Schizophrenia spectrum disorder is a broad term applying to illnesses involving disordered thinking and disturbances in reality orientation and social involvement. Although symptoms of PSYCHOSIS (condition involving hallucinations, delusions, or disorganized thoughts, behavior, or speech) are often intermittently or continuously present, the underlying THOUGHT DISORDER is the most prominent cause of disability associated with this group of psychopathologies. Throughout this chapter, this group of disorders is referred to as schizophrenia spectrum disorders (SSD). The term SCHIZOPHRENIA refers to a diagnostic category within the group of SSD.

This chapter covers the historical aspects and epidemiology of SSD and includes a detailed description of thought disorders. Relevant psychodynamic, cognitive behavioral, genetic, and neurobiological influences are described, along with common pharmacotherapy and nonpharmacotherapy strategies used in the treatment of SSD. Application of the nursing process from an interpersonal perspective is discussed, including a plan of care for a patient with a thought disorder.

HISTORICAL PERSPECTIVES

References to madness in the Bible and in the Atharva Veda (sacred Hindu text) can be found. In addition, some of the symptoms of mental illness were described in ancient history. However, it was not until the beginning of the 19th century that SSD was clearly recorded in the clinical literature. As a result, historians were left with two different interpretations: Either SSD is a relatively new plague of mankind, or, more simply, the descriptions of madness in ancient texts were too vague to identify the syndrome clearly. It should be noted, however, that other mental disorders, particularly depression, mania, and dementia, are identifiable in early historical documents (Torrey, 1980).

The two earliest clinical descriptions of the disorder(s) occurred almost simultaneously in 1809. These descriptions were provided by Philip Pinel in France and John Haslam in England. Just 3 years later, in 1812, Benjamin Rush in the United States addressed the disorder. All three described SSD as a constellation of symptoms that included delusions, hallucinations, and paranoia. In 1860, a French physician, Benedict Morel, found that the disorder was associated with an early age of onset, leading him to believe that it was a type of early dementia. Thus, he named the syndrome dementia praecox. By 1876, Emil Kraepelin, a psychiatrist, began to note similarities in the descriptions of several neurological syndromes in the medical literature of the time. He proposed that all of these syndromes belonged to a group of disorders that shared an early onset, grave prognosis, and list of symptoms. Kraepelin was certain that the symptoms were rooted in a yet-to-be identified neuroanatomical abnormality. More than 30 years later in 1911, Eugen Bleuler, a Swiss physician, renamed the disorder schizophrenia and described both core and associated symptoms of the disorder. Bleuler is credited with recognizing and identifying thought disorders as a primary cause of disability. Unlike his predecessors, Bleuler believed the origin of the disorder was psychological rather than neuroanatomical. These early clinicians influenced current conceptions of schizophrenia.

In 1959, Kurt Schneider, a German psychiatrist, defined a list of symptoms associated with schizophrenia, distinguishing it from other psychotic disorders. This list, which was considered quite reliable, was widely used by professionals and taught in clinical programs throughout Europe and the United States. In 1966, the World Health Organization (WHO) conducted a landmark study titled “International Pilot Study of Schizophrenia,” establishing the clinical picture of schizophrenia and suggesting that the presence of first-rank or positive symptoms does not always predict poor outcomes. Further research has suggested that positive symptoms are not always associated with schizophrenia; however, they tend to be more frequent and severe in patients with schizophrenia (Rosen, Grossman, Harrow, Bonner-Jackson, & Faull, 2011).

The history of targeted and effective treatment for SSD covers a much shorter period of time. Most persons with mental illnesses, presumably including SSD, were treated with banishment and cruelty for the last 200 years. Both Pinel and Rush were early advocates to improve the circumstances of persons in mental asylums. However, even in institutions where benevolent care was provided, effective treatment was not available. Early attempts at intervention included the use of restraints, opium, hydrotherapy, insulin, electroconvulsive therapy (ECT), and crude neurosurgical techniques. It was not until the early 1950s with the discovery of chlorpromazine by French researchers Pierre Deniker, Henri Laborit, and Jean Delay that any effective treatment became available. Many credit the deinstitutionalization of the mentally ill as a major influence on the use of antipsychotic drugs, which rapidly became a mainstay of treatment. Others believe that the entitlement programs of the 1960s, such as Medicare and Medicaid, were a greater impetus to the deinstitutionalization process. Regardless, the use of antipsychotic drugs as treatment for SSD was an extremely influential development.

Psychoanalysis, based on Freud’s theories, as a treatment for SSD was also important. It was the most widely used treatment technique for mental illness in the United States during the first half of the 20th century. Psychoanalysis was considered a legitimate treatment for SSD even beyond the discovery of antipsychotics. However, the number of mental health professionals using it began to dwindle. Its use as a treatment for mental disorders quickly declined in the later 1970s through the 1980s. Today, psychoanalysis is infrequently used as a therapeutic modality for any psychiatric disorder.

Psychoanalysis also was important to the development of psychiatric-mental health nursing. The psychoanalyst Harry Stack Sullivan and his Interpersonal Theory of Psychiatry greatly influenced Hildegard Peplau, often considered the “mother of psychiatric nursing.” Both Sullivan and Peplau were associated with Chestnut Lodge, a private sanitarium outside Washington, DC. The facility staff there was committed to using psychoanalytic techniques. However, Sullivan and Peplau stressed the critical nature of interpersonal relations rather than intrapsychic processes (central to Freudian theory) in the development and treatment of mental disorders including SSD. They reported “good outcomes” for their clientele but it is not clear how the outcomes were determined.

Peplau continues to be an important figure in psychiatric-mental health nursing through her theory describing the development of the nurse–patient relationship as an interpersonal process, and her role in the development of advanced practice psychiatric nursing. Peplau understood the critical nature of communication and use of self when working with persons with SSD. She emphasized the importance of using the nurse–patient relationship to decrease symptoms, reestablish relatedness to the environment, and restore the boundaries of self-identity. She believed that doing so should result in a more fully functioning person (Thelander, 1997). Peplau’s Interpersonal Relations Theory continues to be relevant in relation to recovery in schizophrenia because she describes the helping relationship as one that brings strangers with differing perspectives together. These strangers then evolve into a collaborative dyad focused on the patient’s goals.

EPIDEMIOLOGY

Understanding the epidemiology of a disease is critical to identifying risk factors and possible preventive strategies. It is also important to evaluate disease burden in order to set priorities for appropriate resource allocation.

In the last 10 years, there have been significant breakthroughs in epidemiological methods and thus more is known about all disease processes, including SSD. Many of the old assumptions concerning the epidemiology of SSD have been challenged. Schizophrenia studies are plagued by inconsistency in the definition and changes in diagnostic practices. Schizophrenia is not distributed evenly across cultures and countries. Recent studies across urban and rural areas and systemic reviews have found a wide variation in rates and outcomes (Castle & Buckley, 2011). Interestingly, the outcomes tend to be better in developing countries than those in developed countries, with patients in developed countries having frequent relapses and persisting disability (Juul & Nemeroff, 2012).

Incidence

Incidence refers to the number of newly identified cases in a specific time period. The average incidence of schizophrenia across the world ranges from 7 to 14 per 100,000 per year. Because of the wide range it is safe to assume there is a fairly high variability in rates among locations. In addition, significant differences appeared in the incidence rate between males and females, with males having approximately a 1.4 times higher risk than women. In other words, for every three men affected with SSD, there are two women affected. Also, recent studies confirm that the disease onset peaks earlier in males than in females. The reason for this difference has not been clearly established. It has been speculated that estrogen or neurobiological determinants may play a role (Castle & Buckley, 2011).

Statistics also reveal a significantly higher rate of the disorder among first- and second-generation immigrants than in the native-born populations across societies. Again, the reasons for this difference are not clearly understood. One theory is biological, such as exposure to novel viruses. Another theory suggests psychosocial reasons: migration stress and the experience of discrimination in the adoptive country (Castle & Buckley, 2011).

Economic status does not appear to be a factor. Recent studies have found no difference in the incidence of schizophrenia based on economic status. However, those living in urban areas show a higher incidence rate than those living in rural or suburban settings. Unemployment, lower educational status, and being disabled carry higher odds of acquiring the disease (Juul & Nemeroff, 2012).

Prevalence

Schizophrenia is not uniform in its distribution and there is considerable variation in the prevalence rates (the number of current cases), which range from 1.4 to 4.6 per 1,000 people in the majority of studies (Juul & Nemeroff, 2012). High rates have been found in deprived inner city areas in large cities. Immigrant status does appear to be a factor. As mentioned previously, the prevalence rate for immigrants is higher than for those in the native-born population. In one meta-analysis, migrants whose skin color is considerably darker than the background population were reported to have a relative risk of schizophrenia of 4.8 (Mura, Petretto, Bhat, & Carta, 2012). Economic conditions do appear to influence prevalence rates, with developed countries estimating significantly higher rates of the disorder than that of less-developed countries. Prevalence estimates also differ significantly by latitude, with higher latitudes having greater prevalence rates than lower latitudes. High rates of schizophrenia have been found in Northern Sweden and Western Ireland. Rate differences related to latitude are notable because they signify possible variation in a wide range of influential environmental and economic factors, such as temperature, ultraviolet exposure, precipitation, genetics, and socioeconomic status. Generally the lifetime morbid risk of anyone developing schizophrenia is from 0.5% to 1.0% (Castle & Buckley, 2011).

Mortality

The life span of people with severe mental disorders, including schizophrenia, is shorter compared with the general population. These individuals on average tend to die 10 to 25 years earlier than their non–mentally ill counterparts. This is referred to as premature mortality. The WHO (2013) reports that individuals with schizophrenia are 2 to 2.5 times more likely to die earlier than the general population. While suicide influences the mortality rate for this population, all major causes of death were elevated among those with SSD. A disturbing fact is that the mortality gap (the rate of death for the person with SSD compared with the standard mortality rate) for persons with SSD has increased significantly in the past several decades. Cardiovascular disease is the major single cause of death in people with schizophrenia, with the following risk factors seen in excess among people with schizophrenia: elevated lipids, hypertension, cigarette smoking, obesity, sedentary lifestyle, and diabetes. People with schizophrenia also have higher rates of infectious diseases such as HIV, hepatitis, and tuberculosis (WHO, 2013). Furthermore, the introduction of second-generation antipsychotics has amplified the problem by increasing the risk for metabolic syndrome (a condition associated with insulin resistance, central obesity, and altered serum lipid levels). The rates of diabetes, ketoacidoses, and death have risen dramatically since the late 1990s and early 2000s (Nasrallah, 2012). There is some evidence that people with schizophrenia do not receive adequate health care and treatment. The WHO developed the Mental Health Action Plan 2013 to 2020 to improve access and quality of care for people with severe mental illness, with the specific inclusion of general physical health care. The action plan promotes integrated health care that addresses mental health alongside physical health at all levels of care (WHO, 2013).

Recovery/Remission

The WHO has ranked schizophrenia as the third most disabling illness among people aged 15 to 44 years. Despite the widespread use of antipsychotics, just 1% to 2% of every 100 patients qualify as “recovered” each year (Malhotra, Marder, & Weiden, 2014). According to Castle and Buckley (2011), about 40% of cases have a very poor outcome. Studies of the course of schizophrenia have reported significantly varying rates of recovery/remission and widely different definitions. Remission is defined as a state of improvement in psychosis or reality distortion, disorganization, and negative symptoms for at least 6 months (Castle & Buckley, 2011). Jaaskelainen et al. (2013) defines recovery as an improvement in both clinical and social functioning with some mild residual symptoms. WHO (2013) defines recovery from the perspective of the individual as experiencing hope, healing, empowerment, and connection, and is not synonymous with cure. There has been a recent emphasis on the recovery paradigm in treating schizophrenia. This paradigm places the individual in the center of his or her care and emphasizes a holistic approach. The goal of treatment is not only on symptom amelioration but also on well-being, social integration, vocational success, and achievement of personal life goals (Castle & Buckley, 2011). In simple terms, recovery means having a meaningful life.

In a systemic review Jaaskelainen et al. (2013) found that the median proportion of individuals with schizophrenia who met the recovery criteria was 13.5%. Despite major changes in the treatment options in recent decades they found no evidence that recovery outcomes have improved over time. The majority of people with schizophrenia are unemployed, never marry, do not have college degrees, and struggle socially.

Evidence suggests that regional differences affect the recovery rates for individuals with schizophrenia. Haro et al. (2011) found that the symptom and functional remission rate was higher in low- and middle-income countries than in high-income countries. It has been suggested that sociocultural and environmental factors, such as close family support and interaction, play an important role in the higher recovery rate.

DIAGNOSING A THOUGHT DISORDER

Thought disorders include schizophrenia and its four subtypes: schizophreniform disorder, schizoaffective disorder, delusional disorder, and brief psychotic disorder. Each disorder has a specific set of diagnostic criteria that a patient must meet for diagnosis.

Schizophrenia

SCHIZOPHRENIA is a thought disorder that involves bizarre behavior, thoughts, movements, perceptions, and emotions. There is no single symptom or sign that defines the disorder. Symptoms experienced by the patient are typically divided into positive and negative categories. Positive symptoms are excessive or amplified variations of normal functioning, such as:

Negative symptoms reflect a diminished presentation of emotional expression and include:

For diagnosis, the disease must be present for at least 6 months. During this time frame, the patient must actively demonstrate the symptoms for a significant period of 1 month.

Individuals with schizophrenia display a wide range of symptom types and expressions. Clinicians now use a dimensional approach to diagnose and rate severity for the core symptoms of schizophrenia. The dimensions assessed are delusions, hallucinations, disorganization, negative symptoms, impaired cognition, depression, mania, and psychomotor symptoms including catatonia. Quantitative measurements using a simple rating scale (0–4) can be used to capture the severity of symptoms (Tandon & Bruijnzeel, 2014).

Psychotic symptoms can be assessed within stages or phases of the illness. The prodromal phase of the illness can occur over months or even years. Changes in behavior, such as withdrawal from usual activities, and strange or unusual thinking can occur suddenly or family members may notice subtle changes over several years. It is important to recognize symptoms at this stage as early therapeutic interventions may be employed to halt the progression or reduce the severity of symptoms. The active phase of the illness is associated with the emergence of psychotic symptoms which may include auditory hallucinations, delusions, or disorganized thinking and behavior. Auditory verbal hallucinations are the most frequent and disturbing symptom. According to Tusaie and Fitzpatrick (2013), approximately 60% to 80% of patients experience “hearing voices.” The content of the voices is usually negative, derogatory, and sometimes commands or urges one to act in a negative manner. Delusions typically are persecutory (the feeling that one is being watched, harmed, or plotted against) or GRANDIOSE (one has great wealth, power, or influence). Both types of delusions may also be present. Other common themes are jealousy, religiosity, or somatization. Delusions tend to be organized around a common theme and are sometimes referred to as systematized. Hallucinatory content is also related to the delusions. Persons can be aloof, superior, and patronizing, and predisposed to suicide and violence.

At times, the illness can be characterized by silliness and laughter that is not connected to speech content, and individuals often have trouble with organization and tasks. For example, the person may have difficulty with activities of daily living. Catatonic symptoms are characterized by psychomotor disturbances, which may include immobility, excessive motor activity, extreme negativism, mutism, peculiar voluntary motor movement, echolalia, or echopraxia. Motor immobility may be manifested by catalepsy (waxy flexibility) or stupor. Voluntary movement may be peculiar and include assuming uncomfortable postures or grimacing. During periods of severe stupor or excitement, the person may require careful supervision to avoid injury to self or others. He or she is also at risk for dehydration, malnutrition, and exhaustion.

In the residual phase, the active phase symptoms are no longer prominent. Cognitive impairment, or negative symptoms, usually remain and affect how the patient is able to function in daily life. Treatment is aimed at preventing relapse, maintaining adequate community support, offering vocational rehabilitation, and avoiding isolation.

Schizophreniform Disorder

Schizophreniform disorder shares identical essential features with schizophrenia with two differences. First, the total duration of the illness is at least 1 month but less than 6 months. Second, impaired social or occupational functioning during some part of the illness, although it may occur, is not required as a criterion. If the diagnosis persists beyond 6 months, it is changed to schizophrenia.

Schizoaffective Disorder

Schizoaffective disorder occurs as an uninterrupted period of illness during which there is a major depressive, manic, or mixed episode concurrent with the characteristic symptoms of schizophrenia. In addition, delusions or hallucinations are present. Persons with schizoaffective disorder may have marked difficulties in social contact and self-care. The risk for suicide also is increased. Residual symptoms may be less than in schizophrenia but ANOSOGNOSIA (poor insight) is often present and can result in poor treatment adherence. The incidence of this type of SSD is higher in women. The overall prognosis of schizoaffective disorder is better than that for schizophrenia. In addition, schizoaffective disorder also appears to increase the risk of schizophrenia and mood disorders in first-degree relatives. At times, it may be difficult to distinguish schizoaffective disorder from mood disorder with psychotic features. The distinguishing feature is that in mood disorder with psychotic features, the psychotic symptoms occur within the context of the mood disorder.

Delusional Disorder

Delusional disorder is characterized by the presence of one or more non-bizarre delusions that persist for more than 1 month in a person who has never had a symptom presentation that met the diagnosis of schizophrenia. Hallucinations, if present, are not prominent. Evaluating delusions as non-bizarre can be problematic, especially in relation to cultural differences between the health care professional and the patient. In such cases, the determination can be made by considering plausibility, understandability, and the life experiences of the person. The individual’s functional level may be variable because some behavior surrounding the delusions could diminish functioning. For example, if one believes he or she has a serious disease, he or she may self-isolate and seek medical treatments that could ultimately be harmful. More often, social and interpersonal functioning problems are greater than occupational functioning. The disorder tends to develop later in life compared with schizophrenia. Patients may experience periods when the disorder is fairly quiet. Additionally, the prognosis is often improved when the disorder occurs in response to a stressful event.

Brief Psychotic Disorder

Brief psychotic disorder is a thought disorder that usually has an abrupt onset with at least one positive symptom associated with the characteristics of schizophrenia. This disorder, occurring most often during the second or third decade of life, commonly lasts between 1 and 30 days. The person has a full remission during the specified time period. Although the duration of the disorder is brief, it may be quite intense and require a high level of supervision. The risk for suicide is especially high for younger persons. Individuals diagnosed with certain personality disorders such as borderline, paranoid, narcissistic, and histrionic personality disorders may be at increased risk for this diagnosis. (See Chapter 14 for a discussion on personality disorders.)

ETIOLOGY OF SSD

According to the Global Burden of Disease study in 2010, the burden of mental disorders has increased by 37.6% in the last two decades, with a growing challenge for countries to make prevention and treatment of mental health issues a public health priority (Whitford et al., 2013). In the United States, 12.6% of disability-adjusted life years are caused by mental disorders, with SSD accounting for half of those disability-adjusted years (Murray et al., 2013). SSD affects individuals in nearly all aspects of their lives, including vocational, interpersonal, intrapsychic, and social competencies. These disorders tend to emerge in young adulthood and are lifelong conditions creating stress for families and communities. Unfortunately, the exact etiology of SSD is unknown.

Theories on the etiology of any disorder are important because ascertaining the cause of a disorder is helpful in developing treatment and prevention strategies. Psychosocial and biological theories are described here. However, since the discovery of antipsychotic drugs in the 1950s, the direction of research on the etiology of SSD has radically shifted in favor of biological theories.

Psychosocial Theories

Although the early psychosocial theories have been replaced, evolved, or discredited, their legacy may be important. These etiological conceptualizations of SSD continue to exert some influence on the current understanding. For example, the recognition of the importance of relationships and communication, an appreciation of the conditions under which the diagnosis and treatment take place, and the recognition of family influence and distress in the face of a devastating illness are still viewed as important clinical factors that arose from earlier speculations about the origins of these serious disorders.

In the early years of the 20th century, psychoanalytic theory was used to explain the etiology of a wide range of psychiatric disorders, including SSD. Speculation was that the “schizophrenia process” began in the first few years of life as a result of a faulty maternal relationship. This pathological relationship with the “first love object” created anxiety, leading to the expectation of a world that could not be trusted (Ferriera, 1961). Much of the support for this conceptualization came from case material obtained during the psychoanalysis of schizophrenic patients. The “schizophrenogenic mother” theory that resulted from these case reports negatively affected the relationship between mental health professionals and families during the period of this theory’s acceptance. While this concept has dissipated considerably over the last 30 years, some lingering distrust remains.

In the 1920s, Harry Stack Sullivan, a psychoanalyst by training, began to integrate the theories of anthropology and the newly emerging field of social psychology into an evolving psychodynamic theory emphasizing interpersonal relationships in the etiology of schizophrenia. He theorized that the patient’s observed maladaptive behaviors were the result of a history of faulty communication between the affected individual and the rest of society. Sullivan’s contribution is important because he recognized the critical nature of the individual’s relationships with others and his or her social and interpersonal environment to the development of pathology, rather than viewing it as the result of an intrapsychic experience (Evans, 1996).

During the mid-1950s, early family theories attributed the development of schizophrenia to disordered family communication. The speculation was that in the families of persons with SSD, homeostasis was maintained by a process called pseudomutuality. This process reflects a façade of family harmony maintained by a denial of problems. However, those problems later became manifested as troubled behaviors in the most vulnerable family member, the person who developed schizophrenia. While the family remained together, the burden of unresolved family issues was borne by the person with SSD (Ferriera, 1961). This theory is no longer accepted by mainstream clinicians.

Current research supports that psychological and social factors influence the emergence of symptoms of SSD in vulnerable individuals. No evidence exists to support the belief that psychosocial factors alone can induce SSD in persons without a biological predisposition. Research has consistently supported that proximal stressful life events can influence the emergence of many psychiatric and physical conditions in humans, including SSD. Also, it may be true that early traumatic life events could increase the risk for mental health problems later in life, but again, this is not specific to SSD.

Special psychosocial contexts may exist in which SSD is more likely to emerge through a type of psychosocial “perfect storm.” Here, stressful circumstances work together synergistically to influence symptom emergence. A possible example could be immigration. In such a context, individuals leave their country of origin as a result of fear or actual torture. They arrive in another culture where they do not speak the dominant language and are thus socially isolated and unable to validate their experiences. They may be made to feel unwelcome by officials (police) or neighbors. In addition, they commonly have the added stress of poverty due to poor employment opportunities. In such circumstances, a degree of paranoia may be adaptive for some but it may tip the balance toward illness in especially vulnerable persons.

Family interaction is another possible link to SSD. High levels of negative expressed emotion (EE) in family interaction appear to influence relapse in persons with SSD. Negative EE is characterized by communication that is hostile, critical, and emotionally overintrusive. A negative emotional climate in the family is predictive of relapse. Studies involving high levels of expressed emotion have led to an increased understanding of the importance of family involvement in treatment. In addition, the studies have led to successful family interventions, which have reduced relapse rates (Mura, Petretto, Bhat, & Carta, 2012).

Biological Theories

Despite intense efforts in the recent past in this area, the specific biological etiology of SSD is still unknown. Cannabis appears to be a risk factor but probably needs to act with other vulnerability factors to be a causal cumulative factor (Castle & Buckley, 2011).

Epidemiological studies of SSD point to a number of perinatal risk factors for schizophrenia. These include winter birth; urban birth setting and associated issues such as pollution or crowding; intrauterine infections such as rubella, influenza, or polio; pre-eclampsia (a pregnancy-related condition involving elevated blood pressure); low birth weight; or Rh incompatibility. In addition, maternal stress such as famine, depression, or an unwanted pregnancy is also associated with the later development of SSD. Unfortunately, no common mechanism of injury related to these multiple, contributing, antecedent conditions can account for the development of a disorder, nor do they provide an explanation for why the disease emerges decades after the original insults (Castle & Buckley, 2011).

Genetics

Genetics is the greatest known risk factor predisposing an individual to develop SSD. In a meta-analysis of twin studies on schizophrenia, Sullivan, Kendler, and Neale (2003) quantified the genetic and environmental contribution to the development of schizophrenia as 81% and 11%, respectively. Twin studies have also demonstrated that the concordance rate (presence of the same trait in each twin) for schizophrenia is about 40% to 50% between monozygotic twins and about 10% between siblings, both highly suggestive of an inherited disorder. One particular gene has not been identified as causative; rather, a set of genes likely contributes to development of the disorder. One particular area of scrutiny in the field is those genes that govern neurodevelopment. Recent research seems to strongly suggest that schizophrenia arises from a neurodevelopmental disorder in which the roots of the disease are related to abnormal brain development (Castle & Buckley, 2011).

Neuroanatomical Factors

Various nonspecific macro- and micro-neuroanatomical findings are associated with SSD. The most common macro features are enlargement of the cerebral lateral ventricles, enlarged third ventricle, and reduced overall grey matter volume. In the temporal lobe, there is volume reduction in the amygdala and hippocampus, and appears more marked on the left side. The size of the prefrontal cortex appears diminished in persons with SSD who experience prominent negative symptoms. In monozygotic twins, the overall brain volume of the twin affected by SSD is decreased. Micro-abnormalities have also been observed with widespread cortical and cerebellar atrophy (Castle & Buckley, 2011).

Neurochemical Factors

Currently, two prominent neurochemical theories attempt to explain the etiology of SSD. The first, called the dopamine hypothesis, is supported by the 50-year history of treatment with antipsychotic medications that block dopamine. According to this theory, a dysregulation of dopamine is the underlying etiologic mechanism responsible for SSD. This dysregulation involves overactivity in the mesolimbic dopamine pathway, contributing to positive symptoms, and underactivity in the mesocortical dopamine pathway, contributing to negative and cognitive symptoms. A second neurochemical theory of SSD is the glutamate hypothesis. This theory posits that alterations in the N-methyl-D-aspartate (NMDA) glutamate receptor are the mechanism responsible for all symptoms of SSD (positive, negative, and cognitive) due to its excitatory role in the central nervous system. One of the reasons that the NMDA glutamate hypothesis has captured the attention of researchers is that it plays an important role in neurodevelopmental processes both in utero and during adolescence, critical periods in development according to several current theories. There is also some evidence that gamma amino acid butyric acid (GABA) neurotransmission is dysfunctional in schizophrenia. GABA is the main inhibitory neurotransmitter and it has been suggested that cognitive deficits in schizophrenia may be related to altered GABA transmission (Keshavan, Nasrallah, & Tandon, 2011).

TREATMENT OPTIONS

The treatment of SSD requires medical/pharmacological, environmental, psychosocial, and social interventions. None of these categories of treatment alone is sufficient to assist persons with SSD to live their lives to their fullest potential. Individuals living with SSD will require a combination of interventions across their lifetimes. Depending on their age and the severity and acuity of their condition at a given time, the priority of treatment interventions will vary.

The view of patients with SSD leading productive and satisfying lives traditionally has been pessimistic. Although newer treatment paradigms that combine pharmacological and psychosocial treatment modalities have proved helpful, some of the greatest strides forward are being attributed to the activities of the consumer movement that has given voice to persons with serious mental illnesses. Consumers have sought to de-emphasize the medical model that recognizes symptom reduction as the major goal of all treatment activities in favor of such concepts as empowerment, interpersonal and vocational competency, autonomy, and hope. The recovery paradigm is now widely accepted as the contemporary approach to treating schizophrenia (Compton, 2010). Jaaskelainen et al. (2013) reported that recovery rates can range from 8% to 20% or about one in seven individuals.

Pharmacological Therapy

Following is an overview of pharmacological therapy for SSD; the reader is referred to other pharmacological resources for more in-depth information. Medications used to treat SSD are called antipsychotic agents and typically are classified as first-generation or second-generation antipsychotics. They do not cure the disorder but research has shown that they are effective in managing the symptoms. Typically, medications used for psychiatric-mental health conditions are indicated for use in more than one disorder. For example, the drug olanzapine (Zyprexa) is indicated for use in psychosis and mood instability.

Generally, the therapeutic mechanism of action of antipsychotic drugs involves dopamine blockade in a number of central nervous system receptors. It is theorized that typical or first-generation antipsychotics block dopamine in the mesolimbic pathway, which likely dampens positive symptoms of the disorder. However, they also cause side effects by blocking dopamine in the nigrostriatal pathway and the tuberoinfundibular pathway, leading to parkinsonism and increased prolactin secretion (resulting in galactorrhea, amenorrhea, and decreased libido), respectively. First-generation antipsychotic agents also cause other side effects such as sedation, seizures, arrhythmias, and orthostatic hypotension. However, the most troubling side effects are the extrapyramidal symptoms, which include parkinsonism, akathisia, dystonias, and tardive dyskinesia and neuroleptic malignant syndrome (Box 11-1).

Atypical or second-generation antipsychotics are effective in treating positive symptoms of SSD, and perhaps negative symptoms as well. Their hypothesized action involves a simultaneous blockade of dopamine and serotonin receptors. Available serotonin then inhibits dopamine release to different degrees in different pathways. The greatest inhibition occurs in the desired mesolimbic pathway while decreasing the blockade in the nigrostriatal and tuberoinfundibular pathways. The decreased blockade in the latter two pathways leads to a decrease in the undesirable side effects noted previously. They may cause sedation, anticholinergic effects, orthostatic hypotension, prolongation of the QTc interval, difficulties of sexual arousal, and agranulocytosis. Additionally, second-generation agents are associated with the development of metabolic syndrome (central obesity weight gain, glucose intolerance, and hyperlipidemia) in many patients. Drug Summary 11-1 lists first- and second-generation antipsychotics and implications for the interpersonal process.

 

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DRUG SUMMARY 11-1:
ANTIPSYCHOTIC AGENTS

DRUG	IMPLICATIONS FOR NURSING CARE

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FIRST-GENERATION ANTIPSYCHOTIC DRUGS
chlorpromazine (Thorazine) perphenazine (Trilafon) trifluoperazine (Stelazine) fluphenazine (Prolixin) thioridazine (Mellaril) thiothixene (Navane) haloperidol (Haldol) loxapine (Loxitane)	Work with the patient on measures to reduce anticholinergic effects such as the use of sugarless gum or hard candy to alleviate dry mouth     Institute safety measures to prevent falls     Urge patient to report complaints of dizziness when rising from lying to sitting position or sitting to standing position     Allow patient to verbalize feelings and issues related to drug therapy; work with patient and family to develop a method for ensuring adherence to drug therapy     Monitor the patient for development of extrapyramidal side effects     Be alert that neuroleptic malignant syndrome most often occurs during the first 2 weeks of therapy or after a dosage increase
SECOND-GENERATION ANTIPSYCHOTIC DRUGS
clozapine (Clozaril) risperidone (Risperdal) olanzapine (Zyprexa) quetiapine (Seroquel) ziprasidone (Geodon) aripiprazole (Abilify) paliperidone (Invega) iloperidone (Fanapt) asenapine (Saphris) lurasidone (Latuda)	Instruct the patient using aripiprazole (Abilify) not to take the drug with grapefruit juice     For the patient taking clozapine, obtain baseline white blood cell counts to assess for agranulocytosis; explain to the patient that he or she will receive only a 1-week supply of the drug; assist the patient in arranging for follow-up weekly blood tests for the first 6 months of therapy; monitor the patient closely for signs and symptoms of infection; stress the need for not stopping the drug abruptly     Allow patient to verbalize feelings and issues related to drug therapy; work with patient and family to develop a method for ensuring adherence to drug therapy     Monitor the patient for development of extrapyramidal side effects     Be alert that neuroleptic malignant syndrome most often occurs during the first 2 weeks of therapy or after a dosage increase

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