PSYC1005 Study Guide - Final Guide: Cerebral Circulation, Circadian Rhythm, Seasonal Affective Disorder
Activity-Based Intervention for the Treatment of Psychological Problems
Depression and Anxiety
• Major depression - depressed mood or loss of interest/pleasure in all activities (anhedonia) > 2 weeks +
clinically-significant distress of impairment in social, occupational or other functioning.
• At least 4 other symptoms:
o Somatic symptoms (changes in appetite, sleep, & psychomotor activity, fatigue).
o Neuropsychological change (difficulty thinking, concentrating and making decisions).
o Affective/cognitive changes (feelings of worthlessness/guilt, suicidal ideation).
• Anxiety, eg: Generalised Anxiety Disorder (GAD) - excessive anxieties/worries on most days + difficult to
control (> 6 months).
• At least 3 other symptoms:
o Somatic symptoms (restlessness, tension, disturbed sleep, appetite change, fatigue)
o Neuropsychological change (difficulty concentrating).
o Affective/cognitive changes (Irritability, catastrophizing)
• Anxiety, depression, sleep problems and fatigue are highly comorbid symptoms.
• Anxiety, depression and fatigue have common overlapping symptoms.
• Anxiety (6) and depression (2) are among the top 10 leading causes of disability in Australia.
• 1/5 Australians experience depression (1/4 females).
• People with anxiety/depression die 7.9 years earlier than others and show higher risk of death/hospital
readmission.
• Depression link to sleep disturbances, chronic illnesses (heart disease, diabetes, suicide, Alzheimer's),
cancer and liver disease.
Structural Brain Changes Occur in Depressed people
• Prolonged/repeated stress and major depression are linked to changes in cerebral blood flow, cerebral
metabolism and structural abnormalities in the brain:
o fMRI studies: decreased blood flow and cerebral metabolism in prefrontal cortex and
hippocampus.
o Post-mortem: decreased size (atrophy - cell death) and decreased connectivity of
hippocampus, ant. Cingulate and arbital cortices, dorsolateral prefrontal cortex.
What does this all mean?
• Depression is a state of limbic-cortical dysregulation (i.e. the brain areas most affected) that involves
centres for memory, emotion and motivation, which is caused by brain cell death and immune system
activation.
• What is causing this brain atophy/inflammation?
o Infection - depression is accompanied by activation of the inflammatory response system.
o Cytokines (immune system transmitters).
o Other inflammation sources (eg: autoimmune illness).
o Decreased blood-brain-derived-neurotrophic-factor.
• Antidepressants (AD) increase cerebral blood flow in hippocampus + ant. Cingulate cortex, normalise
cerebral metabolism, decrease atrophy in hippocampus - i.e. ADs may have a neuroprotective (rather
than neurotransmitter) effect.
What is causing the depression?
• Modern environment/society (eg: individualism, lack of collectivism).
• Stress/response to stress - stress can lead to rumination (deep thoughts, going over and over
something) which interferes with sleep thereby potentially contributing to anxiety/depression.
• Comorbid disorders causing each other, eg: sleep problems.
• Unhealthy behaviour, eg: lack of exercise.
• Sleep problems.
Sleep Disturbance and Comorbid Health problems
• Many people with sleep problems are fatigued, depressed, anxious or overweight, or vice versa.
• Eg: Chronic fatigue syndrome is diagnosed only if disabling fatigue occurs in association with a number
of factors.
How do depressed people sleep?
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• Most depressed people experience sleep problems, find it difficult to fall asleep at night, wake early and
experience frequent intense REM sleep that is quick to arrive.
• Most REM dreams especially the negative ones occur near to the time of waking in depressed people,
but fewer non-REM dreams are experienced
• REM dreams tend to be complex, negative, bizarre and memorable - ay orse perso’s orig
mood.
• Antidepressant theory quickly normalises sleep/ decreases REMs sleep - return to normal sleep pattern
occurs before producing a change in mood.
Depression, REM Sleep and Dreaming
• Sleep/dream variables predicted depression levels 1 year after marital separation in depressed
movements.
o Eye movement density in first REM sleep.
o Strength of emotion in firm dream, i.e. emotionality of dream.
o Number of negative dreams recalled from REM awakenings.
o Quality/structure of sleep + valence/content of dreams related to depression severity.
• Depressed patients reported more negative dreams at end of night's sleep than at the start of sleep.
• Late negative dreams often impacted adversely on mood.
Can Circadian rhythm therapies improve mood disorders?
• Bright light therapy is effective in treating seasonal affective disorder (SAD).
• Bright light administered in early morning suppresses melatonin and therefore, advances the circadian
rhythm -> nadir of temperature rhythm occurs earlier in day, whereas bright light in evening delays the
circadian rhythm -> nadir of temperature rhythm occurs later in the day.
How does late night eating interrupt sleep?
• Overweight people experience difficulty in falling asleep at night and sleep less than normal weight
people, and they are more likely to be diagnosed with Night Eating Syndrome or Binge Eating disorder.
• Eating later at night explains much of this relationship.
• Eating increases CBR which interferes with sleep onset.
• Low fibre + high fat + sugar intake related to lighter less restorative sleep and more sleep arousals.
• Fast food intake indicates the relationship body temperature later bedtime → BMI.
• Body temperature is interfered which makes it harder to fall asleep.
o High BMI → night eating → poor sleep.
o Poor sleep quality → binge eating → high BMI.
Longitudinal Predictors of Depression in PWMS
• Unhealthy behaviour: a lack of exercise (67%), recreational drug use (8%), and smoking (20%) predicted
later worse depression.
• Psychological factors - escape-avoidance coping.
• States - anxiety, subjective fatigue.
• High depression levels were not predicted by: stressors, MS relapse, MS disease parameters,
immunotherapy, cognitive factors, sleep disturbance, social support, demographics.
Medical Treatment of Depression: Efficacy of SSRIs
• SSRIs (selective seratonin reuptake inhibitors) are the recommended first-line treatment for moderate -
severe depression.
• 253% increase in antidepressant prescriptions in 1990, mostly SSRIs.
• Meta-analyses of placebo-controlled trials show that SSRIs decrease depression, but small differences
between groups.
• 1/2 depressed patients do not achieve full remission, thus they are at risk of residual symptoms and/or
relapse + low patient compliance.
SSRIS, Depression and Suicide Risk
• Meta-analyses of side-effects of SSRI therapy:
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Document Summary
Activity-based intervention for the treatment of psychological problems. Depression and anxiety: major depression - depressed mood or loss of interest/pleasure in all activities (anhedonia) > 2 weeks + clinically-significant distress of impairment in social, occupational or other functioning, at least 4 other symptoms: People with anxiety/depression die 7. 9 years earlier than others and show higher risk of death/hospital readmission: depression link to sleep disturbances, chronic illnesses (heart disease, diabetes, suicide, alzheimer"s), cancer and liver disease. Infection - depression is accompanied by activation of the inflammatory response system: cytokines (immune system transmitters), other inflammation sources (eg: autoimmune illness), decreased blood-brain-derived-neurotrophic-factor, antidepressants (ad) increase cerebral blood flow in hippocampus + ant. Cingulate cortex, normalise cerebral metabolism, decrease atrophy in hippocampus - i. e. ads may have a neuroprotective (rather than neurotransmitter) effect. What is causing the depression: modern environment/society (eg: individualism, lack of collectivism).
