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Explore psychodynamic, learning, and biological perspectives on schizophrenia, including genetic factors, brain abnormalities, dopamine hypothesis, and familial risks. Uncover truths and fictions surrounding the complex disorder.
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Chapter 12 (Pp 410-422) Schizophrenia and Other Psychotic Disorders
Psychodynamic Perspectives Within the psychodynamic perspective, schizophrenia represents the overwhelming of the ego by primitive sexual or aggressive drives or impulses arising from the id. These impulses threaten the ego and give rise to intense intrapsychic conflict. Under such a threat, the person regresses to an early period in the oral stage, referred to as primary narcissism.
Learning Perspectives Although learning theory does not offer a complete explanation of schizophrenia, the development of some forms of schizophrenic behavior can be understood in terms of the principles of conditioning and observational learning. From this perspective, people with schizophrenia learn to exhibit certain bizarre behaviors when these are more likely to be reinforced than normal behaviors. Social-cognitive theorists suggest that modeling of schizophrenic behavior can occur within the mental hospital, where patients may begin to model themselves after fellow patients who act strangely
Biological Perspectives Although we still have much to learn about the biological underpinnings of schizophrenia, most investigators today recognize that biological factors play a determining role through: Genetic Factors Biochemical Factors Viral Infections Brain Abnormalities
TRUTH or FICTION If you have two parents with schizophrenia, it’s nearly certain that you will develop schizophrenia yourself
Genetic Factors The closer the genetic relationship between schizophrenia patients and their family members, the greater the likelihood (or concordance rate) that the relatives will also have schizophrenia. Overall, first-degree relatives of people with schizophrenia (parents, children, or siblings) have about a tenfold greater risk of developing schizophrenia than do members of the general population. The fact that families share common environments as well as common genes requires that we dig deeper to examine the genetic underpinnings of schizophrenia.
The familial risk of schizophrenia. Generally speaking, the more closely one is related to people who have developed schizophrenia, the greater the risk of developing schizophrenia for oneself. Monozygotic (MZ) twins, whose genetic heritages are identical, are much more likely than dizygotic (DZ) twins, whose genes overlap by 50%, to be concordant for schizophrenia.
Biochemical Factors Contemporary biological investigations of schizophrenia have focused on the role of the neurotransmitter dopamine. The leading biochemical model of schizophrenia, the dopaminehypothesis, posits that schizophrenia involves an overreactivity of dopamine transmission in the brain. Increasing evidence supports the view that schizophrenia involves an irregularity in dopamine transmission in the brain The imbalance seems to be related to D2 neurons in the frontal lobe of the brain. Biochemical factors seem to explain Type I or positive symptoms of schizophrenia.
TRUTH or FICTION Although schizophrenia is widely believed to be a brain disease, evidence of abnormalities in the brains of schizophrenia patients remains lacking
Brain Abnormalities We have compelling evidence of both structural changes (loss of brain tissue) and functional disturbance (abnormalities of functioning) in the brains of schizophrenia patients. However, we have yet to discover any one source of pathology in the brain that is specific to schizophrenia or present in all cases of schizophrenia. The most prominent finding of structural changes is the loss of brain tissue (gray matter) of about 5% on the average in schizophrenia patients as compared to normal controls. These brain abnormalities are responsible for Type II (negative) symptoms of schizophrenia.
Loss of brain tissue in adolescents with early-onset schizophrenia The brains of adolescents with early-onset schizophrenia (right image) show a substantial loss of gray matter. Some shrinkage of gray matter occurs normally during adolescence (left image), but the loss is more pronounced in adolescents with schizophrenia.
Structural changes in the brain of a person with schizophrenia as compared with that of a normal subject The magnetic resonance imaging (MRI) of the brain of a person with schizophrenia (left) shows a relatively shrunken hippocampus (yellow) and relatively enlarged, fluid-filled ventricles (white) when compared to the structures of the normal subject (right).
PET scans of people with schizophrenia versus normal's Positron emission tomography (PET) scan evidence of the metabolic processes of the brain shows relatively less metabolic activity (indicated by less yellow and red) in the frontal lobes of the brains of people with schizophrenia. PET scans of the brains of four normal people are shown in the top row, and PET scans of the brains of four people with schizophrenia are shown below.
An early, but since discredited theory, focused on the role of the schizophrenogenic mother (Fromm-Reichmann, 1948, 1950). In what some feminists view as historic psychiatric sexism, the schizophrenogenic mother was described as cold, aloof, overprotective, and domineering. She was characterized as stripping her children of self-esteem, stifling their independence, and forcing them into dependency on her. Children reared by such mothers were believed to be at special risk for developing schizophrenia if their fathers were passive and failed to counteract the mother’s pathogenic influences.
Today, investigators interested in family influences have turned to consider the effects of: • deviant patterns of communication within the family, and • intrusive, negative comments directed toward the schizophrenic family member
Communication Deviance (CD) A pattern of unclear, vague, disruptive, or fragmented communication that is often found among parents and family members of schizophrenia patients. CD is speech that is hard to follow and from which it is difficult to extract any shared meaning. High CD parents often have difficulty focusing on what their children are saying.
Expressed Emotion (EE) Another form of disturbed family communication, EE is a pattern of responding to the schizophrenic family member in hostile, critical, and unsupportive ways. Schizophrenia patients from high EE families stand a higher risk of relapsing than those with low EE (more supportive) families. High EE relatives typically show less empathy, tolerance, and flexibility than low EE relatives.
Relapse rates of people with schizophrenia in high and low EE families People with schizophrenia whose families are high in expressed emotion (EE) are at greater risk of relapse than those whose families are low in EE. Whereas low-EE families may help protect the family member with schizophrenia from environmental stressors, high-EE families may impose additional stress.
Family Factors in Schizophrenia: Causes or Sources of Stress? No evidence supports the belief that family factors, such as negative family interactions, lead to schizophrenia in children who do not have a genetic vulnerability. Rather, a genetic vulnerability to schizophrenia renders individuals more susceptible to troubled family and social relationships. Within the diathesis–stress model, disturbed patterns of family interaction and communication represent sources of life stress that increase the risks of developing schizophrenia among people with a genetic predisposition for the disorder
The Diathesis–Stress Model Note that the question of whether stress directly triggers the initial onset of schizophrenia in genetically vulnerable individuals is still open to debate (Walker & Diforio, 1997)
Endophenotypes? To better understand how schizophrenia develops, we need to dig under the surface to see how genes affect underlying processes, and how these processes in turn contribute to the development of the disorder. Investigators are studying a number of possible endophenotypes in schizophrenia- measurable processes or mechanisms not apparent to the naked eye, which are the means by which an organism’s genetic code comes to affect its observable characteristics or phenotypes. These phenotypes include disturbances in brain circuitry, deficits in working memory and cognitive abilities, and abnormalities of neurotransmitter functioning.
