Seminar 2 Schizophrenia and Psychosis PDF
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Curtin University
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This document discusses schizophrenia, a chronic and debilitating psychotic disorder. It explores the symptoms, potential causes, and treatments of schizophrenia, highlighting the role of neurotransmitters like dopamine and serotonin. The document also touches upon structural brain changes, genetic risk, and the impact of medication.
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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 experi...
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 and speech Anhedonia - inability to 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