Schizophrenia is a mental disorder characterized by abnormal social behavior and failure to understand what is real. Common symptoms include false beliefs, unclear or confused thinking, hearing voices that others do not hear, reduced social engagement and emotional expression, and a lack of motivation. People with schizophrenia often have additional mental health problems such as anxiety, depressive, or substance-use disorders. Symptoms typically come on gradually, begin in young adulthood, and last a long time. The causes of schizophrenia include environmental and genetic factors. Possible environmental factors include being raised in a city, cannabis use during adolescence, certain infections, parental age and poor nutrition during pregnancy. Genetic factors include a variety of common and rare genetic variants. Diagnosis is based on observed behavior, the person's reported experiences and reports of others familiar with the person. During diagnosis a person's culture must also be taken into account. As of 2013 there is no objective test. Schizophrenia does not imply a "split personality" or " dissociative identity disorder" – conditions with which it is often confused in public perception. The mainstay of treatment is antipsychotic medication, along with counselling, job training and social rehabilitation. It is unclear whether typical or atypical antipsychotics are better. In those who do not improve with other antipsychotics clozapine may be tried. In more serious situations where there is risk to self or others involuntary hospitalization may be necessary, although hospital stays are now shorter and less frequent than they once were. About 0.3–0.7% of people are affected by schizophrenia during their lifetimes. In 2013 there were an estimated 23.6 million cases globally. Males are more often affected than females. About 20% of people do well and a few recover completely. Social problems, such as long-term unemployment, poverty and homelessness are common. The average life expectancy of people with the disorder is ten to twenty-five years less than for the general population. This is the result of increased physical health problems and a higher suicide rate (about 5%). In 2015 an estimated 17,000 people worldwide died from behavior related to, or caused by, schizophrenia.
Signs and symptoms, who had schizophrenia]] Individuals with schizophrenia may experience hallucinations (most reported are hearing voices), delusions (often bizarre or persecutory in nature), and disorganized thinking and speech. The last may range from loss of train of thought, to sentences only loosely connected in meaning, to speech that is not understandable known as word salad. Social withdrawal, sloppiness of dress and hygiene, and loss of motivation and judgment are all common in schizophrenia. Distortions of self-experience such as feeling as if one's thoughts or feelings are not really one's own to believing thoughts are being inserted into one's mind, sometimes termed passivity phenomena, are also common. There is often an observable pattern of emotional difficulty, for example lack of responsiveness. Impairment in social cognition is associated with schizophrenia, as are symptoms of paranoia. Social isolation commonly occurs. Difficulties in working and long-term memory, attention, executive functioning, and speed of processing also commonly occur. In one uncommon subtype, the person may be largely mute, remain motionless in bizarre postures, or exhibit purposeless agitation, all signs of catatonia. People with schizophrenia often find facial emotion perception to be difficult. It is unclear if the phenomenon called " thought blocking", where a talking person suddenly becomes silent for a few seconds to minutes, occurs in schizophrenia. About 30 to 50 percent of people with schizophrenia fail to accept that they have an illness or comply with their recommended treatment. Treatment may have some effect on insight. People with schizophrenia may have a high rate of irritable bowel syndrome but they often do not mention it unless specifically asked. Psychogenic polydipsia, or excessive fluid intake in the absence of physiological reasons to drink, is relatively common in people with schizophrenia.
Positive and negativeSchizophrenia is often described in terms of positive and negative (or deficit) symptoms. Positive symptoms are those that most individuals do not normally experience, but are present in people with schizophrenia. They can include delusions, disordered thoughts and speech, and tactile, auditory, visual, olfactory and gustatory hallucinations, typically regarded as manifestations of psychosis.Kneisl C. and Trigoboff E. (2009). Contemporary Psychiatric- Mental Health Nursing. 2nd edition. London: Pearson Prentice Ltd. p. 371 Hallucinations are also typically related to the content of the delusional theme. Positive symptoms generally respond well to medication.American Psychiatric Association. Task Force on DSM-IV. (2000). Diagnostic and statistical manual of mental disorders: DSM-IV-TR. American Psychiatric Pub. . p. 299 Negative symptoms are deficits of normal emotional responses or of other thought processes, and are less responsive to medication. They commonly include flat expressions or little emotion, poverty of speech, inability to experience pleasure, lack of desire to form relationships, and lack of motivation. Negative symptoms appear to contribute more to poor quality of life, functional ability, and the burden on others than positive symptoms do. People with greater negative symptoms often have a history of poor adjustment before the onset of illness, and response to medication is often limited.
Cognitive dysfunctionDeficits in cognitive abilities are widely recognized as a core feature of schizophrenia. The extent of the cognitive deficits an individual experiences is a predictor of how functional an individual will be, the quality of occupational performance, and how successful the individual will be in maintaining treatment. The presence and degree of cognitive dysfunction in individuals with schizophrenia has been reported to be a better indicator of functionality than the presentation of positive or negative symptoms. The deficits impacting the cognitive function are found in a large number of areas: working memory, long-term memory, verbal declarative memory, semantic processing, episodic memory, attention, learning (particularly verbal learning). Deficits in verbal memory are the most pronounced in individuals with schizophrenia, and are not accounted for by deficit in attention. Verbal memory impairment has been linked to a decreased ability in individuals with schizophrenia to semantically encode (process information relating to meaning), which is cited as a cause for another known deficit in long-term memory. When given a list of words, healthy individuals remember positive words more frequently (known as the Pollyanna principle); however, individuals with schizophrenia tend to remember all words equally regardless of their connotations, suggesting that the experience of anhedonia impairs the semantic encoding of the words. These deficits have been found in individuals before the onset of the illness to some extent. First-degree family members of individuals with schizophrenia and other high-risk individuals also show a degree of deficit in cognitive abilities, and specifically in working memory. A review of the literature on cognitive deficits in individuals with schizophrenia shows that the deficits may be present in early adolescence, or as early as childhood. The deficits which an individual with schizophrenia presents tend to remain the same over time in most patients, or follow an identifiable course based upon environmental variables. Although the evidence that cognitive deficits remain stable over time is reliable and abundant, much of the research in this domain focuses on methods to improve attention and working memory. Efforts to improve learning ability in individuals with schizophrenia using a high- versus low-reward condition and an instruction-absent or instruction-present condition revealed that increasing reward leads to poorer performance while providing instruction leads to improved performance, highlighting that some treatments may exist to increase cognitive performance. Training individuals with schizophrenia to alter their thinking, attention, and language behaviors by verbalizing tasks, engaging in cognitive rehearsal, giving self-instructions, giving coping statements to the self to handle failure, and providing self-reinforcement for success, significantly improves performance on recall tasks. This type of training, known as self-instructional (SI) training, produced benefits such as lower number of nonsense verbalizations and improved recall while distracted.
OnsetLate adolescence and early adulthood are peak periods for the onset of schizophrenia, critical years in a young adult's social and vocational development. In 40% of men and 23% of women diagnosed with schizophrenia, the condition manifested itself before the age of 19. The onset of the disease is usually later in women than in men. To minimize the developmental disruption associated with schizophrenia, much work has recently been done to identify and treat the prodromal (pre-onset) phase of the illness, which has been detected up to 30 months before the onset of symptoms. Those who go on to develop schizophrenia may experience transient or self-limiting psychotic symptoms and the non-specific symptoms of social withdrawal, irritability, dysphoria, and clumsiness before the onset of the disease. Children who go on to develop schizophrenia may also demonstrate decreased intelligence, decreased motor development (reaching milestones such as walking slowly), isolated play preference, social anxiety, and poor school performance.
CausesA combination of genetic and environmental factors play a role in the development of schizophrenia. People with a family history of schizophrenia who have a transient psychosis have a 20–40% chance of being diagnosed one year later.
GeneticEstimates of the heritability of schizophrenia is around 80%, which implies that 80% of the individual differences in risk to schizophrenia is explained by individual differences in genetics. These estimates vary because of the difficulty in separating genetic and environmental influences. The greatest single risk factor for developing schizophrenia is having a first-degree relative with the disease (risk is 6.5%); more than 40% of monozygotic twins of those with schizophrenia are also affected. If one parent is affected the risk is about 13% and if both are affected the risk is nearly 50%. Many genes are known to be involved in schizophrenia, each of small effect and unknown transmission and expression. The summation of these effect sizes into a polygenic risk score can explain at least 7% of the variability in liability for schizophrenia. Around 5% of cases of schizophrenia are understood to be at least partially attributable to rare copy number variants (CNVs), including 22q11, 1q21 and 16p11. These rare CNVs increase the risk of an individual developing the disorder by as much as 20-fold, and are frequently comorbid with autism and intellectual disabilities. There is a genetic relation between the common variants which cause schizophrenia and bipolar disorder, an inverse genetic correlation with intelligence and no genetic correlation with immune disorders.
EnvironmentEnvironmental factors associated with the development of schizophrenia include the living environment, drug use, and prenatal stressors. Maternal stress has been associated with an increase risk of schizophrenia, possibly in association with reelin. Maternal Stress has been observed to lead to hypermethylation and therefore under-expression of reelin, which in animal models leads to reduction in GABAergic neurons, a common finding in schizophrenia. Maternal nutritional deficiencies, such as those observed during a famine, as well as maternal obesity have also been identified as possible risk factors for schizophrenia. Both maternal stress and infection have been demonstrated to alter fetal neurodevelopment through pro-inflammatory proteins such as IL-8 and TNF. Parenting style seems to have no major effect, although people with supportive parents do better than those with critical or hostile parents. Childhood trauma, death of a parent, and being bullied or abused increase the risk of psychosis. Living in an urban environment during childhood or as an adult has consistently been found to increase the risk of schizophrenia by a factor of two, even after taking into account drug use, ethnic group, and size of social group. Other factors that play an important role include social isolation and immigration related to social adversity, racial discrimination, family dysfunction, unemployment, and poor housing conditions. It has been hypothesized that in some people, development of schizophrenia is related to intestinal tract dysfunction such as seen with non-celiac gluten sensitivity or abnormalities in the intestinal flora. A subgroup of persons with schizophrenia present an immune response to gluten different from that found in people with celiac, with elevated levels of certain serum biomarkers of gluten sensitivity such as anti-gliadin IgG or anti-gliadin IgA antibodies.
Substance useAbout half of those with schizophrenia use drugs or alcohol excessively. Amphetamine, cocaine, and to a lesser extent alcohol, can result in a transient stimulant psychosis or alcohol-related psychosis that presents very similarly to schizophrenia. Although it is not generally believed to be a cause of the illness, people with schizophrenia use nicotine at much higher rates than the general population. Alcohol abuse can occasionally cause the development of a chronic, substance-induced psychotic disorder via a kindling mechanism. Alcohol use is not associated with an earlier onset of psychosis. Cannabis can be a contributory factor in schizophrenia, potentially causing the disease in those who are already at risk. The increased risk may require the presence of certain genes within an individual or may be related to preexisting psychopathology. Early exposure is strongly associated with an increased risk. The size of the increased risk is not clear, but appears to be in the range of two to three times greater for psychosis. Higher dosage and greater frequency of use are indicators of increased risk of chronic psychoses. Other drugs may be used only as coping mechanisms by individuals who have schizophrenia, to deal with depression, anxiety, boredom, and loneliness.
Developmental factorsFactors such as hypoxia and infection, or stress and malnutrition in the mother during fetal development, may result in a slight increase in the risk of schizophrenia later in life. People diagnosed with schizophrenia are more likely to have been born in winter or spring (at least in the northern hemisphere), which may be a result of increased rates of viral exposures in utero. The increased risk is about five to eight percent. Other infections during pregnancy or around the time of birth that may increase the risk include Toxoplasma gondi and Chlamydia.
MechanismsA number of attempts have been made to explain the link between altered brain function and schizophrenia. One of the most common is the dopamine hypothesis, which attributes psychosis to the mind's faulty interpretation of the misfiring of dopaminergic neurons.
PsychologicalMany psychological mechanisms have been implicated in the development and maintenance of schizophrenia. Cognitive biases have been identified in those with the diagnosis or those at risk, especially when under stress or in confusing situations. Some cognitive features may reflect global neurocognitive deficits such as memory loss, while others may be related to particular issues and experiences. Despite a demonstrated appearance of blunted affect, recent findings indicate that many individuals diagnosed with schizophrenia are emotionally responsive, particularly to stressful or negative stimuli, and that such sensitivity may cause vulnerability to symptoms or to the disorder. Some evidence suggests that the content of delusional beliefs and psychotic experiences can reflect emotional causes of the disorder, and that how a person interprets such experiences can influence symptomatology. The use of "safety behaviors" (acts such as gestures or the use of words in specific contexts) to avoid or neutralize imagined threats may actually contribute to the chronicity of delusions. Further evidence for the role of psychological mechanisms comes from the effects of psychotherapies on symptoms of schizophrenia.
Neurological(fMRI) showing two levels of the brain; areas in orange were more active in healthy controls than in medicated people with schizophrenia.]] have an association with enlarged lateral ventricles in the brain.]] Schizophrenia is associated with subtle differences in brain structures, found in forty to fifty percent of cases, and in brain chemistry during acute psychotic states. Studies using neuropsychological tests and brain imaging technologies such as fMRI and PET to examine functional differences in brain activity have shown that differences seem to occur most commonly in the frontal lobes, hippocampus and temporal lobes. Reductions in brain volume are most pronounced in grey matter structures, and correlate with duration of illness, although white matter abnormalities have also been found. A progressive increase in ventricular volume as well as a progressive reduction in grey matter in the frontal, parietal, and temporal lobes has also been observed. These differences have been linked to the neurocognitive deficits often associated with schizophrenia. Because neural circuits are altered, it has alternatively been suggested that schizophrenia could be thought of as a neurodevelopmental disorder with psychosis occurring as a possibly preventable late stage. There has been debate on whether treatment with antipsychotics can itself cause reduction of brain volume. Particular attention has been paid to the function of dopamine in the mesolimbic pathway of the brain. This focus largely resulted from the accidental finding that phenothiazine drugs, which block dopamine function, could reduce psychotic symptoms. It is also supported by the fact that amphetamines, which trigger the release of dopamine, may exacerbate the psychotic symptoms in schizophrenia. The influential dopamine hypothesis of schizophrenia proposed that excessive activation of D2 receptors was the cause of (the positive symptoms of) schizophrenia. Although postulated for about 20 years based on the D2 blockade effect common to all antipsychotics, it was not until the mid-1990s that PET and SPET imaging studies provided supporting evidence. While dopamine D2/D3 receptors are elevated in schizophrenia, the effect size is small, and only evident in medication naive schizophrenics. On the other hand, presynaptic dopamine metabolism and released is elevated despite no difference in dopamine transporter. The altered synthesis of dopamine in the nigrostriatal system have been confirmed in several human studies. Hypoactivity of dopamine D1 receptor activation in the prefrontal cortex has also been observed. The hyperactivity of D2 receptor stimulation and relative hypoactivity of D1 receptor stimulation is thought to contribute to cognitive dysfunction by disrupting signal to noise ratio in cortical microcircuits. The dopamine hypothesis is now thought to be simplistic, partly because newer antipsychotic medication ( atypical antipsychotic medication) can be just as effective as older medication ( typical antipsychotic medication), but also affects serotonin function and may have slightly less of a dopamine blocking effect. Interest has also focused on the neurotransmitter glutamate and the reduced function of the NMDA glutamate receptor in schizophrenia, largely because of the abnormally low levels of glutamate receptors found in the postmortem brains of those diagnosed with schizophrenia, and the discovery that glutamate-blocking drugs such as phencyclidine and ketamine can mimic the symptoms and cognitive problems associated with the condition. Reduced glutamate function is linked to poor performance on tests requiring frontal lobe and hippocampal function, and glutamate can affect dopamine function, both of which have been implicated in schizophrenia; this has suggested an important mediating (and possibly causal) role of glutamate pathways in the condition. But positive symptoms fail to respond to glutamatergic medication. Closely related to evidence of glutamate dysfunction in schizophrenia is the observed changes GABAergic transmission. Post-Mortem studies demonstrate decreased expression of GAD67, GAT-1 and GABAA receptor subunits in the prefrontal cortex, although this appears to be restricted to a certain subsets of parvalbumin containing GABAergic neurons. While in vivo imaging of GABAergic signaling appears to be moderately reduced, this may be dependent upon treatment and disease stage.
DiagnosisSchizophrenia is diagnosed based on criteria in either the American Psychiatric Association's (APA) fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM 5), or the World Health Organization's International Statistical Classification of Diseases and Related Health Problems (ICD-10). These criteria use the self-reported experiences of the person and reported abnormalities in behavior, followed by a clinical assessment by a mental health professional. Symptoms associated with schizophrenia occur along a continuum in the population and must reach a certain severity and level of impairment, before a diagnosis is made. As of 2013 there is no objective test.
CriteriaIn 2013, the American Psychiatric Association released the fifth edition of the DSM ( DSM-5). To be diagnosed with schizophrenia, two diagnostic criteria have to be met over much of the time of a period of at least one month, with a significant impact on social or occupational functioning for at least six months. The person had to be suffering from delusions, hallucinations, or disorganized speech. A second symptom could be negative symptoms, or severely disorganized or catatonic behaviour. The definition of schizophrenia remained essentially the same as that specified by the 2000 version of DSM (DSM-IV-TR), but DSM-5 makes a number of changes.
- Subtype classifications – such as catatonic and paranoid schizophrenia – are removed. These were retained in previous revisions largely for reasons of tradition, but had subsequently proved to be of little worth.
- Catatonia is no longer so strongly associated with schizophrenia.As referenced from ,
- In describing a person's schizophrenia, it is recommended that a better distinction be made between the current state of the condition and its historical progress, to achieve a clearer overall characterization.
- Special treatment of Schneider's first-rank symptoms is no longer recommended.
- Schizoaffective disorder is better defined to demarcate it more cleanly from schizophrenia.
- An assessment covering eight domains of psychopathology – such as whether hallucination or mania is experienced – is recommended to help clinical decision-making.
SubtypesWith the publication of DSM-5, the APA removed all sub-classifications of schizophrenia. American Psychiatric Association DSM-5 Work Groups (2010) Proposed Revisions – Schizophrenia and Other Psychotic Disorders . Retrieved 17 February 2010. The five sub-classifications included in DSM-IV-TR were:
- Paranoid type: Delusions or auditory hallucinations are present, but thought disorder, disorganized behavior, or affective flattening are not. Delusions are persecutory and/or grandiose, but in addition to these, other themes such as jealousy, religiosity, or somatization may also be present. (DSM code 295.3/ICD code F20.0)
- Disorganized type: Named hebephrenic schizophrenia in the ICD. Where thought disorder and flat affect are present together. (DSM code 295.1/ICD code F20.1)
- Catatonic type: The subject may be almost immobile or exhibit agitated, purposeless movement. Symptoms can include catatonic stupor and waxy flexibility. (DSM code 295.2/ICD code F20.2)
- Undifferentiated type: Psychotic symptoms are present but the criteria for paranoid, disorganized, or catatonic types have not been met. (DSM code 295.9/ICD code F20.3)
- Residual type: Where positive symptoms are present at a low intensity only. (DSM code 295.6/ICD code F20.5)
- Post-schizophrenic depression: A depressive episode arising in the aftermath of a schizophrenic illness where some low-level schizophrenic symptoms may still be present. (ICD code F20.4)
- Simple schizophrenia: Insidious and progressive development of prominent negative symptoms with no history of psychotic episodes. (ICD code F20.6)