schizophrenia thesis statement

Schizophrenia - Essay Samples And Topic Ideas For Free

Argumentative essays can be prepared on different subjects and reveal different issues of the science branch. Medicine is among the most popular sciences that medical college or university students choose. They can be asked to describe different types of illnesses: a symptom, conditions of progression, and methods to handle them. If you are given to craft an essay about Schizophrenia, we recommend you get familiar with our list of argumentative essay topics to opt for the unique one. Then, you can find some essay examples on Schizophrenia to understand how to accurately provide your research and content.

Schizophrenia is a disease that leads to a psychological disorder. Such diseases affect a person’s health, and they can experience hallucinations. To be able to uncover the entire topic, you should explore many sources and use writing samples. You can also find a documentary movie that reflects the life of people diagnosed with Schizophrenia. We understand how difficult it can be to keep all information in your head. That’s why it is advisable to draw an outline and fix there all your ideas about your topic. It is important to organize your content through an introduction, main body, and conclusion. When determining thesis statements, mention them in the introductory part and conclude them. You can find a research paper example about Schizophrenia on our platform.

Two Different Approaches Used to Explain the Psychological Phenomenon of Schizophrenia

Schizophrenia is a very rare psychological disorder or brain condition that a significantly small number of people. This disorders most common symptoms include hallucinations or hearing voices, and having a hard time with concentrating or thinking. When most people think of someone having Schizophrenia, they think of a person who is crazy or not in their ""right mind,"" which is not really the case. Sometimes, Schizophrenia is also often mistaken for Dissociative Identity Disorder, which can be similar in a […]

Schizophrenia – the Beautiful Mind of John Forbes Nash Jr.

Patient's Information John Forbes Nash, Jr. was born in 1928 in Bluefield, West Virginia to John Forbes Nash Senior, an electrical engineer, and Margaret Virginia Nash, a school teacher. According to his biographer Sylvia Nasar, Nash's upbringing was stable and he benefited from his parents' middle-upper class status. Although socially awkward, Nash excelled in mathematics and was described as a mathematical genius by his professors. After attending the Carnegie Institute of Technology, Nash began graduate school at Princeton University in […]

A Psychological Diagnosis of John Wayne Gacy

In 1942, a baby was born in a Chicago hospital, named John Wayne Gacy. He came from what seemed like a normal family. He grew up with his two sisters, his mother, and his father. However, no one knew that Gacy's father was both verbally and physically abusing him. This would ultimately affect Gacy for the rest of his life. In 1968, Gacy was indicted by a grand jury for allegedly committing the act of sodomy with a young teenage […]

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Cognitive Behavioral Therapy for Schizophrenia

Schizophrenia is a major psychiatric disorder, or cluster of disorders, characterized by psychotic symptoms that alter a person's perception, thoughts, affect and behavior (NICE, 2009). Tai and Turkington (2009) define Cognitive Behavior Therapy (CBT) as an evidence-based talking therapy that attempts cognitive and behavioral change, based on an individualized formulation of a client's personal history, problems and world views. CBT was built on behavioral principles that emphasized clear relationships between cognition, physiology and emotion (Beck, 1952). This essay will look […]

Schizophrenia: Mind and Mental Health

Psychological clarity is something that everyone strives for. A mind that is free from abundant clutter and jumbled thoughts that bring on stress and negativity. Everyone wants a mind that is able to recognize what is presented to it. A reliable psyche that is free from hallucinations and unwanted paranoia. Even though clarity can be achieved, certain illnesses can hinder individuals from reaching it. There are a multitude of disorders that affect the mind in more ways than one. The […]

The Wrongful Conviction of Charles Milles Manson

The first: Charles Manson as the ringleader, the main man, the cult king. He ordered his followers to do everything. The other, a group of middle aged "hippies" caught up in heavy drug use committed all the murders. They later accused a mentally ill man who was a delusional schizophrenic that they took in as a mascot, of orchestrating all the murders. Carrie Leonetti provides a wonderful argument and presents many facts and statistics as to how Charles Manson could […]

The Causes Effects and Treatments of Schizophrenia

Schizophrenia is a very complex, chronic mental health disorder. It is often characterized by displaying multiple symptoms which may include, but are not limited to, delusions, hallucinations, disorganized behavior and/or speech, and impaired cognitive ability. Schizophrenia affects about 1% of the population at some point in their lifetime (Patel, Cherian, Gohil, & Atkinson, 2014). The current Diagnostic and Statistical Manual of Mental Disorders (DSM-V) describes schizophrenia as an illness that displays psychotic symptoms and significant interpersonal or occupational dysfunction that […]

Schizophrenia – a Genetic and Environmental Review

Introduction Schizophrenia is defined as "a severe brain disorder characterized by disturbances of thoughts, perceptions, volition, and cognition, which affects about 1% of the world population today" (Ozawa et al., 2006, p. 546). The disorder can be incapacitating to those who live with it, preventing normal societal function. Despite its frequency in the population, scientists and medical professionals still struggle to find a conclusive explanation for why some people develop schizophrenia. This may be, in part, due to its ties […]

Schizophrenia: Definition, Symptoms, Causes

Schizophrenia alters how a person thinks, feels, and acts, making it hard for them to differentiate between reality and imagination. Individuals with schizophrenia can often become unresponsive or withdrawn, making it difficult to establish personal and professional relationships (Haycoco, 2009). Contrary to popular misconception, schizophrenia is not a split or multiple personality disorder. Most people with schizophrenia are non-violent and do not pose a danger to others (Mental Health America, 2013). People with schizophrenia may conjure up details about people […]

Schizophrenia in the United States

In the United States, schizophrenia is one of the most prevalent mental health disorders that Americans suffer from daily. Those who deal with such a debilitating disorder go through a variety of different symptoms that can be classified in three categories, positive, negative and cognitive. Initial symptoms of schizophrenia-like irritability and the inability to sleep may cause alarm before a diagnosis is made. Positive symptoms of schizophrenia, those symptoms that are not usually present, can include hallucinations and delusions ("How […]

Schizophrenia and Substance Abuse

Up to 60 percent of chronic schizophrenic patients have been reported to be substance abusers (Hambrecht 1). The comorbidity of drugs and alcohol asks the question if one disorder causes another disorder. From a collected sample of 232 schizophrenic patients, alcohol abuse prior to admission was found in 24 percent (Hambrecht 2). Whereas, drug abuse was found in 14 percent. These rates are two times higher than the rates in the general population (Hambrecht 2). Both alcohol and drug abused […]

Emotions and Schizophrenia

Do you know anyone with a mental disorder? Have you ever felt nervous around them? Do you feel it is hard to understand their feelings? Let me tell you about schizophrenia. I decided to further research schizophrenia when one of my brothers was diagnosed with it a couple of years ago. It was weird at first because I didn't feel comfortable around him due to the way he was acting. Even though it wasn't in a harmful way, I never […]

What is Schizophrenia?

Schizophrenia is a chronic mental disease that drastically affects how a person thinks, feels, and behaves. People with schizophrenia often seem disconnected from reality, with a long list of symptoms that significantly change the lives of those it affects. Throughout history, society has held resentment for the mentally ill and discriminated against them in terrible ways. Following the classification of schizophrenia, the disease became gravely misunderstood by the public. Society harshly stigmatized people with schizophrenia because of the extensive list […]

Schizophrenia: Chronic and Severe Mental Disorders

As we know, schizophrenia and its spectrum disorders are chronic and severe mental disorders that affect an individual in many aspects of life. These disorders impact the ability to think and feel and also affect behavior. This means that people with schizophrenia may seem as if they have lost touch with reality. Sometimes, diagnoses can be difficult as there are no specific tests and the only way to identify it is to recognize symptoms that negatively impact an individual's social […]

Portrayals of Schizophrenia by Media

In media portrayal of schizophrenia, such as A Beautiful Mind, schizophrenic characters are depicted as dangerous, violent, distrusting, paranoid, awkward, and unstable people that need to be hospitalized due to exaggerated delusions and hallucinations. Not only does this stigmatize the diagnosis, but it also inflates the reality of knowing someone with the diagnosis. In actuality, schizophrenia shares many of the same characteristics as other disorders such as OCD, depression, anxiety, and ADD, yet none of these disorders have a more […]

Bipolar Disorder and Schizophrenia

Bipolar disorder and schizophrenia affect many people. According to Mahoney (2017), over 2.5 million Americans over the age of 18 are believed to be living with bipolar I or bipolar II disorder. This does not include those who have not been diagnosed properly due to misinformation about symptoms. Schizophrenia affects approximately one percent of people worldwide, impacting men and women equally. Schizophrenia can strike anyone and usually occurs between the late teenage years and thirty years of age. Males typically […]

Living with Schizophrenia

In today's modern world, research has found and diagnosed multiple mental illnesses. Through this spread of information, psychologists generated Schizophrenia. According to the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Schizophrenia involves a range of cognitive, behavioral, and emotional symptoms, and can be difficult to diagnose. There is no test for it, resulting in the diagnoses involving the recognition of negative symptoms that impact social functioning. These symptoms include diminished emotional expression, delusions, and hallucinations, etc. all for […]

Mental Disorder: Schizophrenia

Schizophrenia is a mental disorder that affects many adults all around the world. It is usually diagnosed between the late teenage years and early 20s. Even though Schizophrenia is a mental disorder, it affects the entire body as well. It also has many symptoms that are usually misinterpreted and portrayed incorrectly in movies and everyday life. Schizophrenia is described as a mental disorder that makes the person suffering it seem like they are detached from reality. They usually experience delusions, […]

Schizophrenia and Problems in Everyday Lives

People with schizophrenia have a lot of struggles in their everyday lives. Their minds work differently than the average, mentally sound individual. Schizophrenia is defined as a long-term mental disorder of a type involving a breakdown in the relation between thought, emotion, and behavior, leading to faulty perception, inappropriate actions and feelings, withdrawal from reality and personal relationships into fantasy and delusion, and a sense of mental fragmentation (Oxford English Dictionary). Some examples of schizophrenia symptoms consist of delusion, hallucinations, […]

Modern Plague Vs Schizophrenia

Although the cause is unknown, this mental illness can be developed through factors such as genetics, brain chemistry, brain abnormality and environmental factors."" Schizophrenia affects more than 21 million people worldwide. Scientists are still unable to locate the cause of this disorder. Symptoms of this disorder include hallucinations, abnormal behavior, inability to complete activities, lack of pleasure, and emotional flatness. Although a cure has not yet been discovered, treatments may help. Even though the cause is unknown and the disease […]

Negative Symptoms of Schizophrenia

Mental health illnesses affect many people worldwide, among them is schizophrenia which is a chronic mental health disorder that affects a person's brain. Patients with schizophrenia can experience various symptoms as well as functional impairments. Symptoms include delusions, trouble concentrating, and hallucinations (Parekha, 2017). Schizophrenia also interferes with activities of daily living, social interactions, and occupational performance. Most patients will require financial assistance to help support themselves, because only a very low percentage of people are able to work full […]

Schizophrenia: Mental Illness that Controls how a Person Thinks, Behaves and Feels

When you have schizophrenia you lose touch with reality. You make things up and start to hallucinate and began to get violent. You can start feeling irritated and get mad easily at the person near or by you. It can be hard to handle a person with schizophrenia they can sometimes be intolerable, when dealing with someone with schizophrenia you need to keep an eye on them at all times. Schizophrenia normally starts between the ages of 16 and 30, […]

Growth Patterns and Risk of Schizophrenia

In the introduction of this article called Growth Patterns and Risk of Schizophrenia, it mentions how the growth and nutrition of a fetus can play a part that leads to schizophrenia. It includes, that during the fetal development stage if there is malnutrition can lead a higher risk of the baby developing schizophrenia The studies involve with adult height, weight, or growth patterns. In continuation it mentions that birth weight has an effect when it comes to disorders later in […]

Schizophrenia Symptoms and Treatment in a Beautiful Mind

The film A Beautiful Mind chronicles the adult life of John Nash Jr., a Nobel Prize recipient widely regarded as a brilliant mathematician who greatly influenced modern economic theory. The film focuses on Nash's decades long struggle with paranoid schizophrenia after he receives a diagnosis in 1958. Although it is well known that Nash was diagnosed with schizophrenia in real life, I will use this paper to discuss specific symptoms portrayed in the film, and consider how his treatment and […]

Age of Onset of Schizophrenia

Schizophrenia, which occurs in late adulthood, is characterized as a mental health disorder marked by psychotic features, disrupted relationships, and thought processes that disturb a person's mood, thoughts, and behavior. It affects approximately 1.1% of the world's population, or about three and a half million Americans (About Schizophrenia, 2018). Schizophrenia, a disease that impairs neurocognitive functioning (Snyder, 2013), requires long-term treatment given the varying severity of symptoms across different age groups. Affected individuals may suffer from delusions, false beliefs such […]

Schizophrenia and Stigma

While there are a variety of feasible and effective programs to reduce stigmatization among health professionals in mental health related areas, there are several other strategies that can be put in place by health professionals to counter stigmatization within the population. Thornicroft (2006) identifies some of them. First, health professionals would benefit from getting more involved in the media to properly inform the public about mental health issues. The media, often overly sensational, convey negative images of violence, weakness, and […]

A Beautiful Mind Summary: John Nash’s Struggle with Schizophrenia

A Beautiful Mind Summary: Hallucinations In the movie A Beautiful Mind, they bring forth multiple symptoms of schizophrenia. One of the most apparent symptoms shown is Johns's hallucinations. Hallucinations are "the experiencing of sights, sounds, or other perceptions in the absence of external stimuli." In Johns's case, in the movie, he heard as well as saw things that weren't real. The voices that he heard would talk directly to him, giving him commands and tasks to accomplish as well as […]

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How To Write an Essay About Schizophrenia

Understanding schizophrenia.

Before starting an essay about schizophrenia, it's important to have a comprehensive understanding of this mental disorder. Schizophrenia is a chronic and severe mental disorder that affects how a person thinks, feels, and behaves. It's characterized by distortions in thinking, perception, emotions, language, sense of self, and behavior. Begin your essay by explaining the symptoms of schizophrenia, which can include hallucinations, delusions, disorganized thinking and speech, and impaired cognitive ability. Discuss the known causes of schizophrenia, such as genetic factors, brain chemistry, and environmental influences. Also, explore the impact of schizophrenia on individuals' daily lives, including social interactions, employment, and self-care challenges.

Developing a Thesis Statement

A strong essay on schizophrenia should be centered around a clear, concise thesis statement. This statement should present a specific viewpoint or argument about schizophrenia. For example, you might discuss the challenges in diagnosing and treating schizophrenia, analyze the social stigma associated with the disorder, or explore the latest research in understanding its underlying causes. Your thesis will guide the direction of your essay and provide a structured approach to your analysis.

Gathering Supporting Evidence

To support your thesis, gather evidence from credible sources, such as medical journals, research studies, and healthcare professionals. This might include data on the prevalence of schizophrenia, treatment success rates, or personal narratives from individuals living with schizophrenia. Use this evidence to support your thesis and build a persuasive argument. Remember to consider different perspectives and address potential counterarguments to your thesis.

Analyzing Treatments and Challenges

Dedicate a section of your essay to analyzing the treatments available for schizophrenia and the challenges associated with them. Discuss various treatment methods, such as antipsychotic medications, psychotherapy, and community support. Explore the benefits and limitations of these treatments and the challenges patients face, such as medication side effects and the ongoing need for support and care. Additionally, consider the impact of societal attitudes and healthcare policies on the treatment and management of schizophrenia.

Concluding the Essay

Conclude your essay by summarizing the main points of your discussion and restating your thesis in light of the evidence provided. Your conclusion should tie together your analysis and emphasize the importance of understanding and effectively addressing schizophrenia in society. You might also want to suggest areas for future research or policy improvements that could benefit individuals with schizophrenia.

Reviewing and Refining Your Essay

After completing your essay, review and refine it for clarity and coherence. Ensure that your arguments are well-structured and supported by evidence. Check for grammatical accuracy and ensure that your essay flows logically from one point to the next. Consider seeking feedback from peers or mental health professionals to further improve your essay. A well-crafted essay on schizophrenia will not only demonstrate your understanding of the disorder but also your ability to engage with complex medical and social issues.

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Schizophrenia Research Paper

This sample schizophrenia research paper features: 6600 words (approx. 22 pages), an outline, and a bibliography with 6 sources. Browse other research paper examples for more inspiration. If you need a thorough research paper written according to all the academic standards, you can always turn to our experienced writers for help. This is how your paper can get an A! Feel free to contact our writing service for professional assistance. We offer high-quality assignments for reasonable rates.

Schizophrenia is a psychotic disorder characterized by disturbances in thought, emotion, and behavior. This research paper discusses the symptoms, etiology, treatment, and other pertinent issues concerning this mental illness.

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Get 10% off with 24start discount code, i. description and classification, a. symptoms, 1. delusions, 2. hallucinations, 3. disorganized speech, 4. disorganized or catatonic behavior, 5. negative symptoms, b. variability of symptoms among patients, c. subtypes of schizophrenia, ii. history, iii. demographic characteristics of schizophrenia, a. sex differences, b. social class differences, iv. life functioning and prognosis, a. long-term course, b. premorbid characteristics of schizophrenia, v. etiology: theories and research findings, a. brain abnormalities in schizophrenia, b. biochemical factors, c. genetics, d. obstetrical complications, e. viral infection, f. diathesis-stress model, vi. treatment and therapy, a. antipsychotic medication, b. psychological treatment, vii. summary.

Delusions are the primary example of abnormal thought content in schizophrenia. Delusional beliefs conflict with reality and are tenaciously held, despite evidence to the contrary. There are several types of delusions. Delusions of control is the belief that one is being manipulated by an external force, often a powerful individual or organization (e.g., the FBI) that has malevolent intent. Delusions of grancleur refers to patients’ beliefs that they are especially important and have unique qualities or powers (e.g., the capacity to influence weather conditions). In contrast, some patients express the conviction that they are victims of persecution or an organized plot, and these beliefs are referred to as delusions of persecution. Examples of more specific delusions include thought broadcasting, the patient’s belief that his or her thoughts are transmitted so that others know them, and thought withdrawal, the belief that an external force has stolen one’s thoughts.

Hallucinations are among the most subjectively distressing symptoms experienced by schizophrenia patients. These perceptual distortions vary among patients and can be auditory, visual, olfactory, gustatory, or tactile. The majority of hallucinations are auditory in nature and typically involve voices. Examples include the patient hearing someone threatening or chastising him or her, a voice repeating the patient’s own thoughts, two or more voices arguing, and voices commenting. The second most common form of hallucination is visual. Visual hallucinations often entail the perception of distortions in the physical environment, especially in the faces and bodies of other people.

Other perceptual distortions that are commonly reported by schizophrenia patients include feeling as if parts of the body are distorted in size or shape, feeling as if an object is closer or farther away than it actually is, feeling numbness, tingling, or burning, being hypersensitive to sensory stimuli, and perceiving objects as flat and colorless. In addition to these distinctive perceptual abnormalities, persons suffering from schizophrenia often report difficulties in focusing their attention or sustaining concentration on a task.

It is important to note that in order for an unsubstantiated belief or sensory experience to quality as a delusion or hallucination, the individual must experience it within a clear sensorium (e.g., unsubstantiated sensory experiences that occur only upon awaking from sleep or when falling asleep would not qualify as delusions). Thus, for example, if a patient reports hearing something that sounds like voices when alone, but adds that he or she is certain that this is a misinterpretation of a sound, such as the wind blowing leaves, this would not constitute an auditory hallucination.

The DSM uses the term disorganized speech to refer to abnormalities in the form or content of the individual’s verbalizations. It is assumed that these abnormalities reflect underlying distortions in the patient’s thought processes. Thus the term thought disorder is frequently used by researchers and practitioners to refer to the disorganized speech that often occurs in schizophrenia.

Problems in the form of speech are reflected in abnormalities in the organization and coherent expression of ideas to others. One common abnormality of form, incoherent speech, is characterized by seemingly unrelated images or fragments of thoughts that are incomprehensible to the listener. The term loose association refers to the tendency to abruptly shift to a topic that has no apparent association with the previous topic. In general, the overall content of loosely associated speech may be easier to comprehend than incoherent speech. In perseverative speech, words, ideas, or both are continuously repeated, as if the patient is unable to shift to another idea. Clang association is the utterance of rhyming words that follow each other (e.g., “a right, bright kite”). Patients choose words for their similarity in sound rather than their syntax, often producing a string of rhyming words.

The overt behavioral symptoms of schizophrenia fall in two general areas: motor functions and interpersonal behavior. Motor abnormalities, including mannerisms, stereotyped movements, and unusual posture, are common among schizophrenia patients. Other common signs include bizarre facial expressions, such as repeated grimacing or staring, and repeated peculiar gestures that often involve complex behavioral sequences. As with other symptoms of the psychosis, the manifestation of motor abnormalities varies among individuals. Schizophrenia patients sometimes mimic the behavior of others, known as echopraxia, or repeat their own movements, known as stereotyped behaviors. Although a subgroup of patients demonstrate heightened levels of activity, including motoric excitement (e.g., agitation or flailing of the limbs), others suffer from a reduction of movement. At the latter extreme, some exhibit catatonic immobility and assume unusual postures that are maintained for extended periods of time. Some may also demonstrate waxy flexibility, a condition in which patients do not resist being placed into strange positions that they then maintain. Catatonia has decreased dramatically in recent decades, so that it is now rare. Several researchers have attributed this decline to the introduction of antipsychotic medication (described later).

In the domain of interpersonal interactions, schizophrenia patients frequently demonstrate behaviors that are perceived as bizarre or inappropriate by others. For example, it is not uncommon for patients to use socially unacceptable language and unusual tones of voice, or to show overly dependent or intrusive behavior. Another common symptom, inappropriate affect, involves unusual emotional reactions to events and experiences. For example, patients may laugh at a sad or somber occasion, or be enraged by insignificant events. Finally, many patients manifest increasingly poor hygiene as their illness progresses. Their appearance may also be marked by disheveled clothing or inappropriate clothing, such as gloves and coats in the summer.

The symptoms of schizophrenia can be classified into the general categories of positive and negative. Positive symptoms involve behavioral excesses and most of the symptoms described earlier fall in to this category (e.g., delusions, hallucinations, and bizarre behaviors). In contrast, negative symptoms involve behavioral deficits. Examples include fiat affect (blunted expressions of emotion), apathy, and social withdrawal. In the domain of verbal expression, schizophrenia patients who manifest a very low rate of verbal output are described as showing poverty of speech. Patients whose speech is normal in quantity, but lacks meaning, suffer from poverty of content. Recently, some researchers have suggested that positive and negative symptoms may be caused by different neural mechanisms.

It is important to mention that a reduction in overt displays of emotion does not necessarily imply that patients have less intense subjective emotional experiences than the average person. In fact, recent findings indicate that blunted emotional expressions can coexist with intense subjective feelings of emotion.

According to DSM-IV, patients must show two or more of the preceding five symptoms to meet the diagnostic criteria for schizophrenia. Thus, no one of these symptoms is required for the diagnosis. Furthermore, the following four criteria must also be met: (1) the patient shows marked deterioration in occupational, interpersonal, or domestic functioning; (2) the patient manifests continuous signs of symptoms or dysfunction for at least 6 months; (3) the patient does not manifest predominant signs of mood disturbance (e.g., depression or mania); and (4) the symptoms are not caused by substance abuse or a primary medical condition.

Because the diagnostic criteria for schizophrenia are relatively broad, with no one essential symptom, there is a great deal of variability among patients in their symptom profiles. It has therefore been proposed that schizophrenia is a heterogeneous disorder with multiple causes. It is also the case, however, that patients must show a marked and persistent impairment to meet the diagnostic criteria for schizophrenia. Thus, those who meet criteria for the diagnosis are significantly impaired in everyday functioning. For many individuals who are diagnosed with schizophrenia, independent functioning is never achieved.

The DSM lists five subtypes of schizophrenia. In schizophrenia of the paranoid type, delusional concerns about persecution and/or preoccupation with threat dominate the clinical presentation, although delusions of grandeur are also often present. Disorganized schizophrenia is distinguished by extremely incoherent speech and behavior, as well as blunted or inappropriate affect. In catatonic schizophrenia, the clinical picture is dominated by abnormalities in movement and posture, such as those described earlier. Patients classified as having undifferentiated schizophrenia do not meet criteria for any of the previous subtypes. Finally, the diagnosis of residual schizophrenia is applied to patients who have had at least one episode of schizophrenia and who continue to show functional impairment, but who do not currently manifest any positive symptoms.

During the late 1800s and early 1900s, Emil Kraepelin and Eugen Bleuler provided the first conceptualizations of schizophrenia. Kraepelin defined “dementia praecox,” the original term for schizophrenia, as an endogenous psychosis characterized by intellectual deterioration (dementia) and early onset (praecox). Kraepelin included negativism, hallucinations, delusions, stereotyped behaviors, attentional difficulties, and emotional dysfunction as major symptoms of the disorder. Kraepelin’s work focused on description and phenomenology, leaving subsequent researchers to investigate the cause or causes of the disorder.

In contrast to Kraepelin, Eugen Bleuler, a Swiss psychiatrist, proposed a broader view of dementia praecox, with a more theoretical emphasis. Bleuler contested two of Kraepelin’s defining assumptions: specifically, that the psychosis was typically characterized by early onset and intellectual deterioration. Bleuler attempted to identify an underlying commonality among the diverse variations of what Kraepelin referred to as dementia praecox and concluded that all of the patients suffered from a “breaking of associative threads,” causing a disharmony among communicative and thought processes. He believed this abnormality accounted for the problems of thought, emotional expression, decision making, and social interaction associated with schizophrenia. Guided by the defining principle of disharmonious mental structures, Bleuler renamed the disorder “schizophrenia,” meaning “split mind.”

In the early to mid-1900s, American psychiatrists continued to use a broad definition of schizophrenia. The distinction between process and reactive schizophrenia was considered important, however, because it was assumed to distinguish between cases characterized by gradual deterioration (process) and cases that were precipitated by acute stress (reactive).

During this time, some clinicians and researchers viewed the specific diagnostic criteria for the major mental illnesses (schizophrenia, bipolar disorder, major depression) as artificial and discretionary, and used instead flexible and inconsistent standards for diagnoses. Studies that compared the rates of disorder across nations revealed that schizophrenia was diagnosed at a much higher rate in the United States than in Great Britain and some other countries. This national difference resulted from the use of broader criteria for diagnosing schizophrenia in the United States. Many patients who were diagnosed as having depression or bipolar disorder in Britain were diagnosed with schizophrenia in the United States. Because subsequent revisions in the DSM have included more restrictive criteria for schizophrenia, U.S. diagnostic rates are now comparable with other countries.

In addition to a more restrictive definition of schizophrenia, subsequent editions of the DSM have included additional diagnostic categories that contain similar symptoms. Thus the range of “schizophrenia spectrum disorders” continue to broaden with the description of variants of schizophrenia, such as schizoaffective disorder, which is characterized by a mix of affective and psychotic symptoms. The diagnostic category of schizophreniform disorder was also added. This diagnosis is given when the patient shows the typical symptoms of schizophrenia, but does not meet the criterion of 6 months of continuous illness.

Estimates of the prevalence of schizophrenia converge at around 1% of the population. Although there is evidence of cross-national differences in the rate of schizophrenia, the differences are not large (i.e., 1 to 2% difference). It is, in fact, striking that the rate of occurrence is so consistent across cultures.

The modal age at onset of schizophrenia is in early adulthood, usually before 25 years of age. Thus most patients have not had the opportunity to marry or establish a stable work history before the onset of the illness. As a result of this, and the often chronic nature of the illness, many patients never attain financial independence. It is relatively rare for preadolescent children to receive a diagnosis of schizophrenia. Similarly, it is rare for individuals beyond the age of 40 to experience a first episode of the illness.

Although it has traditionally been assumed that there is no sex difference in the rates of schizophrenia, some recent research findings indicate that a somewhat larger proportion of males than females meet the DSM-IV criteria for the disorder. Nonetheless, the overall rates do not differ dramatically for men and women. It is well established, however, that women are more likely to have a later onset of illness, as well as a better prognosis. Women also show a higher level of interpersonal and occupational functioning during the period prior to illness onset. The reasons for this sex difference are not known, but it has been proposed by several theorists that the female sex hormone, estrogen, may function in attenuating the severity of the illness.

Compared with the general population averages, schizophrenia patients tend to have significantly lower incomes and educational levels. Poor urban inner city districts, inhabited by the lowest socioeconomic class, contain the largest proportion of schizophrenia patients. There is a sharp contrast between the rates of schizophrenia in the lowest socioeconomic class and all other levels, including the next higher level. Findings from various cultures suggest that rates of schizophrenia are almost two times higher in the lowest social class group compared with the next lowest.

These social class differences appear to be a partial consequence of the debilitating nature of the illness. The social-drift theory suggests that during the development of schizophrenia, people drift into poverty. When the incomes and educational levels of the parents of patients are compared with those of the general population, the differences are not as striking.

There is, nonetheless, evidence that patients do come from families where the incomes and educational backgrounds of the parents are slightly below the average. These findings have led researchers to conclude that there may be a causal link between social class and risk for the illness. The sociogenic hypothesis posits that situational factors associated with low social class, such as degrading treatment from society, low levels of education, and few opportunities for achievement and reward, produce stress that contributes to the risk for schizophrenia.

Before the introduction of antipsychotic medications in 1950, the majority of patients spent most of their lives in institutional settings. There was little in the way of programs for rehabilitation. But contemporary, multifaceted treatment approaches have made it possible for most patients to live in community settings.

Of course, during active episodes of the illness, schizophrenia patients are usually seriously functionally impaired. They are typically unable to work or maintain a social network, and often require hospitalization. Even when in remission, some patients find it challenging to hold a job or to be self-sufficient. This is partially due to residual symptoms, as well as to the interruptions in educational attainment and occupational progress that result from the illness. However, there are many patients who are able to lead productive lives, hold stable jobs, and raise families. With the development of greater community awareness of mental illness, some of the stigma that kept patients from pursuing work or an education has diminished.

For about one third of patients, the illness is chronic and is characterized by episodes of severe symptoms with intermittent periods when the symptoms subside but do not disappear. For others, there are multiple episodes with periods of substantial symptom remission. About one third of those who receive the diagnosis eventually show a partial or complete recovery after one or two episodes.

Several factors have been linked with a more favorable prognosis for schizophrenia. Early treatment seems to be important in that the shorter the period between the onset of the patient’s symptoms and the first prescribed medication, the better the clinical outcome. Another indicator of better prognosis is a high level of occupational and interpersonal functioning in the premorbid period. Also, as noted earlier, women and patients who have a later onset of symptoms have a better long-term outcome.

Some of the difficulties experienced by individuals with schizophrenia can be observed before the onset of the clinical symptoms. Deficits in social skills, concentration, emotional expression, motivation, and occupational or academic performance often precede the first clinical symptoms. This period of gradual decline in functioning before the first illness episode is referred to as the prodromal phase.

However, there are often more subtle signs of dysfunction long before the onset of the prodromal period. Controlled studies using archival data sources, such as medical and school records or childhood home-movies, indicate that subtle differences are discernible as early as infancy in some patients. Individuals who succumb to schizophrenia in adulthood sometimes have abnormal motor development and show deficits in emotional expression and interpersonal relationships in early childhood. Cognitive impairment and difficult temperament have also been observed. During middle childhood and adolescence, researchers have found evidence of neurological abnormality, poor emotional control, social immaturity, and academic performance deficits. Premorbid behavioral problems often become marked through the adolescent years, and many exhibit behavioral disturbances and cognitive abnormalities that resemble the clinical symptoms of schizophrenia.

The causes of schizophrenia are unknown, but it is now widely accepted by both researchers and clinicians that schizophrenia is biologically determined. This is in striking contrast to the early and mid-1900s, when many subscribed to the theory that faulty parenting, especially cold and rejecting mothers, caused schizophrenia in offspring.

There are several sources of evidence for the assumption that schizophrenia involves an abnormality in brain function. First, studies of schizophrenia patients have revealed a variety of behavioral signs of central nervous system impairment, including motor and cognitive dysfunctions. Second, when the brains of patients are examined with in vivo imaging techniques, such as magnetic resonance imaging (MRI), many show abnormalities in brain structure. Similarly, postmortem studies of brain tissue have revealed irregularities in nerve cell formation and interconnections.

Laboratory studies of schizophrenia patients have revealed a variety of abnormalities, including irregularities in smooth pursuit eye movements, psychophysiological responses to sensory stimuli, and concentration. Research on the neuropsychological performance of schizophrenia patients was first conducted in the 1950s and continues to the present time. Individual neuropsychological tests are designed to measure functions subserved by specific regions or systems of the brain. An early finding in this area was that schizophrenia patients were the one psychiatric group whose performance on neuropsychological tests was indistinguishable from people with known brain damage. The findings suggested a generalized cerebral dysfunction in schizophrenia. However, patients show the most consistent deficits on tests of attention and memory, indicating dysfunction of the frontal and temporal lobes and the hippocampus. Further evidence of dysfunction in these brain regions is derived from poor performance on tests of executive functions: the ability to formulate, maintain, and adapt appropriate responses to the environment.

Brain-imaging studies of schizophrenia have yielded results that mirror those obtained from neuropsychological research. Some relatively consistent findings are that the brains of schizophrenia patients have abnormal frontal lobes and enlarged ventricles. Enlarged ventricles suggest decreased brain mass, particularly in the limbic regions, which are intimately involved in emotional processing. Furthermore, ventricular size correlates with negative symptoms, performance deficits on neuropsychological tests, poor response to medication, and poor premorbid adjustment. These associations between ventricular enlargement and both premorbid and postmorbid characteristics suggest that the brain abnormalities are long-standing, perhaps congenital.

In addition to brain structure, investigators have examined biological indices of brain function in schizophrenia. Functional brain-imaging studies, with procedures such as positron emission tomography (PET) and measurement of regional cerebral blood flow, reveal that schizophrenia patients have decreased levels of blood flow to the frontal lobes, especially while performing cognitive tasks.

Researchers are now pursuing the question of what causes the brain abnormalities observed in schizophrenia. Although as yet there are no definitive answers, investigators have made continuous progress in identifying factors that are associated with risk for the disorder.

The structural brain abnormalities that have been observed in schizophrenia support the assumption that it is a disorder of the central nervous system. But it has also been shown that similar structural abnormalities (i.e., ventricular enlargement and volume reductions) are present in other disorders, both neurological and psychiatric. It is therefore assumed that specific abnormalities in brain biochemistry may play a role in schizophrenia.

The functioning of the central nervous system is dependent on a host of chemicals that serve as the “messenger substances” among neurons. These chemicals or neurotransmitters have been the subject of intense investigation. Among the various neurotransmitters that have been implicated in the neuropathophysiology of schizophrenia is dopamine. Dopamine is viewed as a likely candidate for two main reasons: (1) drugs that act to enhance the release or activity of dopamine can produce psychotic symptoms, and (2) drugs that have been established to have antipsychotic properties (i.e., reduce psychotic symptoms) reduce the activity of dopamine in the brain. Current theories of the role of dopamine in schizophrenia have focused on dopamine receptors. There is evidence that there may be an abnormality in the number or sensitivity of certain dopamine receptors in the brains of schizophrenia patients. To date, however, this evidence remains inconclusive.

Several other neurotransmitters have also been hypothesized to play a role in schizophrenia. Current theories under investigation include a malfunction of the receptors for a neurotransmitter called glutamate and an abnormality in the balance between dopamine and serotonin (another neurotransmitter which, like dopamine, has been implicated in the pathogenesis of schizophrenia). As research findings on the biochemical aspects of schizophrenia accumulate, it increasingly appears that the illness may involve multiple neurotransmitters, with different biochemical profiles for different patients.

A convincing body of research supports the notion of a genetic predisposition to schizophrenia. Behavioral genetic studies of families, twins, and adopted offspring of schizophrenia patients indicate that an inherited vulnerability is involved in at least some cases of the disorder.

There is an elevated risk of schizophrenia for individuals with a biological relative who suffers from the disorder, and the risk rates increase as a function of the genetic closeness of the relationship. For example, it has been estimated that children of schizophrenia patients have a 9 to 15 % likelihood of developing the illness, siblings of patients have an 8 to 14% likelihood, and cousins have a 2 to 6% likelihood of being diagnosed with schizophrenia. Given the general population rate of approximately 1%, relatives of patients are at statistically increased risk. It must be noted, however, that relatives share common experiences as well as common genes. Therefore, examinations of the prevalence of schizophrenia in the relatives of patients cannot elucidate the relative contributions of environmental and genetic factors.

Some investigators have studied the development of adopted children whose biological mothers had schizophrenia. This approach has the potential to provide more conclusive information than family studies. The results of these investigations show that when biological offspring of schizophrenic mothers are reared from infancy in adoptive homes they are more likely to develop schizophrenia than are adopted children from healthy mothers. Furthermore, these children also exhibit a higher rate of other adjustment problems when compared with controls. Studies of this type have clearly illustrated that vulnerability to schizophrenia can be inherited.

Research on twins examines differences in concordance rates between identical (monozygotic or MZ) and fraternal (dizygotic or DZ) twins. Twin studies rely on the fact that MZ twins essentially share 100% of their genes. Thus, environmental influences account for any behavioral differences between MZ twins. In contrast, DZ twins are no more genetically similar than regular siblings; DZ twins do, however, share more similar environmental factors than do nontwin siblings. To date, the results of twin studies have consistently shown that MZ twins are significantly more likely to be concordant for schizophrenia than are DZ twins.

At the same time, it is important to note that in at least 50% of the cases in which one member of an MZ twin pair has schizophrenia, the other does not. Such “discordant” pairs have been the subject of a recent, comprehensive investigation in the United States. Among the most important findings from this research project are those from the MRI scans conducted on the twins. The ill twins in the pairs showed significantly more brain abnormalities than the healthy twins. Most notable were reductions in the volume of certain brain regions, especially the hippocampus, and increases in the size of the ventricles. These results clearly indicate the importance of environmental factors in the etiology of schizophrenia.

As is the case with many other disorders that involve brain dysfunction, there is evidence that schizophrenia is associated with exposure to prenatal and delivery complications. Obstetrical complications (OCs) are defined as physical deviations from the normal course of events during pregnancy, labor, or the neonatal period. Estimates of OCs in schizophrenics have been as high as 67%, significantly higher than the rate of OCs found in normal controls.

Among the prenatal factors that have been found to be associated with increased risk for schizophrenia are prenatal maternal nutritional deficiency, viral infection, bleeding, and toxemia. Complications of delivery that can result in hypoxia have also been linked with heightened risk for the disorder. Hypoxia, a deficiency in the amount of oxygen available to the fetus, can affect the development of various parts of the brain. Some researchers argue that hypoxia results in hippocampal damage, thus contributing to vulnerability for schizophrenia. Low birth weight, a neonatal complication, is another potential early factor contributing to schizophrenia. There is evidence that low birth weight is related to increased ventricular size, which is a common characteristic of schizophrenia patients.

The findings on prenatal complications support the notion that fetal brain development may be disrupted in individuals who later manifest schizophrenia. A central question raised by these findings concerns the nature of the etiologic role of OCs. Some hypothesize that OCs produce the neural predisposition to schizophrenia, whereas others posit that OCs exacerbate or interact with an existing genetic predisposition.

Findings from prospective, high-risk research projects lend support to the hypothesis that OCs interact with genetic vulnerabilities in the etiology of schizophrenia. High-risk studies involve the repeated assessment of children of schizophrenia patients, based on the expectation that a larger percentage of these children will eventually develop the illness than individuals in the general population. The high-risk method offers some advantages when compared with retrospective studies of the precursors of schizophrenia. One advantage is that it allows for the direct assessment of subjects in the premorbid period, as well as the selection and study of variables that are thought to have prognostic relevance. Furthermore, because a significant portion of the data collection takes place during the premorbid period, this reduces confounds that often occur in the study of diagnosed patients (e.g., medication and institutionalization).

Studies using the high-risk method have shown an interactive effect of genetic risk and exposure to OCs in predicting adult psychiatric outcome. In other words, the correlation between OCs and adult psychiatric symptoms was greater for offspring of schizophrenia parents than for children of healthy parents. The same pattern was apparent for the relation between OCs and adult brain morphology, suggesting that pre- and perinatal factors contribute to brain abnormalities.

As noted earlier, prenatal exposure to maternal viral infection has also been linked with schizophrenia. Specifically, the rate of schizophrenia is increased for cohorts who were in the second trimester during flu epidemics. Another source of evidence for the viral hypothesis is the finding that the births of schizophrenia patients do not seem to be randomly distributed throughout the course of the year. Instead, the births of schizophrenia patients occur more frequently in winter months.

Some researchers have suggested that postnatal viral infection may also be relevant to schizophrenia, and that the illness may be caused by a long-acting virus. This hypothesis claims that “slow viruses,” which are active over a long period of time, interact with a genetic predisposition to produce schizophrenia. Various findings are cited in support of this hypothesis. Some researchers have identified a viral infection in fatal catatonia, a disorder characterized by schizophrenia-like symptoms, suggesting that a similar viral infection may be found for schizophrenia. Other researchers have found signs of viral activity in the cerebrospinal fluid of patients with schizophrenia.

The diathesis-stress model has dominated theories about the etiology of schizophrenia for several decades. This model assumes that certain individuals inherit or acquire a vulnerability to schizophrenia (the diathesis), and that the behavioral expression of this vulnerability is determined or triggered by environmental stressors. Although “stress” was originally conceptualized as psychosocial in origin, contemporary versions of this model broaden the definition of stress to include prenatal and postnatal insults to the central nervous system. Thus the diathesis, combined with exposure to environmental stressors, can produce schizophrenia.

Exposure to stress within the context of the family has been the focus of researchers in the field. Families in which there is a schizophrenia patient show more conflict and abnormalities in communication than do other families. However, it has also been shown that there is greater conflict and more abnormalities of communication in families in which any member has a severe debilitating illness. Thus, family communication styles are unlikely to play a unique causal role in schizophrenia.

There is good evidence, however, that exposure to high levels of criticism from family members can increase the likelihood of relapse in schizophrenia patients. The number of critical comments, expressions of hostility, and emotional overinvolvement comprise a construct referred to as expressed emotion (EE). Recovering schizophrenia patients in families high in EE are much more likely to have a relapse compared with patients in families low in EE. There is also evidence from studies of the adopted offspring of schizophrenia patients suggesting that familial stress can hasten the onset of symptoms.

Before 1900, knowledge of the nature and causes of mental disorders was limited. Individuals with psychiatric symptoms, particularly psychotic symptoms, were typically viewed by others with disdain or amusement. However, social trends and advances in medical knowledge converged to produce greater sympathy for those with mental illness. This led, especially during the early part of the century, to the construction of public and private hospitals devoted to the care of the mentally ill.

Today, most schizophrenia patients experience at least one period of inpatient treatment. This is typically precipitated by the first psychotic episode. During this initial hospitalization, an extensive assessment is usually conducted to determine the most appropriate diagnosis. Treatment is then initiated to reduce symptoms and stabilize patients so that they can return to the community as soon as possible.

In the past, periods of hospitalization were longer in duration than they are today. This is due, in part, to the availability today of better medical treatments. Another factor that has contributed to shorter hospital stays is the deinstitutionalization movement. Initially spurred by concerns that too many of the mentally ill were becoming “institutionalized” and were losing their ability to function in the community, financial support for state psychiatric hospitals was gradually cut. But community support services and transitional living arrangements were not readily available to many patients. As a result, former psychiatric inpatients now constitute a substantial proportion of the homeless found in U.S. cities.

Introduced in the 1950s, antipsychotic medication has since become the most effective and widely used treatment for schizophrenia. Research indicated that the “typical” antipsychotics, such as haloperidol, decreased the symptoms of schizophrenia, especially positive symptoms, and reduced the risk of relapse. However, they were not as effective in reducing the negative symptoms. Furthermore, some patients showed no response to antipsychotic drugs.

Chlorpromazine (Thorazine) was among the first antipsychotic commonly used to treat schizophrenia. Since the 1950s, many other antipsychotic drugs have been introduced. Like chlorpromazine, these drugs reduce hallucinations, delusions, and thought disorder, and engender more calm, manageable, and socially appropriate behavior. As mentioned, all currently used antipsychotic drugs block dopamine neurotransmission. Thus it has been assumed that their efficacy is due to their capacity to reduce the overactivation of dopamine pathways in the brain.

Unfortunately, the benefits of standard or typical antipsychotic drugs are often mitigated by side effects. Minor side effects include sensitivity to light, dryness of mouth, and drowsiness. The more severe effects are psychomotor dysfunction, skin discoloration, visual impairment, and tardive dyskinesia (an involuntary movement disorder that can appear after prolonged use of antipsychotics). It is especially unfortunate that tardive dyskinesia is sometimes irreversible when patients are withdrawn from neuroleptics. Many of these physical signs are known to be caused by chronic blockade of dopamine pathways. Although additional medications can counter some of the negative effects of the typical antipsychotics, schizophrenia patients often resist taking them because of an aversion to the side effects.

Within the past decade, some new, “atypical” antipsychotic drugs have been introduced. It was hoped that these drugs would be effective in treating patients who had not responded to standard antipsychotics. Also, researchers hoped to identify medications that had fewer side effects. One example is Clozapine, released in 1990, which seems to reduce negative symptoms more effectively than typical antipsychotic drugs. Clozapine not only offers hope for patients who are nonresponsive to other medications, but it also has fewer side effects than typical antipsychotics. However, clozapine can produce one rare, but potentially fatal, side effect, agranulocytosis, a blood disorder. Consequently, patients who are on this medication must be monitored on a regular basis. It is fortunate that several other new antipsychotic medications have recently become available, and some of these appear to have no serious side effects.

It appears that it is important to begin pharmacological treatment of schizophrenia as soon as possible after the symptoms are recognized. The longer patients go without treatment of illness episodes, the worse the long-term prognosis. Medication also has the benefit of lowering the rate of mortality, particularly suicide, among schizophrenia patients. Patients who are treated with antipsychotic medication generally require maintenance of the medication to obtain continued relief from symptoms. Medication withdrawal often results in relapse. At the same time, the associated long- and short-term side effects of antipsychotics, especially the typical antipsychotics, are of continuing concern to patients, their families, and physicians. It is possible that future research on the neural mechanisms involved in schizophrenia will lead to the development of novel treatments that eliminate the need for maintenance medication.

Many schizophrenia patients also suffer from depression and, as noted, are at elevated risk for suicide. The reason or reasons for the high rate of co-occurance of depression with schizophrenia is not known. Given the debilitating and potentially chronic nature of schizophrenia, however, it is likely that some patients experience depressive symptoms in response to their condition. For others, depressive symptoms may be medication side effects or a manifestation of a biologically based vulnerability to depression.

Clinicians have used various forms of psychological therapy in an effort to treat schizophrenia patients. Early attempts to provide therapy for schizophrenia patients relied on insight-oriented or psychodynamic techniques. The chief goal was to foster introspection and self-understanding in patients. Research findings provided no support for the efficacy of these therapies in the treatment of schizophrenia.

It has been shown, however, that supportive therapy can be a useful adjunct to medication in the treatment of patients. Similarly, psychoeducational approaches that emphasize providing information about symptom management have proven effective in reducing relapse. Among the most beneficial forms of psychological treatment is behavioral therapy. Some psychiatric hospitals have established programs in which patients earn credits or “tokens” for appropriate behavior and then redeem these items for privileges or tangible rewards. These programs can increase punctuality, hygiene, and other socially acceptable behaviors in patients.

In recent years, family therapy has become a standard component of the treatment of schizophrenia. These family therapy sessions are psychoeducational in nature and are intended to provide the family with support, information about schizophrenia, and constructive guidance in dealing with the illness in a family member. In this way, family members become a part of the treatment process and learn new ways to help their loved one cope with schizophrenia.

Another critical component of effective treatment is the provision of rehabilitative services. These services take the form of structured residential settings, independent life-skills training, and vocational programs. Such programs often play a major role in helping patients recover from their illness.

It is now firmly established that schizophrenia is caused by an abnormality of brain function that in most cases has its origin in early brain insults, inherited vulnerabilities, or both. But the identification of the causal agents and the specific neural substrates responsible for schizophrenia must await the findings of future research. There is reason to be optimistic about future research progress. New technologies are available for examining brain structure and function. In addition, dramatic advances in neuroscience have expanded our understanding of the brain and the impact of brain abnormalities on behavior. We are likely to witness great strides in our understanding of the causes of all mental illnesses within the coming decades.

It is hoped that advances will also be made in the treatment of schizophrenia. New drugs are being developed at a rapid pace, and more effective medications are likely to result. At the same time, advocacy efforts on the part of patients and their families have resulted in improvements in services. But a further expansion of services is greatly needed to provide patients with the structured living situations and work environments they need to make the transition into independent community living.

Bibliography:

• Breier, A. (Ed.). (1996). The new pharmacotherapy of schizophrenia. Washington DC: American Psychiatric Press.
• Keefe, R. S., & Harvey, P. (1994). Understanding schizophrenia: A guide to the new research on causes and treatment. New York: Free Press.
• Miller, G. A. (Ed.). (1995). The behavioral high-risk paradigm in psychopathology. New York: Springer.
• Shriqui, C. L., & Nasrallah, H. A. (Eds.). (1995). Contemporary issues in the treatment of schizophrenia. Washington DC: American Psychiatric Press.
• Torrey, E. F. (1994). Schizophrenia and manic-depressive disorder: The biological roots of mental illness as revealed by the landmark study of identical twins. New York: Basic Books.
• Walker, E. F. (1991). Schizophrenia: A life-course developmental perspective. New York: Academic Press.

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Schizophrenia: An Informative View Essay

Introduction, handling the situation, effects on family and society, reference list.

The brain is undoubtedly one of the most important parts as it is designed to process information and signals projected by the surrounding environment and relay an adequate response to the same throughout the entire body. The brain controls every single muscle of the body whether in an activity as significant as running a marathon or as minute as a twitch.

The brain’s intricate design and the complexity of its operations is something that scientists in general and psychologists in particular find fascinating as each new discovery regarding the functioning of the brain leads to a better understanding of how each part of the body works and most importantly, how to fix it when it stops working either entirely or partially.

However, just like various parts of the body experience difficulty in the performance of their normal functions sometimes, some factors, both internal (within the body) and external, can lead to a disruption of some of the brain’s functions and in severe cases the brain can stop working altogether.

Sometimes, signs and symptoms of such disruptions appear on parts of the body such as the legs causing a lack of mobility or the eyes causing visual disability, while in some cases, they are evident in the behavioral aspect of the person suffering from the disruption.

There are various behavioral disorders caused by the disruption of the brain’s functions including, but not limited to, the bipolar disorder, autism, schizophrenia, and Tourette’s syndrome.

Most people may not be aware of these disorders and may base their knowledge of the disorders on depictions of the same in movies and literary works that often exaggerate the severity of the symptoms for entertainment purposes.

For instance, some writers use their knowledge to write films about possession and people who have the superhuman ability to see things that other people cannot see. In such movies, hallucinations are seen as being good elements and enviable.

This paper looks into schizophrenia, which is caused by various factors either jointly or independently. It discusses the symptoms of the disorder, the cause, and the impact it has on both the individual suffering from it and the people surrounding the victim, both within and outside the family unit.

The word schizophrenia is derived from two Greek words, viz. “ skhein , which translated means ‘to split’ and phrein , which translates to “mind” (Tandon & Maj, 2008, p. 23). Although this etymologizing is mistakenly understood to mean that it is a “split-personality” disorder by many people, schizophrenia is a psychiatric disorder characterized mainly by bizarre delusions, hallucinations, and emotional dissociation.

Unlike in other mental disorders such as Tourette’s syndrome and autism where the victims are aware of their actions, individuals with schizophrenia are clueless as to whether they suffer from symptoms of the disorder. Being a disorder that occurs as a combination of various other disorders, schizophrenia is defined through its characteristic elements.

Tandon and Maj (2008), define schizophrenia as, “A mental illness in which a person is unable to link her or his thoughts and feelings to real life, suffers from delusions and withdraws increasingly form social relationships into a life of the imaginations” (p.23). The American Psychiatric Association has set out a criterion for the determination of the disorder. According to the manual, in order to be diagnosed with the disorder, a person must have:

• Two (or more) of the following, each present for the significant portion of the time during a one-month period: (1) delusions, (2) hallucinations, (3) disorganized speech, (4) grossly disorganized or catatonic behavior, (5) symptoms such as flat affect ( i.e. showing no emotion), or inability to engage in goal-directed behavior
• Social/ occupational dysfunction: one or more major areas of functioning (e.g. work, relationship, and self-care) are markedly lower than when the symptoms began.
• Duration: – continuous signs of the disturbance for at least six months including at least one month of active symptoms.
• Symptoms are not due to another disorder (e.g. major depressive disorder, autism), and are not due to substance use or a medical condition (American Psychiatric Association, 2000, p.308).

Given that different people suffering from the disorder bare unique symptoms from one another coupled with the variation of the symptoms that each of the individuals encounters with the progression of the disorder, a diagnosis on the disorder is made based on observation of behavior and experiences reported to the psychologist concerning an individual.

Schizophrenia usually affects people in their late childhood and early adulthood, and it progresses as people grow older (Marshall & Rathbone, 2009). Some of the known causes of the disorder include genetic factors, environmental factors, drug, and substance abuse. Some scholars also argue that traumatic effects in a person’s life can trigger the onset of the disorder, especially in young adults with a genetic predisposition to the disorder (O’Donovan et al., 2003).

The main course of treatment involves the use of anti-psychotic medication coupled with social rehabilitation through the attendance of individual therapy sessions as well as support groups.

In cases where the disorder advances to such great lengths that the individuals pose danger to themselves and the public in general, involuntary hospitalization is the method of choice, though it is usually used as a last resort. Treatment of the disorder, as is the case with every other disease and disorder, at its earliest point of detection does go a long way in easing the recovery process.

The disorder has a myriad of effects to the individual and the immediate family, as well as the public. Due to the disorder’s interference with the thought process, the majority of people with schizophrenia display some form of disorganization in the way they perform some of the normal activities such as dressing.

They also suffer from disconnection in the train of thought when discussing issues, lack of long-term memory, low attention spans, poor communication skills, and display a lack in cognitive processes such as planning and problem solving. This aspect usually results to long-term job loss and consequently depression and irritability.

Such individuals become withdrawn, thus keeping to themselves most of the time. Living with such a person within the family unit can be frustrating, as although the person suffers an inability to display affection, it does not necessarily mean that he or she does not need it (Broom et al., 2005, p.31).

On the other hand, it is difficult for family members to show their affection to a person who is withdrawn and emotionally detached as it is innate to expect reciprocation when affection is given. Stigma is also common toward people with schizophrenia, mainly because of ignorance and misinformation of what the disorder entails.

Family members are sometimes compelled to hide the fact that one of them suffers from the disorder for fear that most people do not know the disorder as a medical condition, but rather as a personality disorder associated with heinous behavior such as serial killing. Family members also may not know the proper way to explain the intricacies of the disorder, as they are hard to understand even for the family members, as the symptoms keep changing as the disorder graduates.

It is hard for a person with schizophrenia to hide its symptoms because they do not think that they suffer from it. The effect of this element is that it is hard for people to associate with a person who does not readily accept help as he or she does not think it is necessary.

The victims may also take this move as negative criticism of their abilities to conduct normal activities, which leads to resentment and withdrawal. The lack of ability to conduct cognitive processes such as problem solving and planning leads to long-term job losses, which results to the financial frustration to both the individual and the family unit as the family is then tasked to provide for the person’s needs.

This kind of frustration may lead to the individual contemplating and even in some cases attempting suicide. It could also lead to crimes such as murder, with the schizophrenic person justifying this action as a way of punishing people whom he or she thinks are to blame for the problems he or she faces.

Emotional dissociation means that a person is unable to convey emotions, whether verbally or by any other means, and as a characteristic symptom of schizophrenia, it causes the victim to keep emotions, good or bad, bottled up inside. It is also characteristic of schizophrenics to suffer from an inability to experience pleasure, mainly due to their paranoid delusions of persecution.

The combination of these two characteristics is dangerous mainly due to the ways these individuals resort to as means of releasing the bottled up emotions. Most of them result to drug abuse and alcoholism (Perala et al., 2010) while others go to the extremes, experiencing sudden bursts of rage or extreme sorrow, which may cause them to destroy property or even commit suicide.

Although prevention would go a long way in alleviating the disorder, it is not a possibility yet, for the first symptoms of the disorder are not discernible, as they resemble symptoms of normal factors such as stress. The symptoms can be singled out as specific to schizophrenia only at advanced stages. In addition, the fact that the disorder is more predominant in young adults means that it is not easy to differentiate it from normal adolescence characters (Van Os & Kapur, 2009).

The participation of family members in the rehabilitation forums and consequently the recovery process is essential to both the family and the suffering individual. It prepares the family unit mentally and physically on what to expect and what the appropriate reaction would be. It also helps them to prepare financially so that they do not undergo sudden financial strain. In addition, it aids in the acceptance process and helps them learn hoe to deal with stigma and its effects.

Family members are in a position to know that they would have to make social sacrifices in order to keep the family unit strong. About the individual, family support helps to ease the issues of acceptance that surround schizophrenic individuals. Family support also gives the victims comfort in knowing that they are not dealing with the problem alone, but that the family is present to support them along the way.

Although the way the family treats a schizophrenic individual is not necessarily a cause for the trigger or elevation of the disorder, it does help in the recovery process. Family support presumably reduces resentment and anger and thus it plays a role in the reduction of chances of a relapse after recovery.

Knowledge of how to deal with the condition as a family also reduces the chances of involuntary hospitalization, which in moments of paranoid schizophrenia might be interpreted by the schizophrenic individual as an act of rejection by the family, thus causing anger and resentment.

Supportive work environments are also a good way of aiding in the recovery process as such environments give the victims something to concentrate on unlike in situations when they are left alone. The fact that they have the disorder does not negate their sanity and their ability, although restricted by their condition, to be productive.

Although misunderstood by most people as more of a personality disorder, schizophrenia is in fact a medical disorder that disrupts the normal functioning of the individual affected, without the knowledge of the sufferer that he or she does indeed suffer from it.

The attitude of the people surrounding the individual suffering form it plays a big role in the management and recovery of the sufferer. Particularly, family members play a critical role in helping the victims of this condition along the way, which helps one to accept the condition and live positively.

American Psychiatric Association. (2000). Diagnostic and Statistical Manual of Mental Disorders. Washington DC: American Psychiatric Association Press.

Broom, R., Wooley, B., Tabraham, P., Johns, L., Bramon, E., Murray, G., Pariante, C., McGuire, G., & Murray, M. (2005). What Causes the Onset of Psychosis. Schizophrenia Research, 79 (1), 23-34.

Marshall, M., & Rothborne, J. (2009). Early Intervention for Psychosis. Hoboken, NJ: Wiley.

O’Donovan, M., William, M., & Owen, M., J. (2003). Recent advances in Genetics and Schizophrenia. Human Molecular Genetics, 12 (2), 125-133.

Perala, J., Kouppasalmi, K., Pirkola, S., Harkanen, T., Saarni, S., Tuulio-Henrikisson, A., Viertio, S., Suviisari, J. (2010). Alcohol-induced psychotic disorder and delirium in the general population. The British Journal of Psychiatry, 197, 200-06.

Tandon, R., & Maj, M. (2008). Nosological status and definition of schizophrenia: Some considerations for DSM-V and ICD-11. Asian Journal of Psychiatry, 1 (2), 22-27.

Van Os, J., & Kapur, S. (2009). Schizophrenia. Lancet, 374 (9690), 635-645.

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Bibliography

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Schizophrenia, a way of being-in-the-world : a thesis presented in fulfilment of the requirements for the degree of Doctor of Philosophy in Nursing at Massey University

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PERSPECTIVE article

Evolving concepts of the schizophrenia spectrum: a research domain criteria perspective.

• National Institute of Mental Health, Bethesda, MD, United States

Several trends intersecting over the past two decades have generated increasing debate as to how the concepts of schizophrenia, the schizophrenia spectrum, and the psychotic disorders spectrum should be regarded. These trends are reflected in various areas of research such as genomics, neuroimaging, and data-driven computational studies of multiple response systems. Growing evidence suggests that schizophrenia represents a broad and heterogenous syndrome, rather than a specific disease entity, that is part of a multi-faceted psychosis spectrum. Progress in explicating these various developments has been hampered by the dependence upon sets of symptoms and signs for determining a diagnosis, and by the reliance on traditional diagnostic categories in reviewing clinical research grants. To address these concerns, the U.S. National Institute of Mental Health initiated the Research Domain Criteria (RDoC) project, a translational research program that calls for studies designed in terms of empirically-based functions (such as cognitive control or reward learning) rather than diagnostic groups. RDoC is a research framework rather than an alternative diagnostic system, intended to provide data that can inform future nosological manuals. This commentary includes a brief summary of RDoC as it pertains to schizophrenia and psychotic spectra, examples of recent data that highlight the utility of the approach, and conclusions regarding the implications for evolving conceptualizations of serious mental illness.

Introduction

The concept of schizophrenia (SZ) has elicited continual debate since the first descriptions of psychosis appeared in the middle of the nineteenth century. The nature of the concept has fluctuated across the years according to the views of the scientific zeitgeist and various schools of psychopathology, but has always persevered in one form or another ( 1 ). Within the last decade, however, advances in multiple areas of science—genomics, neuroimaging, cognitive science, and epidemiology—have begun to challenge classic conceptions of schizophrenia ( 2 , 3 ).

Progress in expanding these various developments has been hampered by two major obstacles. First, disorders continue to be defined almost exclusively by sets of symptoms and signs; however, the relationships between diagnostic categories and biological or behavioral measures have proven to be modest and inconsistent, frustrating both a more comprehensive understanding of disorders and the development of more effective treatments ( 4 ). Second, research on mental disorders has been constrained by the persistence in grant review committees of a de facto requirement that hypotheses will embody DSM/ICD categories as their scientific focus, thus foiling applications proposing alternative approaches.

To address these problems, the US National Institute of Health (NIMH) initiated the Research Domain Criteria (RDoC) project in 2009 “to develop, for research purposes, new ways of [studying] mental disorders based on dimensions of observable behavior and neurobiological measures” ( 5 ). RDoC was conceived as an experimental framework to support research in psychopathology organized around basic functional domains such as cognition, motivation, and motor activity, most of which are pertinent to multiple disorders as currently defined (and may partially account for the extensive co-morbidity in current disorders).

The various elements of the RDoC framework have been described in detail elsewhere ( 5 – 7 ) and are briefly summarized here. RDoC is intended as an explicitly translational program: The focus is on fundamental operations of adaptive behavioral/cognitive and brain functioning (e.g., working memory, fear behavior), and psychopathology is viewed in terms of dysregulation in these systems rather than starting with clinical syndromes and trying to determine their source. A core desideratum of RDoC is to study entire dimensions of functioning from the normal range to increasingly abnormal extents, and no specific cutpoints for disorders are specified in order to encourage studies of transitions from normality to degrees of pathology. To foster such analyses, RDoC calls for study designs that include a broader range of “healthy controls,” patients with mild/subsyndromal psychopathology, and unaffected relatives of probands.

The basic dimensions of RDoC are organized in six superordinate domains of functioning (negative valence, positive valence, cognition, social processes, arousal/regulatory systems, and sensorimotor systems). Each domain contains multiple constructs, which—central to the entire framework—are defined jointly by data for a behavioral or cognitive/affective function, evidence for a neural circuit or system that plays a primary role in implementing the function, and relevance to psychopathology ( 8 ).

The domains and constructs were defined in a series of workshops attended by experts in both basic and clinical research. This process was essential for two reasons. First, it is important to communicate to the field well-validated constructs from the basic behavioral neuroscience literature that have demonstrated promise for understanding psychopathology. Second (and less evident), it is critical to provide clear guidelines for grant review. Just as established criteria for defining patient groups contributed significantly to the DSM's hegemony in study sections, examples of domains and constructs are essential to serve as standards for both applicants and reviewers in submitting and evaluating RDoC applications. Since RDoC is an experimental framework, applicants are not required to use one of the current constructs, and no claim is made that the current list of constructs is complete; in fact, a major goal of the program is to encourage research that establishes new constructs or domains, based on the premise that promoting diversity of ideas in research is the best way forward (Note that NIMH accepts DSM-oriented grant applications as always, although applicants are encouraged to address pertinent heterogeneity).

In keeping with the basic-to-clinical translational approach, RDoC focuses on relatively specific aspects of disordered functioning rather than syndromal categories. Study designs might include patients from one or more DSM/ICD categories, analyzing dimensions or subgroups in the full sample or examining selected subjects with particular characteristics (e.g., cognitive control or reward-related deficits). Participants in transdiagnostic studies are typically drawn from related areas of psychopathology, such as mood/anxiety disorders or psychotic disorders (plus comparison participants appropriate for exploring dimensions of functioning). An important emphasis concerns individual differences in psychopathology, given the heterogeneity that is now recognized for all syndromal disorders. Studies that include multiple domains/constructs are encouraged, such as the relationship of threat to attention or reward-related activity to social processes. RDoC-related research further advocates the use of multiple classes of measurement, ranging from genomics and circuit measures to behavioral and self-report, in order to seek an integrative understanding of brain-behavior relationships as they relate to particular functions.

RDoC and the Psychotic Spectrum

The RDoC program has consistently emphasized its agnostic position with respect to disorders as defined in the DSM/ICD system: The goal is to stimulate research that can inform revisions to future diagnostic manuals, however similar or divergent to current disorders and their definitions. Recent developments in the field demonstrate novel conceptions across the entire range of psychopathology, employing various types of dimensions, clusters, and hierarchical approaches that align with the RDoC approach ( 9 ).

Research focused on psychotic disorders amply reflects this trend ( 10 ). As one expert recently explained in a publication for psychiatric professionals, “Over the last decade or so, our field has experienced a radical shift in our understanding of schizophrenia and other serious psychotic disorders, such as schizoaffective disorder and bipolar disorder with psychosis. …. Accumulating evidence indicates that psychotic disorders constitute syndromes rather than diseases per se . … Patients with different clinical diagnostic phenotypes … can show similar underlying patterns of cognitive dysfunction and neurobiological abnormalities” ( 11 ). Space allows only a small number of papers to be cited here as examples of RDoC approaches in the psychotic spectrum [which are treated more comprehensively in a recent chapter; ( 7 )].

Transdiagnostic Findings

The current interest in a schizophrenia or psychotic disorders spectrum is consistent with the kinds of trans-diagnostic mechanisms that RDoC prioritizes. There are multiple types of relevant research designs. These include overlaps between traditional diagnostic classes, such as SZ and bipolar Type 1 disorder (BPD), that are frequently used when it is difficult to examine disorder subtypes or dimensions due to the nature of measurement (as in GWAS studies). A second type of design involves transdiagnostic dimensions or gradients; these differ from the prior design in that the analyses focus on how functional domains are arrayed along one or more dimensions across two or more disorders. Finally, cluster or similar analyses use data-driven techniques to reveal groupings that cut across traditional disorder categories.

Psychiatric genetics has provided increasing support for systematically related trans-diagnostic mechanisms as sample sizes grow. Comparisons of GWAS data across disorders have shown results that are consistent with a recently-posited gradient of neurodevelopmental syndromes ordered by the extent of neurodevelopmental impairment (from most to least: intellectual disability, ASD, ADHD, SZ, schizoaffective disorder (SZ-A), BPD, major depressive disorder [MDD]; ( 2 , 12 )). Larger coheritabilities were observed for disorder pairs that were closer on the spectrum; e.g., SZ-BPD and BPD-MDD were larger than SZ-ASD or BPD-ADHD ( 13 ).

More elaborated data emerged from a study comparing eight disorders in a larger sample, resulting in three clusters of disorders based on shared loci—mood and psychotic disorders (SZ, BPD, and MDD), early-onset neurodevelopmental disorders, and compulsive behaviors ( 14 ). As the authors concluded, “… these results indicate a substantial pairwise genetic correlation between multiple disorders along with a higher-level genetic structure that point to broader domains underlying genetic risk to psychopathology. These findings are at odds with the classical, categorical classification of mental disorder.” (14, p. 1475).

A second aspect of trans-diagnostic comparisons involves dimensions that cut across disorders. For example, a recent study from the CNTRACS group employed multiple measures of performance that tapped distinct aspects of cognition (cognitive control, episodic memory, and visual perception) in a large sample consisting of individuals diagnosed with SZ, BPD, or SZ-A ( 15 ). A latent profile analysis returned a solution with three trans-diagnostic clusters of high ability (mostly indistinct from control subjects), medium performance, and low performance. The proportions of patients from the three diagnostic groups were distributed across the three ability clusters, indicating that the latter were not simply proxies for diagnosis. Confirmatory factor analysis was consistent with the presence of an underlying one-dimensional structure across the three cognitive profiles, suggesting a shared mechanism not related to diagnostic classes per se .

Moving toward multi-measure studies that are compatible with the RDoC approach, computational analyses that identify transdiagnostic clusters of patients illustrate the potential of empirically-derived phenotypes that align with particular biological and behavioral functions. In the exemplary B-SNIP study (Bipolar & Schizophrenia Network on Intermediate Phenotypes), investigators recruited a large sample of patients (SZ, SZ-A, or BPD with psychosis) and acquired a wide range of biological, behavioral, and clinical measures ( 16 ). A cluster analysis of factor scores from cognitive and electrophysiological measures grouped patients into three “biotypes” that cut across DSM disorder categories (as in the previous example). The first two biotypes were characterized by impaired cognitive functioning (slightly more severe in Biotype 1) but divergent sensorimotor reactivity (event-related potential responses related to simple stimuli) that was markedly blunted in Biotype 1 and hyper-responsive in Biotype 2; both measures for the third biotype were only slightly different from healthy controls. The biotypes were validated by several different measures not used in the cluster analysis, including gray matter loss as assessed by voxel-based morphometry. This study demonstrated that deriving transdiagnostic clusters based on a combination of behavioral and psychophysiological functions (cognition and perception), consistent with an RDoC approach, have promise in determining data-driven clinical phenotypes with more validity than traditional disorder classes.

Dimensionality

RDoC emphasizes the gamut of normal-to-abnormal functioning. This aspect can be considered both in terms of cross-sectional and longitudinal studies. The latter, in this context, include trajectories of neurodevelopment from conception to risk states and overt psychopathology.

Cross-sectional discussions of psychosis dimensionality date back nearly as far as the concept of schizophrenia itself, with unresolved discussions as to whether the clinical phenomena represent one or more clinical categories, one or more dimensions, or some combination ( 17 , 18 ). More recently, extensive analyses have been adduced to support replacing the schizophrenia concept with a broader “psychosis spectrum” ( 19 ) that reflects a continuous dimension of psychosis proneness from normal to abnormal ( 20 ), although also allowing for a continuous psychometric spectrum that contains one or more latent categorical structures ( 21 ).

This type of normal-to-abnormal dimensional viewpoint comports with the RDoC framework. At the same time, another RDoC principle is to remain agnostic (as with the DSM) and eschew a priori conclusions regarding the number and composition of dimensions and their clinical significance. One of the hurdles that RDoC was created to address concerns the often-modest relationships among the presence/severity of clinical symptoms and various other measures, such as cognitive tests or brain circuit activity. As noted in a recent paper on RDoC and psychosis, “… one must empirically test whether dimensionality of a symptom indicates dimensionality of a mechanism” [( 7 ), p. 32]. In short, the field is just starting to make progress in unpacking the relationships within and across multiple neurocognitive functions, multiple kinds of symptoms, and multiple neurobiological and genetic measures—compounded by the complexities of intermixed clusters and dimensions ( 22 ). In spite of the daunting challenges, the evidence is already strong that the field is moving in positive directions.

Neurodevelopmental Studies

RDoC places a high priority on neurodevelopmental trajectories. While the clinical high-risk state (CHR) state for psychosis is perhaps the most thoroughly researched example of a trajectory leading toward disorder ( 23 ), more recent studies have expanded the scope of neurodevelopment and functions consistent with RDoC principles. For instance, a recent study followed an unselected sample of children from age 8 to late adolescence, collecting a large number of measures including neurocognitive tests and symptoms; children who developed psychotic symptoms later in adolescence were on average 1–2 years behind typically-developing children in cognitive growth, suggesting that early cognitive impairment could be a marker for psychosis risk and that growth charting may be an opportunity for early detection and prevention ( 24 ). Another group has independently begun to implement this concept with a developmental battery of “gamified” tasks (running on a mobile e-platform) that assesses six cognitive domains in young children in India as a first step to developing normative growth curves ( 25 ).

Such promising programs are only the tip of the iceberg for neurodevelopmental studies involving RDoC (which comprise nearly half of RDoC-themed translational grants funded by NIMH). An equally important issue concerns the need to explicate neurodevelopmental changes from birth to adulthood – addressing both substantive and psychometric issues of identifying and assessing functions that emerge at various points in development, as well as relating growth trajectories to the complex effects of multiple environmental influences ( 26 , 27 ).

It is a stimulating time for research on mental disorders. The field is burgeoning with intriguing new results and new ideas – sparked by developments in genomics, neuroimaging, behavioral science, computational approaches, and many other disciplines. The RDoC initiative has been a part of this contemporary zeitgeist, enabling conversations about innovative approaches to psychopathology ( 28 – 30 ) and supporting research projects that represent new avenues for future directions ( 31 – 33 ).

These developments have accelerated progress regarding the schizophrenia (or more broadly, the psychotic) spectrum. Genomic data provide increasing support for the concept of systematic transdiagnostic components of neurodevelopmental spectra ( 2 , 12 ). In this view, schizophrenia represents not so much a distinct disease as one segment of multiple broader spectra. However, the evidence is also clear that a neurodevelopmental gradient is not simply a matter of performance as assessed by the usual cognitive test batteries; it is important to consider multiple functional domains whose combinations comprise potentially significant clinical phenotypes, e.g., biotypes defined by both cognitive performance and sensorimotor reactivity ( 16 ).

A further aspect of the emerging literature, consistent with the RDoC approach, concerns various gradients from normal to abnormal functioning and how these relate to illness and dysfunction. It is now evident that some types of functional impairments are not necessarily tied to manifest clinical features. As two examples, both the B-SNIP and CNTRACS studies (summarized above) reported that patients in one of the three clusters, in spite of meeting criteria for SZ, BPD, or SZ-A, were characterized by functional performance in cognition and perception that was modestly to indistinguishably different from healthy controls ( 15 , 16 ). A necessary agenda for future research is to unravel the complex relationships among the extent of such factors as genetic load, functional impairments, and clinical symptoms.

The current status of evidence about the psychotic disorders spectrum raises significant questions regarding both near-term implications for research on clinical assessment and services, and long-term directions for scientific priorities and perspectives. With respect to clinical practice, the DSM/ICD nosology continues to dominate procedures for diagnosis and treatment. However, there is increasing attention to transdiagnostic approaches for diagnosis and treatment that build upon awareness of heterogeneity and clinicians' wisdom that many (if not most) treatment plans are focused on specific problems (e.g., sleep, attention, interpersonal relationships) irrespective of formal diagnosis ( 34 , 35 ), and at least one case report specifically cites the use of a transdiagnostic, RDoC approach ( 36 ). Further, some clinical programs have explicitly adopted a transdiagnostic process for assessment and treatment of first-episode psychosis in recognition of the change in diagnosis across time in many patients ( 37 ).

Regarding scientifically-driven changes in nosology, there appears to be a clear consensus that traditional disorder classes in this spectrum need to be revamped, and dozens of promising genetic, circuit-based, and behavioral findings provide clues to future classification systems. However, the nature and extent of potential changes to nosology remain far from clear, as different measurement classes and analytical techniques have yet to coalesce. There also remains the question of the granularity of concepts and measurement that are optimal for clinical use; these concerns apply across all areas—e.g., the number and combinations of specific gene abnormalities for molecularly based therapies; the count and locations of voxel-based structural abnormalities ( 38 ); or whether cognitive difficulties are best addressed at the level of broad test batteries, intermediate functional domains (e.g., executive function), or more specific operations (e.g., working memory).

A key question concerns the routes by which research advances can be implemented in diagnostic and treatment practice. Alterations to formal nosological criteria are not likely to be made soon, given conservative approaches to change in diagnostic manuals. Revisions based upon neuroscience and/or systematic behavioral data are yet more difficult to envision since they would involve an overhaul of the long-established reliance on symptoms and signs for diagnosis.

However, it is possible that rapid change may be recognized in other ways. Regulatory agencies, e.g., are well aware of the need for improved treatments and the potential for groupings and/or dimensions that manifest within or across traditional diagnostic categories. For instance, in 2016 the US Food and Drug Administration (FDA) promulgated an innovative new Drug Development Tool (DDT) Qualification program created to evaluate and approve (Qualify) such tools as “a biomarker used for clinical trial enrichment” [e.g., approval of the N170 event-related potential as a biomarker for social processing in ASD ( 39 )] “… and a clinical outcome assessment used to evaluate clinical benefit…” ( 40 ). Further, the tools are developed in a “context of use” that represents “the manner and purpose of use for a DDT,” i.e., essentially the specific impairment to be addressed ( 40 ). Such developments could lead directly to innovative practices that advance treatment while suggesting new conceptions of clinical phenotypes that are validated inherently by their use in patient care.

In sum, the notion of a psychotic spectrum is evolving rapidly, but schizophrenia—as broad concept or specific diagnostic category—remains a core aspect of contemporary psychopathology. Both general and specialty journals continue to publish large numbers of papers devoted directly to SZ, reflecting widespread support from multiple funding agencies across the world. In September, 2020 the National Institutes of Health announced the AMP-SCZ initiative (Accelerating Medicines Partnership-Schizophrenia), bringing together NIH, the US FDA, and multiple non-profit and private organizations to seek biomarkers for the diverse array of clinical trajectories and adverse outcomes observed in individuals identified as at elevated risk of psychosis. Accordingly, there seems to be little doubt that SZ will remain a central concept in mental disorders for some time to come ( 41 ). While future directions remain difficult to predict given the nascent state of the research, novel research frameworks seem likely to foster the continued expansion of research designs and integrative science—and, in turn, to stimulate more precise thinking about the nosology of SZ and the psychosis spectrum.

Data Availability Statement

The original contributions presented in the study are included in the article/Supplementary Material, further inquiries can be directed to the corresponding author/s.

Author Contributions

BC and SM contributed equally to the overall outline and scope of the manuscript. BC wrote the first draft. SM contributed extensive comments and edits that resulted in the final version. All authors contributed to the article and approved the submitted version.

Conflict of Interest

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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Keywords: psychiatric diagnosis, psychiatric nosology, research domain criteria, psychopathology, schizophrenia spectrum, psychosis spectrum

Citation: Cuthbert BN and Morris SE (2021) Evolving Concepts of the Schizophrenia Spectrum: A Research Domain Criteria Perspective. Front. Psychiatry 12:641319. doi: 10.3389/fpsyt.2021.641319

Received: 14 December 2020; Accepted: 01 February 2021; Published: 25 February 2021.

Reviewed by:

Copyright © 2021 Cuthbert and Morris. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY) . The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

*Correspondence: Bruce N. Cuthbert, bcuthber@mail.nih.gov

Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.

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• v.14(4); 2022 Apr

Neurobiology of Schizophrenia: A Comprehensive Review

Enkhmaa luvsannyam.

1 Surgery, Avalon University, School of Medicine, Willemstad, CUW

2 Research, California Institute of Behavioral Neurosciences & Psychology, Fairfield, USA

Molly S Jain

3 Medicine, Saint James School of Medicine, Park Ridge, USA

Maria Kezia Lourdes Pormento

4 Medicine, Ateneo de Manila School of Medicine and Public Health, Quezon City, PHL

Hira Siddiqui

5 Medicine, Windsor University School of Medicine, Cayon, KNA

Angela Ria A Balagtas

6 General Medicine, Global Health Medical Center, Canlubang, PHL

Bernard O Emuze

7 Emergency Medicine, St. James School of Medicine, Fort Worth, USA

Teresa Poprawski

8 Psychiatry and Behavioral Sciences, St. James Medical School, Oakbrook, USA

Schizophrenia is a debilitating disease that presents with both positive and negative symptoms affecting cognition and emotions. Extensive studies have analyzed the different factors that contribute to the disorder. There is evidence of significant genetic etiology involving multiple genes such as dystrobrevin binding protein 1 (DTNBP1) and neuregulin 1 (NRG1). There is no clear link between neurotransmitter changes and the pathophysiology of schizophrenia; however, studies have shown that subcortical dopamine dysfunction is the key mechanism. Specific regions of gray and white matter changes are observed in patients with schizophrenia; gray matter changes being more significant after the onset of psychosis. These pathological changes may be implicated in the impairment of executive functioning, attention, and working memory. The disease can be managed with pharmacological treatments based on individual patient profile, patient compliance, and disease severity. The challenge of disease management sometimes persists due to the side effects. A better understanding of the pathological processes in schizophrenia may lead to more specific and effective therapies.

Introduction and background

Schizophrenia is a chronic illness that causes psychosis with a decline in functioning. It is a multifactorial disorder affecting millions worldwide. Diagnosis of schizophrenia requires at least two or more symptoms, and at least one of the two symptoms must be a positive symptom. Positive symptoms are hallucinations, delusions, disorganized speech, and abnormal movements. Negative symptoms are flattened affect, social withdrawal, anhedonia, apathy, and lack of emotions [ 1 ]. As described in the Diagnostic and Statistical Manual of Mental Disorders, 5th edition (DSM-5), the diagnosis of schizophrenia requires presenting symptoms that cause a decline in both social and occupational functioning for at least six months [ 2 ].

Positive symptoms reflect the presence of exaggerated ideas, perceptions, or actions, whereas negative symptoms reflect the lack of normal mental functioning. The occurrence of these symptoms reflects the interplay of the neurotransmitters, especially dopamine, in the frontal, temporal, and mesostriatal brain regions [ 3 ]. The neurotransmitter release and production is the target of current medical management. Additionally, neuroanatomical changes are seen in the brain of patients with schizophrenia. These changes are seen in the prefrontal, medial, and superior temporal lobes as reduced gray matter volume [ 4 ]. MRI studies of the brain reveal structural changes in the same brain regions that are believed to affect overall functioning in patients with schizophrenia.

The pathophysiology of schizophrenia is complex, and it has been studied for years with many factors yet to be discovered. Genetic studies show that schizophrenia involves different genetic loci and is highly pleiotropic [ 5 ]. Among all neurotransmitters involved in the pathophysiology of schizophrenia, dopamine plays a major role in psychosis.

This review on the neurobiology of schizophrenia aims to explore the current studies on the genetics, neurotransmitters, and neuroanatomy involved in the disease.

Schizophrenia has a complex mode of inheritance involving multiple genes, biological processes, and environmental factors [ 6 ]. There is a significant contribution of genetic factors to the etiology of schizophrenia. The link between multiple genes and specific DNA and protein alterations involved in the etiology of schizophrenia has not yet been identified fully [ 7 ]. However, recent large-scale genomic studies have shown specific DNA variants and how various risk alleles contribute to the disease [ 5 ].

Based on genetic studies, schizophrenia is a highly polygenic syndrome with hundreds or even thousands of distinct genetic loci involved. There are more than 100 distinct genetic loci with common alleles of various effects identified by genomic-wide association studies (GWAS). The genetic risk of the disease appears to be highly pleiotropic; for example, there are common risk variants between schizophrenia and bipolar disorder, major depressive disorder, and an autism spectrum disorder. Another genomic study shows different biological processes where genes encode a variety of synaptic proteins, such as components of the postsynaptic density (PSD) and voltage-gated calcium channel family of proteins. It also involves genes encoding glutamate receptors and dopamine receptor D2 (DRD2) with common variations. Moreover, there is a significant finding from GWAS of schizophrenia that there are multiple correlated variants in the major histocompatibility complex (MHC). These MHC variants are associated with acquired immunity, suggesting that the immune and inflammatory processes are involved in the developmental stages of schizophrenia, such as in utero, adolescence, and adulthood [ 5 ]. Components of brain development such as synapse formation, neurite outgrowth, and homeostatic plasticity are regulated by MHC class I molecules [ 8 ].

The findings from GWAS studies allow us to identify possible genes for targeted treatment and future research regarding the immune mechanisms of schizophrenia [ 9 ]. There are still a number of shortcomings, such as clarification of the pathogenesis, early diagnosis, and the treatment of schizophrenia; hence, the extent of genomics in the treatment of schizophrenia is unclear [ 9 , 10 ].

'Endophenotype' is an alternative approach to investigate phenotypic variation in the identification of the genes involved in schizophrenia [ 6 ]. In epidemiology, endophenotypes are quantitative biomarkers of heritable illness in the population. They are used to connect behavioral symptoms with specific phenotypes and risk genes [ 6 ]. There is extensive central nervous system involvement in the pathology of schizophrenia. These include frontal lobe changes responsible for memory and executive processes and temporal lobe changes responsible for language comprehension, auditory perception, and episodic memory [ 6 ]. These neurological disturbances in schizophrenia are predisposed by many suspected genetic loci. Studies have identified a promising association with candidate genes, including COMT, DISC1, RGS4, PPP3CC, ZDHHC8, AKT1, neuregulin, dysbindin, G72/G30, TRAR4, and alpha-7 nicotinic receptor genes [ 6 , 7 ]. These genes are associated with the regulation of dopamine, contributing to the underlying cause of schizophrenia. Although identifying the exact mechanism of these genetic associations is challenging, the evidence of linkage is strongest for two of these genes: dystrobrevin binding protein 1 (DTNBP1) and neuregulin 1 (NRG1). Both DTNBP1 and NRG1 are expressed at central nervous system synapses and have an impact on glutamate neurotransmission involved in schizophrenia [ 7 ].

Pathophysiology

The primary positive, negative, and cognitive symptoms of schizophrenia have been associated with many neurotransmitters, but the subcortical dopamine dysfunction remains to be the key factor in psychotic symptoms. Presynaptic dopamine dysfunction appears to mediate psychosis in schizophrenia. Stimulants such as amphetamines enhance the dopamine effect and may induce psychotic symptoms in healthy individuals. When people with schizophrenia take stimulants, they are more sensitive to psychotic effects due to increased subcortical synaptic dopamine content, dopamine synthesis, and abnormally high dopamine release following amphetamine administration. Positron emission tomography (PET) studies have shown that the increased synaptic dopamine content is localized in the striatum. In patients with schizophrenia, alterations in dopamine function within the striatum cause delusions and psychosis [ 3 ].

Thalamus is the central relay station that transmits all information from and to the cerebral cortex. The primary circuit responsible for psychotic symptoms forms between the thalamus, cerebral cortex, and associative striatum, where changes in any of these regions can impair the whole network (Figure ​ (Figure1). 1 ). There are many more pathways involved directly or indirectly with this circuit, such as the amygdala and hippocampus, which are responsible for perception and emotion regulation. Dysfunction of the thalamus and cerebral cortex largely affects the striatum and D2 receptors, causing hallucinations and delusional symptoms [ 3 ].

Original image created by the authors.

D1 - dopamine D1 receptor in the excitatory pathway; D2 - dopamine D2 receptor in the inhibitory pathway; SNc - substantia nigra pars compact; GPe - globus pallidus externus; GPi - globus pallidus internus; STN - subthalamic nucleus

Studies have shown that dopamine neurons not only release dopamine in a synaptic signal mode but also release co-transmitters glutamate and gamma-aminobutyric acid (GABA). Glutamate in the excitatory pathway and GABA in the inhibitory pathway transmits various patterns of dopamine neuron activity to the striatum. The N-methyl-D-aspartate (NMDA) receptor antagonists such as ketamine and phencyclidine (PCP) can disrupt the thalamus circuit and lead to cognitive dysfunction and psychotic symptoms [ 11 ]. Similar to amphetamine, individuals with schizophrenia are more sensitive to the effect of these medications. Hypofunction of NMDA receptors may be associated with the pathogenesis of schizophrenia; therefore, treatment with D-serine, glycine, and sarcosine, which modulates NMDA receptors, can be beneficial, especially for negative symptoms [ 12 ]. GABA interneurons such as chandelier neurons have reduced immunostaining for the GABA transporter, which is related to decreased brain-derived neurotrophic factor (BDNF) signaling or NMDA receptor hypofunction. BDNF enhances glutamatergic transmission and reduces GABAergic transmission causing alterations in neuron survival and central nervous system (CNS) function [ 13 ]. The extent to which these changes contribute to the pathophysiology of schizophrenia remains unclear.

Neuroanatomical changes

Schizophrenia is a disorder known for neuroanatomical changes over time. There are various regions of the brain that have been implicated in patients with schizophrenia. In particular, the gray matter of the brain is consistently affected in schizophrenia [ 14 ]. The widespread use of MRI has shown evidence of reduced gray matter volumes within the prefrontal, medial, and superior temporal lobes. This can explain the episodic memory decline and fluctuations in decision-making as the disease progresses [ 4 ].

Along with the respective gray matter changes, the white matter gets affected as well as schizophrenia becomes chronic [ 14 ]. Diffusion tensor imaging (DTI) is used to visualize the structural integrity of white matter using water diffusion patterns in the neural tissue. Specifically, fractional anisotropy (FA) uses the shape of the water diffusion area to assess the integrity of white matter myelination [ 15 ]. Studies on schizophrenia have shown evidence of decreased FA in major tracts such as superior longitudinal fasciculus, cingulate bundle, uncinate fasciculus, inferior longitudinal fasciculus, and hippocampus [ 16 ]. Moreover, as these pathways collaborate in neuronal networks, the increased demyelination observed in schizophrenia can also impact many cognitive abilities. A recent article proposes that the defective differentiation of glial cells is implicated in the deterioration of the working memory in schizophrenia [ 17 ]. However, a study by Dische et al. states that the brains of patients with chronic schizophrenia should be investigated carefully due to the confounding effects of antipsychotics [ 18 ]. The study confirms the decrease in the gray matter within the brain but reported less evidence of white matter abnormalities [ 17 ]. Similarly, a study by Liang et al. on the classification of schizophrenia with neuroimaging also showed significant gray matter changes compared to white matter [ 19 ].

Furthermore, CT imaging has demonstrated generalized brain tissue loss along with ventricular enlargement in schizophrenic patients as compared to controls [ 15 ]. The lateral and third ventricles progressively enlarge in size with the duration of the disease [ 16 ]. Changes associated with negative symptoms are also related to volume loss in the superior temporal lobe, medial temporal lobe, and thalamus [ 4 ]. Additionally, executive function impairment has been related to structural abnormalities in the striatum, thalamus, cerebellum, anterior cingulate gyrus, hippocampus, medial temporal lobe, medial frontal, and posterior parietal cortex [ 18 ]. Finally, it is concluded that the brain dysfunction in schizophrenic patients is due to a range of brain networks rather than a single brain region [ 16 , 18 ].

Neurobiology of first onset, late-onset, and relapse

A meta-analysis by Hajima et al. of medication-naive schizophrenic patients found intracranial volume decrease with chronic and recent-onset schizophrenia. The meta-analysis demonstrates that schizophrenic patients start having brain volume abnormalities in the early teenage with the first episode, which continues to a larger extent after the onset of the disease [ 20 ]. However, gray matter changes do seem more significant after the onset of psychosis and show a direct relationship with medication use and psychotic relapse [ 21 ]. Specifically, with the first episode of schizophrenia, there was evidence for both white and gray matter changes at different rates [ 20 , 21 ]. In both patients with or without antipsychotics, white matter changes were reflected by FA studies suggesting axonal damage or demyelination in the uncinate and arcuate fasciculi [ 22 ]. Furthermore, the most significant gray matter changes were found in the frontal and temporal lobes, including the insula, anterior cingulate gyrus, and superior temporal gyrus [ 23 ].

Late-onset schizophrenia is associated with increased ventricle-to-brain ratio, structural abnormalities in the frontal, subcortical and temporal areas, along with white matter demyelination [ 23 ]. Interestingly, late-onset schizophrenia presents with a heterogeneous set of symptoms ranging from delusions and hallucinations to cognitive impairment associated with memory declines and executive dysfunction compared to early-onset schizophrenia [ 24 ]. Studies report persecutory delusions, misidentification, and visual hallucinations as initial symptoms of late-onset schizophrenia. Other studies found an association of hallucinations representing neurocognitive disorders such as Lewy body dementia and Alzheimer's disease [ 25 ]. Memory dysfunction and cognitive abilities precede paranoid delusions. Visual and auditory hallucinations often occur concurrently with misidentification delusions, and these symptoms are associated with parietal, medial temporal, and frontal lobes dysfunction. Overall, frontotemporal abnormalities are implicated in late-life schizophrenia [ 24 ].

Schizophrenia relapse is multifactorial in nature, involving several genetic, biological, and environmental factors. It can be idiopathic or secondary to medication non-compliance or substance abuse. Clozapine seems to be an exception that has worked well for patients with relapse and treatment resistance. Overall, relapse as a whole cannot be explained by a single brain anatomical abnormality or by medication non-adherence, but it requires detailed patient history and clinical picture to account for specific reasons [ 26 ].

Neuropsychology

To understand neuropsychological impairments of schizophrenia, various psychological processes, their relativity to the area of the brain affected, and its functions need to be considered. Negative symptoms along with cognitive dysfunction are the primary reason for functional disability [ 27 ]. Even though there are various overlapping symptoms, not everyone with schizophrenia displays identical symptoms as there are distinct subtypes. This can be observed through the research conducted on paranoid versus non-paranoid schizophrenics. The patients in the paranoid group performed significantly better than those in the non-paranoid group on measures of executive functions and learning/memory [ 27 ]. When testing cognitive functions, it is evident there is impairment in working memory, verbal memory, learning, executive functions, attention, processing speed, and general intellectual disability when compared to individuals not affected by schizophrenia. Some theories state that these cognitive dysfunctions are due to impairment in connectivity between the cortices and neurotransmitter inputs [ 28 , 29 ].

Executive functioning is a multifaceted process where different areas of the brain function together to accomplish goal-directed behavior [ 30 ]. A study by Orellana and Slachevsky demonstrated neuroimaging with a prefrontal cortex dysfunction and further concluded that patients with schizophrenia scored relatively low on conceptualization, planning, cognitive flexibility, verbal fluency, and the ability to solve complex problems [ 31 ]. Another study explains that patients with schizophrenia exhibit reality distortion, disorganization, and psychomotor poverty, which were strongly correlated to the occupational and social impairment seen with the illness [ 32 ]. Four subtypes of attention include sustained attention, selective attention, alternating attention, and divided attention [ 33 ]. A study found that schizophrenic patients scored lower in tests such as the Stroop test for attention compared to the control group [ 29 ]. The Stroop Color-Word Test has three components: word reading, color naming, and interference (color names printed in conflicting colors), and patients with schizophrenia scored lower, possibly due to their inability to selectively focus and filter [ 34 ]. Working memory functions to gather information, code it for short or long-term storage, and apply information to attain tasks that require learning, reasoning, and comprehension [ 28 , 35 ]. According to a study by Perry et al., the following five measures of working memory were administered in patients with schizophrenia: digital span forward and backward, spatial span forward and backward, and letter-number sequencing, where the patients scored significantly below average [ 36 ]. Several studies have shown severe deficits in phonological, visuospatial, and central executive areas of the working memory in schizophrenia patients. However, it is still unclear if the dysfunction is due to a specific region of the brain or the inability to synchronize the system of complex networks [ 28 ].

The neuropsychology underlying the positive and negative symptoms of schizophrenia is quite complex. The negative symptoms demonstrate a lack of initiation of emotions causing withdrawal, while positive symptoms are due to abnormal internal monitoring systems for thought and voluntary actions. The prefrontal cortex, basal ganglia, and the hippocampus are major brain regions involved in the neuropsychology of positive and negative symptoms seen in schizophrenia [ 37 ].

Pharmacology

Among many clinical trials of antipsychotic medications for schizophrenia management, the history began with first-generation antipsychotics (FGAs). The mechanism of action of the FGA is predominantly blocking the D2 receptor in the mesolimbic pathway antagonizing dopamine. Additionally, it blocks noradrenergic, cholinergic, and histaminergic actions. Moreover, first-generation antipsychotics are effective in treating positive symptoms but have no effect on negative symptoms [ 38 ]. The most common side effects of FGAs are extrapyramidal symptoms which are associated with antagonism of D2 receptors in the nigrostriatal pathway. Acute extrapyramidal symptoms include acute dystonia, akathisia, and parkinsonism, while prolonged use can lead to tardive dyskinesia [ 39 ].

Second-generation antipsychotics (SGAs) were developed for the management of both positive and negative symptoms of schizophrenia. SGAs have the added effect of antagonizing 5HT serotonin receptors along with D2 receptors causing fewer extrapyramidal symptoms in comparison to the FGAs [ 38 ]. However, there are still limitations in terms of side effects such as metabolic syndrome and hypotension. Due to metabolic syndrome, especially with olanzapine, patients with diabetes mellitus, increased BMI, and dyslipidemia should be monitored regularly [ 39 ]. Clozapine is reserved for treatment-resistant schizophrenia. It has undesirable side effects of agranulocytosis and leukopenia that may cause severe infections. The therapeutic treatment with clozapine should be halted immediately if the absolute neutrophil count drops below 1,000 cells/mm 3 or below 500 cells/mm 3 in those with benign neutropenia. Other possible side effects of both FGAs and SGAs include hyperprolactinemia, anhedonia, sedation, cardiac arrhythmias such as QT prolongation, and disturbances of thermoregulation. The neuroleptic malignant syndrome is a rare phenomenon that can occur within 24 to 72 hours and presents with increased temperature, severe muscular rigidity, confusion, elevation in white blood cell count (WBC), elevated creatine phosphokinase, and myoglobinuria [ 39 ].

Multiple articles report that the effect of SGAs on managing negative symptoms is debatable [ 40 ]. Clinical trials evaluating SGAs for patients with both positive and negative symptoms eventually found that the effect of these antipsychotics on negative symptoms was quite unclear. Although SGAs have more advantages for treating patients with negative symptoms compared to FGAs, it is still not the most promising treatment [ 40 ]. Lumateperone is a recently developed atypical antipsychotic that modulates serotonin, dopamine, and glutamate neurotransmission simultaneously [ 41 ]. It inhibits serotonin reuptake, antagonizes the 5-HT2A receptor and postsynaptic D2 receptor. It also acts as a partial agonist of presynaptic D2 receptors and a modulator of D1 receptor-dependent glutamate. The long-term side effects of lumateperone are currently unknown. However, it has the advantage of having fewer adverse effects due to the lack of interaction with other receptors that cause common side effects seen in most antipsychotics [ 41 , 42 ]. Moreover, a new drug, SEP-36385 with agonistic action on the trace amine-associated receptor 1 (TAAR1) and 5-hydroxytryptamine type 1A (5-HT1A) receptor is under investigation [ 43 ]. The SEP-363856 medication exhibited a significant decrease in psychotic symptoms in comparison to the placebo group. In a randomized controlled trial, the SEP-363856 group had gastrointestinal symptoms; however, there is no significant difference in the incidence of extrapyramidal symptoms, change in lipids, HbA1c, and prolactin level compared to the control group [ 43 ]. Therefore, longer and larger trials will be needed to confirm the potential side effects of SEP-363858 along with its efficacy in relation to the existing treatment for schizophrenia.

A new atypical antipsychotic, pimavanserin, was FDA approved in 2016 in the U.S. for Parkinson's disease psychosis (PDP), including management of hallucinations and delusions. Pimavanserin is the first drug with antipsychotic actions without dopamine D2 blocking activity. The mechanism of action of this drug involves an antagonist and an inverse agonist at the 5HT2A and 5HT2C receptors. Pimavanserin is also being studied for the management of schizophrenia, Alzheimer's disease psychosis, and major depressive disorder [ 44 ]. 

Conclusions

Although schizophrenia is a complex syndrome that is difficult to manage, recent advances in ongoing research studies and clinical trials are contributing to the management of schizophrenia. Investigating the neurobiological processes behind behavioral disorders, including schizophrenia, will facilitate a better understanding of the pathogenesis and targeted therapy. Numerous genes have yet to be identified and may be associated with the variations in the disease, severity of cognitive impairment, and effectiveness of treatment. Further studies should integrate different domains, including genetics, biochemistry, and anatomy. A combination of all these factors will provide a deeper understanding of the pathophysiology of schizophrenia for clinicians, therefore, will contribute to the development of treatment for the illness.

Acknowledgments

Enkhmaa Luvsannyam and Molly S. Jain contributed equally to the work and should be considered co-first authors.

The content published in Cureus is the result of clinical experience and/or research by independent individuals or organizations. Cureus is not responsible for the scientific accuracy or reliability of data or conclusions published herein. All content published within Cureus is intended only for educational, research and reference purposes. Additionally, articles published within Cureus should not be deemed a suitable substitute for the advice of a qualified health care professional. Do not disregard or avoid professional medical advice due to content published within Cureus.

The authors have declared that no competing interests exist.

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30 schizophrenia research topics, rachel r.n..

• September 9, 2022
• Essay Topics and Ideas

Schizophrenia is a mental disorder that affects how a person thinks, feels, and behaves. People with schizophrenia may seem like they have lost touch with reality. Although there is no cure for schizophrenia, it can be treated with medication, therapy, and support. In this article, we will provide an overview of some current research topics in schizophrenia.

What You'll Learn

Thirty Schizophrenia Research Topics

1. The causes of schizophrenia. 2. The symptoms of schizophrenia. 3. The relationship between schizophrenia and creativity. 4. The link between schizophrenia and violence. 5. The role of genetics in schizophrenia. 6. The role of the environment in schizophrenia. 7. The prevalence of schizophrenia in different cultures. 8. The impact of schizophrenia on the family. 9. The economic cost of schizophrenia. 10. The treatment options for schizophrenia. 11. The effectiveness of medication for treating schizophrenia. 12. Alternative treatments for schizophrenia. 13..The challenges of living with schizophrenia. 14..How to cope with the symptoms of schizophrenia 

15..The role of support groups in managing schizophrenia 16. The importance of early diagnosis and treatment of schizophrenia 17. The long-term outlook for people with schizophrenia 18. The impact of schizophrenia on employment 19. The effect of schizophrenia on relationships 20. Having a baby when you have schizophrenia21. Parenting with schizophrenia 22. Schizophrenia and substance abuse 23. Schizophrenia and self-harm 24. Schizophrenia and suicide 25. The role of the media in reporting on schizophrenia 26. The use of service user involvement in mental health research 27. The experiences of people from black and minority ethnic groups with schizophrenia 28. The experiences of carers of people with schizophrenia 29. Improving access to services for people with schizophrenia 30. Developing new treatments for schizophrenia

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Thesis statement for schizophrenia research paper

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