12.4 Schizophrenia: Blurring What is Real and What is Not.

Learning Objectives

Categorize and describe the major symptoms of schizophrenia.
Describe positive and negative symptoms of schizophrenia as well as other behaviors common in schizophrenia.
Describe the diagnostic criteria for schizophrenia.
Identify the biological and environmental factors that contribute to the development of schizophrenia.

The term schizophrenia, which in Greek means “split mind,” was first used to describe a psychological disorder by Eugen Bleuler (1857–1939), a Swiss psychiatrist who was studying patients who had very severe thought disorders. People with schizophrenia experience a blurring between their own thoughts and experiences and speech or other information from outside themselves. Schizophrenia is a serious psychological disorder marked by delusions, hallucinations, loss of contact with reality, inappropriate affect, disorganized speech, social withdrawal, and deterioration of adaptive behavior.

Figure 12.14

People with schizophrenia may exhibit disorganized behavior, as this person does.

Source: Photo courtesy of Max Avdeev, http://www.flickr.com/photos/avdeev/4203380988.

Schizophrenia is the most chronic and debilitating of all psychological disorders. It affects men and women equally, occurs in similar rates across ethnicities and across cultures, and affects at any one time approximately 3 million people in the United States (National Institute of Mental Health, 2010). Onset of schizophrenia is usually between the ages of 16 and 30 and rarely after the age of 45 or in children (Mueser & McGurk, 2004; Nicholson, Lenane, Hamburger, Fernandez, Bedwell, & Rapoport, 2000).

Symptoms of Schizophrenia

Schizophrenia is accompanied by a variety of symptoms, but not all people have all of them (Lindenmayer & Khan, 2006). As you can see in Table 12.5 "Positive and Negative Symptoms of Schizophrenia" , the symptoms are divided into positive symptoms, and negative symptoms (American Psychiatric Association ( later "APA"), 2013). Positive symptoms refer to the presence of abnormal behaviors or experiences (such as hallucinations) that are not observed in normal people, whereas negative symptoms (such as lack of affect and an inability to socialize with others) refer to the loss or deterioration of thoughts and behaviors that are typical of normal functioning. Finally, cognitive features are the changes in cognitive processes that accompany schizophrenia (Skrabalo, 2000). Psychologists describe individuals with schizophrenia as having psychosis, or being psychotic, which is a psychological condition characterized by a loss of contact with reality.

Table 12.5 Positive and Negative Symptoms of Schizophrenia

Positive symptoms	Negative symptoms
Hallucinations	Flat or blunted affect
Delusions (of grandeur or persecution)	Avolition- lack of goal-directed activity
Disorganized Speech	Limited speech- "poverty of speech
Grossly disorganized behavior	Incoherent speech
Inappropriate affect
Movement disorders

Positive Symptoms

People with schizophrenia almost always suffer from hallucinations—imaginary sensations that occur in the absence of a real stimulus or which are gross distortions of a real stimulus. Auditory hallucinations are the most common and are reported by approximately three quarters of people (Nicolson, Mayberg, Pennell, & Nemeroff, 2006). Individuals frequently report hearing imaginary voices that curse them, comment on their behavior, order them to do things, or warn them of danger (National Institute of Mental Health (later "NIMH"), 2009). Visual hallucinations are less common and frequently involve seeing God or the devil (De Sousa, 2007).

Another common symptom is delusions, which are false beliefs not commonly shared by others within one’s culture, and maintained even though they are obviously out of touch with reality. People with delusions of grandeur believe that they are important, famous, or powerful. They often become convinced that they are someone else, such as the president or God, or that they have some special talent or ability. Some claim to have been assigned to a special covert mission (Buchanan & Carpenter, 2005). People with delusions of persecution believe that a person or group seeks to harm them. They may think that people are able to read their minds and control their thoughts (Maher, 2001). If a person suffers from delusions of persecution, there is a chance that he or she will become violent, and this violence is typically directed at family members (Buchanan & Carpenter, 2005). However, overall, the risk of violence is small (NIMH, 2009). People with schizophrenia generally try to withdraw from others, which decreases the likelihood of interaction with others and thus the risk of violence against others. People with schizophrenia are more likely to commit violence against themselves; the risk of suicide is substantially greater than in the general population (NIMH, 2009).

People suffering from schizophrenia also often suffer from the positive symptom of disorganized speech (APA, 2013). There are a number of ways that the disorder may affect speech. One is derailment—the shifting from one subject to another, without following any one line of thought to conclusion-- and another involves the person speaking in nonsense words, called neologisms (NIMH, 2009). A third involves the person speaking in words that together make no sense- this is termed word salad. If you wish to get an idea of word salad, read aloud every third or fourth word in this paragraph- the words themselves are fine, but put together they make no sense.

In addition, people with schizophrenia may exhibit grossly disorganized behavior including inappropriate sexual behavior, peculiar appearance and dress, unusual agitation (e.g., shouting and swearing), strange body movements, and awkward facial expressions. It is also common for schizophrenia sufferers to experience inappropriate affect. For example, an individual may laugh uncontrollably when hearing sad news. Movement disorders typically appear as agitated movements, such as repeating a certain motion again and again, but can in some cases include catatonia, a state in which a person does not move and is unresponsive to others (Janno, Holi, Tuisku, & Wahlbeck, 2004; Rosebush & Mazurek, 2010). Other motor disturbances, may include random and frenzied motor activity during which they become hyperactive and incoherent (Kirkpatrick & Tek, 2005).

Negative Symptoms

Negative symptoms of schizophrenia include flat or blunted affect, incoherent speech, and avolition. Individuals often suffer from flat affect, which means that they express almost no emotional response (e.g., they speak in a monotone and have a blank facial expression) even though they may report feeling emotions (Kring, 1999). Blunted affect is also possible, in which the person demonstrates a far smaller emotional response than expected for the situation. Another negative symptom is the tendency toward incoherent language, for instance, to repeat the speech of others (“echo speech”). Other individuals exhibit "poverty of speech" in which they use too few words. Finally, they may also show avolition, a condition where the person shows a lack of motivation to do "goal-directed" activities (APA, 2013).

Other common negative feature of schizophrenia include social withdrawal, poor hygiene and grooming, poor problem-solving abilities, and a distorted sense of time (Skrabalo, 2000). These features may well be caused by the symptoms. So someone who has difficulty communicating or a delusion of persecution might engage in social withdrawal in order to feel safer. Avolition may prevent the person from self-care, and result in the person having poor hygiene and grooming.

Not all people with schizophrenia exhibit negative symptoms, but those who do also tend to have the poorest outcomes (Fenton & McGlashan, 1994). Negative symptoms are predictors of deteriorated functioning in everyday life and often make it impossible for sufferers to work or to care for themselves. As well, medications used to treat schizophrenia generally don't have an effect on negative symptoms.

Cognitive and Other Features

There are also cognitive features associated with schizophrenia. These features are not part of the diagnosis of schizophrenia, and are difficult for outsiders to recognize. These features can make it extremely difficult for the sufferer to lead a normal life. These symptoms include difficulty comprehending information and using it to make decisions (the lack of executive control), difficulty maintaining focus and attention, and problems with working memory (the ability to use information immediately after it is learned) (NIMH, 2009).

Another significant feature is “poor insight” in which the individual is not aware that they have schizophrenia (APA, 2013). Poor insight is associated with greater problems as the individual sees no reason to seek or continue treatment.

Diagnosing Schizophrenia

Now that you have some general background, let's move on to how to tell schizophrenia from other disorders and eccentric or unusual behavior. As mentioned previously, psychologists and psychiatrists use the Diagnostic and Statistical Manual of Mental Disorders (DSM) as the main reference for diagnosis. The DSM is in its fifth edition, so it is called "DSM-V."

In order to diagnose schizophrenia, certain criteria must be met. The below are the current diagnostic criteria from the DSM-V. In section A, the first three are the most critical since at least one is required for a person to meet the diagnosis of schizophrenia (APA,2013).

Diagnostic Criteria for Schizophrenia

A. Two or more of the following:

Delusions
Hallucinations
Disorganized Speech
Disorganized or Catatonic behavior
Negative Symptoms

B. The person’s functioning at work, home, personal relationships, or self care must be significantly impacted for “a significant portion of the time since the onset of the disturbance” (p.99).

C. The disorder must be present for at least 6 months, and must include one month of full-blown (“active phase”) symptoms. Symptoms can be less severe for the rest of the time however. Less severe symptoms can be present before or after the period of active phase symptoms.

D. Other psychological disorders have been ruled out, such as depression or schizoaffective disorder.

E. The disorder is not due to drug effects, use of illegal drugs, or another medical condition.

F. Individuals with a history of autism spectrum disorder or a communication disorder of childhood only can be diagnosed If they also have prominent delusions or hallucinations along with the other required symptoms of schizophrenia. (This criterion is to differentiate these disorders from schizophrenia. Individuals with these disorders may suffer from similar kinds of social withdrawal and/or speech difficulties, though for very different reasons.)

Explaining Schizophrenia

Overview

Generally, researchers consider schizophrenia to be the outcome of an interaction between biological and environmental factors (Schmidt-Kastner, et al., 2012). Beyond that basic statement matters get murky and complicated. Four concepts may help you organize your understanding of this web of factors. These are levels of explanation, development, the diathesis stress model, and epigenetics.

Levels of Explanation

Any model of causes is likely to be complex and operate on multiple levels of explanation (See discussion in the Scientific Inquiry module for more on levels of explanation.) In this case, it seems likely that the higher level causes are the ultimate causes. They bring about the cascade of events that create the changes at the lower level that are the proximal causes of the disorder. At the higher level, there are factors such as famine, poverty, prenatal stress, hypoxia (oxygen deprivation at birth), and prenatal infection, to name a few (Brown et al., 2004; Cannon, et al, 2002; Murray & Bramon, 2005; Susser et al., 1996; Waddington, Lane, Larkin, O’Callaghan, 1999). At the lower level, there is evidence for structural anomalies in the brain as well as abnormalities in neurotransmitters such as dopamine. So, for example, difficulties during prenatal development may cause biochemical changes in the developing fetus that, along with other factors, ultimately affect brain structure, and thus bring on the disorder (Brown & Susser, 2008).

The Diathesis Stress Model

The Diathesis Stress Model indicates that biological and environmental factors combine to create disorders, including schizophrenia (OpenStax, 2014). The individual with schizophrenia has a generally biological preexisting vulnerability, but just that is not enough to create the disorder. It is some other factor (the “stressor”) that causes the disorder to be expressed. People are generally diagnosed between the ages of 16 and 30 (NIMH, 2009). Researchers have suggested the challenges of starting adult life as a possible "stressor" to bring about the disorder. There is evidence for this role of stress. Stress increases the likelihood that a person will develop symptoms of schizophrenia; as well, onset and relapse of schizophrenia typically occur during periods of increased stress (Walker, Mittal, & Tessner, 2008).

Development

Development refers to the process of change or growth over time. Schizophrenia is considered to be a neurodevelopmental disorder, meaning that the causes of the disorder are rooted in changes in the brain over the course of prenatal development (Schmidt-Kastner, et al., 2012; Xu, et al, 2009). Certain events occurring development have been linked to later development of schizophrenia. It is possible that these developmental events create the biological vulnerability described in the Diathesis Stress model. Alternatively, the events may simply add to the "stressor" aspect of the model, becoming the initial stressor. Later difficulties simply bring the disorder into "full blown" being. There are certainly several prenatal factors that have been associated with the development of schizophrenia (Bale, et al., 2010). Some possible prenatal stressors are maternal infections, stress, season of birth, malnutrition, and hypoxia, which refers to a lack of oxygen to the fetus, either during prenatal development or during birth.

Epigenetics

The last piece of the puzzle is epigenetics. Epigenetics is one mechanism by which the environment can affect the structure and function of the brain. Epigenetic effects are mechanisms that turn genes on and off. They essentially “program” the operation of genes and are themselves affected by environmental conditions (Bale, et al., 2010). It makes sense to have a means for the organism to change its functioning in response to environmental conditions. For example, if a fetus is developing during a time of food scarcity, it would promote survival for that fetus to develop a more efficient metabolism, to make best use of whatever food supplies were available. The way epigenetics works is that there are other proteins in the cell nucleus along with the DNA. Among other functions, these proteins act to create and regulate the folding of DNA in the nucleus (Tsankova, et al,, 2007). These other proteins affect whether or not a particular gene or set of genes is available for transcription, the process by which the cell uses the genes to make proteins (Tsankova, et al,, 2007). Changing those proteins changes which genes are available, or "on" and changes the functioning of the cell, which can eventually affect complex behavior, such as those in schizophrenia (Tsankova, et al,, 2007). There is direct evidence of epigenetic changes in humans, from studies of how antipsychotic medications work (Tsankova, et al,, 2007).

Putting it All Together

These four concepts give an organization to the bewildering mass of data on schizophrenia. So first, there is an individual, developing in the womb. At the low level of explanation, she or he has a genetic abnormality (diathesis). Later, at the higher levels, some event occurs that along with the previous genetic abnormality, epigenetically changes her or his brain's development, and ultimately structure and/or function. Finally, those changes are not fully seen until the individual is older, when some additional stressor(s) bring out the symptoms of schizophrenia. Below you will see more details of research on these various contributors to schizophrenia. Keep these concepts in mind as you are thinking about these research findings.

As described above, there are a variety of explanations for schizophrenia. Below is a selection of research describing the evidence for those explanations, organized by level of explanation and the diathesis stress model.

Diathesis: The Role of Genes

Genes play a significant role in schizophrenia. A person in the general population has about a 1% chance of developing schizophrenia, but if they have a parent or sibling with schizophrenia, their risk increases to about 10% (NIMH, 2007). If they have an identical twin with schizophrenia, their risk increases to between 40% and 65% (NIMH, 2007). Researchers are "on the hunt" for the particular genes responsible for schizophrenia. A number of new tools have been developed, including the SzGene database, which centralizes data on specific genes and their relationships with schizophrenia symptoms (Schmidt-Kastner, 2012). Traditional methods, such as family, twin, and adoption studies also indicated that genetics are important (Walker & Tessner, 2008). Figure 12.15 shows the increase in risk that comes with different degrees of relatedness.

Figure 12.15 Genetic Disposition to Develop Schizophrenia

Source: Adapted from Gottesman, I. I. (1991). Schizophrenia genesis: The origins of madness. New York, NY: W. H. Freeman.

Researchers, however, have known for decades that schizophrenia wasn’t just genes, however. Even if a person has an identical twin with schizophrenia, he or she still has less than a 50% chance of getting it, and over 60% of all people with schizophrenia have no first- or second-degree relatives with schizophrenia (Gottesman & Erlenmeyer-Kimling, 2001; Riley & Kendler, 2005). Thus, researchers have searched for the other factors involved in developing schizophrenia as described later in this section.

Many of the genetic studies have involved animal models, commonly mice. Animals are helpful in this work for a number of reasons. First they can be bred to either have or lack certain genes researchers believe are involved in a disease, then the behaviors and/or biology of those animals can be examined. Second, animals like mice have short lifespans, so many generations of mice can be studied in a few years, unlike humans.

There are two major limitations of mouse models and animal models in general. First, some behaviors, like hallucinations, can’t be observed in a mouse, and second, even behaviors that look like human behaviors, like poor social interaction or hyperactivity, are not the same behaviors as in humans (Robertson & Feng, 2011). We should be careful in comparing the two sets of behaviors. Mice are pretty similar in many ways to humans, though, so there is still value in studying them, even if they are inexact models. Two of these models are the DISC-1 (Disrupted in Schizophrenia-1) gene deletion and deficits in a glutamate receptor known as NMDA (Blanke & VanDongen, 2013; Robertson & Feng, 2011). In both cases, the behavioral problems these abnormalities create can be treated with medications used to treat schizophrenia in humans (Robertson & Feng, 2011) which leads credence to the idea that these abnormalities are also present in humans with schizophrenia.

High Level Stressors: Prenatal Environmental Factors

There are a number of other factors that play a role in schizophrenia. The most important are prenatal environmental factors, specifically maternal stress, restricted oxygen (hypoxia), exposure to infection, and malnutrition. All have been shown to increase risk for schizophrenia via epigenetic means (Bale, et al, 2010; Schmidt-Kastner, 2012).

Maternal Stress

In a study of 1.38 million people from Denmark, researchers found a greater risk of schizophrenia among people whose mother had had a close relative die during the first trimester, but only during the first trimester (Kashan, et al, 2008). In that case “close relative” was a parent, partner, sibling, or older child (Kashan, et al, 2008). Maternal stress in the first trimester is associated with an increased risk of schizophrenia in males (Bale, et al, 2010).

Malnutrition

Multiple studies have found a link between prenatal exposure to famine, which is extreme malnutrition, and later risk of schizophrenia. Famine is a tragic event, and is fortunately rate in the developed world, but there have been two large-scale famines for which there are data which could be used to study a link with schizophrenia. The first is the Dutch Hunger Winter of 1944-45, reported in Brown & Susser (2008). That famine was caused by a combination of a German blockade of a portion of Holland during World War Two and a winter that froze the canals used to transport food. The second is the Chinese Famine of 1959-61, which was caused by Mao’s “Great Leap Forward” and spanned the entirety of China (Xu, et al., 2009). To give an idea of the severity of this famine, in the area used for one study the population dropped from approximately 1.7 million in 1958 to 1.45 million in 1961 (St. Clair, et al., 2005). All three studies found approximately a doubling of the risk of schizophrenia in adults who had been in the early stages of prenatal development during the famine (Brown & Susser, 2008; St. Clair, et al., 2005, Xu, et al., 2009). Adding further support to the idea that nutrition matters is a study reported in Brown & Susser (2008) that found a similar increase in the risk of Schizoid Personality Disorder in the same population from the Dutch Hunger Winter. There is clearly a correlation between famine and the “Schizoid Spectrum Disorders,” including schizophrenia. Researchers have hypothesized that a lack of certain nutrients such as folate, iron, vitamin A may be the cause, but data for those links is tentative and mixed (Brown & Susser, 2008).

Maternal Infection

There is significant research demonstrating a link between a variety of maternal infections and development of schizophrenia (Buka, et al., 2001a; Buka, et al., 2001b). Researchers Stephen Buka and colleages (2001a) found a link between mothers who had children who later developed schizophrenia and infection. Those mothers had higher levels of antibodies in their blood than matched mothers of children who did not develop schizophrenia (Buka, et al., 2001a).

Researchers have identified a number of specific infectious agents with links to schizophrenia. Studies have linked Herpes Simplex Virus type 2 (HSV-2) (Buka, et al., 2001a, Kashan, et al, 2008), Influenza, and Toxoplasmosis (Brown, et al, 2009), respiratory infections and genital-reproductive infections (Brown, et al, 2009b) to later schizophrenia. Timing may also matter; one study found a link between third trimester (the last approximately 3 months of pregnancy) infections and later development of schizophrenia (Buka, et al., 2001b). Many of these studies have used blood testing to determine infection, thus decreasing the chance of reporting error. Large-scale population studies are needed for this kind of research, since schizophrenia is a rare condition a large number of births need to be studied to find a small number of people with schizophrenia. For instance, one study of 12,000 births found 71 people with schizophrenia who met all the study criteria (Brown, et al, 2009). That study, involving over 12,000 births in California found an association between infection, schizophrenia, and executive function deficits (Brown, et al, 2009). Executive function problems are common contributors to the difficulties many people have with schizophrenia, even if they are not diagnostic criteria for schizophrenia (APA, 2013, Brown, et al, 2009), so they are an important area of study. Researchers using animal models have shown a link between infections during pregnancy and later schizophrenia-like behaviors (Bale et al., 2010). It may be that inflammation due to the infection epigenetically “programs” specific genes in ways that create the behaviors involved in schizophrenia or it may be that the infection itself is the cause(Bale et al., 2010; Buka, et al., 2001b).

Hypoxia

Hypoxia has the strongest relationship to schizophrenia of any of the environmental factors (Cannon, et al., 2002). Hypoxia refers to oxygen deprivation during development, whether that deprivation happens for an extended period during development or during birth. One study found the risk of developing schizophrenia increased as the number of hypoxia-related pregnancy complications increased (Cannon, et al., 2000). A 19-year longitudinal study found that the risk of developing a psychotic disorder doubled in people who experienced prenatal hypoxia vs. controls (Zornberg, et al., 2000). Also, a large-scale study of 524 people with schizophrenia and 1043 controls found a similar relationship (Dalman, et al., 2001).

It is not entirely clear how hypoxia and schizophrenia are related. One puzzle is that ninety percent of infants who experience hypoxia, even severe hypoxia, don’t develop schizophrenia (Cannon, et al., 2002). Two studies may show the answer. First, Besovich (2010) described research indicating that hypoxia creates changes in neuronal development, and that those changes led to abnormal connections between neurons, and thus abnormal behaviors, feelings, or sensation, which we identify as mental illness. Second, Schmidt-Kastner and colleagues (2012) found that many genes related to schizophrenia are also related to the kinds of cellular responses to hypoxia that are likely to create later schizophrenia. So it may be that only in these individuals with a specific set of genes (the diathesis) does hypoxia bring about the changes that can later result in schizophrenia.

Changes in Brain Structure and Function

All the research above details high level contributors to schizophrenia. What they seem to cause are changes in the structure of the brain and how the brain works. This section details some of the research evidence for these topics.

Brain Structure

There is evidence, from neuroimaging studies, that there are some differences in brain structure between people with schizophrenia and normal controls. Researchers find these differences in the open, fluid-filled spaces in the brain as well as in actual brain structures.

There is evidence for changes in two spaces in the brain. These are the cerebral ventricles and the cavum septum pellucidum. Thinking about problems with a space may seem strange, but in this case, a problem with a space indicates a problem in the brain structures that border that space. Researchers have long found that the cerebral ventricles (fluid-filled spaces in the brain) are enlarged in some people with schizophrenia. (Suddath, Christison, Torrey, Casanova, & Weinberger, 1990). Another indicator of structural problems in the brain is a space called the Cavum Septum Pellucidum (CSP), which borders on the corpus callosum and limbic system (Winter, et al., 2010). In normal development, the CSP is very small due to areas of the brain fusing together (Farrugia & Babcock, 1981). When the CSP is larger, those areas of the brain are smaller, and that is an indicator of a problem in development (Winter, et al., 2010). Researchers have found a link between greater CSP size, and certain prenatal infections, including Influenza, Toxoplasmosis, serious respiratory infection (second trimester only) and specific genitourinary infections (Brown, et al., 2009b) Finally, there is a strong association between increased length of the CSP and later schizophrenia (Brown, et al., 2009b). Researchers hypothesize that an abnormal CSP may indicate abnormalities in the development of the limbic system and corpus callosum (Brown, et al., 2009b; Winter, et al., 2010). Both of these brain areas may well be involved in the symptoms of schizophrenia, such as inappropriate emotional responses.

There are also issues with specific brain structures. People with schizophrenia also frequently show an overall loss of neurons in the cerebral cortex, and some show less activity in the frontal and temporal lobes, which are the areas of the brain involved in language, attention, and memory. Cannon and colleagues (2002) found a decrease in gray matter (neurons and neuronal connections) in the temporal lobes of people with schizophrenia. These findings seem to explain the deterioration of functioning in language and thought processing that is commonly experienced by individuals with schizophrenia (Galderisi et al., 2008).

Brain Function

Many researchers believe that schizophrenia is caused in part by excess dopamine, and this theory is supported by the fact that most of the drugs useful in treating schizophrenia inhibit dopamine activity in the brain (Javitt & Laruelle, 2006). Levels of serotonin may also play a part (Inayama et al., 1996). But recent evidence suggests that the role of neurotransmitters in schizophrenia is more complicated than was once believed. It also remains unclear whether observed differences in the neurotransmitter systems of people with schizophrenia cause the disease, or if they are the result of the disease itself or its treatment (Csernansky & Grace, 1998).

Conclusions

It is clear that schizophrenia, like most or even all, psychological disorders is extraordinarily complex, involving a developmental path, Indeed, there is development even after the individual has developed the disorder. Some people do better than others, and environmental factors play a role in this as well. The degree to which one or more of the individual’s relatives is highly critical or highly emotional in their attitude toward the person has significant impact on their later outcomes. Hooley and Hiller (1998) found that people who ended a stay in a hospital and returned to a family with high expressed emotion were three times more likely to relapse than those who returned to a family with low expressed emotion. It may be that the families with high expressed emotion are a source of stress.

Schizophrenia is highly complex. both in its development and in diagnosis.. It is a developmental disorder, involving interactions between genetics, epigenetics, and a wide variety of environmental factors such as malnutrition, hypoxia, and maternal infection. These interactions all take the individual on a tragic path to schizophrenia. Researchers and clinicians use the DSM-V to diagnose schizophrenia and other psychological disorders. Diagnosis is often the first step for treatment.

Key Takeaways

Schizophrenia is a serious psychological disorder marked by delusions, hallucinations, and loss of contact with reality (psycholsis).
Schizophrenia is accompanied by a variety of symptoms, but not all individuals have all of them.
Positive symptoms of schizophrenia include hallucinations, delusions, disorganized speech, disorganized behavior, inappropriate affect, and catatonia.
Negative symptoms of schizophrenia include avolition, decreased speech, and blunted or flat affect.
Cognitive features of schizophrenia include difficulty comprehending and using information and problems maintaining focus.
Other features of schizophrenia may include poor hygiene and social withdrawal.
Schizophrenia is a neurodevelopmental disorder, with origins in prenatal development as well as genetics.
There is evidence for a complex interplay of factors in the development of schizophrenia, including prenatal exposure to infection, stress, hypoxia and malnutrition, which may interact with or program genetic abnormalities that later result in developing schizophrenia.

Exercise and Critical Thinking

How should society deal with people with schizophrenia? Is it better to keep people in psychiatric facilities against their will, but where they can be observed and supported, or to allow them to live in the community, where they may be a danger to self or others? What factors influence your opinion?

References

American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.). Washington, DC: Author.

Bale, T. L., Baram, T.Z., Brown, A. S., Goldstein, J. M., Insel, T.R., McCarthy, M.M., Nemeroff, C.B., Reyes, T.M., Simerly, R.B., Susser, E. S., and Nestle, E. J. (2010). Early Life Programming and Neurodevelopmental Disorders. Biological Psychiatry, 68, 314-319.

Blanke, M. L. , and Van Dongen, A. M. J. (2009). Activation Mechanisms of the NMDA Receptor. (Chapter 13.) In: Van Dongen, A.M., editor. Biology of the NMDA Receptor. Boca Raton (FL): CRC. Available from: http://www.ncbi.nlm.nih.gov/books/NBK5274/

Brown & Susser (2008). Prentatal nutritional deficiency and risk of schizophrenia. Schizophrenia Bulletin, 34, 1054-1063.

Brown, A. S., Begg, M. D., Gravenstein, S., Schaefer, C. S., Wyatt, R. J., Bresnahan, M., Susser, E. S. (2004). Serologic evidence of prenatal influenza in the etiology of schizophrenia. Archives of General Psychiatry, 61, 774–780.

Brown, A. S., Deicken, R. F., Vinogradov, S., Kremen, W. S., Poole, J. H., Penner, J. D., Kochetkova, A. Kern, D., and Schaefer, C. A. (2009b). Prenatal infection and cavum septum pellicidum in adult schizophrenia, Schizophrenia Research, 108, 285-287.

Brown, A. S., Vinogradov, S., Kremen, W. S., Poole, J. H., Deicken, R. F., Penner, J. D., McKeague, I. W., Kochetkova, A. Kern, D., and Schaefer, C. A. (2009a). Prenatal exposure to maternal infection and executive dysfunction in adult schizophrenia. American Journal of Psychiatry, 166, 683-690.

Buchanan, R. W., & Carpenter, W. T. (2005). Concept of schizophrenia. In B. J. Sadock & V. A. Sadock (Eds.), Kaplan & Sadock’s comprehensive textbook of psychiatry. Philadelphia, PA: Lippincott Williams & Wilkins.

Buka, S.L.., Tsuang, M. T., Torrey, E.F., Klebanoff, M.A., Berenstein, D., & Yolken, R.H. (2001a). Maternal infections and subsequent psychosis among offspring. Archives of General Psychiatry, 58, 1032-1037.

Buka, S.L.., Tsuang, M. T., Torrey, E.F., Klebanoff, M.A., Wagner, R.L., & Yolken, R.H.(2001b) Maternal cytokine levels during pregnancy and adult psychosis. Brain, Behavior, and Immunity, 15, 411-420.

Cannon T. D., Rosso I. M., Hollister J. M., Bearden C. E., Sanchez L. E. , and Hadley T. (2000). A prospective cohort study of genetic and perinatal influences in the etiology of schizophrenia. Schizophrenia Bulletin, 26, 351-366.

Cannon, T. D., vanErp, T. G. M., Rosso, I. M., Huttunen, M., Lonnqvist, J., Pirkola, T., Salonen, O., Valanne, L., Poutanen, V-P., and Standertskjold-Nordenstam, C-G. (2002). Fetal hypoxia and structural brain abnormalities in schizophrenic patients, their siblings and controls. Archives of General Psychiatry, 59, 35-41.

Csernansky, J. G., & Grace, A. A. (1998). New models of the pathophysiology of schizophrenia: Editors’ introduction. Schizophrenia Bulletin, 24(2), 185–187.

Dalman C., Thomas H. V., David A. S., Gentz J,, Lewis G., and Allebeck, P. (2001). Signs of asphyxia at birth and risk of schizophrenia. Population-based case-control study. British Journal of Psychiatry, 179, 403-408.

De Sousa, A. (2007). Types and contents of hallucinations in schizophrenia. Journal of Pakistan Psychiatric Society, 4(1), 29.

Farruggia, S., Babcock, D.S., 1981. The cavum septi pellucidi: its appearance and Incidence with cranial ultrasonography in infancy. Radiology, 139(1). 147-150.

Fenton, W. S., & McGlashan, T. H. (1994). Antecedents, symptom progression, and long-term outcome of the deficit syndrome in schizophrenia. American Journal of Psychiatry, 151, 351–356.

Galderisi, S., Quarantelli, M., Volper, U., Mucci, A., Cassano, G. B., Invernizzi, G., Maj, M. (2008). Patterns of structural MRI abnormalities in deficit and nondeficit schizophrenia. Schizophrenia Bulletin, 34, 393–401.

Gottesman, I. I., & Erlenmeyer-Kimling, L. (2001). Family and twin studies as a head start in defining prodomes and endophenotypes for hypothetical early interventions in schizophrenia. Schizophrenia Research, 5(1), 93–102; Riley, B. P., & Kendler, K. S. (2005). Schizophrenia: Genetics. In B. J. Sadock & V. A. Sadock (Eds.), Kaplan & Sadock’s comprehensive textbook of psychiatry (pp.1354–1370). Philadelphia, PA: Lippincott Williams & Wilkins.

Hooley, J. M., & Hiller, J. B. (1998). Expressed emotion and the pathogenesis of relapse in schizophrenia. In M. F. Lenzenweger & R. H. Dworkin (Eds.), Origins and development of schizophrenia: Advances in experimental psychopathology (pp. 447–468). Washington, DC: American Psychological Association.

Inayama, Y., Yoneda, H., Sakai, T., Ishida, T., Nonomura, Y., Kono, Y., Asaba, H. (1996). Positive association between a DNA sequence variant in the serotonin 2A receptor gene and schizophrenia. American Journal of Medical Genetics, 67(1), 103–105.

Janno, S., Holi, M., Tuisku, K., & Wahlbeck, K. (2004). Prevalence of neuroleptic-induced movement disorders in chronic schizophrenia patients. American Journal of Psychiatry, 161, 160–163.

Javitt, D. C., & Laruelle, M. (2006). Neurochemical theories. In J. A. Lieberman, T. S. Stroup, & D. O. Perkins (Eds.), Textbook of schizophrenia (pp. 85–116). Washington, DC: American Psychiatric Publishing.

Kirkpatrick, B., & Tek, C. (2005). Schizophrenia: Clinical features and psychological disorder concepts. In B. J. Sadock & S. V. Sadock (Eds.), Kaplan & Sadock’s comprehensive textbook of psychiatry (pp. 1416–1435). Philadelphia, PA: Lippincott Williams & Wilkins.

Kring, A. M. (1999). Emotion in schizophrenia: Old mystery, new understanding. Current Directions in Psychological Science, 8, 160–163.

Lindenmayer, J. P., & Khan, A. (2006). Psychological disorder. In J. A. Lieberman, T. S. Stroup, & D. O. Perkins (Eds.), Textbook of schizophrenia (pp. 187–222). Washington, DC: American Psychiatric Publishing.

Maher, B. A. (2001). Delusions. In P. B. Sutker & H. E. Adams (Eds.), Comprehensive handbook of psychological disorder (3rd ed., pp. 309–370). New York, NY: Kluwer Academic/Plenum.

Mueser, K. T., & McGurk, S. R. (2004). Schizophrenia. Lancet, 363(9426), 2063–2072.

Murray, R. M., & Bramon, E. (2005). Developmental model of schizophrenia. In B. J. Sadock & V. A. Sadock (Eds.), Kaplan & Sadock’s comprehensive textbook of psychiatry (pp. 1381–1395). Philadelphia, PA: Lippincott Williams & Wilkins.

National Institute of Mental Health. (2009, September 8). What are the symptoms of schizophrenia? Retrieved from http://www.nimh.nih.gov/health/publications/schizophrenia/what-are-the-symptoms-of-schizophrenia.shtml

National Institute of Mental Health. (2010, April 26). What is schizophrenia? Retrieved from http://www.nimh.nih.gov/health/topics/schizophrenia/index.shtml

Nicolson, R., Lenane, M., Hamburger, S. D., Fernandez, T., Bedwell, J., & Rapoport, J. L. (2000). Lessons from childhood-onset schizophrenia. Brain Research Review, 31(2–3), 147–156.

Nicolson, S. E., Mayberg, H. S., Pennell, P. B., & Nemeroff, C. B. (2006). Persistent auditory hallucinations that are unresponsive to antipsychotic drugs. The American Journal of Psychiatry, 163, 1153–1159. doi:10.1176/appi.ajp.163.7.1153

OpenStax College (2014, December 16), Perspectives on Psychological Disorders. OpenStax CNX. Retrieved from http://cnx.org/contents/7d74e56c-c750-4da5-a42c-50da0e5c5cb2@5.

Rosebush, P. I., & Mazurek, M. F. (2010). Catatonia and its treatment. Schizophrenia Bulletin, 36(2), 239–242. doi:10.1093/schbul/sbp141.

Schmidt-Kastner, R., van Os, J., Esquivel, G., Steinbusch, H. W. M., and Rutten, B.P.F., 2012. An environmental analysis of genes associated with schizophrenia: hypoxia and vascular factors as interacting elements in the neurodevelopmental model. Molecular Psychiatry, 17, 1194-1205.

Skrabalo, A. (2000). Negative symptoms in schizophrenia(s): The conceptual basis. Harvard Brain, 7, 7–10.

St Clair, D, Xu M, Wang P, Yu, Y., Fang, Y., Zhang, F., Zheng, Y, Gu, N, Feng, G, Sham, P, He, L. (2005). Rates of adult schizophrenia following prenatal exposure to the Chinese famine of 1959-1961. Journal of the American Medical Association, 294, 557-562. doi:10.1001/jama.294.5.557. Retrieved from: http://jama.jamanetwork.com/article.aspx?articleid=201329#ArticleInformation

Suddath, R. L., Christison, G. W., Torrey, E. F., Casanova, M. F., & Weinberger, D. R. (1990). Anatomical abnormalities in the brains of monozygotic twins discordant for schizophrenia. New England Journal of Medicine, 322(12), 789–794.

Susser, E. B., Neugebauer, R., Hock, H.W., Brown, A. S., Lin, S., Labowitz, D., & Gorman, J. M. (1996). Schizophrenia after prenatal famine: Further evidence. Archives of general psychiatry, 53, 25–31.

Tsankova N., Renthal W., Kumar A., and Nestler, E. J. (2007) Epigenetic regulation in psychiatric disorders. Nature Reviews: Neuroscience 8, 355–367.

Waddington J. L., Lane, A., Larkin, C., & O’Callaghan, E. (1999). The neurodevelopmental basis of schizophrenia: Clinical clues from cerebro-craniofacial dysmorphogenesis, and the roots of a lifetime trajectory of disease. Biological Psychiatry, 46(1), 31–9.

Walker, E., & Tessner, K. (2008). Schizophrenia. Perspectives on Psychological Science, 3(1), 30–37.

Walker, E., Mittal, V., & Tessner, K. (2008). Stress and the hypothalamic pituitary adrenal axis in the developmental course of schizophrenia. Annual Review of Clinical Psychology, 4, 189–216.

Winter, T. C., Kennedy, A. M., Byrne, J. and Woodward, P. J. (2010). The Cavum Septi Pellucidi: Why Is It Important? Journal of Ultrasound in Medicine, 29, 427-444. Retrieved November 3, 2015, from: http://www.jultrasoundmed.org/content/29/3/427.long

Xu, M-Q, Sun, W-S, Liu, B-X, Feng, G-Y, Yu, L., Yang, L. He, G., Sham, P. Susser, E., St.Clair, D., & He, L. (2009). Prenatal malnutrition and adult schizophrenia: Further evidence from the 1959-1961 Chinese famine. Schizophrenia Bulletin, 34, 568-576.

Zornberg G. L., Buka S. L., and Tsuang M. T. (2000) Hypoxic-ischemia-related fetal/neonatal complications and risk of schizophrenia and other nonaffective psychoses: A 19-year longitudinal study. American Journal of Psychiatry, 157, 196-202.

The content of this page is licensed under a Creative Commons Attribution Non-Commercial Share-Alike License except for any elements that may be licensed differently. The content of this page includes:

Introduction to Psychology (Links to an external site.) was created by Saylor Foundation under a Creative Commons Attribution Non-Commercial Share-Alike License
Original content contributed by Glenn E "Bert" Fox, Jr., PhD of Tidewater Community College.
Research assistance provided by Ylisha Morgan, of William and Mary College.

If you believe that a portion of this Open Course Framework infringes another's copyright, contact us.