Disorders (Affective Disorder) Flashcards
Affective disorders
Affective Disorders are complex human experiences
As complex humans there are many ways in which affective disorders can be studied and many parts of human experience can be impacted.
As this is a lecture on brain-behaviour, we are going to focus on the biological elements associated with affective disorders.
What is an Affective Disorder?
- Depression (post partum, atypical, SAD, dysthymia, substance abuse, pre-menstrual dysphoria)
- Mood cycling with mania (Bi-polar, cyclothymia)
- Anxiety ( GAD, Panic, Phobia, OCD, separation, selective mutism, social, panic, agoraphobia, substance induced)
- Trauma/Stressor induced (attachment disorder, PTSD, Acute stress disorder, adjustment disorder)
- Often characterised by going on for a certain period of time
- Be impairing in the day to day function of the person
- Can be mild, moderate and severe
- A person can have co-morbid disorders – i.e. its pretty depressing to have OCD
- Can be caused by external factors, e.g., specific experience and a biological predisposition e.g. genetic, regulation of neurotransmitters, injury, etc
The concept of stress
•A fourth response in humans has also been observed called “fawn”.
•This in when someone engages in behaviour that aims to please, appease and pacify the threat in an effort to keep themselves safe from further harm.
•Stress has many dimensions and is an ongoing process.
•The concept of allostasis
–The active process of adapting and maintaining stability (or homeostasis) through the production of mediators, like cortisol, that promote adaptation.
•Allostatic load/overload
–Allostatic load refers to the price the body pays for being forced to adapt to adverse psychosocial or physical situations
Depressive Disorders
- Depression (post partum, SAD, dysthymia, substance abuse, pre-menstrual dysphoria, due to a medical condition)
- 2-week period
- Loss of interest or pleasure,
- Low mood
- Weight loss or gain
- Sleep changes
Mood Cycling Disorders
- Mania – 1 week, hypomania – 4 days
- Inflated self esteem, grandiosity,
- Decreased need for sleep
- Talkative
- Flight of ideas racing thoughts, distractibility, increase in goal directed behaviour
- Excessive involvement in activities with risky and painful consequences.
Anxiety Disorders
- Excessive fear due to the anticipation of a future threat
- Threat may not be named or may be clearly identified
- Behavioral disturbance
- Surges of anxiety, increased autonomic arousal, escape behaviors – Fight Flight - Panic
- Passive avoidance behaviors - Freeze/Fawn - OCD
Trauma/Stress Induced
- Marked by a specific event; threatened death, serious injury or sexual violation,
- direct experience
- Witnessed
- Learning of the event happening to a loved one
- Repeated or extreme exposure to aversive details
- Recurrent distressing memories
- Recurrent distressing dreams
- Dissociative reactions
- Anhedonia
- Avoidance
- Arousal symptoms- disturbed sleep, hypervigilance, poor concentration, exaggerated startle response
Neural Correlates of Affective Disorders: Part 1
HPA Axis and Cortisol:
•Neuroendocrine system; sleep, digestion, immune system, mood, sexuality and energy, cardiovascular and reproductive systems
•Mediates stress response – hormonal and chemical cascade through the brain
•Anatomical connections to amygdala, hippocampus and pre-frontal cortex.
•Periventricular nucleus of the hypothalamus – release peptides
Neural Correlates of Affective Disorders: Part 2
- Anterior lobe of the pituitary gland -
- Adrenal cortex - releases glucocorticoid hormones
- Feedback loop
- Connections to the limbic system hippocampus, amygdala and cingulate gyrus – emotions and behaviour
- Connections to the prefrontal cortex – attention, working memory, planning organization and personality and takes a long time to reach maturation
Neural Correlates of Affective Disorders: Part 3
- Prolonged exposure to glucocorticoids can cause atrophy in the hippocampus
- Changes in volume, cells, plasticity in the amygdala, hippocampus anterior cingulate cortex and areas of the prefrontal cortex
- The HPA can begin to have difficulty regulating the functions it modulates impacting immune responses, inflammatory reactions, hyper and hypo responses.
- Cortisol becomes down regulated over time and people who experience intergenerational trauma have been shown to have have lower than expected levels of cortisol and increased rates of inflammation.
Gaba
- Low GABA is possible inherited biological marker of vulnerability to mood disorders
- Reduces neuronal excitability by inhibiting neuronal transmission
- GABA receptors found in the hippocampus, amygdala thalamus, basal ganglia, hypothalamus and brain stem
- Decreased GABA function is associated with depressive and manic states, lower levels found in blood plasma
- But – do not normalize after remission of mood disorder ??
- Benzodiazepines –GABA inhibitory neurotransmitter that reduces neuronal excitability
Imaging
- GAD - Changes in ventro lateral and dorsolateral prefrontal cortex, anterior cingulate, posterior parietal regions and amygdala in adults and children
- Mega analysis – No difference between female GAD and healthy controls, some small difference between men but small and not a major component of pathology
- Social – cortical volume reduction left inferior parietal cortex, CBT success associated with decreased volume in the bilateral dorsomedial prefrontal cortex and increased connectivity in the fronto-limbic networks
Epigenetics
•Gene modification across generations can increase risk for an affective disorder
•Low SES during adolescence is associated with increased methylation of the proximal promoter of the serotonin transporter genes
•Which predicts greater threat-related amygdala reactivity
•Histone acetylation – seterotonin, norepinephrine
•Methylation - serotonin, dopamine, adrenaline, norepinephrine and melatonin
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