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104 Cards in this Set
- Front
- Back
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Classification of Preventions
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Individual vs Population
Primary vs Secondary vs Tertiary Universal vs Selective vs Indicated |
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In mental health we think of risk factors vs _____________
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protective factors
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RF
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Parental mental illness
Genetic predisposition Affectionless parenting Parental discord Adverse life events Perinatal problems Low intelligence |
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Protective Factors
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Belief in own effectiveness
Success/Achievement “Easy” temperament Sense of humour and optimism Positive school life Good peer relations High intelligence Positive relation with a caregiver |
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Triple P
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Positive Parenting Program
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Observed negative child behaviour (%)
Triple P vs Wait list |
it also INC. parenting sense of competency cf to wait list
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Risk Factors for Schzo
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45% monozygotic twin studies
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Children of Parents with Mental Illness
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21-23% of children living in Australian households have a least one parent with a mental health issue.
i.e. over 1 million children under 18 in Australia. |
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Parent with mental illness
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Social isolation
Social withdrawal (e.g. depression, psychosis) Paranoid/Persecutory delusions Agoraphobia, social anxiety disorder Depression, “Negative symptoms” of schizophrenia, medication side effects Difficulty with communication Difficulty with intimacy Difficulty teaching social norms to children |
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Example sof family intervention
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SMILES (Simplifying Mental Illness + Life Enhancement Skills)
"Family Talk” |
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Burden of disease
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Genes and causes of mental health
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Example:
Gene & envirnoment interaction |
cannibus exposure on COMT gene and risk of schizo
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Burden of disease in 15y
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Adolescent onset of major disorders
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all seem to relate to prefrontal cortex development
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Normal brain development and grey matter shifting
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Early onset vs Late onset
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›Early Onset:
-Typically age 15-25 -Typically with anxious phenotype -Complicated by substance abuse -Including other forms (bipolar, somatic) -Goals: - EARLY PRESENTATION -Evaluation on universal and selective interventions -Minimizie long-term biological and social complicatons |
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Clinical Late life depression Changes
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Pathogenesis of major psychiatric disorders
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Ideally for genetic studies to yeild good results you need them to be
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depression is a nightmare for genetic studies; its common and wide when optimally for genetics you need something rare and fixed (thus start looking for new phenotypes)
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Path1: Anxiety- Depression
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›1. Concept of Brain Over-reactivity to environmental stressors:
›1. Genetics of Central Nervous System Reactivity – family history of anxiety-depression, alcohol misuse ›2. Environmental exposures and Fear Conditioning ›3. Brain-Circuitry – Frontal- Temporal lobe structures that moderate fear and anxiety ›4. Childhood Expression as Anxiety with later anxiety and depression ›5. Later use of alcohol and other substances ›6. Treatment Approaches based on reducing reactivity (mainly behaviourally or secondary pharmacologically) and avoidance behaviour through cognitive and behavioural techniques |
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Path 2: Circadian - Depression
Circadian-Depression (about 40% of clinical cases) |
›1. 24-hour sleep-wake and circadian systems as the fundamental biology
›2. Depression characterised by daytime fatigue, non-restorative sleep, oversleeping, weight gain rather than mood disturbance – „Atypical‟ ›2. Relationships with „unipolar and bipolar‟ depressions (mania-fatigue) ›3. Unique Genetic and Environmental Risks – linked to the circadian system – Family History of Bipolar, Psychosis, Substance misuse ›4. Novel Assessment Techniques ›5. Novel Interventions – behaviourally on sleep-wake and pharmacologically on melatonin systems |
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disturbed circadian function
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›Non-restorative sleep
›Daytime fatigue (early morning prior to activity, daytime napping) ›Impaired cognition ›Depressive symptoms – „atypical‟ ›Irritability ›Light sleep, nightime ‘sweats’ ›Musculoskeletal pain |
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Circadian systems effects on physiology and behaviour
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Normal Entrainment of cortisol, melatonin and body temp
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Heritability of Mood Disorders and Traits
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Neurobiological pathways linking circadian and sleep-wake disruption with mood disorders and bipolar disorder
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Pathways linking infection with circadian, fatigue and depressive disorders
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Path 3: Brain Developmental Risks and Depression
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›1. Markers of altered brain development in childhood (autism, learning developments, ADHD)
›2. Genetic and early environmental risks ›3. Assessment Techniques ›4. Treatment Approaches – Novel learning, glutamate, neuropeptides |
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Describe the key neurotransmitters and neural circuitry regulating mood
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- 5HT and NA
- at amygdala, hippocampus. limibic system... |
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Understand the pathophysiology of depression relating to the monoamine hypothesis
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Depression is caused by a functional deficit of monoamines at certain sites in the brain
- it came about when the MOA of drugs was discovered |
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Appreciate the role of trophic factors in depression
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Recent evidence suggests that depression may be associated with defective monoamine transmission, neurodegeneration and reduced neurogenesis
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What is Depression
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Mood disorder
1 in 4 females & 1 in 6 males will experience depression at some time in life (beyondblue.org.au) 45% of Australians aged 16-85 years experienced at least one anxiety disorder, mood disorder or substance use disorder (ABS, 2007) Leading cause of suicide (15%) Familial pattern: •1.5-3 times more common among 1st degree relatives •Increased risk of alcohol dependence in adult 1st degree relatives |
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Depression Disorders - DSMIV
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Major depression (episode or disorder)
•At least 2 weeks of depressed mood/anhedonia + additional symptoms Dysthymic disorder •2 years depressed mood for more days than not + additional symptoms that don’t meet criteria for Major depression Bipolar disorder (manic depression) Cyclothymic disorder •2 years hypomanic and depressed moods that don’t meet criteria for Bipolar or Major depression |
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Clinical Features - Major Depression
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A. Depressed mood and anhedonia + 3 other symptoms for 2 weeks:
Depressed mood: sad or empty, hopeless, tearful, irritable Inability to experience pleasure (anhedonia) Significant weight loss or gain/decrease or increase in appetite Insomnia or hypersomnia Psychomotor agitation or retardation Feelings of worthlessness/excessive or inappropriate guilt Inability to concentrate/indecisive Recurrent thoughts of death/suicide B. Symptoms affect social and occupational functioning C. Symptoms NOT due to drugs or general medical condition D. Symptoms not better accounted for by bereavement |
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Neural Circuitry of Mood
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Depression and HPA
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- in depression the -ve feedback on the hippocampus to hypothalamus isnt effective
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Neurochemistry of Depression
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Major neurotransmitters:
•Noradrenaline •Serotonin (5-HT) •Dopamine •GABA |
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Monoamines
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NA and 5HT
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Diffusely projecting neurotransmitters
•Released from varicosities rather than synapses Specific stimuli can elicit rapid bursts, superimposed on baseline “tone” |
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NA pathways
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5HT pathways
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NA & 5-HT Uptake
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Active transport into neurons via Na+-dependent membrane transporter protein
•electrochemical gradient for Na+ is the driving force Then active transport into vesicles Neuronal uptake (NAT, SERT) is main mechanism for terminating NA & 5-HT neurotransmitter actions |
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Degradation (5HT, NA)
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In neurons by oxidative deamination by monoamine oxidase (MAO)
•MAO bound to neuronal and non-neuronal cell mitochondria MAO isoforms: •MAO-A (degrades 5-HT, NA, Adr, DA) •MAO-B (degrades DA) |
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Monoamine theory evidence FOR & AGAINST
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FOR:
Reserpine (disrupts storage of monoamines) causes depression Antidepressants act on monoamine systems AGAINST: NA & 5-HT are augmented straight away while symptoms take weeks to diminish Delayed effect coincides with receptor downregulation |
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Monoamine theory REvISED 1980s
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Revised in 1980s to suggest the hypoNA/hypo5-HT state leads to receptor hyperresponsiveness
•Antidepressants increase synaptic levels of NA & 5-HT to normal levels •Down-regulating receptors to normal levels accounts for slow action of drugs |
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MOA revised EVIDENCE
for and against |
Evidence FOR
Decrease in NA metabolites (via MAO-A, COMT) i.e VMA, MHPEG in CSF and urine in depression Decrease in 5-HT and metabolites (via MAO-A, aldehyde dehydrogenase) i.e 5-HIAA in CSF and brainstem in depression |
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Neuroplasticity/Neurotrophic Hypothesis
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Depression is associated with neuronal loss in the hippocampus and prefrontal cortex
•Imaging studies of patients show regional neurodegeneration in these regions Antidepressants enhance BDNF signalling and neurogenesis •BDNF stimulates gene transcription of SERT and tryptophan hydroxylase in raphe nuclei •5-HT receptor activation stimulates BDNF expression •Antidepressants increase 5-HT synthesis, release and cell |
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List the range of disorders that may be part of the syndrome of psychosis
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Schizophrenia spectrum
Schizophrenia Schizophreniform Paranoid Disorder Organic Dementias Substance induced Cannabis Amphetamines Hallucinogens Phencyclidine Mood disorders Bipolar disorder Psychotic Depression Other Hysterical & cultural forms Folie à deux Brief and atypical forms |
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Describe the symptoms and signs of psychosis
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Hallucinations & Delusions
Disorganisation (Formal thought disorder) Loss of insight Negative symptoms Cognitive impairment Excitement / Aggression Disturbance of mood |
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Discuss neurodevelopmental and gene x environment models of psychosis
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Genes affect sensitivity to environmental factor
MZ twins have 50% concordance rate Genetic risk interacts with developmental and environmental factors |
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Outline the biopsychosocial approach to treatment in schizophrenia
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Describe the social marginalisation of people with a psychosis
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Psychosis is the box: a syndrome
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Symptomatology of psychosis
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Positive Sx
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hallucinations
delusions insight |
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Lack of insight in schizo
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Hallucinations
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“a perception in the absence of an external stimulus”
Illusion – a misinterpretation of an external stimulus |
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Activation of Heschl’s Gyrus
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When they heared the hallucination the same areas of brain light up
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Delusions
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“a false unshakeable belief that is out of keeping with the person’s cultural and educational background”
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Negative Sx
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1. Alogia: change in cognitive fn
Poverty of thought & content of thought Slowness of thought and movement Social withdrawal Apathetic Loss of meaning of social connections 2. Affective blunting : Loss of the personal ife and charm of the person Loss of the modulation and expression of affect 3. Amotivation 4. Asociality |
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Excitement Sx
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1.Hostility
2.Aggression; - worse at illness onset - risk INC. with substance abuse 3.Disorganisation |
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Cognitive Sx
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Attention
Memory Planning Problem solving Social cognition Stable over initial 5 years Deterioration “dementia” less commonly seen (5%) as against 15% in older series |
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Anxiety in psychosis
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High rates of anxiety with approximately 60% of people with psychosis complaining of symptoms of anxiety over the past year
Social anxiety 42% Anxiety 49% Obsessions or compulsions 28% |
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Pattern of symptoms overlap
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Cognitive and negative symptoms suggestive of schizophrenia
Positive symptom severity no guide to diagnosis Diagnoses are determined by the longitudinal course of the illness Time course of mood symptoms help with diagnosis Psychotic illness have high levels of functional impairment, however schizophrenia has the most marked deterioration in level of functioning |
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Epidemiology of schizophrenia
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Incidence of 0.16 – 0.42 / 1000, morbid risk of 0.50 – 1.60%,
slight preponderance of males Female has later onset Population risk no longer thought to be consistent across the globe. Family History of schizophrenia single greatest significant risk factor MZ concordance approx. 50% DZ concordance approx. 10% |
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Risk factors for developing schizophrenia
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Family history strongest predictor
Other risk factors point to a neurodevelopmental cause Obstetric Maternal infection Starvation |
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Schizophrenia - Aetiology
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Schizophrenia (and psychosis) is a brain disease, however
No specific localised “psychosis” area. Clinical picture can vary widely Manifestations can change over time Brain as a distributed network |
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Neurodevelopmental model of schizophrenia
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Substance abuse and SChizo
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↑ rate of schizophrenia in Swedish conscripts who smoked (Andreassen et al, 1987)
Early adolescent use leads to increased risk of psychosis (Arseneault et al 2004) COMT val/val allele increased risk of developing Sz (OR=10.9). Cannabis had no effect on individuals with met/met allele No effect for initiation of cannabis use as an adult |
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Dopaminergic & other neurotransmitter dysfunction
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Lots of speed; in truck drivers developing psychosis (INC> DA in the striatum linkage with Schizo)
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Neuropathology of schizophrenia
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Gray matter Deficits in early cf to late Achizo
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Although severe parietal, motor, and diffuse frontal loss has already occurred (Upper) and subsequently continues (Figs. 1 and 2), the temporal and dorsolateral prefrontal loss characteristic of adult schizophrenia is not found until later in adolescence (Lower), where a process of fast attrition occurs over the next 5 years
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Treatment of Schizophrenia
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Positive & excitement Pharmacotherapy
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2nd generation & 1st generation antipsychotics effect
Onset rapid Sustained 80-90% response Heavy burden of side effects |
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Anxiety & Depression Pharm
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Initially note effects of antipsychotics
Additional treatment with antidepressants or psychological intervention may be needed |
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Negative & Cognitive Pharm
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Antipsychotics have a small effect on negative sx and minimal on cognitive sx
Other pharmacological treatments have had little effect |
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Initial treatment regimen
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Antipsychotic SE
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Extrapyramidal
Akathisia Tardive Dyskinesia Cholinergic Sedation Cardiovascular Endocrine Cognitive Neuroleptic Malignant Syndrome Mood Blood dyscrasias Hepatic Dermatological |
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Other health problems in Psychosis
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49% meet criteria for metabolic syndrome. Highly sedentary.
Triple the population rates of smoking, alcohol and other drug abuse Leading to a mortality rate of 2.5 times the community rate and 20 year reduction in life spans DIABETES: due to weight, lifestyle and medications |
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Psychosocial Treatments
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Case management
Assertive Psychoeducation Family therapy Communication Problem solving Cognitive behavioural therapy Social Skills training Supported Employment/Education Cognitive Remediation |
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Income in Psychosis
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remain isolated
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Dualism theory
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There is something about the mental that is necessarily forever beyond the reach of a scientific understanding.
PROBLEMS: 1. The problem of influence. 2. The problem of brain injury. 3. The problem of evolution of consciousness. |
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Substance Dualism
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Mental processes take place
outside the physical realm of the brain, in a non-physical (spiritual) mind-stuff. |
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Materialism
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The seat of mental life rests solely in the material world and is no less amenable to scientific understanding than any other phenomenon.
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Identity Theory
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came about the same time as computers came out (just like you needed to have invented pumps first to understand that the heart was a pump
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Identity theory and changing mind states
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Functionalism
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the brain is demoted just hardware to run a program
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What is Bipolar Disorder?
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Recurrent episodes of both mania or hypomania and depression
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Bipolar Disorder
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DSM IV - one episode mania/mixed
Common Equal sex distribution Familial - 20% risk in 10 family members Early age of onset but late diagnosis Comorbidity common Underdiagnosed Delayed diagnosis - 8 years High suicide risk - 15% Major burden is depression Progressive cognitive impairment |
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Bipolar Disorder Prevalence
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Prevalence: Bipolar I 0.5 - 2.4% Bipolar II 0.2 - 5% “Bipolar Spectrum” (subsyndromal mania) 3.0 - 6.5% No gender difference Mean age of onset 17 - 21 years |
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Comorbidity
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High rates of Axis I comorbidity (McElroy 2001)
42% have lifetime comorbid substance abuse 42% have lifetime comorbid anxiety Personality disorder Medical - vascular disease, migraine, diabetes, obesity, hypertension |
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Burden of Bipolar
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Majority had been hospitalised Half reported worsening illness over time 2/3 not asymptomatic between episodes 1/3 attempted suicide at least once 30% had current suicidal ideation |
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Onset of Bipolar
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Onset <17 associated with rapid cycling, worse course of illness and history of early abuse First treatment delayed 10 years from onset 62% experienced moderate/severe impact on occupational function 15% reported continuous depression, mania or mixed symptoms 53% reported rapid cycling |
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Systematic Treatment Enhancement Program for Bipolar Disorder (STEP-BD)
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48% recurrence rate <2 years (despite best available Tx and its mainly depression) Depression 34.7%, manic/hypo/mix 13.8% Residual symptoms predicted recurrence Results not much different from early Li follow-up studies! |
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Bipolar Disorder - Classification
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Bipolar I At least 1 episode of mania Bipolar II Recurrent depression with at least one episode of hypomania, but no mania or mixed episodes Mixed affective state Features of both mania (hypomania) and depression concurrently |
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Secondary Mania |
Due to medical illness - neurological, endocrine Due to drugs - amphetamines, stimulants, steroids, antidepressants |
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Mania - Signs and Symptoms
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Activity and behaviour:
hyperactive, restless ‘unlimited’ energy pressure of speech decreased need for sleep erratic, unpredictable, risk-taking increased social contact, increased libido, hypersexuality excessive spending, overgenerous Thought form: racing thoughts, flight of ideas overfamiliar, disinhibited distractible Thought content: grandiosity, unrealistic plans, creative mood congruent delusions and hallucinations |
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The Risks of Mania
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Impulsive recklessness Risk taking - speeding, accidents Drug and alcohol abuse Promiscuity - STD Aggression and violence Financial distress Irrational life changes - marriage, divorce Damage to reputation Criminal charges |
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Characteristics of Bipolar Depression
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May be different from unipolar depression but often clinically indistinguishable Equal gender prevalence Presence of atypical features (hypersomnia, hyperphagia, weight gain, anergia ++) Psychotic features common May be recurrent for years before mania appears >50% experience depression as index episode Depressed BP patients seek treatment 2-3 times more than in manic state Depression is chronic in 20% Greater cause of disability and decreased quality of life than any other phase Depression more refractory to treatment esp. rapid cyclers Suicide risk greater during depression and with more frequent depressive episodes |
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Different Phases, Different Treatments
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Antimanics Antidepressants Antipsychotics - oral and parenteral, typical and atypical Sedatives and hypnotics Mood stabilisers ECT Psychosocial and educative |
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Summary of Pharmacological Treatments (RCT Evidence)
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Mania:
Lithium, valproate, atypical antipsychotics, carbamazepine Depression: Lithium, lamotrigine, olanzapine, olanzapine + fluoxetine, quetiapine, antidepressants, ECT Maintenance: Lithium, olanzapine, valproate, lamotrigine, carbamazepine |
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Summary Bipolar Tx
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There is as yet no single drug which is effective in all phases of BPD (i.e. mood stabiliser) Lithium is closest to the ideal but has limitations Combination therapy is likely to be required at each phase and often for prophylaxis Pathophysiology of BPD needs research |
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Non-pharmalogical Tx Bipolar
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Establish therapeutic alliance Psychoeducation Family involvement and support Assess and manage comorbidity CBT, IPT, social rhythms therapy Occupational/career rehabilitation Role of consumer groups |
