Schizophrenia
Schizophrenia is a mental disorder often characterized by abnormal social behavior and failure to recognize what is real. Common symptoms include false beliefs, unclear or confused thinking, auditory hallucinations, reduced social engagement and emotional expression, and lack of motivation. Diagnosis is based on observed behavior and the person's reported experiences.
Genetics and early environment, as well as psychological and social processes, appear to be important contributory factors. Some recreational and prescription drugs appear to cause or worsen symptoms. The many possible combinations of symptoms have triggered debate about whether the diagnosis represents a single disorder or a number of separate syndromes. Despite the origin of the term, from Greek skhizein, meaning "to split", and phrēn, meaning "mind", schizophrenia does not imply a "split personality" or "multiple personality disorder" — a condition with which it is often confused in public perception. Rather, the term means a "splitting of mental functions", reflecting the presentation of the illness.
The mainstay of treatment is antipsychotic medication, which primarily suppresses dopamine receptor activity. Counseling, job training and social rehabilitation are also important in treatment. In more serious cases—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.
Symptoms begin typically in young adulthood, and about 0.3–0.7% of people are affected during their lifetime. In 2013 there was estimated to be 23.6 million cases globally. The disorder is thought to mainly affect the ability to think, but it also usually contributes to chronic problems with behavior and emotion. People with schizophrenia are likely to have additional conditions, including major depression and anxiety disorders; the lifetime occurrence of substance use disorder is almost 50%. 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 the average life expectancy. This is the result of increased physical health problems and a higher suicide rate (about 5%). In 2013 an estimated 16,000 people died from behavior related-to or caused by schizophrenia
Violence
Individuals with severe mental illness including schizophrenia are at a significantly greater risk of being victims of both violent and non-violent crime. Schizophrenia has been associated with a higher rate of violent acts, although this is primarily due to higher rates of drug use. Rates of homicide linked to psychosis are similar to those linked to substance misuse, and parallel the overall rate in a region. What role schizophrenia has on violence independent of drug misuse is controversial, but certain aspects of individual histories or mental states may be factors.
Media coverage relating to violent acts by individuals with schizophrenia reinforces public perception of an association between schizophrenia and violence. In a large, representative sample from a 1999 study, 12.8% of Americans believed that individuals with schizophrenia were "very likely" to do something violent against others, and 48.1% said that they were "somewhat likely" to. Over 74% said that people with schizophrenia were either "not very able" or "not able at all" to make decisions concerning their treatment, and 70.2% said the same of money management decisions. The perception of individuals with psychosis as violent has more than doubled in prevalence since the 1950s, according to one meta-analysis.
Mechanisms
Psychological
Many 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
Schizophrenia is associated with subtle differences in brain structures, found in 40 to 50% 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 most commonly occur in the frontal lobes, hippocampus and temporal lobes. Reductions in brain volume, smaller than those found in Alzheimer's disease, have been reported in areas of the frontal cortex and temporal lobes. It is uncertain whether these volumetric changes are progressive or preexist prior to the onset of the disease. 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 should be thought of as a collection of neurodevelopmental disorders. 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. 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, have suggested an important mediating (and possibly causal) role of glutamate pathways in the condition. But positive symptoms fail to respond to glutamatergic medication.