Our understanding of schizophrenia has evolved since its symptoms were first catalogued by German psychiatrist Emil Kraepelin in the late 19th century (Andreasen, 1997a). Even though the cause of this disorder remains elusive, its frightening symptoms and biological correlates have come to be quite well defined. Yet misconceptions abound about symptoms: schizophrenia is neither split personality nor multiple personality. Furthermore, people with schizophrenia are not perpetually incoherent or psychotic (DSM-IV; Mason et al., 1997) (Table 4-6).
Schizophrenia is characterized by profound disruption in cognition and emotion, affecting the most fundamental human attributes: language, thought, perception, affect, and sense of self. The array of symptoms, while wide ranging, frequently includes psychotic manifestations, such as hearing internal voices or experiencing other sensations not connected to an obvious source (hallucinations) and assigning unusual significance or meaning to normal events or holding fixed false personal beliefs (delusions). No single symptom is definitive for diagnosis; rather, the diagnosis encompasses a pattern of signs and symptoms, in conjunction with impaired occupational or social functioning (DSM-IV).
Symptoms are typically divided into positive and negative symptoms (see Table 4-7) because of their impact on diagnosis and treatment (Crow, 1985; Andreasen, 1995; Eaton et al., 1995; Klosterkotter et al., 1995; Maziade et al., 1996). Positive symptoms are those that appear to reflect an excess or distortion of normal functions (Peralta & Cuesta, 1998). The diagnosis of schizophrenia, according to DSM-IV, requires at least 1-month duration of two or more positive symptoms, unless hallucinations or delusions are especially bizarre, in which case one alone suffices for diagnosis. Negative symptoms are those that appear to reflect a diminution or loss of normal functions (Roy & DeVriendt, 1994; Crow, 1995; Blanchard et al., 1998). These often persist in the lives of people with schizophrenia during periods of low (or absent) positive symptoms. Negative symptoms are difficult to evaluate because they are not as grossly abnormal as positives ones and may be caused by a variety of other factors as well (e.g., as an adaptation to a persecutory delusion). However, advancements in diagnostic assessment tools are being made.
Diagnosis is complicated by early treatment of schizophrenias positive symptoms. Antipsychotic medications, particularly the traditional ones, often produce side effects that closely resemble the negative symptoms of affective flattening and avolition. In addition, other negative symptoms are sometimes present in schizophrenia but not often enough to satisfy diagnostic criteria (DSM-IV): loss of usual interests or pleasures (anhedonia); disturbances of sleep and eating; dysphoric mood (depressed, anxious, irritable, or angry mood); and difficulty concentrating or focusing attention.
Currently, discussion is ongoing within the field regarding the need for a third category of symptoms for diagnosis: disorganized symptoms (Brekke et al., 1995; Cuesta & Peralta, 1995). Disorganized symptoms include thought disorder, confusion, disorientation, and memory problems. While they are listed by DSM-IV as common in schizophreniaespecially during exacerbations of positive or negative symptoms (DSM-IV)they do not yet constitute a formal new category of symptoms. Some researchers think that a new category is not warranted because disorganized symptoms may instead reflect an underlying dysfunction common to several psychotic disorders, rather than being unique to schizophrenia (Toomey et al., 1998).
These cognitive problems vary from person to person and can change over time. In some situations it is unclear whether such deficits are due to the illness or to the side effects of certain neuroleptic medications (Zalewski et al., 1998). As research on brain functioning grows more sophisticated, some models posit dysfunction of fundamental cognitive processes at the center of schizophrenia, rather than as one of numerous symptoms (Andreasen, 1997a, 1997b; Andreasen et al., 1996). On the basis of neuropsychological and neuroanatomical data, for example, some researchers posit that schizophrenia is a disorder of the prefrontal cortex and its ability to perform the essential cognitive function of working memory (Goldman-Rakic & Selemon, 1997). Problems in such fundamental areas as paying selective attention, problem-solving, and remembering can cause serious difficulties in learning new skills (social interaction, treatment and rehabilitation) and performing daily tasks (Medalia et al., 1998); treatment of such deficits is discussed in later sections of the chapter.
Clinicians can misinterpret and misdiagnose patients whose cognitive style, norms of emotional expression, and social behavior are from a different culture, unless clinicians become culturally competent (see Chapter 2 and Center for Mental Health Services [CMHS], 1997). For example, clinicians may misinterpret a clients deferential avoidance of direct eye contact as a sign of withdrawal or paranoia, or a normal emotional reserve as flattened affect if they are unaware of the norms of cultural groups other than their own. There is some empirical evidence that such misinterpretations happen widely. One finding is that African-American patients are more likely than white patients to be diagnosed with severe psychotic disorders in clinical settings (Snowden & Cheung, 1990; Hu et al., 1991; Lawson et al., 1994, Strakowski et al., 1995). The overdiagnosis of psychotic disorders among African Americans is interpreted by some as evidence of clinician bias.
People with differing cultural backgrounds also may experience and exhibit true schizophrenia symptoms differently (Brekke & Barrio, 1997; Thakker & Ward, 1998). Culture shapes the content and form of positive and negative symptoms (Maslowski et al., 1998). For example, people in non-Western countries report catatonic behavior among psychiatric patients much more commonly than in the United States. How culture, societal conditions, and diagnosing tendencies among clinicians in various countries interact to create these differences is being studied but is not yet well understood.
No description of symptoms can adequately convey a persons experience of schizophrenia or other serious mental illness. Two individuals with very different internal experiences and outward presentations may be diagnosed with schizophrenia, if both meet the diagnostic criteria (Brazo & Dollfus, 1997; Kirkpatrick et al., 1998). Additionally, their symptoms and presentation may vary considerably over time (Ribeyre & Dollfus, 1996). This considerable variation (Basso et al., 1997; Sperling et al., 1997) has led to the naming of several subtypes of schizophrenia, depending on what symptoms are most prominent. Currently these are seen as variations within a single disorder. Similarly, the diagnosis is often difficult because other mental disorders share some common features. Diagnosis depends on the details of how people behave and what they report during an evaluation, the diagnostician, and variations in the illness over time. Therefore, many people receive more than one diagnostic label over the course of their involvement with mental health services. Refining the definition of schizophrenia and other serious mental illnesses to account for these individual and cultural variations remains a challenge to researchers and clinicians.
Prevalence of Comorbid Medical Illness
It is difficult to study the course of schizophrenia and other serious mental illnesses because of the changing nature of diagnosis, treatment, and social norms (Schultz et al., 1997). Overall, research indicates that schizophrenias course over time varies considerably from person to person (DSM-IV; Wiersma et al., 1998) and varies for any one person (Moller & von Zerssen, 1995). The variability may emanate from the underlying heterogeneity of the disease process itself, as well as from biological and genetic vulnerability, neurocognitive impairments, sociocultural stressors, and personal and social factors that confer protection against stress and vulnerability (Liberman et al., 1980; Nuechterlein et al., 1994). Most individuals experience periods of symptom exacerbation and remission, while others maintain a steady level of symptoms and disability which can range from moderate to severe (Wiersma et al., 1998).
Most people experience at least one, often more, relapse after their first actively psychotic episode (Herz & Melville, 1980; Falloon, 1984; Gaebel et al., 1993; Wiersma et al., 1998). Often these are periods of more intense positive symptoms, yet the person continues to struggle with negative symptoms in between episodes (Gupta et al., 1997; Schultz et al., 1997). However, whether such exacerbations have the same degree of disabling and distressing effects each time depends greatly on the persons coping skills and support system. Over time, many people learn successful ways of managing even severe symptoms to moderate their disruptiveness to daily life (e.g., Hamera et al., 1992). Therefore, earlier years with the illness are often more difficult than later ones. Additionally, gradual onset and delays in obtaining treatment seem to raise the risk of longer episodes of acute illness over time (Wiersma et al., 1998). Early treatment with antipsychotic medications has been found to predict better long-term outcomes for people experiencing their first psychotic episode, as compared with a variety of control groups, including those in more advanced stages (Lieberman et al., 1996; Wyatt et al., 1997, 1998; Wyatt & Henter, 1998).
The course of schizophrenia is also influenced by personal orientation and motivation, and by supports in the form of skill-building assistance and rehabilitation (Lieberman et al., 1996; Awad et al., 1997; Hafner & an der Heiden, 1997). These, in turn, are heavily influenced by regional, cultural, and socioeconomic factors in addition to individual factors (Dassori et al., 1995).
Family factors also are related to the course of illness. Following hospitalization, patients who return home are more likely to relapse if their family is identified as critical, hostile, or emotionally overinvolved than if their family is not so identified (Jenkins & Karno, 1992; Bebbington & Kuipers, 1994). This is a controversial finding because it appears to blame family members (Hatfield et al., 1987). However, recent studies suggest an interaction between families and the patient (Goldstein, 1995b), suggesting that the negative emotions of some family members may be a reaction to, more than a cause of relapse in, the family member. Blaming either the family or the patient overlooks important ways both parties interact and how such interactions are associated with the course of schizophrenia. In addition, there is a need to examine what part the role of families prosocial functioning (family warmth and family support) plays in the course of schizophrenia to identify how family factors can serve as protective factors (Lopez et al., in press).
Despite the variability, some generalizations about the long-term course of schizophrenia are possible largely on the basis of longitudinal research. A small percentage (10 percent or so) of patients seem to remain severely ill over long periods of time (Jablensky et al., 1992; Gerbaldo et al., 1995). Most do not return to their prior state of mental function. Yet several long-term studies reveal that about one-half to two-thirds of people with schizophrenia significantly improve or recover, some completely (for a review see Harding et al., 1992). These studies were important because they began to dispel the traditional view, dating back to the 19th century, that schizophrenia had a uniformly downhill course (Harding et al., 1992). Several other longitudinal studies, however, found less favorable patient outcomes with other cohorts of patients (Harrow et al., 1997). The differences in outcomes between the studies are thought to be explained on the basis of differences in patient age, length of followup, expectations about prognosis, and types of services received (Harrow et al., 1997).
The importance of a rehabilitation focus in shaping patient outcome was supported by one of the only direct comparisons between patient cohorts. The Vermont cohort consisted of the most severely affected patients from the back wards of the state hospital (Harding et al., 1987). As part of a statewide program of deinstitutionalization, the cohort was released in the 1950s to a hospital-based rehabilitation program and then to what was at the time an innovative, broad-based community rehabilitation program, which incorporated social, residential, and vocational components13. Patients degree of recovery at followup after three decades was measured by global functional improvement and other functional measures. One-half to two-thirds of the Vermont cohort significantly improved or recovered (Harding et al., 1987). The receipt of community-based rehabilitation was considered key to their recovery on the basis of a study comparing their progress with that of a matched cohort of deinstitutionalized patients from Maine. The Maine cohort did not function as well after receiving more traditional aftercare services without a rehabilitation emphasis (DeSisto et al., 1995a, 1995b). Although the findings from the Vermont cohort, as well as those from a cohort in Switzerland (Ciompi, 1980), are widely cited by consumers as evidence of recovery from mental illness, a topic discussed in detail in Chapter 2, it bears noting that patients in the Vermont cohort represented a less rigorously defined conceptualization of schizophrenia than is common today, which may account, in part, for the more favorable outcomes.
In summary, schizophrenia does not follow a single pathway. Rather, like other mental and somatic disorders, course and recovery are determined by a constellation of biological, psychological, and sociocultural factors. That different degrees of recovery are attainable has offered hope to consumers and families.
Gender and Age at Onset
Current research (e.g., Hafner & an der Heiden, 1997; Hafner et al., 1998) suggests that some of the apparent gender differences in course and outcome occur because for some women schizophrenia does not develop until after menopause. This delay is thought to be related to the protective effects of estrogen, the levels of which diminish at menopause. According to this line of reasoning, men have no such delay because they lack the protective estrogen levels. Therefore, a higher proportion of men develop schizophrenia earlier.
Generally, early onset (younger than age 25 in most studies) is associated with more gradual development of symptoms, more prominent negative symptoms across the course (DSM-IV), and more neuropsychological problems (Basso et al., 1997; Symonds et al., 1997), regardless of gender. Early onset also usually involves more disruption of adult milestones, such as education, employment achievements, and long-term social relationships (Nowotny et al., 1996). People with later onset often have reached these milestones, cushioning them from disruptive sequelae and enabling better coping with symptoms (Hafner et al., 1998). Therefore, early onset (more men than women) often yields a more difficult first several years, although not necessarily a worse long-term outcome.
However, it must be emphasized that group probabilities do not necessarily speak to individual cases.
13 These are the vital components of most contemporary rehabilitation programs (see section on service delivery).