Schizophrenia neuropsychological disorder

Schizophrenia neuropsychological disorder

Summative assessment: You will be required to complete an essay examining a neuropsychological disorder Due: July 25th 2018 12.00 noon Coursework – Essay (1200wds) Choose one of the following disorders: ? Schizophrenia ? Depression ? Parkinson’s disease ? Alzheimer’s disease Outline the physiological changes that occur during the course of your chosen disorder, in addition to how these changes are related to the symptoms and potential treatments of the disorder from a modern perspective.

Learning outcomes assessed by this work 2. Critically appraise research in the area of comparative approaches to biological psychology including the role of brain functioning. 3. Enter into theoretical and evidential debates, and evaluate positions taken by researchers on key issues in biological psychology 4. Critically appraise how biological psychology and comparative perspectives can be applied to wider society and specialist areas in psychology and their cognate disciplines. Synopsis Assessment Criteria The following criteria will be used in marking the synopsis. A (70%+)

Provides a concise, yet detailed overview of the physiological mechanisms involved in the chosen disorder, providing a sophisticated evaluation of the evidence in support of (and against) each mechanism. It will also indicate an in-depth understanding of relevant theoretical underpinnings and acknowledge the role of different approaches/research methods in evaluation of the evidence. There will be a clear indication of how the physiological changes (within the disorder) impact psychological outcomes, through their impact on symptoms and how treatments alleviate the symptoms via these physiological mechanisms. The synopsis will provide a discussion (and comparison, where appropriate) across the different types of mechanism (neurochemical, neurophysiological and hormonal) that have been discussed in the module. B (60-69%)

Provides a clear overview of the physiological mechanisms involved in the chosen disorder, with attempts at evaluation of the evidence in support of (and against) each mechanism. Highlights some understanding of relevant theory and approaches/research methods in evaluation of the evidence. There will be some indication of the link between the physiological changes (within the disorder) and psychological outcomes. Both the symptoms and treatment of the particular disorder will receive some discussion in light of the physiological mechanisms. C (50-59%) A largely descriptive account of the physiology associated with the chosen disorder, with little to no evaluation of the evidence regarding these mechanisms. Shows a basic account of relevant theory and/or research methods, with relatively little indication of the link between physiology and psychological outcomes within the disorder. D (40-49%)

A descriptive account of the physiology associated with the chosen disorder, with no evaluation and a number of inaccuracies. Misunderstood or inaccurate discussion of related theory and/or research methods, with little to no attempts to discuss symptoms and/or treatment related to the disorder. E (30-39%) Displays largely inaccurate understanding of physiology associated with the chosen disorder at best. Very inaccurate and/or no discussion of relevant theory/research methods. No discussion of symptoms and/or treatment related to the disorder.

Choose one of the following disorders: Schizophrenia Depression Parkinson’s disease Alzheimer’s disease Outline the physiological changes that occur during the course of your chosen disorder, in addition to how these changes are related to the symptoms and potential treatments of the disorder from a modern perspective. Critically appraise research in the area of comparative approaches to biological psychology including the role of brain functioning. 3. Enter into theoretical and evidential debates, and evaluate positions taken by researchers on key issues in biological psychology

4. Critically appraise how biological psychology and comparative perspectives can be applied to wider society and specialist areas in psychology and their cognate disciplines. A 1st essay provides a concise, yet detailed overview of the physiological mechanisms involved in the chosen disorder, providing a sophisticated evaluation of the evidence in support of (and against) each mechanism. It will also indicate an in-depth understanding of relevant theoretical underpinnings and acknowledge the role of different approaches/research methods in evaluation of the evidence. There will be a clear indication of how the physiological changes (within the disorder) impact psychological outcomes, through their impact on symptoms and how treatments alleviate the symptoms via these physiological mechanisms. The synopsis will provide a discussion (and comparison, where appropriate) across the different types of mechanism (neurochemical, neurophysiological and hormonal) that have been discussed in the module Provides a clear overview of the physiological mechanisms involved in the chosen disorder, with attempts at evaluation of the evidence in support of (and against) each mechanism. Highlights some understanding of relevant theory and approaches/research methods in evaluation of the evidence. There will be some indication of the link between the physiological changes (within the disorder) and psychological outcomes. Both the symptoms and treatment of the particular disorder will receive some discussion in light of the physiological mechanisms. 2:2(50-59%) A largely descriptive account of the physiology associated with the chosen disorder, with little to no evaluation of the evidence regarding these mechanisms. Shows a basic account of relevant theory and/or research methods, with relatively little indication of the link between physiology and psychological outcomes within the disorder. Pass (40-49%) A descriptive account of the physiology associated with the chosen disorder, with no evaluation and a number of inaccuracies. Misunderstood or inaccurate discussion of related theory and/or research methods, with little to no attempts to discuss symptoms and/or treatment related to the disorder. Fail (30-39%) Displays largely inaccurate understanding of physiology associated with the chosen disorder at best. Very inaccurate and/or no discussion of relevant theory/research methods. No discussion of symptoms and/or treatment related to the disorder. Which disorder did you choose? schziophrenia Any particular reason? Partner had it and committed suicide What did you find out since the lecture that you hadn’t known before? so much more than i knew Had you known something about the disorder before? yes Background Relevant Neurotransmitters, Anatomy & Hormones Schizophrenia & Depression Introduction/Symptoms Genetics & Heritability Anatomical pathways Psychopharmacology & Treatment Endocrine influences Cognitive Difficulty in sustaining attention Low psychomotor speed Deficits in learning Poor problem solving and abstract thinking Impairs attention, memory & executive function (Heinrichs & Zakzanis, 1998) About 1 SD below the norm (Fioravanti et al. 2005) Time course Late adolescence Negative & Cognitive Positive symptoms High heritability rate (Van Os & Kapur, 2009; Gejman, 2010) Up to 80%, MZ twin concordance ~40% BUT environmental factors exist Positively related to how urban the environment is Immigrant ethnic groups more likely (more so in isolation) Cannabis use Also epigenetic factors Paternal age > 40 years Distinction between GLOBAL anatomy & FUNCTIONAL anatomy People with schizophrenia lose grey matter faster… Globally, not sited in one area Enlarged ventricles Also globally Evidence from MRI scans shows structural abnormalities in: Frontal Lobes Medial & Lateral temporal lobe structures Parietal lobe Corpus callosum Hypofrontality (Weinberger, 1988) Consistent decreased activity of the dorsolateral prefrontal cortex What symptoms might these abnormalities explain? The DOPAMINE HYPOTHESIS of Schizophrenia One of the major theories of the disorder Overactivity of dopaminergic neurons in the Ventral Tegmental Area (VTA), Nucleus Acumbens (NA) and Amygdala Decreased activity in the prefrontal cortex Chloropromazine discovered to be an antipsychotic Eliminates positive symptoms Dopamine antagonist Neuro transmission The DOPAMINE HYPOTHESIS of Schizophrenia One of the major theories of the disorder Overactivity of dopaminergic neurons in the Ventral Tegmental Area (VTA), Nucleus Acumbens (NA) and Amygdala Decreased activity in the prefrontal cortex Chloropromazine discovered to be an antipsychotic Eliminates positive symptoms Dopamine antagonist Additional evidence Euphoria prior to an episode Psychotomimetic effect of dopamine agonists (Guillin et al. 2002) D2 Receptors Anti-psychotic drugs work by blocking Kestler et al. (2001) review modest increases of D2 receptors in brains of schizophrenics A lot of evidence, but some issues Explanatory power largely for positive symptoms Some Cognitive symptom links Neuroleptic medication does not help all schizophrenic individuals Therefor, other important factors… The role of Glutamate/GABA Psychotic symptoms can be triggered by Phencyclidine (PCP) and Ketamine These block NMDA neural channel Effects persist even in the absence of dopamine activity Hypofunction at glutamate (NMDA) receptors Increased function elsewhere Increased, disorganised pattern of activity The role of Glutamate/GABA Post mortems of schizophrenia patients have shown reduced expression of NMDA receptors Especially in the PFC and hippocampus (Harrison et al. 2003) But findings are inconsistent And glutamate remains widespread through the cortex Post mortem shows reduced levels of GABA expression in the PFC (Lewis et al. 2005) Symptoms Positive symptoms linked to increased Dopaminergic Activity (DA) In the NA Negative symptoms linked to decreased DA in the PFC Glutamate and DA Hypoactivity in the PFC => positive symptoms in the NA? PFC Glutamatergic neurons => GABA neurons in VTA. VTA GABA neurons inhibit DA neurons => NA (Carr & Sesack, 2000) “First generation” (Typical) Anti-Psychotics e.g. Haloperidol & Chloropromazine May result in Tardive dyskinesia “Second generation” (Atypical) Anti-Psychotics e.g. Olanzapine, Rispirdone Same mechanism – Less pronounced symptoms? Tyrer & Kendall (2009) No clear distinction, worrying lack of clarity in findings Negative & Cognitive symptoms? Other treatments? Clozapine > Agranulocytosis Anti-depressants & glutamate modification Stress hypothesised as trigger for schizophrenia Evidence Urinary cortisol prior to psychotic episodes (Sachar et al. 1970) Dexamethasone levels higher in schizophrenic patients relative to controls (Yergani, 1990) Elevated cortisol secretion linked with greater symptoms (Walder et al. 2000) Baseline cortisol levels predict severity of adolescent schizotypal symptoms 1 and 2 years later (Walker et al. 2001) Puberty = Increased hormones and HPA axis activation Stress hypothesised as trigger for schizophrenia Mechanisms? Stress augmenting DA activity (Walker & Diforio, 1999) Increase in Glutamate makes NA hyper-responsive to stress Corticosteriods can result in psychotic symptoms (Walker et al. 2008) Deppression Characterised by disordered feelings (Mood/Affect) Unipolar or Bipolar Depressive symptoms Depressed mood, Irritability Anhedonia Neurovegetative symptoms Mania Unjustified euphoria Non stop speech & activity Delusions, but not disorganisation of schizophrenia Difficult to diagnose Substantial co-morbidity Depression is moderately heritable (Levinson, 2006) e.g. neurotransmission & stress vulnerabilities Estimates of ~40% heritability rates Higher concordance for monozygotic twins Especially for bipolar type disorders Regardless of being reared apart or together Twin study stats suggest a genetic predisposition of some kind Anotomical pathways Substantial reductions in grey matter volume in PFC and hippocampus (Drevets, 2001; Harrison, 2002) Thought to mediate cognitive aspects Hippocampal neurogenesis implicated Brain-derived neurotrophic factor? BDNF production decreases with stress in rats, leading to hippocampal atrophy – decrease in positive affect? (Warner-Schmidt & Duman, 2006) Findings inconsistent (complicated by co-morbidity) E.g. Hippocampus links with disorders of memory, amnesia (HM case) and affect fMRI and PET studies Increased amygala activity Increased subgenual cingulate cortex activity (Ressler & Mayberg, 2007) Linked to emotional inhibition Influenced by DA projections from the VTA Serotonin from the Dorsal Raphe (Primary serotonin contributor to the forebrain) Noradrenaline from the locus coeruleus (In the pons; linked to stress/panic) What symptoms might these abnormalities explain? Early clinical observations Decreased monoamine function in the brain – dopamine, noradrenaline and serotonin Neuoro transmission Monoamine oxidase inhibitors (e.g. Zellar et al. 1952) Iproniazid was developed for the treatment of tuberculosis (TB). Ineffective in treating TB Further support The Monoamine Hypothesis of Depression Insufficient activity of monoaminergic neurons BUT not dopamine… Tryptophan depletion procedure (Delgado et al. 1990) No effect in healthy subjects OR people with a family history of depression Thus got to be other factors Serotonin is also positively related to neurogenesis (see Mahar et al. 2014) Changes in treatment – Fewer side effects 1st gen: Tricyclic antidepressants – Effective but prone to a long list of minor and major side effects 2nd gen: SSRIs (e.g. Prozac) – selective serotonin re-uptake inhibitor SNRIs (e.g. Milnacipran) – serotonin norepinephirine re-uptake inhibitor MAOIs (e.g. Ipronaizid) – Monoamine oxidase inhibitors MAOIs were popular, became unpopular due to diet-drug interaction difficulties evaluate moanimine theory Recently regaining popularity as the interaction is better understood Anti-depressant time lag Weeks of treatment needed, often no short- term change is noticed Autoreceptor sensitivity theory Agonists overstimulate autoreceptors Must be other factors… Monoamines depletion only affects unmedicated depressed patients (Ruhe, Mason & Schene, 2007) And not all patients respond to 5HT (serotonin) agonists (Albert et al. 2012) Neuroendocrine Influence Stress implicated as a causal factor (Lupien et al. 2009) Glucocorticoid release > HPA dysregulation/Toxicity Hyperactive in depression (Steckler et al. 2009) Higher negative feedback from cortisol (Modell et al. 2007) Innate 5HT neurotransmission vulnerability linked to stress vulnerability (Firk & Marcus, 2007) Neuroendocrine influences Stress implicated as a causal factor (Lupien et al. 2009) Glucocorticoid release > HPA dysregulation/Toxicity Hyperactive in depression (Steckler et al. 2009) Higher negative feedback from cortisol (Modell et al. 2007) Innate 5HT neurotransmission vulnerability linked to stress vulnerability (Firk & Marcus, 2007) Theories Stress downregulates hippocampal neurogenesis (Kemperman & Kronenbourg, 2003) Vicious cycle > Neurogenesis can regulate HPA activity (Schlosser et al. 2009) Anti-depressants increase neurogenesis (Banasr et al. 2006) Stress influences monoamine neurotransmission (Lanfumey et al. 2009) Stress globally depletes 5 HT levels (Ahmed et al. 2010) Serotonin influences HPA activation CRH overactivation results in depressive-like behavior CRH antagonists have anti-depressive properties (Hauger et al. 2006) Learning outcomes Background HPA axis Schizophrenia & Depression Introduction/Symptoms Genetics & Heritability Anatomical pathways Psychopharmacology & Treatment Endocrine influences reading Carlson’s Physiology of Behaviour book – Chapter 16, Schizophrenia and Affective Disorders Also some good info in chapter 17- Stress 4 papers available under the “Resources” Tab on Moodle (Lecture 2 now available), including a systematic review These are a good start for researching your essay, but be sure not to rely on them as your only evidence!

Schizophrenia neuropsychological disorder

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