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This chapter provides an in-depth exploration of schizophrenia, including its definition, symptoms (positive, negative, and cognitive), course, possible causes, and the dopamine hypothesis. It also discusses drug treatments and their effectiveness, as well as the potential brain abnormalities associated with the disorder.
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Chapter 15 The Biological Basis of Affective Disorders and Schizophrenia
Schizophrenia • First described in 1883 by Emil Kraepelin – dementia praecox, premature insanity • The Swiss psychiatrist, Eugen Bleuler, coined the term, "schizophrenia" in 1911. He was also the first to describe the symptoms as "positive" or "negative." • Bleuler renamed it schizophrenia for three reasons: • The deteriorization doesn’t always begin in adolescence, it can begin later in life • Mental functioning may actually improve rather than deteriorate after it is diagnosed • The disorder seems to reflect a splitting of the psyche’s functions: emotion and perception
Schizophrenia: a definition • Mental disorder characterized by loss of contact with reality; disturbances in perception, emotion, cognition, motor behavior. • Characterized by positive, negative, and cognitive symptoms: • Positive Symptoms - Behaviors exhibited by a person with schizophrenia but absent in people without the disorder • Negative Symptoms - Normal behaviors that are absent in people with schizophrenia • Cognitive Symptoms – Deficits in learning, reasoning or perception
Positive Symptoms • Thought disorders - tangentiality, neologisms, loosening of associations, word salad, rambling monologues • Delusions – grandeur, persecution, control • Hallucinations – visual, tactile, auditory, olfactory, gustatory • Movement - high levels of motor excitement, catatonic behaviors, repetitive motor activities
Negative Symptoms • Disturbances in affect - blunted or flat affect • Lack of interest in life, low motivation • Anhedonia – inability to experience pleasure • Social withdrawal or emotional detachment • Low energy • Alogia – poverty of speech • Inappropriate social skills or lack of interest or ability to socialize with other people • Inability to make friends or keep friends, or not caring to have friends
Cognitive Symptoms • Disorganized thinking • Slow thinking • Difficulty sustaining attention • Difficulty understanding • Poor concentration and problem solving • Poor memory • Difficulty expressing thoughts • Difficulty integrating thoughts, feelings and behavior
Course of Schizophrenia • Prodromal phase - The phase which the person becomes socially withdrawn and school or work performance declines. • Active phase -The phase in which the more acute symptoms of the disorder appear, such as hallucinations and delusions. • Residual phase - The phase in which some recovery of functioning occurs.
Schizophrenia: The Dopamine Hypothesis and Drug Treatments • Dopamine hypothesis of schizophrenia -The view that an excess of activity in the dopamine system results in the positive symptoms of schizophrenia. • Chlorpromazine (a DA antagonist) blocks postsynaptic DA receptors and improves positive symptoms in schizophrenics. • Therapeutic effectiveness is directly related to the ability to bind tightly to the receptors
Schizophrenia: Drug Treatments • Effect of DA agonists • Amphetamine and cocaine produce positive symptoms of schizophrenia. • Amphetamine use exacerbates positive symptoms in people already diagnosed with schizophrenia. • L-Dopa (used to treat Parkinson’s) is a DA agonist which can induce a psychosis which is responsive to clozapine.
Evidence Against a DA Hypothesis of Schizophrenia • Approximately 30% of people with schizophrenia do not experience relief of positive symptoms with DA antagonists. • There are also lower levels of GABA and glutamate in brains of people with schizophrenia. Some studies suggest the NMDA receptor may be involved.
Problems with DA Antagonists • Tardive dyskinesia - A motor disorder with facial tics and involuntary limb movements; often appears after long-term use • Relief from negative symptoms is not experienced with DA antagonists • A new family of antipsychotic drugs, which block D4 receptors, relieve positive and negative symptoms without causing tardive dyskinesia • A hypothesis of brain damage may explain the negative symptoms
Brain Damage and Schizophrenia • Lateral ventricles of many people are enlarged. • Loss of dendritic material in the prefrontal cortex. • Reduced numbers of neurons in the thalamus and hippocampus. • Hippocampus connections with the prefrontal cortex are connected in a more disorganized fashion than normal.
Possible Causes of Brain Abnormalities • Epidemiological studies • Season of birth • Viral epidemics • Population density • Vitamin D deficiency • Prenatal malnutrition • Substance abuse • Complications of pregnancy and childbirth • Fetal growth retardation • Hypoxia • Rh factor incompatability
Hypofrontality Theory • Theory that the negative symptoms of schizophrenia are caused by decreased activity in the prefrontal cortex. • PET scans show decreased activity in the frontal area of the brain • People with schizophrenia have difficulty with tasks requiring working memory. • Metabolic hypofrontality in people with schizophrenia can be reversed with DA agonists but at what cost? • Third generation antipsychotic – partial agonist • Some people do not exhibit hypofrontality, so results are mixed with regard to this theory.
Role of Genetics • What is inherited is only a susceptibility or genetic predisposition to develop schizophrenia. • The concordance rate for identical twins is not 100% but about 50% indicating that a particular gene is not by itself sufficient to produce schizophrenia. • No single gene for schizophrenia • Children of older fathers • Epigenetic influences inhibit or promote gene expression
Schizophrenia: No Definitive Explanations • Neither the DA theory nor the hypofrontality theory provide a complete explanation. • Several brain structures are dysfunctional and act together to produce symptoms. • Schizophrenia may be several related disorders rather than a single disorder • Some patients have prefrontal dysfunctions, others do not • DA antagonists help some patients but not others. • What role, if any, does puberty play • Much more research is necessary