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8 Schizophrenia Spectrum and Other Psychotic Disorders

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Chapter Objectives

After reading this chapter, you should be able to do the following:

• Describe and explain how schizophrenia is diagnosed.

• Describe and explain what causes schizophrenia.

• Describe and explain how schizophrenia is treated.

• Describe the other schizophrenia spectrum and psychotic disorders and differentiate them from schizophrenia.

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Schizophrenia is among the most catastrophic of all psychological disorders, with a lifetime prevalence ranging from about 0.3% to 0.7% (American Psychiatric Association [APA], 2013) and about 2.5 million cases in the United States alone (Lambert & Kinsley, 2005). This means that approximately 1 of every 100 people in the world suffers from schizophrenia during his or her lifetime (Lindenmayer & Khan, 2012; Long et al., 2014). One meta-analysis shows the worldwide lifetime prevalence at 0.48% (Simeone, Ward, Phillip, Collins, & Windish, 2015). According to the National Institute of Mental Health (2010), an estimated 24 million people worldwide are afflicted with the disorder. It typically strikes young adults, who may suffer for decades as schizophrenia wrecks their social relationships, impairs their thinking and health, and robs them of the ability to enjoy life. Schizophrenia also represents a massive drain on society’s resources. Many patients cannot work, many require public assistance, and most require expensive treatment (Wu et al., 2005). Faced with numerous difficulties, not only psy- chological and behavioral but also economic, many individuals with schizophrenia attempt suicide (at least 25% to 50% may attempt it, and about 4% to 13% may successfully complete it; Lee, Lee, Koo, & Park, 2015). These tragic deaths add to the guilt and pain already borne by the families of individuals with schizophrenia. However, with proper intervention, family involvement in treatment, better education (especially through mass media), and perhaps most important, early identification, many individuals with schizophrenia can lead meaning- ful lives.

Schizophrenia falls under the category of schizophrenia spectrum disorders. The other disor- ders in this category are discussed later in this chapter. The signs and symptoms of schizo- phrenia are not simply more extreme forms of everyday behavior, as with anxiety, depressive, or bipolar and related disorders. Some of the symptoms associated with schizophrenia are rarely, if ever, encountered in daily life. Still, it is important to remember that no matter how bizarre their behavior, people with schizophrenia are human beings who experience love, hurt, joy, grief, and all the other human emotions and feelings. To help us keep in mind the human side of the tragedy that is schizophrenia, this chapter refers frequently to the story of Jennifer Plowman. Let’s begin with Part 1 of her case study.

8.1 The Genesis of Schizophrenia We can all identify with people who are depressed or anxious. Most of us have been there ourselves, in the sense that at some time or another we have all experienced the “blues” or felt nervous and worried about events occurring in our daily lives. There is nothing baffling or impenetrable about depression, or anxiety, or even mania. Schizophrenia is different. Schizo- phrenia is not a personality disorder (these will be discussed in Chapter 9), and as discussed in Chapter 5, it is definitely not a dissociative disorder, such as dissociative identity disorder. People with schizophrenia behave in ways that most of us find incomprehensible. They may believe that other people can read their thoughts or that friends and neighbors are engaged in elaborate plots against them. In different historical periods, people who have displayed these behaviors have been given pejorative labels such as “mad,” “crazy,” “insane,” and “lunatic,” but such behaviors can be more accurately and appropriately categorized as symptoms of a group of disorders known as the psychoses, disorders characterized by gross distortions of reality.

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The Case of Jennifer Plowman: Part 1

Transcript of a Commitment Hearing for Jennifer Plowman COUNTY COURT

COURT TRANSCRIPT

Marion County

Presiding: Hon. Richard Harding

JUDGE: You are requesting that your daughter, Jennifer, be involuntarily committed to University Hospital? Are you represented by legal counsel?

ANNE PLOWMAN: No, Your Honor. I can’t afford a lawyer.

JUDGE: I can see that you receive public assistance.

ANNE PLOWMAN: I do not want my daughter to wait for public assistance. Jenny refuses to go to the hospital on her own, and she desperately needs help.

JUDGE: Why do you say this?

ANNE PLOWMAN: Jenny has not left the house for days. She has not washed or changed her clothes. She just sits in her room. Sometimes I hear her talking to herself. Other times I can hear her laughing and swearing. Jenny says that she cannot come out of her room because people can read her thoughts. Your Honor, she desperately needs help.

JUDGE: Has she threatened you or anyone else?

ANNE PLOWMAN: No.

JUDGE: Has she harmed herself ?

ANNE PLOWMAN: She won’t wash or change her clothes.

JUDGE: But has she tried to hurt herself, cut herself, or something similar?

ANNE PLOWMAN: No. She says that there is nothing wrong with her.

JUDGE: I do not want to deprive Jenny of her liberty unless there is some good reason. Jenny is a 21-year-old adult. If she is not dangerous to herself or anyone else, then she should choose for herself whether she needs treatment.

ANNE PLOWMAN: Please, Your Honor. I’m so worried. Isn’t there something you can do to help?

JUDGE: Perhaps we can talk her into going voluntarily into University Hospital. If not, I will commit her, but only for 72 hours so that she may be examined by Mental Health Services. Once I receive their report, I will decide how to proceed.*

*Note: The requirements for involuntary commitment vary from state to state. In general, they include the presence of a mental illness, dangerous behavior toward self or others, grave disability, and the need for treatment. A person can be involuntarily committed for 72 hours and must be released if there are no reason(s) to retain the individual.

See appendix for full case study.

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Emil Kraepelin (1856–1926) devised a classification system for psychotic conditions. After examining a group of hallucinating and delusional patients, he distinguished between two types of psychotic disorders. In the first type, serious mental symptoms began in adolescence or early adulthood and followed a deteriorating course. In the second type, symptoms fol- lowed a cyclical course in which periods of remission alternated with psychotic episodes. Kraepelin named the cyclic psychosis manic-depressive disorder. Kraepelin called the continu- ously deteriorating psychosis dementia praecox (translated from Latin, means “premature dementia”). Kraepelin believed that the deterioration he observed in dementia praecox was the result of a progressive organic brain syndrome that began early in life.

In contrast to Kraepelin, Swiss psychiatrist Eugen Bleuler (1857–1939) rejected the idea that the course of a disorder, alone, could ever distinguish one psychosis from another. Bleuler pre- ferred to classify psychological disorders on the basis of their characteristic signs and symp- toms, rather than on their course and outcome (Bleuler, 1911/1952). The DSM–5 adopted Bleuler’s approach.

Bleuler proposed that the name dementia praecox be replaced with schizophrenia, a term derived from the Greek words for “split” (schizo) and “mind” (phrene). It is important not to confuse Bleuler’s concept of schizophrenia with dissociative identity disorder (formerly called multiple person- ality disorder, as discussed in Chapter 5). Bleuler’s “split” was not among personali- ties but among cognitions within a single personality. In schizophrenia, thoughts become split (disconnected) from one another. People race from one idea to the next, often with no obvious connection. Bleuler believed that a “loosening of asso- ciative threads” among cognitions was the common link among a set of heterogeneous disorders that he loosely grouped together and called the “schizophrenias.”

Bleuler’s symptoms for schizophrenia included hallucinations (sensory experi- ences in the absence of external stimuli), delusions (unsubstantiated beliefs), odd motor movements, and bizarre behavior. For example, individuals with schizophre- nia might walk around in public wearing a lion’s pelt in the middle of summer and talk- ing to themselves, or they might sit in the middle of a busy street beating the ground

Vlue/iStock/Thinkstock The term schizophrenia derives from the Greek words for “split” (schizo) and “mind” (phrene) in order to demonstrate the disconnected, or split, thoughts that occur within the mind.

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with drumsticks. They might be combative or easily agitated. Bleuler always referred to “the schizophrenias” rather than simply to “schizophrenia.” He insisted on the plural because he believed that several different but related disorders were responsible for psychotic behav- ior. Although this chapter uses the more common singular term schizophrenia, Bleuler was undoubtedly correct; schizophrenia is far from a homogeneous diagnostic category.

Signs and Symptoms The DSM–5 diagnostic criteria for schizophrenia are relatively narrow (see Table 8.1). Yet, despite this narrowing, there is no single symptom or set of symptoms that describes all people with schizophrenia. The schizophrenic syndrome is heterogeneous (mixed or var- ied or different; homogeneous means “the same”) in the presentation of symptoms, course, response to treatment, and outcome. These differences among people may mean that Bleuler was correct: Schizophrenia is not a single disorder but a syndrome or series of disorders with different etiologies and outcomes (Cuesta & Peralta, 2016).

In addition to schizophrenia, the DSM–5 describes seven other psychotic disorders, each of which shares some characteristics with schizophrenia (see Table 8.2).

Table 8.1 Main DSM–5 diagnostic criteria for schizophrenia

A. Characteristic symptoms: two (or more) of the following, each present for a significant portion of time during a one-month period (or less if successfully treated). At least one of these must be (1), (2), or (3): 1. Delusions 2. Hallucinations 3. Disorganized speech (frequent derailment or incoherence) 4. Grossly disorganized or catatonic behavior 5. Negative symptoms (diminished emotional expression or avolition)

B. For a significant portion of the time since the onset of the disturbance, level of functioning in one or more major areas, such as work, interpersonal relations, or self-care are markedly below the level achieved prior to the onset (or when the onset is in childhood or adolescence, failure to achieve expected level of interpersonal, academic, or occupational functioning).

C. Continuous signs of the disturbance persist for at least six months. This six-month period must include at least one month of symptoms (or less if successfully treated) that meet criterion A (active-phase symptoms) and may include periods of prodromal or residual symptoms. During these prodromal or residual periods, the signs of the disturbance may be manifested by only negative symptoms or two or more symptoms listed in criterion A present in an attenuated form (for example, odd beliefs or unusual perceptual experiences).

D. Schizoaffective disorder and depressive or bipolar disorder with psychotic features have been ruled out because either (1) no major depressive or manic episodes have occurred concurrently with the active- phase symptoms; or (2) if mood episodes have occurred during active-phase symptoms, they have been present for a minority of the total duration of the active and residual periods.

E. The disturbance is not due to the direct physiological effects of a substance (for example, a drug of abuse or a medication) or another medical condition.

F. If there is a history of autism spectrum disorder or a communication disorder of childhood onset [see Chapter 11], the additional diagnosis of schizophrenia is made only if prominent delusions or hallucinations, in addition to the other required symptoms of schizophrenia, are also present for at least a month (or less if successfully treated).

Source: APA (2013, p. 99).

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At first glance, it might appear to the untrained eye that all schizophrenia spectrum and other psychotic disorders are similar, if not almost identical. After all, most, if not all, include hal- lucinations and delusions among their diagnostic criteria. However, this is not the case. The accompanying Highlight briefly examines two disorders that appear similar to schizophrenia but are not.

Although the DSM–5 contains diagnostic criteria for each of the schizophrenia spectrum and other psychotic disorders, researchers have tended to neglect the other disorders in favor of schizophrenia. For this reason, this chapter focuses on schizophrenia, although the other disorders are mentioned when appropriate.

Positive Versus Negative Symptoms Schizophrenic symptoms are divided into two main categories: positive and negative. In this context, positive and negative do not mean good or bad. Instead they mean the presence (posi- tive) or absence (negative) of something. Positive symptoms reflect an excess or distortion of normal cognitive and emotional functions; negative symptoms reflect a reduction or loss of normal functions. The most common positive symptoms are delusions, hallucinations, dis- organized speech and thinking, inappropriate affect, and bizarre motor movements. The neg- ative symptoms are loss of initiative, lack of emotional expression, and impoverished speech.

Although the distinction between positive and negative symptoms may have some practical value in predicting who will respond to treatment, it is a rather crude dichotomy (Velligan et al., 1997). Positive symptoms can occur in people who have major depressive disorder,

Table 8.2 Main DSM–5 psychotic disorders

Schizophrenia: A psychotic disturbance lasting more than six months that includes one or more of the following: delusions, hallucinations, disorganized speech, or odd movements.

Schizophreniform disorder: A disorder with symptoms similar to schizophrenia but with a shorter duration (between one and six months).

Schizoaffective disorder: A combination of a mood disorder and symptoms similar to those found in schizophrenia.

Delusional disorder: A disorder characterized by at least one month of delusions that are not bizarre in character and with none of the other symptoms of schizophrenia.

Brief psychotic disorder: A disturbance in which psychotic symptoms last for less than one month.

Psychotic disorder due to another medical condition: A disturbance in which psychotic symptoms develop directly from a medical condition, such as a seizure disorder (epilepsy), migraine headaches, or multiple sclerosis.

Substance/medication-induced psychotic disorder: A disorder in which psychotic symptoms are the result of substance abuse or exposure to a toxin.

Catatonia: A disorder in which the individual displays at least three symptoms including stupor (no psychomotor activity), waxy flexibility (slight resistance to a professional’s attempt to change the individual’s body position), and mutism (no or very little verbal response).

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bipolar I disorder, delusional disorder, and schizoaffective disorder, among other conditions. In schizophrenia, positive symptoms do not seem to be closely related to one another. Some people with schizophrenia have only one positive symptom; others have many. Similarly, neg- ative symptoms are not specific to schizophrenia (they are also found in depressive, and bipo- lar and related disorders). Approximately 60% of individuals with schizophrenia exhibit pos- itive symptoms such as hallucinations and delusions (Lindenmayer & Kahn, 2006), whereas approximately 41% display at least two negative symptoms (Patel et al., 2015).

Delusions Delusions are odd or unusual ways of thinking that lie outside the realm of reality or do not have rational explanations. To be considered a potential symptom of schizophrenia, a delu- sion must be contrary to a person’s background and must not be held by members of the person’s cultural or ethnic group. For example, members of a cult who believe that the world will come to an end on a certain date are probably not showing signs of schizophrenia. By

Highlight: Differentiating Among Schizophrenia and Schizoaffective and Delusional Disorders

In schizoaffective disorder the individual must have a major mood episode (this means a major depressive or manic episode) along with criterion A of schizophrenia (delusions, hallucinations, disorganized speech, negative symptoms, and/or grossly disorganized or catatonic behavior; see Table 8.1). In addition, the delusions or hallucinations must be present for at least two weeks while a depressive or manic episode is not present. Third, the manic or depressive episode must be present for most of the total length of the active portion of the mental illness (APA, 2013). In other words, the individual must have symptoms of schizophrenia as well as a major mood episode during the illness, unlike schizophrenia, where a major mood episode has not occurred with the active-phase symptoms. In addition, schizoaffective disorder is rather rare, affecting 0.3% of the population, making it a third as likely to occur as schizophrenia (APA, 2013). Although it is difficult to differentiate schizoaffective disorder from schizophrenia, one need only assess if the criteria are being met for a manic or a major depressive episode during the majority of the active phase of the illness. If so, then one is most likely seeing schizoaffective disorder.

Delusional disorder differs from schizophrenia in one key aspect: Criterion A for schizophrenia has never been met. If hallucinations are present, they are not a prominent feature and are related to the delusion’s theme (for example, an individual who constantly hears voices saying that his or her every move is being closely watched and recorded in association with the delusion of persecution). In addition, the individual’s functioning is not very bizarre or odd. Also, if the individual has manic or major depressive episodes, they are brief. Delusional disorder is less common than schizophrenia and is a bit rarer than schizoaffective disorder, occurring in about 0.2% of the population.

Perhaps the most important differentiation among these three disorders is that schizophrenia is the most debilitating of the three disorders, oftentimes defying treatment progress or success. Individuals with schizophrenia often end up among the nation’s homeless population.

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contrast, educated middle-class Americans who believe that mice are scientifically advanced aliens who were sent to colonize the Earth and destroy humanity most probably are.

According to her mother, Jennifer Plowman believed that “people” could “read her mind.” This belief was explored by Dr. Stuart Berg, the psychologist who evaluated Jennifer on her second day in the hospital. Part of their discussion appears here.

The Case of Jennifer Plowman: Part 3

Transcript From an Interview Between Dr. Berg and Jennifer Plowman DR. BERG: Jenny, your mother says that you refused to leave your house. How come?

JENNIFER: Come, lum, rum is a drink that sailors like.

DR. BERG: But, why did you refuse to go outside?

JENNIFER: I am fine. Why do I need to be here? The walls protected me at home.

DR. BERG: From what?

JENNIFER: Selegonite cannot get out of lead. There is lead in the bed and the walls and halls. Outside, they can get through.

DR. BERG: Who can get through?

JENNIFER: They can hear my thoughts. Without the lead, they leak out, and they can hear them. I can hear them laughing. They find out what I am thinking, and they laugh at their success.

DR. BERG: You believe that lead in the walls of your house keeps people from reading your mind. While you are outside of the house, without the lead to protect you, people will read your thoughts and laugh when they manage to get what they want.

JENNIFER: Yes. Like Superman. I know the secret because I am a rocket scientist. I have flown to space. I can develop new rockets that run on special minerals. I am too smart for this place. I should be at home.

Additional Transcript of Jennifer Plowman’s “Background Chatter” at Her Intake Interview Men need sex. I have had sex 10,000 times. That window is in the room because you want patients to know the color of the world. I know the president. He lives in town. I didn’t like his movie. He just wants to win the Academy Award. His movie is my life. I made a movie once. It had lots of stars. The cameraman was my friend. The sound technician was excellent. Where are the mics and cameras hidden? Is this logomouth here to get me nervous? My father died last year, leer, jeer, tears on my pillow, pain in my heart over you, what can I do? There is nothing wrong with me, you know. I don’t know why I am here. I’m fine.

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Although Jennifer’s delusions are relatively vague and incoherent, this is not always the case (Maher & Spitzer, 1993). For some individuals with schizophrenia, delusions can be system- atic, be elaborate, and have a common premise. Persecutory delusions (also called paranoid delusions) are beliefs held by people who insist that someone is out to get them. Thought insertion delusions (sometimes called delusions of influence) are a category of delusion in which people believe thoughts are being inserted into their heads. Grandiose delusions, when people believe they have some extraordinary talent or power, are also relatively com- mon. For example, they may think they can control the weather or the stock market, or that they are Christ or Bill Gates.

In Capgras syndrome, people believe that someone they know has been replaced by a dou- ble (Moschopoulos, Kaprinis, & Nimatoudis, 2016), and in Cotard syndrome, the individual believes he or she is dead (Cannas et al., 2017). Both of these kinds of delusions are very rare. Incorrect but plausible delusions (for example, “my assistant is plotting to get my job”) may also be seen in individuals with schizophrenia, but bizarre delusions have greater diagnostic value. The problem with plausible delusions is that they may not be delusions at all. After all, even delusional people can have enemies.

Interestingly, most people with schizophrenia find it difficult to believe that others consider their ideas hard to believe and perhaps even outlandish. They cling to their beliefs even in the face of compelling negative evidence.

Delusions vary in the extent to which they disrupt everyday functioning. Some individuals with schizophrenia are totally preoccupied with their odd beliefs, whereas others are only minimally impaired. In fact, you may never even know that some people have delusions because they are perfectly rational and can get along well except when someone brings up the subject of their delusion. For example, one person might believe that she is a religious demi- god, or perhaps Batwoman, who will save her city from being overrun with crime. Another might believe that he is a famous artist and paint, and display his works on the sidewalk for all to enjoy, even though to a trained eye they are just scrawls on canvas. Something to consider: Do these kinds of delusions pose a danger to the individual or to others? Keep this question in mind as we continue the discussion.

Hallucinations We all have sensory illusions. If you’re alone in your house at night, you may think you hear a burglar when there is no one around. Walking across campus, you think you hear your name being called, and yet there is no one there. These experiences do not mean that you have schizophrenia. It is only your imagination “playing tricks.” In contrast, people who have schizophrenia consider such sensory illusions quite real.

Hallucinations are perceptions that occur without any external stimuli. Auditory hal- lucinations, such as hearing external voices,

Thomas J Peterson/Exactostock-1672/SuperStock Some individuals with schizophrenia believe that people can read their minds, or insert thoughts into their heads, common delusions. To guard against this, they may cover their head with tin foil.

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are the most common type, occurring in as many as 70% to 80% of individuals with schizo- phrenia (Chhabra et al., 2016; Gram-Henriksen, Raballo, & Pamas, 2015). Different cultures tend to produce different hallucinations: Visual, olfactory (particularly rotten odors), and tactile (touch) hallucinations (such as the feeling that bugs are crawling under one’s skin) are associated with schizophrenia in the United States (Bauer et al., 2011; Larøi et al., 2014). Another example of a culture-specific hallucination involves an Amazonian people called the Bororo. In this culture, the novice shaman is identified when he has a dream of soaring high above the earth, like a vulture, and seeing the fiery cloud of smoke that indicates an attacking illness (Larøi et al., 2014). To the person with active schizophrenia, these voices, odors, and sounds are not imaginary; they are real.

Imaging techniques have given researchers insight into what is going on in the brains of people when they hallucinate. One study found that the part of the brain most active during schizo- phrenic auditory hallucinations is the area responsible for speech production, not the brain area responsible for speech comprehension (Donata-Wolf et al., 2011). This finding suggests that when people with schizophrenia hallucinate, they are not “hearing” voices in their brain but instead are reporting their own thoughts. In effect, they are listening to their own voices and thoughts and cannot differentiate these from someone else talking to them (Chhabra et al., 2016).

Disorganized Speech As you can see from the earlier interview excerpts, Jennifer Plowman’s speech was distinctly odd. She made up words, such as selegonite (these are known as neologisms). She also jumped from one topic to the next, a phenomenon known as thought derail- ment. Jennifer also linked words together according to their sound, as in “come, lum, rum.” These sound- based sequences are known as clang associations. Like Jennifer, people with schizophrenia often give irrelevant responses to questions, a phenomenon known as tangentiality. When the disorganization becomes extreme, the result is word salad, a mass of disconnected words (for example, “I saw a rat earlier yet it really smells in here yabba glick morch blargh”). In contrast to Jennifer, many people with schizophrenia speak very little; others are exces- sively literal or concrete.

The incoherent speech produced by Jennifer, and other people with schizophrenia, is often taken as a sign of an underlying “thought disorder” (Wens- ing et al., 2017). However, disorganized speech is not found in all people with schizophrenia, nor is it unique to schizophrenia. It may also be present dur- ing the manic phase of bipolar I disorder, although the disorganized speech and communication typi- cally is much more severe and common in schizo- phrenia (Wensing et al., 2017; Yalincetin et al., 2017).

Remik44992/iStock/Thinkstock Schizophrenia patients may create their own words, called neologisms, and jump from one topic to the next, a phenomenon classified as thought derailment. Disorganized speech is also linked to the manic phase of bipolar disorder, but it is more severe in schizophrenia patients.

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For an example of Jennifer’s odd speech, look at Part 3 of Jennifer’s case study, in the section on delusions. It contains a transcript of what Dr. Kahn called Jennifer Plowman’s “background chatter,” recorded during Jennifer’s intake interview. The excerpt illustrates what Bleuler meant by a breakdown in associations. Note how Jennifer jumps from one idea to the next and how the word year produces the clang associations leer, jeer, and tear, which then conjures up an old song lyric.

Inappropriate and Flat Affect Many people with schizophrenia display what is called inappropriate affect: Emo- tions that are inappropriate or not properly fit to the current situation, such as laughing when one is very nervous (see, for instance, Gard et al., 2011). For example, if they are told, in a worst-case scenario, that their entire family was murdered in a grotesque way, they would smile or perhaps laugh. Similarly, if they were told they won a huge amount in Powerball they might cry, not tears of happiness but sadness (to know for certain what the tears meant, you would have to ask the person). They also might exhibit inappropriate mood shifts during a short timeframe. These shifts should not be confused with bipolar I or II disorder, as the mood changes are rapid and do not involve a shift from mania to depression.

Flat affect refers to having a blank facial expression that is devoid of emotion. Flat affect is also reflected in a monotonous speaking voice with few inflections. People with schizo- phrenia lose pleasure in previously enjoyable activities (anhedonia, a symptom also found in depression).

There is evidence that affective symptoms are associated with a poorer prognosis and are more common in men (Gur et al., 2006). In one interesting yet dated study, home movies of children who develop schizophrenia later in life show that they displayed fewer positive emo- tions than their siblings years before the appearance of their schizophrenia (Walker, Grimes, Davis, & Smith, 1993).

Disorganized or Catatonic Behavior (Catatonia) Left alone, some people with schizophrenia may not move a muscle for hours. At such times, they seem indifferent to events going on around them. This condition is known as cata- tonic stupor. Catatonic stupor may be accompanied by waxy flexibility, in which people with schizophrenia place or allow their limbs to be placed in uncomfortable positions (sitting with their hands on their heads, for example). They seem able to maintain these uncomfortable positions for long periods without apparent distress. Schizophrenia can also produce aimless,

Purestock/Thinkstock People with schizophrenia may spend most of their time alone and withdrawn from social activities.

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repetitive activity, such as pacing the floor or rocking back and forth in a chair (catatonic frenzy). These repetitive movements may be accompanied by odd mannerisms, such as facial grimaces. Catatonic behavior (catatonia) can also be displayed in bipolar disorder (especially bipolar I) as well as in depressive disorders, especially major depressive disorder. As we will see, catatonic schizophrenia used to be considered a subtype of schizophrenia. These sub- types were eliminated in the DSM–5.

The range of schizophrenic behavior is fairly wide: Patients may imitate other people’s move- ments, act like robots, or refuse to cooperate with even simple requests (negativism). Many people with schizophrenia neglect their personal hygiene, and some behave in socially unac- ceptable ways (shouting obscenities, for instance). Note that Tourette’s disorder will also pro- duce this phenomenon, yet Tourette’s begins in childhood and does not involve hallucinations and delusions.

Social Withdrawal and Lethargy Most people with schizophrenia spend their time alone, withdrawn from normal social activities. This further distances them from reality and seems to lead to or increase deficits in interpersonal skills (Ten- hula & Bellack, 2008). Indecisiveness, ambivalence, and apathy are among the most debilitating negative symptoms of schizophrenia because, put together, they rob people of the energy they need to keep up with the activities of everyday life.

Phases of Schizophrenia Individuals with schizophrenia typically go through several phases in the course of the disorder. Progress through the phases can vary widely from person to person.

Prodromal Phase The prodromal phase precedes the disorder and is marked by deterioration from some higher level of functioning. Friends and relatives almost always notice personality changes—flattened affect, social withdrawal, and other negative symptoms—well before any positive symptoms appear.

Mary Evans Picture Library/Everett Collection A 19th century depiction of someone demonstrating catatonia.

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Active Phase In contrast to those in the prodromal phase, patients in the active phase do not seem to be aware that they are behaving strangely. They deny that their peculiar ideas are delusional or that their sensory experiences may only be hallucinations. Because they are shunned by oth- ers, and partly for self-protection, most schizophrenic people withdraw into their own lonely and isolated worlds. The active phase can persist for weeks, months, or even years.

Residual Phase In most cases, active symptoms eventually respond to treatment. However, a minority of patients never get beyond the active phase. Their course is said to be “continuous.” Usually, negative symptoms and mild levels of positive symptoms persist in the residual phase. When negative symptoms alternate with active-phase positive symptoms, the course of the disorder is said to be “episodic.” In single episodes, the active phase is followed by a period in which there are either no symptoms or only negative ones.

Additional Symptoms and Signs In addition to the characteristic symptoms listed in criterion A, the DSM–5 includes several other important diagnostic criteria (see Table 8.1). First, the symptoms must affect the per- son’s work or social life, or, in the case of a child or adolescent, the symptoms must cause a failure to achieve the age-expected level of interpersonal, academic, or occupational function- ing. Second, the symptoms must persist for at least six months, including prodromal, active, and residual. In the prodromal and residual phases, only negative symptoms, or two or more symptoms in criterion A, may appear in a less severe form. The main effect of the six-month diagnostic criterion is to restrict schizophrenia to chronic cases, as in Kraepelin’s original formulation.

Kraepelin proposed three subtypes of schizophrenia, all of which were in use until publica- tion of the DSM–5. These subtypes are catatonic, paranoid, and disorganized (formerly known as hebephrenic, which means silly and immature emotionality). These subtypes were elimi- nated due to their limited diagnostic stability, low reliability, and poor validity (APA, 2013). Instead, an eight-item severity specifier is used, as measured by a psychosis rating scale (a checklist) completed by the clinician. The DSM–5 notes that the specifier’s use is optional (APA, 2013). In sum, schizophrenia is now considered a spectrum disorder, meaning that its severity can range from not present to present and severe, depending on the symptoms dis- played and their duration.

The DSM–5 also requires that schizoaffective disorder and depressive or bipolar disorder with psychotic features be ruled out before a person can be diagnosed as having schizo- phrenia. When a major depressive episode or manic episode is present with schizophrenic symptoms for a major portion of the active and residual phases, then the correct diagnosis is schizoaffective disorder, not schizophrenia. Finally, the DSM–5 criteria require that schizo- phrenia be kept separate from autism spectrum disorder or a communication disorder of childhood onset. Oftentimes people confuse schizophrenia with autism spectrum disorder. There are two critical differences: Autism spectrum disorder onsets in childhood, and people with autism spectrum disorder do not have hallucinations or delusions.

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8.2 Prevalence and Course of Schizophrenia

Incidence As explained in Chapter 5, the incidence of a dis- order is technically defined as the number of new cases that appear during a given period of time. Most incidence estimates are obtained by counting the number of new cases seen at treatment facilities (usually mental hospitals, but also doctors’ offices and counseling centers) over the period of a year. This approach assumes that all cases are seen at these treatment centers and that the clinicians who work in them are perfectly accurate diagnosti- cians. However, neither assumption is likely to be true. Hospitalization is less common today than in the past, and many people with schizophrenia live among the homeless and never come into contact with a mental health facility. In developing coun- tries and in the poorer parts of industrialized coun- tries, many people with schizophrenia lack access to treatment services. For those who do get to treat- ment, there is no guarantee that they will be diag- nosed accurately.

Using the standard DSM and International Statis- tical Classification of Diseases and Related Health Problems (ICD) criteria for schizophrenia, incidence rates are remarkably similar around the world. A review of 50 epidemiological studies (Warner & de Girolamo, 1995) conducted in both developing and developed countries, with many different age groups and clinicians, found the incidence of schizophrenia to be between 0.21 and 0.24 new cases per 1,000 people per year (Comer, 2007).

Age of Onset The typical age of onset for the psychotic symptoms of schizophrenia (hallucinations, delu- sions, and negative symptoms) is between the late teenage years and mid-30s. As the DSM–5 notes, onset prior to adolescence is rare (APA, 2013). One study noted that the average age of onset for schizophrenia is between 15 and 25 for men and between 15 and 30 for women, with negative symptoms making their appearance around four years before the first hospi- tal admission (Eranti, MacCabe, Bundy, & Murray, 2013; Huang et al., 2017; Lewine, 1991). According to the APA (2013), the first psychotic episode appears in men in their early to mid-20s, and in women in their late 20s. By the age of 60, the cumulative incidence for men and women is equal, and almost no new cases of schizophrenia are identified after age 60

Mrk movie/Marka/SuperStock The film A Beautiful Mind (2001) was based on the life of John Nash and showcased not only Nash’s mathematic genius but also his struggle with paranoid schizophrenia.

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(Gottesman, 1991). Thus, although men show signs of schizophrenia earlier in life, women eventually catch up. The finding of an earlier onset for men, which was first noted by Kraepelin, has been con- firmed many times (APA, 2013; Howard, Castle, Wessely, & Murray, 1993; Reicher, Maurer, Loffler, & Fatkenheuer, 1991). A more recent study found that the sex difference in the age of onset is negligible or perhaps even absent in developing countries, when certain known risk factors are taken into consid- eration (such as birth complications and family his- tory; van der Werf et al., 2013). The earlier onset for males does not seem to be related to diagnostic pro- cedures, nationality, occupational status, or help- seeking differences between the sexes (Warner & de Girolamo, 1995). Instead, the striking cross-cul- tural similarity of the sex difference in age of onset points toward a biological explanation (Eranti et al., 2013). It has been suggested, for example, that the female hormone estrogen may reduce vulnerability to schizophrenia (Huang et al., 2017; Kulkarni et al., 2015; van der Werf et al., 2013) and has potential use for treatment (Kulkarni et al., 2015).

Prognosis We now know that Bleuler was correct—some patients do recover, perhaps as many as 25% or more (Roe & Davidson, 2008), and even severely affected patients may improve (Breier, Schreiber, Dyer, & Pickar, 1991; Hegarty, Baldessarini, Tohen, Waternaux, & Oepen, 1994). The best predictors of outcome are the level of premorbid functioning and the severity of symptoms in the active phase (Diaz-Caneja et al., 2015). Given two people with good pre- morbid functioning, the one whose symptoms are predominantly negative is likely to have a poorer outcome than the one with mainly positive symptoms (Diaz-Caneja et al., 2015).

Although the prognosis for those with schizophrenia is less pessimistic than Kraepelin thought, it is still not very good. Many will relapse more than once and will have remaining or irregular symptoms for the rest of their lives (Emsley, Chiliza, Asmal, & Harvey, 2013). The relapse rate is worst for those whose first episode occurred at a young age, probably because they never had the opportunity to develop adequate coping skills (Gomez-Revuelta et al., 2017). Life expectancy is also lower among people with schizophrenia. This is partly the result of a high rate of suicide (Kredentser, Martens, Chochinov, & Prior, 2014) and partly from deaths aris- ing from cold weather exposure among the schizophrenic homeless. In addition, individuals with schizophrenia may be at increased risk for cardiovascular disease, respiratory disorders, diabetes, tuberculosis, and other infectious diseases (Kredenster et al., 2014). On the other hand, one earlier, rather dated study revealed that 60% of those with schizophrenia who do manage to survive into middle and old age have a good chance of a reasonable quality of life free of active symptoms (Torrey, 2001).

BananaStock/BananaStock/Thinkstock Many people with schizophrenia may not have access to a mental health facility and live among the homeless.

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Cultural Considerations The cultures of developing countries may be more accepting of different or deviating behav- ior than those of developed countries. For this reason, observers in developing countries (for example, Tunisia) may rate the same schizophrenic behavior as more tolerable than observ- ers in developed countries, such as Germany (Angermeyer et al., 2015). Overall, outcomes are better in developing countries than in the developed world, perhaps because of the greater tolerance of psychotic behavior in developing areas (Hopper, Harrison, Janca, & Sartorius, 2007). Vahia and Vahia (2008) found that, according to World Health Organization data, 25 million individuals with schizophrenia who live in developing countries (India and Nige- ria, for example), have better recovery rates than those who live in Western and other devel- oped countries, such as Germany. The hypothesis here, again, is that in developing countries the environments tend to be more supportive and therapeutic than in, say, the United States. More family may be available via extended family, less critical judgments might occur, and family may be more willing, and more available, to help out. For example, the Nigerian culture, according to Matsumoto and Juang (2008), tends to be more accepting of hearing voices than are Western cultures.

8.3 Etiology of Schizophrenia: Genetics One possible reason why the prevalence of schizophrenia is so similar from one country to the next is that it is an inherited condition. Franz Kallman (1938) examined the family mem- bers of more than 1,000 people with schizophrenia, all of whom were patients in a Berlin psy- chiatric hospital. He found that the more severe a person’s disorder, the more likely it was that a member of the person’s family would also show signs of a mental disorder. Decades later, a Danish study reported on a 30-year follow-up of 207 high-risk children, whose mothers were schizophrenic, and 104 low-risk children, whose family members showed no signs of mental illness (Mednick & Schulsinger, 1968). Thirty-one members of the high-risk group developed schizophrenia, whereas only two members of the low-risk group developed it. Over the years, there have been numerous investigations into the genetics of schizophrenia. The vast major- ity of these studies have confirmed the connection between genetics and schizophrenia. (To read more about Jennifer Plowman’s family background and to see if schizophrenia runs in her family, see Part 4 of her case in the appendix.)

Twin Studies Twin studies are one way to try to separate the effects of heredity from those produced by the environment. Specifically, if environmental factors determine who develops schizophrenia, we would expect the rate of concordance for schizophrenia between monozygotic (identi- cal) twins who are reared together to be similar to that for dizygotic (fraternal) twins reared together (monozygotic twins have the same genes, whereas dizygotic twins share only about 50% of their genes). By contrast, if genetics play a larger role, we should expect to find a higher concordance rate among monozygotic twins (who share both their genes and their environments) than among dizygotic twins.

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Twin studies have produced mixed results. Still, the majority of studies have found that mono- zygotic twins have much higher concordance rates for schizophrenia than do dizygotic twins (about a 33% chance for monozygotic twins versus about a 7% chance for dizygotic twins; Hilker et al., 2017). This suggests that genetics is a more important determinant of schizo- phrenia than is the environment. However, it is always possible that schizophrenia may be present in some form from birth (congenital) without being genetic. For example, the antipsy- chotic medications given to pregnant women with schizophrenia may produce an abnormal intrauterine environment, which may affect the brain development of their children. It is pos- sible that such children may be predisposed to develop schizophrenia in response to stress. Alternatively, a virus during pregnancy could affect neurological development and make chil- dren susceptible to schizophrenia (Lambert & Kinsley, 2005; Torrey, 2001). Both of these con- genital causes would produce a higher concordance among twins than among other siblings because twins are exposed to the same intrauterine environment (Davis & Phelps, 1995).

To separate congenital from genetic causes of schizophrenia, Gottesman and Bertelsen (1989) studied the children of monozygotic twins where only one twin had schizophrenia. They found that the probability of finding schizophrenia in the next generation is 17%. It did not matter whether it was a parent who had schizophrenia or a parent’s identical sibling (an aunt or uncle). In both cases, the probability of a child’s developing schizophrenia was the same, 17% (see Figure 8.1). This is a striking finding. Children of parents without schizophre- nia whose aunts or uncles had schizophrenia have the same probability of developing schizo- phrenia as their cousins, whose parents actually had schizophrenia. This study suggests that genetics rather than events during pregnancy are responsible. The identical twin aunts and uncles who did not have schizophrenia seem to be “carriers” who pass on the condition to their children.

If schizophrenia were entirely a function of heredity, we would expect to find a concordance of 100% among identical twins because they share all of their genes. Yet, despite the wide- spread evidence for the inheritance of schizophrenia, no study has produced a concordance rate of 100% among monozygotic twins. Therefore, it seems obvious that factors other than genetics must be involved. Perhaps being raised by a mentally ill parent or alongside a sibling with schizophrenia determines who among those with “schizophrenic genes” will develop the disorder and what form it will take. In other words, if a child’s biological mother had schizophrenia and the child’s adoptive family was dysfunctional, the child would be more likely to “contract” schizophrenia (Tienari, Wahlberg, & Wynne, 2006; the quotes are ours). This hypothesis is consistent with the results of a case study of one set of quadruplets, the Genain sisters. All four developed schizophrenia between the ages of 22 and 24. This seems compelling evidence for the genetic transmission of schizophrenia. Yet there were differ- ences among the girls. Even though they shared 100% of their genes, each sister had a differ- ent course, symptoms, and outcome (Rosenthal, 1963). For example, two of the four sisters were floridly psychotic, showing severe symptoms, whereas the other two were much better adjusted. One of the four sisters eventually married and had children, two had fluctuating good periods and bad periods during which they had to be hospitalized, and the fourth sister spent her life in the hospital. These differences suggest that differences in the sisters’ respec- tive environments influenced the way they expressed their genetically identical disposition toward schizophrenia, even though their environments were quite similar.

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Adoption Studies Heston (1966) found that the risk of schizophrenia among the offspring of mothers with schizophrenia who were adopted early in life was 16.6%. This figure is not much different from the average morbid risk for children raised by their own mothers diagnosed with schizo- phrenia (Gottesman, 1991). In other words, being raised by a mother with schizophrenia does not increase the risk of developing schizophrenia. Over the years, other adoption studies have confirmed that the children of mothers with schizophrenia tend to resemble their biological mothers in terms of behaviors and traits more than their adoptive ones (Tienari et al., 2006).

One possible confounding variable in this research is the effect of adoption itself. Perhaps being adopted predisposes a person to develop schizophrenia. The implication is that being

Percentage

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Parents

0 5 10 15 20 25 30 35 40 45 50

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Dizygotic twins

Siblings with 1 schizophrenic parent

Offspring of 2 schizophrenic parents

Monozygotic twins

Figure 8.1: Risk of developing schizophrenia for relatives of people with schizophrenia

Source: Adapted from Gottesman and Shields (1972), as appearing in S. Schwartz, Abnormal Psychology: A Discovery Approach. Mountain View, CA: Mayfield Publishing Company, 2000, Figure 9.1, p. 389.

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Section 8.3 Etiology of Schizophrenia: Genetics

raised by a parent with schizophrenia does not increase the probability of developing the dis- order. Further support for this idea comes from the finding that identical twins who are raised apart have the same concordance rates for schizophrenia as do those who are raised together by their natural parents (Gottesman, 1991).

Markers Underlying genotypes (the specific genetic makeup of an individual) are often reflected in phenotypic traits (behaviors or observable characteristics of an individual) known as mark- ers. These markers are present not only in people with schizophrenia but also in their rela- tives. Prospective studies, in which people with the supposed markers are followed longitudi- nally to see if they develop schizophrenia, can help researchers pinpoint the specific genetic causes of schizophrenia. Two potential cognitive markers for schizophrenia are attentional dysfunction and eye-tracking abnormalities.

Attentional Dysfunction Kraepelin (1919) viewed distractibility as one of the most common features of dementia praecox. Because attentional deficits not only run in fami- lies but also appear before any schizophrenic-like symptoms, they may reflect a genetic vulnerability to schizophrenia. For example, an inability to focus attention impairs a person’s ability to perceive affect (Combs & Gouvier, 2004) and engage in appropri- ate social functioning. However, because most of the family members who exhibit attentional deficits will never show any schizophrenic symptoms, sen- sory deficits alone are clearly not sufficient to cause schizophrenia; other factors must also be involved.

Eye Movement (Tracking) Dysfunction In his clinical descriptions, Kraepelin noted that people with dementia praecox had difficulty track- ing a moving stimulus, such as a pendulum. Instead of smooth eye movements from side to side, Krae- pelin’s patients had frequent, jerky eye movements. Kraepelin’s observations have been repeated many times over the decades. On each occasion, patients with schizophrenia were found to have eye-tracking abnormalities, whereas only a small number of peo- ple without schizophrenia displayed any eye-track- ing problem (Demler et al., 2016). These abnormali- ties in eye movement are also apparent in people at risk of developing schizophrenia (Demily et al., 2016). Specifically, about 35% of the relatives of people with schizophrenia have similar abnormalities (Lenzenweger, McLachlan, & Rubin,

Zoonar RF/Zoonar/Thinkstock Behaviors or observable character- istics are known as markers, and researchers have identified eye- tracking abnormalities as a potential cognitive marker for schizophrenia. Kraepelin discovered that patients with dementia praecox had difficulty following a moving stimulus, like the pendulum shown here.

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Section 8.4 Etiology of Schizophrenia: Nongenetic Risk Factors

2007). Imaging studies seem to indicate the presence of some defect in the frontal lobes of at least some people with schizophrenia (Mubarik & Tohid, 2016; Watanabe, Urakame, Hongo, & Ohtsubo, 2014).

How Many Genes Are Involved in Schizophrenia? On average, children get half their genes from their mother and half from their father. This means that, if schizophrenia is the result of a single dominant gene, we should expect to find that 50% of children with one schizophrenic parent develop schizophrenia. The actual figure is only 17%, however.

Also, if schizophrenia is the result of a single dominant gene, then it might be possible to identify its specific chromosomal location. However, researchers have not yet been able to replicate initial positive findings that have pointed toward potential “schizophrenic” genes (Hamilton, 2008). There is always the chance that researchers are seeking something that does not exist. There may not be a schizophrenic gene. Instead, schizophrenia may be poly- genic, the unlucky result of inheriting a number of interacting genes (Gottesman, 1991; Har- rison & Weinberger, 2005).

There are several reasons to believe that schizophrenia is polygenic. Polygenic inheritance would explain why only 17% of the offspring of a parent with schizophrenia develop the con- dition. (The probability of inheriting more than one schizophrenia-related gene is lower than the probability of inheriting only one.) Polygenic inheritance may also account for schizo- phrenia’s varied course and symptoms, which seem too diverse to be caused by a single domi- nant gene. Finally, when several genes are responsible for a condition, we would not expect any single genetic marker to be present in all cases, and they are not.

Whether schizophrenia is caused by one gene or many, there is little doubt that nongenetic factors play an important role. An inherited vulnerability is not sufficient on its own to pro- duce schizophrenia. Nongenetic factors must also be present. The best explanation is one derived from the diathesis-stress model. That is, the symptoms of schizophrenia are the result of an interaction between genetic and nongenetic factors. (See the accompanying Highlight.)

8.4 Etiology of Schizophrenia: Nongenetic Risk Factors It is possible to identify risk factors associated with a greater vulnerability to schizophrenia. In the sections that follow, we will examine several nongenetic risk factors that have been proposed to make schizophrenia disorders more likely to onset or to recur.

Viral Infection The idea that schizophrenia is the result of a brain infection comes partly from observing the rapid increase in the number of diagnosed cases during the 19th century. Schizophrenic-like conditions were considered rare in the 18th century, but their incidence increased dramati- cally in the late 1800s (Warner & de Girolamo, 1995). It is possible that some biological event

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(the birth of a new virus, for example) occurred sometime in the 1800s, producing the mod- ern condition we know as schizophrenia (Hare, 1988).

The notion that schizophrenia may be the result of a virus that affects brain development in the fetus is consistent with the findings of research on fingerprints. When only one identi- cal twin has schizophrenia, he or she has significantly greater or fewer fingerprint ridges than the twin without schizophrenia. This suggests that some process has interfered with the normal biological development of the twin with schizophrenia (Van Os, Fananas, Cannon, Macdonald, & Murray, 1997).

Although some researchers have found a relationship between maternal exposure to viral epidemics during pregnancy and later development of schizophrenia in offspring (Khanda- ker, Zimbron, Lewis, & Jones, 2013), others have failed to confirm such a relationship (Selten & Termorshuizen, 2017). One possible reason for the discrepant results is uncertainty about whether a specific woman contracted a virus during pregnancy. Just because an epidemic

Highlight: The Face of Schizophrenia You surely recognize this face: The Joker, perhaps the comics’ most famous villain. Why is his picture here? Good question! Is this how schizophrenia appears: a man in clown makeup who kills people solely for pleasure? The Joker does not hallucinate, but is he delusional? Do people with schizophrenia kill because they enjoy it? What about John Nash, whose life was the basis for the film A Beautiful Mind? Does the film present a true and accurate portrayal of someone

with schizophrenia? If you’ve seen the film One Flew Over the Cuckoo’s Nest, do you think Jack Nicholson’s character has schizophrenia? If you had no knowledge of this disorder, what would you think after seeing those movies and knowing about The Joker? Interviews with Batman’s current head writers have called The Joker a psychotic killer, a psychotic clown, and a schizophrenic clown. How accurate are these portrayals? If you’re familiar with Batman, chances are you know about The Joker’s girlfriend, Harley Quinn. Did you know she is considered psychotic, yet in her former life she was a psychiatrist? How often do psychiatrists develop schizophrenia?

The questions raised here are all relevant yet difficult to answer. Many of the Highlight boxes focus on how the media portray the disorders discussed in the text. Invariably it seems as though the media portray people with these disorders as raving madmen and madwomen, killers like Leatherface from the Texas Chainsaw Massacre movies or Jason Voorhees from Friday the 13th, or characters like The Joker. Is this just what most people expect? Is portraying people who have schizophrenia as chainsaw killers simply good for ticket sales or television ratings? Or do writers truly believe that these portrayals are accurate depictions of mental illness? What did you think before you took this class and began reading the text?

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occurred in an area does not mean that every pregnant woman who lived in the affected area contracted the illness. One study that used doc- tors’ records to substantiate that specific pregnant women had contracted influenza failed to find any increase in the prevalence of schizophrenia among the offspring of affected mothers, even after a period of 30 years (Crow & Done, 1992). Unfortu- nately, this negative finding does not settle the mat- ter completely because it remains possible that an infection other than influenza (or the drugs used by expectant mothers to combat illness) produced a delayed effect on the fetus.

Looking at the viral issue in a different way, researchers have published dozens of articles on the season of birth of people with schizophrenia. Most report an excess of births in late winter or early spring, which means that their mothers were pregnant during the winter virus season (Meyer, Feldon, Schedlowski, & Yee, 2005; Tamminga, Shad, & Ghose, 2008). The most common view is that the excess of late winter/early spring births among those with schizophrenia is the result of viruses such as influenza, which are more common dur- ing winter. Specifically, viral exposure at a critical

period of prenatal development may be causing subtle brain damage, which, in turn, pro- duces a vulnerability to schizophrenia (Stahl, 2007). In particular, respiratory infections dur- ing the second trimester are associated with an increased risk of schizophrenia spectrum and other psychotic disorders (Brown et al., 2000).

One way to test this coincidental relationship is to examine season of birth in the Southern Hemisphere, where January and February are summer months and winter occurs in July and August. If more individuals with schizophrenia are born in July and August in the Southern Hemisphere, then the “coincidence” explanation is not likely to be correct. Unfortunately, the results of studies conducted in Australia and South America are equivocal; some find an excess of schizophrenic births in the winter months of July and August; others do not (Lewis, 1992).

Life-Stress Studies that have followed people with schizophrenia over time have often found that active- phase episodes are preceded by significant life-stress (Docherty, Feldon, Schedlowski, & Yee, 2009). For instance, it is possible that the stress of being homeless contributes to the devel- opment of schizophrenia. Alternatively, though, people with schizophrenia may be unable to look after themselves and therefore become homeless. Some researchers have found sup- port for the hypothesized link between the immune system and schizophrenia, positing that a weak or weakened immune system may make one more susceptible (Ripke et al., 2014).

Dan ionut Popedcu/Hemera/Thinkstock The study of fingerprints has given researchers insight into the formation of schizophrenia. If one identical twin has schizophrenia, he or she will have greater or fewer fingerprint ridges than the twin without schizophrenia.

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One particular form of social stress that has received special attention is the stigma of being labeled “schizophrenic.” Goffman (1961) and Scheff (1966) have argued that once people are labeled as such, they are forced into a “sick” social role. They are denied employment, consid- ered incapable of looking after themselves, and subjected to treatment (sometimes against their wishes). Eventually, such people come to believe that they are sick and act accordingly. Although it is important not to discount the social stigma associated with being labeled schizophrenic, few researchers today believe that hallucinations, delusions, and other schizo- phrenic behaviors are simply the result of having been called schizophrenic.

Demographic and Socioeconomic Status Schizophrenia has been associated with several intriguing demographic and socioeconomic findings (see Figure 8.2). For example, schizophrenia is more common among people born and raised (up to the age of 15) in large cities than among people brought up in rural areas or small towns (Kirkbride et al., 2006; Lewis, Davis, Andreasson, & Allebeck, 1992). New immigrants have higher than average prevalence rates and so do divorced and single people (Cantor-Graae & Selten, 2005; Eaton, 1985). It is easy to explain why schizophrenia is more common among single than among married people—people with schizophrenia simply do not make good mar- riage prospects. Social class is a particularly important variable in schizophrenia research. It is a standard finding that schizophrenia is more common among those in the lower social and economic groups (Lambert & Kinsley, 2005; Werner, Malaspina, & Rabinowitz, 2007).

Economic status

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Figure 8.2: Socioeconomic class and schizophrenia

Lower- and lower-middle-class people in the United States are more likely than wealthy people to experience schizophrenia.

Source: From R. J. Corner, Abnormal Psychology, 6th ed. New York: Worth Publishers, 2007, Figure 14.1, p. 412. Reprinted by permission.

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Traditionally, two theories have been put forward to account for the relationship between social class and schizophrenia. The previously mentioned social drift theory blames the debilitating effects of mental illness. People with schizophrenia are impaired in their ability to compete economically, so they “drift” down the socioeconomic ladder. In other words, the social drift theory argues that membership in the lower social classes is simply an offshoot of having schizophrenia.

Social stress theory proposes a direct causative role for social class. According to social stress theory, poor people are exposed to more economic and social problems than are those who are better off. However, in developing countries, the better educated are under greater social stress with industrialization because they must learn to become part of a new and unfa- miliar economic system, whereas the poor are left to their traditional subsistence living. This extra stress may be responsible for a higher prevalence of schizophrenia among the upper socioeconomic groups in those countries.

Family Communication Early on, many adherents of psychoanalytic theory harbored the belief that family interac- tions were somehow responsible for psychoses. The so-called schizophrenogenic mother, for example, was thought to produce schizophrenia by her cold, domineering, and aloof attitude toward her children (Fromm-Reichmann, 1948; Hartwell, 1996). Parents of schizophrenic children were accused of sending confused messages to their offspring. For example, moth- ers might scold their children for speaking without permission and then accuse them of not wanting to share their thoughts with their parents. Such messages allegedly place children in a psychological “double-bind” from which they cannot escape except by schizophrenic breakdown (Bateson, 1959; Wynne & Singer, 1963). The evidence for this theory was always tenuous, however (Willick, 2001). Few researchers even bothered to study parent-child inter- actions. After all, it is always possible that the causal direction is the other way around—psy- chologically disturbed children affect the communication style of their parents. These blame- the-family theories placed an additional burden of guilt on parents, and there is no research to support either of these two concepts.

Although these early communication-based hypotheses were overstated, we do know that stressful family relationships influence the course of schizophrenia (Boye, Bentsen, & Malt, 2002; Schiffman et al., 2001, 2002). Patients discharged to their own homes are more likely to return to the hospital or have an exacerbation of their symptoms if family members are hostile, critical, and/or overbearing.

Brain Structure and Function If viruses and birth injuries play a causative role in schizophrenia, they probably exert

Utah778/iStock/Thinkstock Brain imaging studies on patients with schizophrenia have shown that the most common brain abnormality is enlarged lateral ventricles.

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their effects by causing some form of brain damage (Gilmore & Murray, 2006). Brain imaging studies have attempted to identify these injuries. The most commonly reported abnormality is enlarged lateral ventricles (the cavities on each side of the brain that are filled with cerebro- spinal fluid; Raz & Raz, 1990). The ventricles of people with schizophrenia have been found to be enlarged even before treatment, so the defect is not the result of receiving antipsychotic medication (Belger & Dichter, 2006; Lawrie, McIntosh, Hall, Owens, & Johnstone, 2008). The problem is that we do not have any good theory for why people with enlarged ventricles should develop the negative (or any other) symptoms of schizophrenia (Staal et al., 2001). Enlarged ventricles tell us only that these people’s brains have failed to develop normally.

Enlarged ventricles are not the only observed abnormality in people with schizophrenia. Researchers have also reported that people with schizophrenia have a smaller hippocampus and amygdala than people without schizophrenia. The hippocampus and the amygdala are part of the brain’s limbic system, a part of the brain that is thought to be concerned with cog- nition and emotion (Barker et al., 2016).

Brain Chemistry Although the idea that body chemistry affects behavior goes back about 1,900 years, modern attempts to link schizophrenia to brain chemistry date to the 1950s. For at least the last 30 years, researchers have focused on and implicated serotonin, glutamate, and dopamine in schizophrenia (for example, Javitt & Laruelle, 2006; Tan et al., 2007). However, most research- ers have focused on dopamine. Their research can be summarized by three important findings:

1. If taken over a long period of time, antipsychotic medications known as phenothi- azines may produce symptoms similar to those found in the movement disorder Parkinson’s disease (that is, tremors and jerky movements). We know that Parkin- son’s disease results from the destruction of dopamine-producing neurons. It is pos- sible, therefore, that antipsychotic medications work because they somehow reduce dopamine activity in the brain.

2. The drug L-dopa, which is used to treat Parkinson’s disease, works by increasing dopamine activity. Because L-dopa can produce some of the positive symptoms of schizophrenia, this is further evidence that some schizophrenic symptoms are related to increased dopamine activity.

3. Finally, because some types of antipsychotic medications ameliorate the positive symptoms of schizophrenia (and seem to work by reducing dopamine activity in the brain), it seems reasonable to conclude that excess dopamine activity is somehow responsible for the positive symptoms.

Put simply, drugs known to increase dopamine activity seem to provoke schizophrenic symp- toms, whereas drugs that reduce dopamine activity tend to ameliorate them.

The evidence does not demonstrate conclusively that people with schizophrenia have a higher level of dopamine activity than others. Instead, it seems that people with schizophrenia have more dendritic dopamine receptors than do people without schizophrenia (see Figure 8.3). These excess receptors make them more responsive to dopamine, even though their overall levels of dopamine are no different from those of people without schizophrenia. Before we con- clude that extra dopamine receptors are somehow responsible for schizophrenic symptoms,

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Section 8.4 Etiology of Schizophrenia: Nongenetic Risk Factors

however, there is one complication. Some antipsychotic drugs themselves can increase the number of dopamine receptors. Because most people with schizophrenia receive drug treat- ment, it is possible that the excess number of dopamine receptors observed by researchers is caused by drug treatment and, therefore, could not be responsible for the initial development of schizophrenic symptoms.

D5D4

D2 D3

Low expression

Background color

Neocortex

Hippocampus

Caudate Putamen

Nucleus accumbens Retrorubral

field Ventral

tegmental area

Pars compacta of the substantia nigra

Entorhinal cortex

Key

High expression

2 2

3 3

5 5

Figure 8.3: Areas of dopamine receptor activity

Five dopamine receptors have been identified to date. As shown, each one is more common in some parts of the brain than others. The D2 receptor is particularly implicated in schizophrenia.

Source: From S. Schwartz, Abnormal Psychology: A Discovery Approach. Mountain View, CA: Mayfield Publishing Company, 2000, Figure 9.4, p. 402.

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Even if we could provide definitive evidence for an overabundance of dopamine receptors among untreated people with schizophrenia, the relationship between schizophrenia and dopamine would still be ambiguous. For example, among those patients who do respond to medication, it usually takes anywhere from five days to six weeks before any improve- ment is noticed (Rosenbaum et al., 2005). Yet conventional antipsychotic medications have an immediate effect on dopamine activity. The lag before symptoms improve and the finding that some people do not improve at all suggest that schizophrenic symptoms reflect more than just dopamine activity. Perhaps it is the balance among different neurotransmitters that is important in schizophrenia rather than the absolute level of any particular neurotransmit- ter (Bach, 2007).

8.5 Treatment Let us establish one main point at the outset: There is no cure for schizophrenia—no pill, no operation, and no psychotherapy. Nevertheless, the quality of life of people with schizophre- nia can be improved by medical, psychological, and social interventions.

Hospitalization and Milieu Treatment For at least 100 years, mental hospitals were considered to be the best place to treat psychotic individuals. Not only could drug and psychological treatment be delivered in the hospital, but the hospital environ- ment (or milieu) itself was thought to have beneficial effects of its own. Patients were sheltered from the everyday world, while doctors, nurses, and other staff created a culture in which patients interacted socially and gained a sense of independence by participating in ward government. Milieu treatment was considered to be an impor- tant factor in patient outcome. Even today, most people with schizophrenia spend at least some time in a hospital milieu pro- gram, although long-term hospitalization has fallen out of favor. In 1830, approxi-

mately 200 mentally disturbed people were hospitalized in the United States. By the 1950s, the number was 500,000. The numbers of hospitalized patients did not begin to fall off until the 1960s, when antipsychotic medications made it possible for people with schizophrenia to live outside the hospital. People who had spent most of their lives in mental hospitals were discharged in a process known as deinstitutionalization, the result of an act passed by Con- gress in 1963. This act, known as the Community Mental Health Act, provided funding to cre- ate community mental health centers.

UNITED ARTISTS/SuperStock Ken Kesey’s 1962 novel, One Flew Over the Cuckoo’s Nest, compared mental hospitals to jails and portrayed the institutionalized as citizens robbed of their freedom. Many people who spent most of their lives in mental hospitals were discharged after Congress passed the Community Mental Health Act in 1963.

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There were two general ideas driving deinstitutionalization (Scull, 1989). The first was the belief that mental patients are better cared for in their home communities, where they are known and where they can participate in everyday life. The second idea grew out of 1960s radical politics. Mental hospitals were portrayed as tools by which the state robbed citizens of their freedom. Books and movies such as One Flew Over the Cuckoo’s Nest portrayed men- tal hospitals as no different from jails. Hospitals were alleged to create more problems than they solved. What was formerly supposed to be a therapeutic milieu came to be seen as a repressive regime that enforced rigid conformity to rules and made patients apathetic, pas- sive, withdrawn, and helpless. Deinstitutionalization became a romantic crusade to give back to “oppressed” patients their rights and their freedom. Arguing that care should be provided in the least restrictive environment possible, the courts began to require that patients who could survive outside the hospital be discharged.

Ironically, however, the deinstitutionalization movement, which saw as one of its missions the restoration of freedom to hospitalized mental patients, produced a situation in which people were simply allowed to wallow on the streets or in jails. One psychiatrist summarized the situation by saying, “Freedom to be insane is an illusory freedom, a cruel hoax perpe- trated on those who cannot think clearly by those who will not think clearly” (Torrey, 1988, p. 34). Meanwhile, little has been done to improve the situation. What has become clear is that people who cannot look after themselves, who may be violent, or who do not have access to the services they require to live in the community need protection. The best place for them is probably in a hospital, at least during the active phase of their disorders.

Somatic Treatments Perhaps the most important development in the somatic treatment of schizophrenia took place in the 1940s with the development of antihistamines. These drugs were found not only to relieve the symptoms of allergies such as hay fever but also to be useful in preparing people for surgical procedures. Antihistamines made people sleepy and less anxious. Attempts to maximize the tranquilizing effects of antihistamines in the 1950s resulted in the discovery of chlorpromazine (Thorazine) followed by other phenothiazines. The phenothiazines were the first neuroleptic drugs (neuroleptic is derived from an ancient Greek term meaning “take hold of nerves”). They act by blocking certain dopamine receptors. The phenothiazines were soon followed by the butyrophenones (haloperidol [Haldol]) and the thioxanthenes (thiothix- ene [Navane]).

Studies have shown neuroleptic drugs to be effective in reducing the positive symptoms of schizophrenia, but they have a smaller effect on the negative symptoms (Julien, 2008). Neu- roleptics seem to be equally effective for people from different racial backgrounds (Levin- son & Simpson, 1992), although people of Asian origin may require lower doses than other people (Lin et al., 1989). Some people respond to one neuroleptic; some to another (Virani, Bezchlibnyk-Butler, & Jeffries, 2009). This is a bit mysterious because the neuroleptic drugs in each category are very similar to one another (Kane & Marder, 1993). Unfortunately, some people with schizophrenia do not respond to any neuroleptics at all (around 25%) and others respond only partially (Julien, 2008).

Even among those who do respond, neuroleptics present a risk because of their potential side effects (see the accompanying Highlight). The most troubling are the motor side effects that

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arise in the extrapyramidal neural pathways that connect the spinal cord to the brain. These include a shuffling walk, expressionless face, writhing, and other various odd movements. These side effects may be controlled by lowering the dosage or by administering additional drugs (Pereira & Albert, 2017).

To reduce the probability of a relapse, individuals with schizophrenia are often kept on neu- roleptic medication for long periods (Rosenbaum et al., 2005). Because patients sometimes choose to discontinue their neuroleptic medication when they are feeling better, neuroleptics may also be administered by periodic injections rather than as tablets or pills. This is done to ensure that the patients comply with medication protocols and, in effect, to take dosing con- trol away from the patient. Long-term neuroleptic treatment, whether by injection or tablet, is associated with a movement disorder known as tardive dyskinesia (Salem, Pigott, Zhang, Zeni, & Teixeira, 2017). The symptoms include facial grimaces, jerky movements, lip chewing, and a host of other tics and odd movements. Tardive dyskinesia is often irreversible, particu- larly in women (Salem et al., 2017).

Atypical neuroleptics, which work on serotonin as well as dopamine, have a lower probability of producing extrapyramidal symptoms while also having equal or better therapeutic effects (Divac, Prostran, Jakovcevski, & Cerovac, 2014). One of these is clozapine (Clozaril). This drug seems to reduce symptoms in patients who do not respond to traditional neuroleptics (Dem- ler, Morabito, Meyer, & Opler, 2016). Clozaril has one serious problem, though—it produces a potentially lethal blood condition known as agranulocytosis in about 1% of patients (Demler et al., 2016). In agranulocytosis, there is a dramatic lowering in the number of white blood cells and a consequent loss of immune function. People become prone to infections that they cannot fight off. For this reason, frequent white blood cell counts are required so that treat- ment may be discontinued before an infection takes hold. Table 8.3 lists several atypical anti- psychotic medications.

Highlight: Is the Treatment Worse Than the Disorder?

A common question students ask, and one you should consider, is the following: Is the treatment for schizophrenia, specifically the use of antipsychotic medications, worse than the disorder itself ? As you have just read, antipsychotic medications can produce significant side effects, sometimes leading to suicidal behaviors. Is this more problematic than perhaps hallucinations and/or delusions?

Another question: The medications control and reduce, perhaps eliminating, these symptoms. They do not, however, cure schizophrenia. We saw the same situation in Chapter 6, in our discussion of bipolar I and II. Does it make sense, then, for patients to take these medications when they do not cure schizophrenia?

There is a saying among many oncologists (cancer specialists): We can kill the cancer, but sometimes the patient dies also. Can that occur with schizophrenia? Should we, and psychiatrists, think carefully before prescribing, or advocating, medication use?

Finally, let’s assume that you were an individual with schizophrenia who was high functioning (that is, you have insight into your symptoms and can verbalize this). Suppose your health care provider recommended that you take Thorazine based on your medical history. How would you respond?

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Psychological Treatment Few, if any, psychologists believe that schizophrenia can be cured by psychotherapy alone. Instead, the aim of psychological interventions is to delay relapse and to improve the quality of life for people with schizophrenia and for those who care for them.

Initially talk therapy was not very successful with individuals with schizophrenia. An inter- esting example is provided by Frieda Fromm-Reichmann (1950). She would tell her patients that they could continue to stay in their world and stay there as long as they wished, in effect condoning the disorder. She believed, and wrote, that eventually the patients would accept, trust, and grow attached to her and begin to talk to her about their problems (Fromm-Reich- mann, 1950). Today, talk therapy is successful much more often than in Fromm-Reichmann’s time (Miller et al., 2012; Swartz et al., 2012). In combination with antipsychotic medications, cognitive-behavioral therapy and family therapy help patients to relieve thought and per- ceptual disturbances and help them to make behavioral changes and cope with life’s various stressors. Let’s examine each of these.

Cognitive-Behavioral Therapy Cognitive-behavioral techniques are based on the premise that people with schizophrenia have hallucinations due to biology. Patient try to make sense of these sensations and conclude that the hallucinations are coming from external sources, that people are out to get them, that people are putting thoughts into their head, and so on (Hagen et al., 2011; Howes & Murray, 2014). Techniques that can be used include educating patients about the biological causes of their hallucinations, and helping the patients learn to identify which situations (usually

Table 8.3 Atypical (second-generation) antipsychotic medications

Common U.S. Trade Name Generic Name

Abilify aripiprazole

Saphris asenapine maleate

Clozaril clozapine

Fanapt iloperidone

Latuda lurasidone

Zyprexa olanzapine

Symbyax olanzapine/fluoxetine

Invega paliperidone

Seroquel quetiapine

Risperdal risperidone

Geodon ziprasidone

Source: U.S. Food and Drug Administration

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stressful) set off the hallucinations. The clinician can also work with patients to challenge the hallucinations, for example, asking patients what would occur if they did not follow the voice’s orders? This helps to weaken the hallucinations’ power. Clinicians might also teach patients to more accurately interpret their hallucinations. Patients may conclude, “It’s not a real voice; it’s my illness.” Patients can also be taught to use relaxation techniques and to be distracted from the hallucinations when they occur. This can reduce any physical arousal that occurs, reducing the patient’s stress (Veiga-Martínez et al., 2008). The main issue is that these techniques do not eliminate the hallucinations, though they may reduce their frequency.

Family Therapy According to Tsai et al. (2011), more than 50% of those who are recovering from schizophre- nia live with their families. Not surprisingly, a patient’s recovery may be strongly influenced by the behavior and reactions of his or her relatives at home (Macleod et al., 2011). People with schizophrenia who feel positive toward their relatives do better in treatment (Okpokoro et al., 2014). Research has demonstrated that patients in recovery who live with relatives who are very critical, emotionally overinvolved, and hostile, similar to Minuchin’s enmeshed fam- ily, often have a much higher relapse rate than those living with more positive and supportive relatives. Some researchers have also discovered that family members may be very upset by the social withdrawal and unusual behaviors of a relative with schizophrenia (Friedrich et al., 2014; Quah, 2014).

Typically, clinicians will attempt to involve family members in the treatment of schizophrenia. This should include guidance, education about the disor- der, and emotional support and empathy (Burbach, Fadden, & Smith, 2010). Communication patterns often are examined and if need be worked on to improve them.

Expressed emotion refers to the frequency and quality of negative emotions, such as anger or hos- tility, expressed by family members that often lead to a high relapse rate with individuals with schizo- phrenia. Research has shown that relapse is at least in part determined by how people with schizophre- nia are received by their immediate families when they are discharged from the hospital (Ritsner & Gibel, 2007). Treatment programs usually begin by educating families and other caregivers about schizophrenia and what types of behavior they should expect. They are also taught about anti- psychotic medications and their side effects. Fam- ily assistance is enlisted in helping patients to stay on their medication because noncompliance is an important determinant of relapse (Saba, Mekaoui, Leboyer, & Schurhoff, 2007).

digitalskillet/iStock/Thinkstock Expressed emotion may contribute to a higher relapse rate of individuals with schizophrenia. Treatment programs educate family members and caregivers about schizophrenia and what types of behavior to expect.

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Chapter Summary

Token Economies Token economies are behavior modification programs used in psychiatric hospitals to rein- force desired behaviors (making one’s bed, for example). In these programs, staff reward each occurrence of a desired behavior with a token, which can be exchanged for privileges such as time watching television. Patients who disrupt others or who act inappropriately are not rewarded and may even be fined. Some research has found these programs to be effective (Combs, Basso, Wanner, & Ledet, 2008).

Social Skills and Cognitive Training Individuals with schizophrenia who spend long periods in hospitals (or out of the hospital but removed from social interaction) may lack social skills (Ridgeway, 2008). They need to learn the specific skills required to hold a conversation, go through a job interview, express their feelings, and maintain relationships. This is supplied by clinicians either on an inpatient or outpatient basis (Ridgeway, 2008).

In sum, a combination of antipsychotic medications, psychological treatment that includes family support, and social skills training, among other approaches, allows us to best treat schizophrenia. Current research continues to focus on antipsychotic medications as well as ways to more effectively treat this disorder (Conley et al., 2005).

Chapter Summary

The Genesis of Schizophrenia • Schizophrenia is the most common of the schizophrenia spectrum disorders (disor-

ders characterized by gross distortions of reality). • The precise definition of schizophrenia has varied over the decades. • The DSM–5 diagnostic criteria for schizophrenia require that two of five symptoms

be present (positive symptoms include delusions, hallucinations, disorganized speech, and grossly disorganized or catatonic behavior, whereas negative symptoms include limited speech and flat affect). At least one of the symptoms must include hallucinations, delusions, or disorganized speech.

• The diagnosis also requires evidence of a decline from a previous level of function- ing and the presence of disturbed behavior over a period of at least six months.

Course • The course of schizophrenia is divided into three stages: prodromal, active, and

residual. • The syndrome’s first appearance is usually in adolescence or early adulthood, with

alternating active and residual phases over many years.

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Chapter Summary

Etiology of Schizophrenia • The evidence from family, twin, and adoption studies suggests that there is a genetic

factor that determines vulnerability to schizophrenia; however, the inherited trait appears to have variable expression (relatives may not be schizophrenic but may have related disorders).

• Because even identical twins have a concordance of less than 50%, it seems clear that heredity is not a sufficient explanation for schizophrenia. Heredity must interact with other causal factors.

• Among the many risk factors that have been related to schizophrenia are season of birth, social class, life-stress, and expressed emotion in families.

• Etiology has been attributed to brain damage and neurochemical abnormalities (in dopamine, for example).

Treatment • Milieu treatment in hospitals, once the therapeutic mainstay, is now mostly limited

to brief stays during the active phase of the disorder. • Deinstitutionalization has resulted in an emptying out of psychiatric hospitals. • Schizophrenia is usually treated with drugs, although medications (both old and

new) may have serious side effects.

Critical Thinking Questions

1. Reread the case of Jennifer Plowman. Jennifer was adopted by parents who evidently have no history of mental illness and who raised her in a supportive environment. Jennifer’s biological mother, however, had schizophrenia. Discuss which causal factor(s) of schizophrenia Jennifer’s case supports. Justify your response.

2. Jennifer Plowman’s mother asked the court to commit her daughter to a psychiat- ric hospital, which meant she could be held for 72 hours for observation. The judge was initially reluctant to do so. Discuss the pros and cons of this, and also discuss whether you think “forcing” someone into a hospital or into treatment would be effective.

3. Scientists and practitioners have been researching and trying to understand schizo- phrenia better for decades now, yet successful treatment remains difficult. Give some reasons why this is the case.

4. How would you differentiate between a delusion and an actual belief ? That is, would you classify someone who claims to receive messages from a deity (for example, Christ) as having delusions? Why or why not?

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Chapter Summary

Key Terms active phase The phase in schizophrenia in which symptoms are present.

Capgras syndrome A condition in which an individual with schizophrenia believes that someone he or she knows has been replaced by a double; one type of delusion.

catatonic stupor A condition in which some people with schizophrenia do not move a muscle for hours. At such times, they seem indifferent to events going on around them.

chlorpromazine Known more commonly as Thorazine; the first antipsychotic medica- tion, developed in the early 1950s.

Cotard syndrome A type of delusion in which an individual with schizophrenia believes that he or she is dead.

deinstitutionalization A movement during which psychiatric patients were released from hospitals to be cared for in their home communities, where they are known and where they can participate in everyday life.

delusions Unsubstantiated beliefs; a symp- tom of schizophrenia.

dementia praecox The term that Kraepelin used to denote what he called the “continu- ously deteriorating psychosis”; this is analo- gous to schizophrenia.

expressed emotion The frequency and quality of negative emotions, such as anger or hostility, expressed by family members that often lead to a high relapse rate with schizophrenic patients.

flat affect Little to no emotional expression.

grandiose delusions A person’s beliefs that he or she has some extraordinary talent or power.

hallucinations Perceptual experiences in the absence of external stimuli.

inappropriate affect Emotions that are inappropriate or not properly fit to the cur- rent situation, such as laughing when one is very nervous.

milieu treatment Therapy for schizo- phrenic individuals in a psychiatric hospital with a complete daily program; designed to provide the patient optimal support.

negative symptoms Signs of schizophrenia that reflect a reduction or loss of normal functions, including loss of initiative, lack of emotional expression, and impoverished speech.

neuroleptic drugs Another term for phenothiazines, a class of antipsychotic medications.

persecutory delusions Also called para- noid delusions; a person’s beliefs that some- one is out to get him or her.

phenothiazines A class of antipsy- chotic medications; Thorazine is the most well-known.

polygenic inheritance A condition in which an individual inherits more than one gene that may be a causal factor for schizophrenia.

positive symptoms Signs of schizophrenia that reflect an excess or distortion of normal cognitive and emotional functions, including delusions, hallucinations, and bizarre motor movements.

prodromal phase The phase that precedes schizophrenia; marked by a deterioration from some higher level of functioning.

psychoses Disorders characterized by gross distortions of reality.

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Chapter Summary

residual phase The phase in schizophre- nia in which only negative symptoms, or mild versions of the positive symptoms, are present.

risk factors Features, genetic or otherwise, that are associated with a greater vulnerabil- ity to schizophrenia.

schizophrenia A psychotic disorder typi- cally characterized by hallucinations, delu- sions, and a loss of contact with reality.

social drift theory A theory proposing that schizophrenia affects a person’s social and economic condition; people with schizo- phrenia are impaired in their ability to compete economically, so they “drift” down the socioeconomic ladder.

social stress theory A theory proposing a direct causative role for schizophrenia: Poor people are exposed to more eco- nomic and social problems than are those who are better off and therefore are more likely to become schizophrenic. Although they also need to have a predisposition for schizophrenia, their social situation makes it more likely that symptoms will present themselves.

tardive dyskinesia A movement disorder with symptoms that include facial grimaces, jerky movements, lip chewing, and many other tics and odd movements.

thought insertion delusions Sometimes called delusions of influence; a person’s beliefs that thoughts are being inserted into his or her own head.

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