peer group (e.g., bullying), culture birth cohort and gender, diet, family discord exposure to domestic abuse, socio-economic status, parenting style. Anxiety has additional of parent internalising or other psychopathology, and a specific anxiogenic event e.g., for specific phobia. (Brook & Schmidt, 2008)
- Anxiety negatively associated with popularity and social competence, and positively associated with victimisation (Giora et al., 2005)
- Twin studies child anxiety consistently suggest majority of variance in anxiety attributed to environmental features unique to each twin (Gregory & Eley, 2007), but evidence is inconsistent (Rapee et al., 2009)
Behaviour
- Behavioural inhibition, tendency respond fearfully to, or withdraw from novel or unfamiliar objects, people and situations for both anxiety (Gladstone et al., 2005) and may be linked with depression (Gladstone & Parker, 2006). Linked to genetics, as offspring depressed/anxious parents more likely to have high BI than those psychiatrically healthy parents (Lau & Waters, 2016). Environmental factors too, infants high BI insecurely attached (Shamir-Essakow et al., 2005) or experience permissive parenting (Williams et al., 2009) have higher anxiety *
- Neuroticism - adolescents high neuroticism increased risk developing anxiety and depression across time (Aldinger et al., 2014) and may reflect genetic risks for anxiety and depression (Luciano et al., 2012)
Genetics
- MDD 40-50% heritable (Eley, 1997), childhood onset less heritable than adolescent onset (Rice, 2009) perhaps due to new genetic influences in adolescence, effect of gene-environment correlation?
- Anxiety - 30-40% heritable (Kessler, 2002) greater heritability anxiety in girls than boys (Fegion et al, 2001)
- Molecular genetics MDD - GWAS indicated 44 genetic differences associated, usually expressed in brain regions indicated to be structurally different (Wray et al., 2018)
Examples:
Social Anxiety
- Persistent fear of one or more social or performance situations, exposed to unfamiliar people or possible scrutiny by others, fear will act in a way that will be embarrassing and humiliating.
- Exposure to feared situation provokes anxiety, person recognises fear is unreasonable and excessive, feared situation avoided or else are endured with intense anxiety and distress.
- Condition interferes with daily life and typically lasts 6+ months.
- Not due to another condition or drugs/medication
GAD
- Excessive anxiety and worry occurring more days than not for 6+ months about a number of events or activities.
- Finds difficult to control the worry as can’t avoid everything, - Associated with at least one (in children) of restlessness, easily fatigued, difficulty concentrating, irritability, muscle tension, sleep disturbance.
- Interferes with daily life
- Not due to another condition or drugs/medication
MDD
- 5+ following over 2-week period: depressed mood (irritable in kids), diminished pleasure daily activities, weight loss or gain (failure to meet expected weight in kids), insomnia/hypersomnia, psychomotor agitation or retardation, loss of energy, feelings guilt or worthlessness, diminished ability to think or concentrate, suicidal ideation.
- Interferes with daily life
- Not due to condition, no episodes of mania.
Prevalence in Development
- MDD diagnoses 15-16 y/os doubled since 1980s (Nuffield Foundation, 2013), gender ratio approximately 2:1 F:M, onset around 13.
- Children 5-16, 3% anxiety, 1% MDD (2-8% adolescence), (Green et al., 2004).
- Rare to be diagnosed with these disorders if there were no symptoms in childhood (Paus et al., 2008). Young people meeting criteria anxiety disorder at one time are at moderate-to-high risk to meet criteria for anxiety disorders as move from childhood to adolescence (Bittner et al., 2007) and adolescence to early adulthood (Pine et al., 1998)
- Female preponderance anxiety disorders showed steady increase over development, starting before 5 years of age and building in child and adolescent years (Roza et al., 2003)
- Shy and anxiety-disordered children continue to show above-average levels of life interference into early adulthood (Caspi et al., 1998)
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