Psychopathology Flashcards
(19 cards)
Prevalence in Adolescence
Casey and Powers 2015: High incidence rate in A of mood disorders, conduct disorders and anxiety disorders and schizophrenia- critical period. Around the onset of puberty conduct disorders manifest. Substance abuse is also typically high but is generally co-morbid with other disorders.
Hypothalamic-pituitary-adrenal-axis
Stress response triggers the H-P-P-A. The hypothalamus triggers the pituitary gland which triggers adrenal gland to release cortisol= fight or flight response. Works via a negative feedback loop- this system is more sensitive during A therefore heightened/prolonged stress may further influence this system.
Romeo 2013
In rats that are restrained, cortisol levels return to normal quicker than those who are pre-pubertal. Cortisol stays in the system longer in pre-pubescent rats.
Dendritic arborisation is reduced in hippocampus, mPFC and increased in amygdala, when exposure to corticosterone is maintained. Operates in a region dependent manner.
Depression: Forbes et al 2009
Very simple gambling task (higher or lower), controls showed heightened activation in reward centre (VS), those with major depressive disorder there was no such rewards related activity- was altered in mPFC.
With fMRI cause and effect can’t be established- don’t know which ones cause the other. A self-reported positive affect correlates to how activated the VS is activated- brain behaviour relationship.
Op de Macks et al 2011
Gambling tasks- engagement of VS was mediated by the amount of bio-available testosterone (index of pubertal stage) infer that this high prevalence of testosterone may be related to mood disorders in A. Clinical brain behaviour relationship.
Atypical Neurodevelopmental Trajectories
Many psychopathologies can be linked to altered trajectories of GM/WM development:
Delayed: change in time
Deviant: completely altered pattern to typical
Velocity: peak not reached
ADHD
Between 5-10% of school aged children, typical onset start of puberty through to A. Characterised by attention deficit and hyperactivity.
Shaw et al 2007
Between 7-12 ADHD relative to controls show delayed cortical thinning in GM up to 2 years in lPFC and temporal cortex. These areas are implicated in suppress responses, executive control of attention, working memory- all linked to pathogenesis of ADHD.
Contrastingly show increases rate in motor cortex- linked to excessive and poorly controlled motor activity.
Ellison and Wright 2008
VS is linked to ADHD as there are significant decreases in volume.
Hart et al 2013
Go/no go task impulse control VS, STS and mPFC are all consistently engaged- areas which are delayed in ADHD, structure impacting on function of areas- less able to restrict impulses.
Rubia 2018
Stroop task with instructions switching- socially not switching is impaired and has behavioural implications. Less ability to inhibit motor interference which implicates social cognition. Cold executive functions impact hot executive functions.
Co-morbities
ADHD rarely presents its own, high co-morbidities including ODD (67%), Conduct disorder (46%), mood disorders, anxiety, depression and substance abuse. Developmental trajectories show co-morbidity increases with age.
Shaw et al 2011
Conduction Co-morbidities where ADHD may bot be an all or nothin disorder, evidence of it being a spectrum of increasing symptom severity. The slower the rate of cortical thinning is characteristic of the symptoms severity for both symptoms and the syndrome.
Dual systems model
Casey and powers 2015: Dual systems model shows that the imbalance between PFC and limbic system may dive atypical trajectories and cause symptoms in multiple disorders.
Conduct Disorder
Characterised by repetitive and persistent pattern of atypical behaviours without empathy- reducing prosocial behaviour. Aggression, violation of rules, resulting in anti-social behaviour. Hyperactivity is also seen, with blunted affect and atypical behaviour in social situations.
Oppositional Defiant Disorder
Noordermer et al 2016: Co-morbid with ADHD, characterised by angry and irritable mood and being argumentative. Separate from bi-polar and depression. Less control in the amygdala and ACC which is linked to empathy and feeling others pain. Brain function is altered by brain structure resulting in psychopathologies.
Schizophrenia
Many factors contribute to schiz including: genetics, environment, synapses, neurotransmitters etc. Global morphology of COS, symptoms are magnified.
Gogtay et al 2008
Relative to healthy controls, those with COS show reduced WM increase but there is an increase in the ventricles- characteristic of schiz. They also fund that those with reduced WM perform worse on the child global assessment scale- day to day functioning.
Herting et al 2012
Difference in WM development can differentiate between typical individuals and those with COS. In the same areas WM tracts are undergoing localised changes with age/bioavailable testosterone- link to imbalance of pubertal hormones and COS?
Also get a sex by pubertal stage interaction, with 2:1 males diagnosed with schiz as females. Linked to short and long androgen receptors- testosterone has massive impact on WM integrity…. SPECULATION
