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Steve Joordens

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Symptoms Self-portrait of a person with schizophrenia, representing that individual's perception of the distorted experience of reality in the disorder A person diagnosed with schizophrenia may experience hallucinations (most reported are hearing voices), delusions (often bizarre or persecutory in nature), and disorganized thinking and speech. The latter may range from loss of train of thought, to sentences only loosely connected in meaning, to incoherence known as word salad in severe cases. Social withdrawal, sloppiness of dress and hygiene, and loss of motivation and judgment are all common in schizophrenia.[8] There is often an observable pattern of emotional difficulty, for example lack of responsiveness.[9] Impairment in social cognition is associated with schizophrenia,[10] as are symptoms of paranoia; social isolation commonly occurs.[11] Difficulties in working and long-term memory, attention, executive functioning, and speed of processing also commonly occur.[2] In one uncommon subtype, the person may be largely mute, remain motionless in bizarre postures, or exhibit purposeless agitation, all signs of catatonia.[12] About 30% to 50% of people with schizophrenia do not have insight; in other words, they do not accept their condition or its treatment.[13] Treatment may have some effect on insight.[14] People with schizophrenia often find facial emotion perception to be difficult.[15] Schneiderian classification In the early 20th century, the psychiatrist Kurt Schneider listed the forms of psychotic symptoms that he thought distinguished schizophrenia from other psychotic disorders. These are called first-rank symptoms or Schneider's first-rank symptoms. They include delusions of being controlled by an external force; the belief that thoughts are being inserted into or withdrawn from one's conscious mind; the belief that one's thoughts are being broadcast to other people; and hearing hallucinatory voices that comment on one's thoughts or actions or that have a conversation with other hallucinated voices.[16] Although they have significantly contributed to the current diagnostic criteria, the specificity of first-rank symptoms has been questioned. A review of the diagnostic studies conducted between 1970 and 2005 found that they allow neither a reconfirmation nor a rejection of Schneider's claims, and suggested that first-rank symptoms should be de-emphasized in future revisions of diagnostic systems.[17] Positive and negative symptoms Schizophrenia is often described in terms of positive and negative (or deficit) symptoms.[18] 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.[19] Hallucinations are also typically related to the content of the delusional theme.[20] Positive symptoms generally respond well to medication.[20] Negative symptoms are deficits of normal emotional responses or of other thought processes, and respond less well to medication.[8] They commonly include flat or blunted affect and emotion, poverty of speech (alogia), inability to experience pleasure (anhedonia), lack of desire to form relationships (asociality), and lack of motivation (avolition). Research suggests that negative symptoms contribute more to poor quality of life, functional disability, and the burden on others than do positive symptoms.[21] People with prominent negative symptoms often have a history of poor adjustment before the onset of illness, and response to medication is often limited.[8][22] Onset Late adolescence and early adulthood are peak periods for the onset of schizophrenia,[2] critical years in a young adult's social and vocational development.[23] In 40% of men and 23% of women diagnosed with schizophrenia, the condition manifested itself before the age of 19.[24] 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.[23] Those who go on to develop schizophrenia may experience transient or self-limiting psychotic symptoms[25] and the non-specific symptoms of social withdrawal, irritability, dysphoria,[26] and clumsiness[27] during the prodromal phase. Causes Main article: Causes of schizophrenia A combination of genetic and environmental factors play a role in the development of schizophrenia.[2][3] People with a family history of schizophrenia who suffer a transient psychosis have a 20–40% chance of being diagnosed one year later.[28] Genetic Estimates of heritability vary because of the difficulty in separating the effects of genetics and the environment.[29] The greatest risk 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.[3] A child of two parents with schizophrenia has a 46% chance of developing the disorder.[30] It is likely that many genes are involved, each of small effect and unknown transmission and expression.[3] Many possible candidates have been proposed, including specific copy number variations, NOTCH4, and histone protein loci.[31] A number of genome-wide associations such as zinc finger protein 804A have also been linked.[32] There appears to be significant overlap in the genetics of schizophrenia and bipolar disorder.[33] Evidence is emerging that the genetic architecture of schizophrenia involved both common and rare risk variation.[34] Assuming a hereditary basis, one question from evolutionary psychology is why genes that increase the likelihood of psychosis evolved, assuming the condition would have been maladaptive from an evolutionary point of view. One idea is that genes are involved in the evolution of language and human nature, but to date such ideas remain little more than hypothetical in nature.[35][36] Environment Environmental factors associated with the development of schizophrenia include the living environment, drug use and prenatal stressors.[2] Parenting style seems to have no major effect, although people with supportive parents do better than those with critical or hostile parents.[3] 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,[2][3] even after taking into account drug use, ethnic group, and size of social group.[37] 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.[3][38] Drug use Amphetamine, cocaine, and to a lesser extent alcohol, can result in psychosis that presents very similarly to schizophrenia.[3][39] Although it is not generally believed to be a cause of the illness, people with schizophrenia use nicotine at much greater rates than the general population.[40] About half of those with schizophrenia use drugs or alcohol excessively.[41] Evidence supports a link between earlier onset of psychotic illness and cannabis use; alcohol use is not associated with an earlier onset of psychosis.[42] Other drugs may be used only as coping mechanisms by individuals who have schizophrenia to deal with depression, anxiety, boredom, and loneliness.[41][43] There is evidence that alcohol abuse via a kindling mechanism can occasionally cause the development of a chronic substance induced psychotic disorder, i.e. schizophrenia.[44] The more often cannabis is used, the more likely a person is to develop a psychotic illness,[45] with frequent use being correlated with twice the risk of psychosis and schizophrenia.[46] Whether cannabis use is a contributory cause of schizophrenia, rather than a behavior that is simply associated with it, remains controversial.[31][47] Developmental factors Factors 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.[2] 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.[3] This difference is about 5 to 8%.[48] Mechanisms Main article: Mechanisms of schizophrenia A number of attempts have been made to explain the link between altered brain function and schizophrenia.[2] One of the most common is the dopamine hypothesis, which attributes psychosis to the mind's faulty interpretation of the misfiring of dopaminergic neurons.[2] 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.[49] Some cognitive features may reflect global neurocognitive deficits such as memory loss, while others may be related to particular issues and experiences.[50][51] 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.[52][53] 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.[54][55][56] The use of "safety behaviors" to avoid imagined threats may contribute to the chronicity of delusions.[57] Further evidence for the role of psychological mechanisms comes from the effects of psychotherapies on symptoms of schizophrenia.[58] Neurological Functional magnetic resonance imaging (fMRI) and other brain imaging technologies allow for the study of differences in brain activity in people diagnosed with schizophrenia. The image shows two levels of the brain, with areas that were more active in healthy controls than in schizophrenia patients shown in orange, during an fMRI study of working memory. Schizophrenia is associated with subtle differences in brain structures, found in 40 to 50% of cases, and in brain chemistry during acute psychotic states.[2] 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.[59] 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.[60] These differences have been linked to the neurocognitive deficits often associated with schizophrenia.[61] Because neural circuits are altered, it has alternatively been suggested that schizophrenia should be thought of as a collection of neurodevelopmental disorders.[62] 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.[63] 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.[64] 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,[65] and the discovery that glutamate-blocking drugs such as phencyclidine and ketamine can mimic the symptoms and cognitive problems associated with the condition.[66] 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.[67] But positive symptoms fail to respond to glutamatergic medication.[68] Diagnosis Main article: Diagnosis of schizophrenia John Nash, a U.S. mathematician and joint winner of the 1994 Nobel Prize for Economics, who had schizophrenia. His life was the subject of the 2001 Academy Award-winning film A Beautiful Mind. Schizophrenia is diagnosed based on criteria in either the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders, version DSM-IV-TR, or the World Health Organization's International Statistical Classification of Diseases and Related Health Problems, the ICD-10.[2] 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 before a diagnosis is made.[3] As of 2009 there is no objective test.[2] Criteria The ICD-10 criteria are typically used in European countries, while the DSM-IV-TR criteria are used in the United States and to varying degrees around the world, and are prevailing in research studies. The ICD- 10 criteria put more emphasis on Schneiderian first-rank symptoms. In practice, agreement between the two systems is high.[69] According to the revised fourth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR), to be diagnosed with schizophrenia, three diagnostic criteria must be met:[70] Characteristic symptoms: Two or more of the following, each present for much of the time during a one- month period (or less, if symptoms remitted with treatment). Delusions Hallucinations Disorganized speech, which is a manifestation of formal thought disorder Grossly disorganized behavior (e.g. dressing inappropriately, crying frequently) or catatonic behavior Negative symptoms: Blunted affect (lack or decline in emotional response), alogia (lack or decline in speech), or avolition (lack or decline in motivation) If the delusions are judged to be bizarre, or hallucinations consist of hearing one voice participating in a running commentary of the patient's actions or of hearing two or more voices conversing with each other, only that symptom is required above. The speech disorganization criterion is only met if it is severe enough to substantially impair communication. Social or occupational dysfunction: For a significant portion of the time since the onset of the disturbance, one or more major areas of functioning such as work, interpersonal relations, or self-care, are markedly below the level achieved prior to the onset. Significant duration: Continuous signs of the disturbance persist for at least six months. This six-month period must include at least one month of symptoms (or less, if symptoms remitted with treatment). If signs of disturbance are present for more than a month but less than six months, the diagnosis of schizophreniform disorder is applied.[70] Psychotic symptoms lasting less than a month may be diagnosed as brief psychotic disorder, and various conditions may be classed as psychotic disorder not otherwise specified. Schizophrenia cannot be diagnosed if symptoms of mood disorder are substantially present
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