Psychiatry: Schizophrenia U0

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The first assignment is available now from WebCT. Read the article that was posted on WebCT. The how to read a research paper by next class. Schizophrenia Clinical manifestation. o The Diagnostic and statistical manual of mental disorders (DSM-IV) o Mental illnesses do not have concrete observations. Based more on behaviour. What are we classifying? Classifies behaviour into Normal vs. abnormal. It is made by neurologists and sociologists, not an omnipotent force. Therefore, it may contain bias standpoints. o The DSM-IV lists concrete and observable behaviours to categorize conditions. o The diagnostic requirement for schizophrenia : Characteristic symptoms of the active phase, two of the following should be present for significant portion of time: Types of Delusions Hallucinations Disorganized speech Grossly disorganized or catatonic behaviour Negative symptoms, ie affective flattening, algoia or avolition. Having two or more of them is sufficient for the diagnosis of schizophrenia. o Positive symptoms: an existing result. These symptoms are thought to be normally not present. The manifestation of any of them suggests schizophrenia Delusions, hallucination, bizarre behaviour, disorganized thinking. Types of Delusions: o Holding beliefs that the rest of the society would generally disagree with. o Delusions of control The belief that others can interfere with ones thoughts o Delusions of persecution: Believe that others are deliberately cheating, harassing, poisoning, spying upon, or plotting against them or the people they care about. o Delusions of grandeur Think they are famous historical figures.

Psychiatry: Schizophrenia U0
o Thought broadcast Types of Hallucination: o Positive symptoms o Dramatic distortions of perceptions; sensory experiences in the absence of any stimulation o Hearing Voices: Coment on behaviour, order to do things, warn of impending danger, talk to each other o Seeing people or objects that are not there o Smell odours that no one else detects o Feeling things like invisible fingers touching their bodies when no one else is near. Hallucinations are formed by ones own brain, but the front of the brain that determines the source of the hallucination, is quiet. Negative symptoms: the lack of normal symptoms of an individual. Affective flattening is the lack of inflections and emotions. Lack of emotions. Algoia Poverty of speech, of content, delays before responding Avolition: Apathy, lack of interest or drive, innatention to grooming and hygiene Anhedonia: Asociality; inability to experience pleasure of interacting socially. Negative symptoms often preset the positive symptoms. Cognitive Deficit Overall performance deficit: 1.2-2 standard deviations below healthy controls. Verbal learning & memory: up to 3 standard deviation lower than the persons performance previously Deficits in cognitive functions requiring controlled and active information Motor Symptoms: Disorganized behaviour Reflect difficulty with goal directed behaviour Stereotypic behaviour: The repetition of one incoherent movement for a long period of time. Catatonic behaviour: The maintenance of unusual positions for a long period of time. Course of symptoms: Course: permorbid decline, acute psychotic episodes, periods of stability and possible psychotic relapse.

Psychiatry: Schizophrenia U0
A more chronic condition with periods of progression nand periods of remission. Typical onset: 16-30 years, infrequently: 45+ First signs, change of friends, drop in grades, sleep problems, irritability. The DMS IV example of differentiation: o Schizoaffective disorder and mood disorder with psychotic features have been ruled out because either no major depressive, manic, or mixed episodes have occured concurrently with the active-phase symptoms, or, if mood episodes have occured during active-phase symptoms, their total duration have been brief relative to the duration of the active and residual periods. A measurement of severity is based on how it affects functioning of the individual. In terms of work, interpersonal relations or self-care. Compared to the levels prior to the onset. Prognosis: o Predicted by the leve of social development attained at the onset of psychosis: o Developped by the amount of information acquired at that moment. o If there is a great different between the prior functional levels compared to the present levels, then the prognosis will not be good. Endurance o Some impairment is usually present throughout most life. o Psychotic symptoms tend to be episodic over time. Anti-psychotic drugs are available to reduce the affects of positive symptoms.

The Medical Causes of Schizophrenia: Genetic factors o Prevalence rate of 1% in the general population. o 10% of people with a first degree relative with disorder o 40% - 65% identical twins of a person with schizophrenia. o Most view how much is environmental factors. o It is naive to map one gene to one disorder. It is a combination of genes and genetic traits that may relate to one disorder. Therefore, it is called a poly-genetic disorder. Environmental Factors: Biological o Prenatal: Maternal influenza, rubella, malnutrition, diabetes mellitus and smoking during pregnancy o Perinatal: Obstetric complications (hypoxia) Environmental Factors: Socio-demographic Factors: o Socio-demographic factors: poverty, lower social class. o Social causation: Stress-vulnerability Model:

Psychiatry: Schizophrenia U0
o Biological and psychosocial factors interact with underlying psychobiological vulnerability (genetic and early environmental factors) to determine the onset of the illness and its course.

Neurodevelopmental Hypothesis Abnormal early brain development -> structural changes -> emergence of psychosis later in life. Something went wrong BIOLOGICALLY early on. An early biological problem. Evidence: o Structural changes are apparent before the first episode and in first-degree biological relatives o Histopathological evidence consistent with errors in brain development.

Epigenetics: how environmental factors may block or express certain genes. Neuropathology: Focus on frontal and temporal regions. Enlargment of ventrical system in the brain. o Ventricals secrete cerebrospinal fluid which is suspended in the skull. Overall reductions in brain volume and cortical grey matter Many subtle molecular changes

Neurodegeneration vs Neurodevelopmental Hypothesis. Cause vs result. The dopamine hypothesis: Too much dopamine that is flooding the brain. Antipsychotic medications: block Dopamine D2 receptors Dopamine agonists, amphetamine induced psychosis Neuroimaging: increased pre-synaptic stores of D2? By removing dopamine excess, the positive symptoms of schizophrenia are alleviated. However, the negative symptoms are not improved. Lack of glutamine However, dopamine is needed in other parts of the brain, such as the hippocampus. Needs to diminish levels in the frontal cortex.

Intervention: Early detection and comprehensive treatment of first episode.

Psychiatry: Schizophrenia U0
Treatment for the positive treatment must start right away! Psychosocial interventions: family interventions, social interventions. Therapy for comorbid conditions.

Neurodevelopmental Models Pharmacology presumably will largely be constrained to producing compensatory changes to minimize functional effects of disordered brain circuits.

Biochemical Models: Medication corrects an excess of deficit of neurotransmitters.

Pathology of schizophrenia is progressive or neurodegenerative Pharmacology halts progression of illness and prevent full expression of the disease based on interventions initiated early in the course of the illness.

Genes: If the alterations of an enzymes activity improves the functions of the patient.

First generation anti-psychotics: Psychotic drugs have side effects. Must balance positive and negatives

Second generation anti-psychotics Reducing facial expressions, vocal intonations, and affective responsiveness.

Pharmagenetics.

Psychiatry: Schizophrenia U0
Prevention: Precautions taken to reduce the possible rates of schizophrenia

Summary: Devastating brain disorder, early onset, profound psychosocial morbidity Abnormalities in Dopamine, brain structure, cortical cytoarchitecture and physiology, and cognition Polygenetic disorder, a variety of potential intermediate neurobiological phenotypes Several promising genetic mechanisms now emerging