GMED Seminar 1-3 PDF

WHO – Mental health The positive dimension of mental health is stressed in WHO's definition of health as contained in its constitution: "Health is a state of complete physical, mental and social well-being and not merely the absence of disease or infirmity.“ Mental health is defin...

WHO – Mental health The positive dimension of mental health is stressed in WHO's definition of health as contained in its constitution: "Health is a state of complete physical, mental and social well-being and not merely the absence of disease or infirmity.“ Mental health is defined as a state of well-being in which every individual realizes his or her own potential, can cope with the normal stresses of life, can work productively and fruitfully, and is able to make a contribution to her or his community. http://www.who.int/features/factfiles/mental_health/en/ WHO – Mental disorders Mental disorders comprise a broad range of problems, with different symptoms characterized by some combination of abnormal thoughts, emotions, behaviour and relationships with others. Examples are schizophrenia, depression, intellectual disabilities and disorders due to drug abuse. Most of these disorders can be successfully treated. http://www.who.int/mental_health/management/en/ “Mental Disorder” versus “Mental Illness” Terms are often used interchangeably but are different concepts Mental disorder - a disturbance or dysfunction in mental health Mental illness - suggests a disease process, a pathological condition of a body part, an organ, or a system resulting from a distinguishable cause (e.g. infection, genetic defect, or environmental stress) and characterized by an identifiable group of signs or symptoms. Models of mental disorders Spiritual (supernatural, religious) Moral Biological/neurophysiological Psychological Psychodynamic Behavioural Sociological Cognitive Mental disorders “Mental disorders can best be understood as a complex interplay between biological, psychological, social and lifestyle factors: a classic bio-psycho-social-lifestyle model”. (Boyce, P. M., & Berk, M. 2016). “Brain” versus “mind” Brain Mind Physical structure The consciousness – comprising tissue, blood thoughts, feelings and and neurons. behaviours Can be investigated The product of firing (dissected, stained, X- neurons rayed, photographed) Observed behaviourally Can be measured (activity electrical, Not necessarily confined glucose/oxygen to the brain (adrenal metabolism) cortex, brainstem) GMED3008 – “Brain” versus “mind” Brain Mind Structure and function of the Diagnosis and classification of brain mental illness Substance addiction and Psychosis and schizophrenia withdrawal Affective disorders (depression, Psychopharmacology bipolar disorder, anxiety disorders) Seizures Head injuries Normal brain functioning Maintains homeostatic body functions Allows psychological functioning  process information  plan and initiate action (to detect and react)  experience emotion (positive and negative)  control behaviours  interpret and interact with our environment  communicate and interact with others  make decisions, exercise judgement Two mainstream schools of thought on mental disorders Biologic psychiatry Mental disorders are due to anatomic, developmental, and functional disorders of the brain Psychosocial psychiatry Mental disorders are due to impaired psychological development, a consequence of poor child rearing, or environmental stress Bio-psycho-social model The bio-psycho-social model (abbreviated "BPS") is a general model or approach that posits that biological, psychological (which entails thoughts, emotions, and behaviors), and social factors, all play a significant role in human functioning in the context of disease or illness. Health is best understood in terms of a combination of biological, psychological, and social factors rather than purely in biological terms. Diathesis-stress model The diathesis-stress model is a psychological theory that explains behaviour as both a result of biological and genetic factors ("nature") and life experiences ("nurture"). Mental disorders can arise from a combination of both sources (predisposing factor) and environmental stress (precipitating factor). In many cases there is no single accepted or consistent cause currently established. A common view is that disorders result from genetic vulnerabilities exposed by environmental stressors. Mental illness across the lifespan Estimated that up to 20% of adults have a mental illness Estimated that up to 25% of children and adolescents have a mental illness A total of 45% of the Australians 16-85 will have a mental illness at some point in their lifetime Most people with a mental illness live in the community and receive care from primary health or community mental health services Mental illness is responsible for almost 13% of the total burden of disease in Australia placing it third as a disease group after cancer and cardiovascular diseases Some mental disorders in childhood Intellectual disability Learning disorders Motor skills disorders Communication disorders Autism Attention deficit disorders Conduct disorders Feeding, eating and elimination disorders Tic Disorders Some mental disorders in adulthood Psychotic Disorders Delusional disorders Schizophrenia Schizoaffective disorder Mood Disorders Unipolar depression Bipolar disorder Anxiety Disorders Substance disorders Mental disorders in older adulthood Delirium Dementia Cognitive disorders Amnesic disorders Unspecified cognitive disorders  Dementia Impairment of short- and long-term memory, associated with abstract thinking, impaired judgment, other higher cortical functions, or personality change Caused by any disorder that permanently damages large association areas serving memory and learning Diagnosis Assessment History Complete physical Cognition Functional status Laboratory and imaging studies Types of dementia Lewy body Alzheimer disease Vascular dementia Frontotemporal dementia Creutzfeldt-Jakob disease Wernicke-Korsakoff syndrome Huntington disease Common types Mental Disorders Mental disorders are characterised by disturbances in  perception (senses)  cognition (thoughts)  affect (emotion)  behaviour (actions)  memory Perception Alterations in processing of information taken in through our senses  Visual  Auditory  Olfactory  Gustatory  Tactile  Hallucinations, distortions, misinterpretations Cognition (thoughts) Disturbances in processing information; thought processes Storage (memory) and recall Encoding and decoding Sequencing (order) Contextualising Sorting relevant from irrelevant information Logic and reasoning Abstracting thinking and planning Judgement and insight For example: Formal thought disorder, delusions, flight of ideas, bizarre or magical thinking Image: http://www.ufodigest.com/news/0808/images/cbt.jpg  Affect (emotion) Disturbances in  Regulating of emotions  Experiencing emotions  Expressing emotions  Congruity  Controlling fight or flight responses Some terms used to describe affect: Flat ,blunted, restricted, elevated Behaviour Behaviour disturbances (observed by others)  Change from normal development  Outside social norms (context)  Primal instincts  Idiosyncratic or bizarre  Reflected in self-expression  Egocentric (unaware of others’ responses, and judgements)  Not concerned about the consequences Behavioral anatomy of the brain Cortex Parietal lobe Thalamus Occipital lobe Prefrontal cortex Limbic association area Frontal lobe Prefrontal association area Temporal lobe  Steps of neurotransmission Synthesis of a transmitter substance Storage and release of the transmitter Binding of the transmitter to receptors on the postsynaptic membrane Removal of the transmitter from the synaptic cleft Image: https://en.wikipedia.org/wiki/Neurotransmission Neurotransmitters important in mental disorders Acetylcholine Dopamine Noradrenaline and adrenaline Serotonin γ-Aminobutyric acid (GABA), glutamate, aspartate, and glycine Neural pathways  In biological terms the mental illness is considered to be disturbances in either brain functioning or the communication pathways between the brain areas  The communication pathways are neural pathways or neurotransmitter pathways  The neurotransmitter pathways of interest in mental illness are the Dopamine, Serotonin, Noradrenergic, and Cholinergic Pathways Association areas Lobes of the brain Parietal lobe Frontal lobe Occipital lobe Temporal lobe Functions of the frontal lobe Abstract vs. concrete reasoning Motivation/volition Concentration Decision making Purposeful behavior Memory, sequencing, making meaning of language Speech organization and production Aspects of emotional response Functions of the temporal lobe Visual-spatial recognition Attention Motivation Emotional modulation and interpretation Impulse and aggression control Interpretation & meaning of social contact Aspects of sexual action and meaning Functions of the parietal lobe Sensory integration and spatial relations Bodily awareness Filtration of background stimuli Personality factors and symptom denial Memory and nonverbal memory Concept formation Function of occipital lobe Vision Possible information-holding area Learning and memory (thoughts) Thought processes involve patterns of stimuli from many parts of the nervous system simultaneously for example: Cerebral cortex Thalamus Limbic system Reticular formation Memory traces New or reactivated pathways transmit neural circuits Biological influences What are the biological factors that can influence our perception, cognition, affect and behaviour? Genetics Neuro-chemical disturbances , e.g. increased dopamine Brain abnormalities (either through injury or defect). e.g. Reduced grey matter or increased ventricles Disease process, e.g. viruses, degeneration etc. Environmental factors, e.g. neglect, stressful, unstimulating environment Heredity in mental disorders Complex influences of genetic and environmental factors on neural development and function Nurture versus nature Genetic vulnerability and environmental influences play significant roles in the development of mental illness. Other factors are involved. Origin of the manifestations of mental disorders Alterations in brain neuron functioning Destruction of those neurons Alteration in the neural connections among the brain regions Diagnosing mental disorders There is no medical diagnostic test available to diagnose mental illness -diagnosis made on observed behaviour in social context Clinical classification into diagnostic categories is still debated Two major diagnostic methods used ICD11 (WHO) DSM-5 (American Psychiatric Association) Classification of disorders DSM-5 Diagnostic and Statistical Manual of Disorders (fifth Edition) Produced by the American Psychiatric Association ICD-11 International Classification of Disease European classification World Health Organisation Current Day Improved brain imaging technologies and advances in neuroscience have improved care and treatment Current Day New medications continue to be trialled – improved efficacy and reduced side-effects Medications commonly used in mental health Antipsychotics Antidepressants Benzodiazepines Mood stabilizers Anxiolytics Current Day Modified ECT – improved protocols and guidelines for use Current Day Combined use of biological treatment (medications and ECT) with emotional therapies. Cognitive Behavioural therapies Psycho-social-interventions Counselling 60% of mental illness is treated outside the hospital setting Current Day Improved public policy and treatment guidelines Current day - Challenges Mental health in the 21st Century has its challenges Dangerous medication side effects Lifestyle issues that lead to poor physical health Increasing chronic disease burden Co-occurring substance use/abuse Health issues related to homelessness and poverty Side effects to medications Side effects to medications Patients with severe mental illnesses, including schizophrenia, major depressive, and bipolar disorders have higher mortality rate and shorter life expectancy compared to the general population People with a severe mental illness are 2.5 times more likely to die from preventable physical illness than people in the general population (Stanley & Laugharne, 2010). Metabolic syndrome Metabolic syndrome and its components, including obesity, glucose intolerance, dyslipidemia, & hypertension, are highly prevalent & and associated with an increased risk of cardiovascular disease. Metabolic syndrome – “an insidious inflammatory state with impaired inflammation, impaired inflammation, endothelial function & coagulation, predisposing individuals to cardiovascular disease”. (Byrant et al., 2019) Obesity, inactivity, aging, and food containing trans-fats, ethanol and fructose promote insulin resistance & excessive insulin excretion leading eventually to T2DM and increased morbidity and mortality from chronic cardiovascular disease and kidney disease (Byrant et al., 2019) Side effects to medications Prolonged Q-T interval refers to an abnormality seen on an electrocardiogram. This abnormality reflects a disturbance in how the heart's ventricles conduct electricity QT represents ventricular depolarisation and repolarisation and prolongation may lead to life- threatening complications (arrhythmias) Torsades de Pointes and Ventricular Fibrillation Image: https://www.mayoclinic.org/diseases-conditions/long-qt- syndrome/symptoms-causes/syc-20352518 Chronic Diseases / https://healthjade.com/the-metabolic-syndrome Psychosis Definition - Inability to distinguish what is real; a loss of contact with reality (SANE Australia). Presence of confused thinking, delusions or hallucinations 3% of general population experience psychosis in their lifetime (mostly in late teens and early adulthood) Multiple causes – stress, substance, medical conditions Often a feature of other mental illness such as depression and bipolar disorder Psychosis There are a number of types of psychosis Brief reactive psychosis Drug induced psychosis Psychosis associated with the major mental disorders e.g. schizophrenia, bipolar affective disorder or major depression Can be brief (1-2 days), more frequent or be associated with a long term illness such as schizophrenia Psychosis DSM-5 Presence of one or more of the following symptoms Hallucinations Delusions Disorganised speech + or - Disorganised or catatonic behaviour Duration of at least one day but less than a month. Disturbance is not explained by other diagnoses and is not attributed to effects of substances or medical conditions. What causes psychosis? The causes of psychosis are not fully understood and is multifactorial. Combination of hereditary and other factors Neurochemical changes/ disturbance Structural or functional changes (Illness or trauma) Certain drugs (for example, marijuana, speed or LSD) can trigger the first episode of psychosis Risk factors Biological and psychosocial Often interlinked DSM 5 / ICD 11 Schizophrenia & Psychotic Disorders Curtin University is a trademark of Curtin University of Technology CRICOS Provider Code 00301J ICD-11-CM Codes Schizophrenia, schizotypal, delusional, and other non-mood psychotic disorders F20-F29 Codes F20 Schizophrenia F21 Schizotypal disorder F22 Delusional disorders F23 Brief psychotic disorder F24 Shared psychotic disorder F25 Schizoaffective disorders F28 Other psychotic disorder not due to a substance or known physiological condition F29 Unspecified psychosis not due to a substance or known physiological condition F20 Schizophrenia Codes F20 Schizophrenia F20.0 Paranoid schizophrenia F20.1 Disorganized schizophrenia F20.2 Catatonic schizophrenia F20.3 Undifferentiated schizophrenia F20.5 Residual schizophrenia F20.8 Other schizophrenia F20.81 Schizophreniform disorder F20.89 Other schizophrenia F20.9 Schizophrenia, unspecified DSM 5 Schizophrenia Spectrum and Other Psychotic Disorders Schizotypal (Personality) Disorder Delusional Disorder Brief Psychotic Disorder Schizophreniform Disorder Schizophrenia Schizoaffective Disorder Substance/Medication-Induced Psychotic Disorder Psychotic Disorder Due to Another Medical Condition Catatonia Catatonia Associated With Another Mental Disorder Catatonia Specifier) Catatonic Disorder Due to Another Medical Condition Unspecified Catatonia Other Specified Schizophrenia Spectrum and Other Psychotic Disorder Unspecified Schizophrenia Spectrum and Other Psychotic Disorder Schizophrenia Curtin University is a trademark of Curtin University of Technology CRICOS Provider Code 00301J Schizophrenia Often chronic, a debilitating psychotic disorder that involves the disconnection between thought and language Affects the thinking, feeling, perceiving, behaving, and experiencing of the environment Onset between 17 and 25 years Men seem to be more affected than women First-degree relatives of a person with schizophrenia have a 10-fold greater prevalence of the illness. Early conceptions Eugene Bleuler (1857-1939) coined the term schizophrenia (schizen = split, phren = mind). However Schizophrenia DOES NOT mean split personality Split-mind implied; a) fragmented thoughts b) incongruity of thoughts & emotions, c) withdrawal from reality & not split personality. DSM 5 diagnosis of schizophrenia Two or more of the following present for a significant portion of time within 1 month period : Hallucinations Delusions Disorganised speech + or - Catatonic or disorganised behaviour Negative symptoms Reduced level of functioning (work, self-care or relationships) Continuous signs of the disturbance for at least six months, with at least 1 month of which includes symptoms in full & active form Affective disorder has been ruled out Not caused by the effects of a substance or another medical condition Two types of symptoms Positive symptoms (Outward signs of psychosis) Associated with increased numbers of dopamine D2 receptors in the striatum, limbic system, and cortex. Acute onset, good neuroleptic treatment response. Better prognosis than type negative type Negative symptoms (Deficit symptoms) Thought to be due to more D1 dopamine receptors in the prefrontal cortex Slower onset, Poorer response to neuroleptics but respond to atypical anti-psychotics. Schizophrenia What are the positive and negative symptoms of schizophrenia? https://www.youtube.com/watch?v=r_MFpzWHKGk Positive and negative symptoms Positive Negative Delusions Social Withdrawal Hallucinations (auditory, Flat or blunted affect and visual, tactile, olfactory emotion, and gustatory) Alogia - poverty of speech Disordered thoughts Anhedonia - inability to and speech experience pleasure Movement disorders Avolition - lack of motivation. Dopamine hypothesis The dopamine hypothesis of schizophrenia proposes increased levels of exogenous dopamine striatum and cortex. Increased numbers of dopamine receptors (D2) in the striatum and frontal cortex (postmortem studies) Meso-limbic system thought to be involved in positive symptoms of schizophrenia through an overactive dopamine system Meso-cortical system is thought to be involved in the negative symptoms of schizophrenia through an underactive dopamine system The nigrostriatal pathway is involved with extrapyramidal effects such as tremors, slurred speech, and dystonia Dopamine pathways 4 major dopamine pathways Mesocoritcal, Important for cognition, memory, attention and problem solving. Mesolimbic, “pleasure centre of the brain”. Motivation and reward Nigrostriatal - Modulates the control of voluntary movement Tuberoinfundibular – Hormone regulation, and some sensory processes Support for the dopamine hypothesis Strong correlation between antipsychotic medication and affinity for D2 receptors The best drugs to treat schizophrenia resemble dopamine and completely block dopamine receptors. Drugs that block dopamine have side effects similar to Parkinson's disease. Parkinson's disease is caused by a lack of dopamine in the basal ganglia. Support for the dopamine hypothesis High doses of amphetamines cause schizophrenia-like symptoms and make symptoms of schizophrenia worse. Amphetamine psychosis is a model for schizophrenia because drugs that block amphetamine psychosis also reduce schizophrenic symptoms. Children at risk for schizophrenia may have brain wave patterns similar to adults with schizophrenia. These abnormal brain wave patterns in children can be reduced by drugs that block dopamine receptors.  Evidence against the dopamine hypothesis Amphetamines do more than increase dopamine levels – they alter other neurotransmitter levels. Drugs that block dopamine receptors act quickly, however, these drugs may take days to change behaviour in a person with schizophrenia Atypical antipsychotics (e.g. Clozapine, Olanzapine, and Quetiapine) block receptors for both serotonin and dopamine. Serotonin in schizophrenia The serotonin–dopamine hypothesis has been followed by a number of theories proposing that interaction among multiple neurotransmitter systems may play an important role in the mechanism of action for atypical antipsychotic drugs. Thought that projections in the serotonin pathways may inhibit dopamine pathways, therefore, leading to the negative symptoms seen in schizophrenia Atypical antipsychotics with a low affinity for dopamine support this notion Stabilisation of 5HT2a receptor firing of cortical pyramidal neurons improves perceptions of reality Serotonin pathway Serotonin (5- HT) Originates in the brainstem (Raphe nuclei) to the cerebellum, forebrain and limbic system. Regulates sleep, mood, emesis, libido, appetite, pain perception, body temperature, blood pressure and hormonal activity Too little serotonin caused low mood, depression, poor sleep, decreased appetite, poor concentration, low motivation. Too much serotonin results in irritable mood (can lead to aggressive behaviour), over activity, increased energy, little sleep. Brain abnormalities Areas of the brain implicated forebrain , hindbrain and limbic system Disruption in some of the functional circuits Frontal lobe temporal lobe limbic system, (specifically the cingulate gyrus , the amygdala and the hippocampus ) Thalamus Cerebellum Image: https://sites.google.com/site/brainandabnormalbehavior/schizophrenia Structural changes Reductions in the volume of grey matter in the frontal lobe Decreased brain volume and activity Ventricles larger than normal, as are the basal nuclei Hippocampus & amygdala smaller Alterations in blood flow to certain areas of the brain Ventricle enlargement The image to the left shows an MRI image of unaffected and schizophrenic identical twins. The brain structures pointed out are the ventricles (which are much larger in the person affected by schizophrenia). Genetic risk for schizophrenia Relationship Risk of developing schizophrenia Identical twin affected 50% Fraternal twin affected 15% Brother or sister affected 10% One parent affected 15% Both parents affected 35% 2nd degree relative affected 2-3% No relative affected 1% Table source: Craft et al., (2019) page 1206. Table 39.2 Genetic risk for schizophrenia Depression World Health Organisation: Depression is a common mental disorder, characterized by persistent sadness and a loss of interest in activities that you normally enjoy, accompanied by an inability to carry out daily activities, for at least two weeks. In addition, people with depression normally have several of the following: a loss of energy; a change in appetite; sleeping more or less; anxiety; reduced concentration; indecisiveness; restlessness; feelings of worthlessness, guilt, or hopelessness; and thoughts of self-harm or suicide. Depression is treatable, with talking therapies or antidepressant medication or a combination of these. Depression Five main types of depression include: major depressive disorder major depressive disorder (with melancholia) psychotic depression persistent depressive disorder (or dysthymic disorder) perinatal depression (also called antenatal and postnatal depression). Additional information: https://www.blackdoginstitute.org.au/clinical-resources/depression/types-of- depression Major Depression - DSM 5 Criterion A 5 or more of the following for 2 weeks and represent a change from previous level of function (must have either depressed mood or loss of interest or pleasure to reach DSM-V diagnosis) Depressed mood most days (tearful or appears low) Markedly diminished pleasure in almost all daily activities Significant weight loss (5% body weight in 1 month) Insomnia or hypersomnia nearly every day Psychomotor agitation or retardation Fatigue or loss of energy Feeling of worthlessness or inappropriate guilt Poor concentration nearly every day Recurrent thoughts of death (suicide) Symptoms of depressive disorders Symptoms must be present for most of the day, for at least 2 weeks and cause significant distress or impairment of functioning. Symptoms not better accounted for by other factors (e.g. bereavement, substances) Symptoms may last for several weeks to months followed by a period of relatively normal mood. No history of a manic or hypomanic episode Vincent Van Gough’s 1890 painting ‘At Eternity’s gate’ Other depressive disorders DSM 5 Persistent Depressive Disorder (Dysthymia) A consolidation of DSM-IV-defined chronic major depressive disorder and dysthymic disorder. Depressed mood for most of the day, for more days than not, as indicated by either subjective account or observation by others, for at least 2 years. Presence, while depressed, of two (or more) of the following: Poor appetite or overeating. Insomnia or hypersomnia. Low energy or fatigue. Low self-esteem. Poor concentration or difficulty making decisions. Feelings of hopelessness. Other depressive disorders DSM 5 Persistent Depressive Disorder (Dysthymia) Never been a manic episode or a hypomanic episode The disturbance is not better explained by another condition. Symptoms are not attributable to the physiological effects of a substance Other depressive disorders DSM 5 Depressive Disorder Due to Another Medical Condition  A prominent and persistent period of depressed mood or markedly diminished interest or pleasure in all, or almost all, activities that predominate in the clinical picture.  Evidence from the history, physical examination, or laboratory findings that the disturbance is the direct pathophysiological consequence of another medical condition.  Not better explained by another mental disorder (e.g., adjustment disorder, with depressed mood, in which the stressor is a serious medical condition).  The disturbance does not occur exclusively during the course of a delirium Other depressive disorders DSM 5 Substance/Medication-Induced Depressive Disorder  A prominent and persistent disturbance in mood that predominates in the clinical picture and is characterized by depressed mood or markedly diminished interest or pleasure in all, or almost all, activities.  There is evidence from the history, physical examination, or laboratory findings of both (1) and (2): The symptoms in Criterion A developed during or soon after substance intoxication or withdrawal or after exposure to a medication. The involved substance/medication is capable of producing the symptoms in Criterion A. Pathophysiology Genetic factors Gene-environment interaction Neurochemical factors Hormonal systems Circadian rhythms Environment factors Neurochemical factors Biogenic Amine Hypothesis A monoamine is a molecule containing one amino acid. Monoamines of interest in depression include the neurotransmitters serotonin, dopamine and noradrenaline. Depression is caused by a deficiency of monoamines, particularly noradrenaline and serotonin Monoamines and brain function Adrenergic Pathway Serotoninergic pathway  Biogenic amine hypothesis Depression can be alleviated by drugs that increase the availability of noradrenaline and serotonin. MAOI – blocks the metabolism of noradrenaline and serotonin via the inhibition of MAO (monoamine oxidase) TCA (Tri-cyclic Antidepressants) – block the reuptake of neurotransmitters into the neuron for re-synthesis However, these drugs work relatively quickly yet the therapeutic benefit is not noticed for 6-8 weeks. Permissive hypothesis Control of emotional behavior results from a balance between noradrenaline and serotonin 5HT NA Both the manic phases and the depressive phases are characterized by a dysregulated level of serotonin. Permissive hypothesis Serotonin controls noradrenaline levels Depression Low serotonin and low noradrenaline Mania High serotonin and high noradrenaline 5HT NA Antidepressant drugs affect the relative concentration of serotonin compared to noradrenaline, thus restoring the critical balance that controls emotional behaviour. Permissive hypothesis NE and serotonin circuit dysfunction together may mediate many of the symptom clusters of depression, such as: NE -- poor attention and memory, decreased concentration, reduced socialization, and altered states of arousal; and Serotonin -- poor impulse control, low sex drive, decreased appetite, and irritability (see Figure) Image: https://www.medscape.org/viewarticle/412866_4 Permissive hypothesis However, the permissive hypothesis does not reflect the full picture of the pathophysiology of depression because: Acute elevation of synaptic transmitter levels are not sufficient to improve mood and takes at least 2-6 weeks before therapeutic effects Drugs that antagonise the central serotonin receptors does not induce depression Therefore there is now an understanding that depression may result in or is a result of other physiological changes  Brain-derived neurotrophic factor (BDNF) BDNF is a neuronal growth hormone that acts on certain neurons of the central nervous system and the peripheral nervous system, helping to support survival of existing neurons, and encouraging growth and differentiation of new neurons and synapses BDNF is active and binds to the TrkB receptor in the hippocampus, cortex, and basal forebrain—areas vital to learning, memory, and higher thinking. In depression, BDNF may be deficit due to various reasons, for example Image: https://cranemedicine.files.wordpress.com/2015/05/6fde6- bdnf.jpg stress Stress and depression Depression is can be a result of Noradrenergic and serotonergic activation of the hypothalamic-pituitary- adrenal system (HPA Axis) Kolb, B. a. (2016). An introduction to brain and behavior / Bryan Kolb, Ian Q. Whishaw, G. Campbell Teskey (Fifth edition.. ed.): New York, New York : Worth Publishers. Stress and depression Stress = HPA axis stimulated to secrete corticotrophin-releasing hormone which stimulates pituitary land to produce cortisol Normally cortisol helps us deal with stress Excessive stress = high cortisol concentrations damage the feedback loop that turns off the release of cortisol so the HPA axis becomes overstimulated. Over secretion of cortisol is associated with depression. Kolb, B. a. (2016). An introduction to brain and behavior / Bryan Kolb, Ian Q. Whishaw, G. Campbell Teskey (Fifth edition.. ed.): New York, New York : Worth Publishers. Brain abnormalities in Depression When the hypothalamic hormone corticotropic- releasing factor is chronically elevated, it can induce cortisol secretion from the adrenal gland Changes in the level of BDNF and hypothalamic hormone corticotropic-releasing factors correlate with a decrease size of hippocampus MRI scans - evidence for smaller hippocampal volumes ? a link between depression and neurogenesis of the hippocampus (center for both mood and memory). Loss of hippocampal neurons is found in some depressed individuals and correlates with impaired memory and dysthymic mood. Image: https://core.ac.uk/download/pdf/43167242.pdf Brain abnormalities in depression Hypertensive lesions Hyperintensities are areas of high intensity shown on MRI scans. They are generally seen as a bright white spot. Hyperintensities are a normal part of aging but occur more frequently in patients with depression and bipolar affective disorder. Led to the development of the theory of vascular depression (demyelination due to reduced blood flow). Image: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4072809/figure/F1/?report=objectonly Treatment - Depression Treatment pharmacotherapy and/or psychotherapy. Medications used to treat this disorder include tricyclic antidepressants, SSRIs, SNRIs etc. Electroconvulsive therapy ECT Improve personal factors - maladaptive coping skills, a poor social support system, and difficulties related to finances or employment. Treatment of underlying disease process/condition Bipolar disorder Curtin University is a trademark of Curtin University of Technology CRICOS Provider Code 00301J Bipolar Disorder – DSM 5 Bipolar 1 Disorder  One or more manic episode  Manic episode may have been preceded by and be followed by hypomanic or major depressive episodes Bipolar 2 Disorder  Current or past hypomanic episode and a current or past major depressive episode Bipolar disorder NOS (not otherwise specified) Bipolar Disorders – DSM 5 Categories: Bipolar disorder 1 One or more manic episode Bipolar disorder 2 Never been a manic episode Most recent episode of hypomania Most recent episode of mixed Most recent episode of depression DSM 5 Manic episode Distinct period of abnormally persistently elevated, expansive or irritable mood lasting at least 1 week (or any period of duration if hospitalised). Mood disturbance causes marked social, occupational dysfunction or psychotic features Symptoms not due to substances or medical condition DSM 5 Manic episode During period of mood disturbance must have 3 or more of the following;  Inflated self-esteem or grandiosity  Decreased need for sleep  More talkative than usual, the pressure of speech  Flight of ideas or racing thoughts  Distractibility  Increased goal-directed activity or psychomotor agitation  Excessive involvement in pleasurable activities DSM 5 Hypomanic episode Similar to mania except; Elevated, expansive or irritable mood lasting at least 4 days (which is different from normal nondepressed mood) Elevated mood does not result in hospitalisation Mood disturbance is a change in usual social, and occupational function when not symptomatic, however, no psychosis occurs. The change in mood may be observed by others but not cause marked dysfunction DSM 5 Mixed episode Criteria are met for mania and major depressive episodes (except duration) nearly every day for 1 week The mood disturbance causes marked impairment in social or occupational functioning, to necessitate hospitalisation to prevent harm, or there are psychotic features Symptoms not due to substances or medical condition DSM 5 Bipolar related disorders Cyclothymic Disorder For at least 2 years (at least 1 year in children and adolescents) there have been numerous periods with hypomanic symptoms that do not meet criteria for a hypomanic episode and numerous periods with depressive symptoms that do not meet criteria for a major depressive episode. During the above period, the hypomanic and depressive periods have been present for at least half the time and the individual has not been without the symptoms for more than 2 months at a time. DSM 5 Bipolar related disorders Cyclothymic Disorder cont. Criteria for a major depressive, manic, or hypomanic episode have never been met. Symptoms are not better explained by schizoaffective disorder, schizophrenia, schizophreniform disorder, delusional disorder, or other specified or unspecified schizophrenia spectrum and other psychotic disorder. Symptoms are not attributable to the physiological effects of a substance (e.g., a drug of abuse, a medication) or another medical condition (e.g., hyperthyroidism). Symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning. DSM 5 Bipolar related disorders Substance/Medication-Induced Bipolar Related Disorder Bipolar and Related Disorder Due to Another Medical Condition The typical mood fluctuations over time of a person with bipolar disorder, adapted from Muzina et al, 2007 Brain abnormalities in BPAD Ventral Striatum The ventral striatum of a bipolar person, which aids the brain in processing rewards tends to be overactive, which may contribute to the loss of judgment and overly involved in socially rewarding stimuli during manic episodes. Image: http://ravensongtarot.com/brain-structure-and-aggression/brain-structure-and- aggression-fabulous-placebo-parkinsons-pain-and-pet-a-neuroimaging/ Brain abnormalities in BPAD Hippocampus Reduction in size of the hippocampus. Because the hippocampus plays a main role in regulating stress response, the reduction may create a constant state of anxiety. Affects emotional, attentional and memory functions Thalamus People with Bipolar have an average of 31% more monoamine binding sites (signal-sending cells) in the brain's thalamus region (participates in regulatory functioning).  Poor judgement  Brain abnormalities in BPAD Brain Stem (ventral) Patients with Bipolar disorder have an average of 28% more monoamine binding sites in the ventral (anterior side) brain stem message relay center between the brain and spinal cord). Irritability and restlessness Brain Stem (raphe) The raphe nucleus in the brain stem, which is home to serotonin cells, is 40% smaller for persons with bipolar disorder.  This may contribute to the person's low moods and depressive episodes. Other Biological Causes Neurotransmitter hypothesis: Increased levels of norepinephrine dopamine serotonin in acute mania Endocrine correlations: Some indications of elevated thyroid hormones in acute mania Vitamin Deficiency Mania may be secondary to vitamin B12 deficiency appeared +/- overt clinical features of pernicious anaemia and resolved with B12 replacement. Management of affective disorders Depends on the category and presentation of symptoms; Short term treatment  Depressive phase - traditionally antidepressants have been used, although caution is needed to assess for induced mania or rapid cycling.  Manic phase - Benzodiazepines and antipsychotics Long-term treatment  Mood stabilizers – Lithium, Lamotrigine and Sodium valproate  Atypical antipsychotic – Olanzapine, Quetiapine Anxiety disorders Anxiety disorders can also affect your mood and often occur along with depression. Research shows about half of the people with an anxiety disorder also develop depression (a mood disorder), if the anxiety is left untreated. Depression and anxiety are not the same. They do have some overlapping symptoms including nervousness, irritability, and problems with sleep and concentration. Anxiety disorders An anxiety disorder is a medical condition characterised by persistent, excessive worry. Anxiety disorders can take a number of forms. Common to all of these is anxiety so distressing it can interfere with a person’s ability to carry out, or take pleasure in, day-to-day life. A person may experience more than one anxiety disorder. Some people may also experience depression with anxiety, or have problems with alcohol or drug abuse. Anxiety disorder A person with an anxiety disorder will feel distressed a lot of the time, even if there seems to be no obvious reason. An episode can be so severe it is immobilising. The person might have: persistent, excessive, or unrealistic worries (generalised anxiety disorder) compulsions and obsessions which they can't control (obsessive- compulsive disorder) intense excessive worry about social situations (social anxiety disorder) panic attacks (panic disorder) an intense, irrational fear of everyday objects and situations (phobia). Other symptoms of anxiety disorders may include a pounding heart, difficulty breathing, upset stomach, muscle tension, headache, sweating or choking, and feeling faint or shaky. Causes of Anxiety Disorders Genetic Biological Neurotransmitters -Serotonin and Dopamine Structural changes – (hyperactive amygdala and number of other brain regions) Personality/temperament Environmental Trauma Learnt response Twin studies Correlation of schizophrenia between identical twins, who have identical genomes, is less than one-half. This indicates that schizophrenia is NOT entirely a genetic disease. Therefore, there must be some environmental factors Activity Please complete the tutorial activity People with mental disorders may have disturbances in their perception, cognition, affect, behaviour and memory that are characteristic to the disorder they suffer: 1. What type of dysfunction in terms of perception, cognition, affect, behaviour and memory would be associated with the following disorders: Schizophrenia Depression Mania 2. Which brain areas would be involved in olfactory, tactile, visual and auditory hallucinations seen in schizophrenia? 3. Which brain areas would you expect to be functioning abnormally when someone experiences “formal thought disorder” as seen in psychosis?