Biological Explanations for Schizophrenia

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  AQA Psychology A Level Paper Three: Schizophrenia

  • Phil Gorman(Author)
  • 2020(Publication Date)
  • Routledge

    (Publisher)

  Chapter 3

  Biological Explanations for Schizophrenia

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  Biological Explanations for Schizophrenia: genetics, the dopamine hypothesis and neural correlates.

  AO1 (Knowledge and understanding): What are the Biological Explanations for Schizophrenia?

  How does biology influence mental health?

  Mental disorders are generally regarded to be different from physical disorders in that they are problems with the way a person’s mind is working. According to the World Health Organisation:

  Mental disorders comprise a broad range of problems, with different symptoms. However, they are generally characterized by some combination of abnormal thoughts, emotions, behaviour and relationships with others.

  (www.who.int/mental_health/management/en/ )

  This definition seems to place mental disorders in the area of the mind and behaviour as it mentions thoughts, feelings and relationships with others, however, it is questionable whether we can separate our minds from our physical bodies and, in particular, from our brains. This is part of a long-standing debate in psychology concerning whether we can separate our mind and body or whether they are the same thing. Biological psychologists are confident in arguing that the mind is ultimately just another part of the brain and therefore we can locate the cause of all mental disorders in the brain and the body.

  This is important to our attempt to understand the Biological Explanations for Schizophrenia because it helps us to understand the arguments made about the causes of mental disorders put forward by these biological psychologists. These arguments can essentially be divided into three types:

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  Molecular Neurobiology for the Clinician

  • Dennis S. Charney(Author)
  • 2008(Publication Date)
  • American Psychiatric Association Publishing

    (Publisher)

  Molecular Neurobiology and Schizophrenia 75 Chapter 3 Molecular Neurobiology and Schizophrenia Implications for Etiology and Treatment Andrew R. Gilbert, M.D. David W. Volk, Ph.D. David A. Lewis, M.D. Schizophrenia is a complex disorder with a pathogenesis and pathophysiology that remain to be elucidated. With a 1% lifetime incidence and substantial morbidity, schizophrenia is a wide- spread and disabling condition. As the fields of neuroscience and behavioral science evolve, the diagnosis, treatment, and under- standing of schizophrenia continue to develop. The heterogene- ity characteristic of the clinical presentation of schizophrenia is consistent with the variety of neurobiological abnormalities observed in affected individuals, which appear to arise from the interactions of multiple genetic and environmental factors. In this chapter, we summarize recent findings from research on the neurobiology of schizophrenia. First, we provide a brief over- view of the genetic, environmental, and developmental factors that appear to be involved in the pathogenesis of schizophrenia. Second, we present four examples of susceptibility genes that may contribute to the liability for schizophrenia. Third, we con- sider the alterations in several molecular systems that appear to be relevant to the pathophysiology of schizophrenia. Finally, we discuss the implications of these findings which, when synthe- sized, may both inform etiopathogenic models of the illness and suggest novel approaches to its treatment. 76 MOLECULAR NEUROBIOLOGY FOR THE CLINICIAN Etiological Factors and Schizophrenia Genetic Risk Factors Although the roles of specific susceptibility genes remain elusive, inheritance clearly contributes to the etiology of schizophrenia. Family, twin, and adoption studies indicate that the morbid risk of schizophrenia in the relatives of affected individuals increases with the percentage of shared genes (see Gottesman 1991; Lewis and Levitt 2002 for review).

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  The SAGE Handbook of Mental Health and Illness

  • David Pilgrim, Anne Rogers, Bernice Pescosolido, David Pilgrim, Anne Rogers, Bernice Pescosolido(Authors)
  • 2010(Publication Date)
  • SAGE Publications Ltd

    (Publisher)

  Over the period of the study they found an increase in public acceptance of biomedical explanations of psychosis, associated with public desire for increased distance from people with a diagnosis of schizophrenia. These time trends did not hold for major depressive disorder. Read et al., (2006) have recently subjected the literature on stigma and schizophrenia to a comprehensive review to assess whether the ‘schizophrenia is an illness like any other’ approach helps reduce prejudice and stigma towards those with the diagnosis. They found a recent increase in biological causal beliefs across Western countries, suggesting that this approach is gaining hold. However, biological attributions for psychosis were overwhelmingly associated with negative public attitudes in 18 of 19 studies, whereas psychosocial attributions were associated with positive attitudes in 11 of 12 studies. Biological attributions are thus strongly linked to negative public attitudes, or stigma. This appears particularly to be the case for the diagnosis of schizophrenia. CONCLUSIONS Although biomedical explanations of psychosis have become extraordinarily influential over the last fifty years, they have yet to yield convincing evidence that biological differences between people with a diagnosis of schizophrenia actually exist, or that they may lead to more rational interventions. No less an authority than the clinical neuroscience and genetics research agenda group for DSM-V has recently concluded that: Although the past two decades have produced a great deal of progress in neurobiological investigations, the field has thus far failed to identify a single neurobiological phenotypic BIOLOGICAL EXPLANATIONS FOR AND RESPONSES TO MADNESS 307 marker or gene that is useful in making a diagnosis of a major psychiatric disorder or for predicting response to psychopharmacological treatment.

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  Controversies in Schizophrenia

  Issues, Causes, and Treatment

  • Michael Farrell(Author)
  • 2023(Publication Date)
  • Routledge

    (Publisher)

  3 A Biopsychosocial Perspective of Schizophrenia

  DOI: 10.4324/9781003413554-3

  Introduction

  An orthodox biopsychosocial understanding of schizophrenia identifies it as a brain disorder understood, approached, and described in medical terms. At the same time, psychological and social factors are taken into account in understanding causation, and in treatment.

  Critics of an orthodox approach to schizophrenia may emphasise the physical aspects of a biopsychosocial perspective, conveyed by the term, ‘medical model’ used with negative connotations. Accordingly, they may claim that regarding schizophrenia as a physical illness, assumes that it therefore requires solely physical treatment like medication, or electroconvulsive therapy (ECT). However, an orthodox position recognises not only physical causal factors, but also environmental and social triggers that can precipitate schizophrenia. Furthermore, it recognises the place of nonphysical treatments.

  Another criticism is that a medical approach is pessimistic about the chances of recovery from schizophrenia. The condition is depicted as an incurable illness, and a life-long brain disease in which life events and circumstances can play no causal role. However, evidence of the long-term progress of people with schizophrenia does not support this position.

  Critics may take a subjectivist view in which knowledge is personal and there is no external or objective truth. Accordingly, positions are not examined for evidence of whether they are true or correct. On the contrary, they are presented as what ‘some people’ think or feel and what ‘others’ think or feel as though personal and subjective views and experiences imply objective, agreed truth. Relatedly, understanding schizophrenia as an illness is regarded as just another theory. Criticism is sometimes expressed in rhetoric such as an emphasis on the simplistic, outdated, reductionist, unsubstantiated, contextless, and crude, and a resort to emotive language.

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  Epilepsy and Schizophrenia

  • (Author)
  • 2014(Publication Date)
  • College Publishing House

    (Publisher)

  ________________________ WORLD TECHNOLOGIES ________________________ Chapter 10 Causes of Schizophrenia Data from a PET study suggests that the less the frontal lobes are activated (red) during a working memory task, the greater the increase in abnormal dopamine activity in the striatum (green), thought to be related to the neurocognitive deficits in schizophrenia. While the reliability of the diagnosis introduces difficulties in measuring the relative effect of genes and environment (for example, symptoms overlap to some extent with severe bipolar disorder or major depression), evidence suggests that genetic and environmental factors can act in combination to result in schizophrenia. Evidence suggests that the diagnosis of schizophrenia has a significant heritable component but that onset is significantly influenced by environmental factors or stressors. The idea of an inherent vulnerability (or diathesis ) in some people, which can be unmasked by biological, psychological or environmental stressors, is known as the stress -diathesis model . An alternative idea that biological, psychological and social factors are all important is known as the biopsychosocial model. Genetic Estimates of the heritability of schizophrenia tend to vary owing to the difficulty of separating the effects of genetics and the environment although twin and adoption studies have suggested a high level of heritability (the proportion of variation between ________________________ WORLD TECHNOLOGIES ________________________ individuals in a population that is influenced by genetic factors). It has been suggested that schizophrenia is a condition of complex inheritance, with many different potential genes each of small effect, with different pathways for different individuals. Some have suggested that several genetic and other risk factors need to be present before a person becomes affected but this is still uncertain.

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  Schizophrenia (Mental Disorder)

  • (Author)
  • 2014(Publication Date)
  • The English Press

    (Publisher)

  However, regarding psychosis itself, it is well understood that methamphetamine and cocaine use can result in methamphetamine- or cocaine-induced psychosis that present very similar symptomatology (sometimes even misdiagnosed as schizophrenia) and may persist even when users remain abstinent. The same can also be said for alcohol-induced psychosis, though to a somewhat lesser extent. The causes of schizophrenia have been the subject of much debate, with various factors proposed and discounted or modified. The language of schizophrenia research under the medical model is scientific. Such studies suggest that genetics, prenatal development, early environment, neurobiology and psychological and social processes are important contributory factors. Current psychiatric research into the development of the disorder is often based on a neurodevelopmental model (proponents of which see schizophrenia as a syndrome.) However, schizophrenia is diagnosed on the basis of symptom profiles. Neural correlates do not provide sufficiently useful criteria. Current research into schizophrenia has remained highly fragmented, much like the clinical presentation of the disease itself. ________________________ WORLD TECHNOLOGIES ________________________ Although no common cause of schizophrenia has been identified in all individuals diagnosed with the condition, currently most researchers and clinicians believe it results from a combination of both brain vulnerabilities (either inherited or acquired) and life events. This widely adopted approach is known as the 'stress-vulnerability' model, and much scientific debate now focuses on how much each of these factors contributes to the development and maintenance of schizophrenia. Schizophrenia is most commonly first diagnosed during late adolescence or early adulthood, suggesting it is often the end process of childhood and adolescent development.

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  Biological Psychiatry

  • Edward Bittar(Author)
  • 1999(Publication Date)
  • Elsevier Science

    (Publisher)

  The Biological Basis of Schizophrenia 253 This lack of consistency, the failure to find a reliable neurological marker of schizophrenia, is disappointing given the effort that has been expended. It is pos-sible to claim that progress has been made in that certain structures have been implicated fairly well while others have not. The failure to find consistent evi-dence of damage or dysfunction in the schizophrenic brain has led many neurosci-entists to look at the brain in different ways: PET scans are used to examine it functionally, and the microcircuitry is examined in ever closer detail with the rationale that if there is no gross pathology, then there must be a microscopic one. Alternatively, however, one might consider whether the lack of consistency itself has become the issue to investigate. One substantial problem is that schizophrenia is not, at least at a symptomatic level, a unitary disease. There is a wide range of signs and symptoms that many have tried to classify in different ways. Some of the signs and symptoms are abnormal by their presence, while others are abnormal by their absence; some are typically associated togethermothers not so. It is possible that specific signs and symptoms are associated with particular forms of damage or dysfunction. For instance, negative symptoms are thought to be associated particularly with pre-frontal deficits, while positive symptoms are more closely associated with dopam-inergic abnormality than are negative symptoms, which are not responsive to antipsychotic drugs. Different authors have tackled this problem in radically dif-ferent ways. Some have adopted the argument that schizophrenia has no real value as a diagnostic entity and that it would be better to concentrate on the spe-cific signs and symptoms that are the cause of distress in schizophrenia (Bentall, 1990; Boyle, 1990). Eliminate these and the patients' problems would disappear. The use of the label schizophrenia has, in this argument, no value.

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  Abnormal Psychology

  • Gordon L. Flett, Nancy L. Kocovski, Gerald C. Davison, John M. Neale(Authors)
  • 2018(Publication Date)
  • Wiley

    (Publisher)

  Thaker (2007) noted that the hunt for schizophrenia- related genes turned out to be more difficult than expected for several reasons, including: 1. Lack of preciseness in defining the boundaries of the clinical phenotype 2. Absence of biological tests that confirm diagnostic catego- rization 3. Clinical heterogeneity and the complex nature of schizo- phrenia One of the most remarkable emerging findings from genome-wide analyses is that five major psychiatric disorders including schizophrenia may all stem from several specific TABLE 11.3 Characteristics of Participants Separated from Their Mothers in Early Infancy Assessment Offspring of Schizophrenic Mothers Control Offspring Number of participants 47 50 Mean age at follow-up 35.8 36.3 Overall ratings of dis- ability (low score indi- cates more pathology) 65.2 80.1 Number diagnosed schizophrenic 5 0 Number diagnosed mentally defective 4 0 Number diagnosed psychopathic 9 2 Number diagnosed neurotic 13 7 Source: From Heston (1966). 11.3 Etiology of Schizophrenia 319 the longest standing biologically based theory of schizophre- nia and it has predominated for over four decades. Initially, the hypothesis that schizophrenia is related to excess activity of dopamine is based principally on the knowledge that drugs effective in treating schizophrenia reduce dopamine activity. Antipsychotic drugs, in addition to being useful in treating some symptoms of schizophrenia, produce side effects resem- bling the symptoms of Parkinson’s disease. Parkinsonism is known to be caused in part by low levels of dopamine in a particular nerve tract of the brain. It has been confirmed that because of their structural similarities to the dopamine mole- cule (Figure 11.3), molecules of antipsychotic drugs fit into and thereby block postsynaptic dopamine receptors. The dopamine receptors that are blocked by first-generation or conventional antipsychotics are called D2 receptors.

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  Evolutionary Psychiatry

  Current Perspectives on Evolution and Mental Health

  • Riadh Abed, Paul St John-Smith(Authors)
  • 2022(Publication Date)
  • RCPsych Publications

    (Publisher)

  Chapter 10 Evolutionary Perspectives on Schizophrenia Spectrum Disorders Martin Bru ¨ne Abstract The term ‘schizophrenia’ refers to a group of disorders that seem to occur worldwide, with clinical pictures being strikingly similar across cultures. Evolutionary explanations of these disorders are warranted for at least two reasons: the first concerns their prevalence in all known ethnicities; the second relates to the need to explain the paradox as to why the conditions are maintained despite the greatly decreased fecundity of the affected individuals. Accordingly, a plethora of heterogeneous hypotheses – unparalleled among other psychiatric disorders – have been put forth, some of which deal with genetic considerations, others with environmental risk factors, and a few consider the adaptive advantages associated with the genes that predispose to schizophrenia. None of the evolutionary scenarios has the potential to account for the diversity of the symptomatol- ogy or to cover all of the biological and non-biological aspects of schizophrenia or schizophrenia spectrum disorders. This chapter aims at discussing the most relevant evolutionary hypotheses of schizophrenia, arguing that a symptom-based approach to psychotic disorders from an evolutionary perspective may improve upon the existing models of schizophrenia. Keywords dysconnectivity, genetics, human evolution, immunology, schizophrenia, social cognition, symptom-related approach, trade-off Key Points  Schizophrenia is a severe mental illness that occurs worldwide and is associated with a reduction in life expectancy and reproductive success.  The evolutionary questions as to why genes predisposing to or associated with schizophrenia are maintained in human gene pools remain unresolved.  Among the most plausible scenarios, genes conferring increased risk for schizophrenia are preserved because they have been sexually selected or are relevant for immune function.

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  Cognitive Impairment in Schizophrenia

  Characteristics, Assessment and Treatment

  • Philip D. Harvey(Author)
  • 2013(Publication Date)
  • Cambridge University Press

    (Publisher)

  Biological Psychiatry, 64, 739–749. 222 Section 3: Genetic and biological contributions to cognitive impairment Durstewitz, D., Seamans, J. K., & Sejnowski, T. J. (2000). Dopamine-mediated stabilization of delay-period activity in a network model of prefrontal cortex. Journal of Neurophysiology, 83, 1733–1750. Edwards, B. G., Barch, D. M., & Braver, T. S. (2010). Improving prefrontal cortex function in schizophrenia through focused training of cognitive control. Frontiers in Human Neuroscience, 4, 32. Elvevåg, B. & Goldberg, T. E. (2000). Cognitive impairment in schizophrenia is the core of the disorder. Critical Reviews in Neurobiology, 14, 1–21. Enticott, P. G., Upton, D. J., Bradshaw, J. L., et al. (2011). Stop task after-effects in schizophrenia: behavioral control adjustments and repetition priming. Neurocase [Epub ahead of print]. Finkelstein, J. R., Cannon, T. D., Gur, R. E., et al. (1997). Attentional dysfunctions in neuroleptic-naive and neuroleptic- withdrawn schizophrenic patients and their siblings. Journal of Abnormal Psychology, 106, 203–212. Fleming, K., Goldberg, T. E., Binks, S., et al. (1997). Visuospatial working memory in patients with schizophrenia. Biological Psychiatry, 41, 43–49. Fletcher, P. C. (2011). Hurry up and wait: action, distraction, and inhibition in schizophrenia. Biological Psychiatry, 70, 1104–1106. Fox, M. D., Snyder, A. Z., Vincent, J. L., et al. (2005). The human brain is intrinsically organized into dynamic, anticorrelated functional networks. Proceedings of the National Academy of Sciences of the United States of America, 102, 9673–9678. Funahashi, S., Bruce, C. J., & Goldman-Rakic, P. S. (1989). Mnemonic coding of visual space in the monkey’s dorsolateral prefrontal cortex. Journal of Neurophysiology, 61, 331–349. Fusar-Poli, P., Perez, J., Broome, M., et al. (2007). Neurofunctional correlates of vulnerability to psychosis: a systematic review and meta-analysis. Neuroscience and Biobehavioral Reviews, 31, 465–484.

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