Schizophrenia Research Paper

View sample Schizophrenia Research Paper. Browse other  research paper examples and check the list of research paper topics for more inspiration. If you need a religion 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 research paper writing service for professional assistance. We offer high-quality assignments for reasonable rates.

Schizophrenia is a psychosis—a severe mental disorder in which the person’s emotions, thinking, judgment, and grasp of reality are so disturbed that his or her functioning is seriously impaired. The symptoms of schizophrenia are often divided into ‘positive’ and ‘negative.’ Positive symptoms are abnormal experiences and perceptions like delusions, hallucinations, illogical and disorganized thinking, and inappropriate behavior. Negative symptoms are the absence of normal thoughts, emotions, and behavior; such as blunted emotions, loss of drive, poverty of thought, and social withdrawal.

Despite common features, different forms of schizophrenia are quite dissimilar. One person, for example, may be paranoid, constantly bothered by voices warning him or her about plots or threats, but able to show good judgment and high functioning in many areas of life. Another may be bizarre in manner and appearance, preoccupied with delusions of bodily disorder, passive and withdrawn. So marked are the differences that many researchers believe that the illness will eventually prove to be a set of different conditions which lead to somewhat similar consequences.

1. Diagnostic Difficulties

It is difficult to define schizophrenia precisely. The two most common functional psychoses are schizophrenia and bipolar disorder (also known as manic-depressive illness). The distinction between the two is not easy to make and psychiatrists in different parts of the world at different times have drawn the boundaries in different ways. Bipolar disorder is an episodic disorder in which psychotic symptoms are associated with severe alterations in mood—at times elated, agitated episodes of mania, at other times depression, with physical and mental slowing, despair, guilt, and low self-esteem. The course of schizophrenia, by way of contrast, though fluctuating, tends to be more continuous, and the person’s display of emotion is likely to be incongruous or lacking in spontaneity. Markedly illogical thinking is common in schizophrenia. Auditory hallucinations may occur in either bipolar disorder or schizophrenia, but in schizophrenia they are more likely to be commenting on the person’s actions or to be conversing one with another. Delusions, also, can occur in both conditions; in schizophrenia they may give the individual the sense that he or she is being controlled by outside forces or that his or her thoughts are being broadcast or interfered with.

2. Schizophrenia Is Universal

Schizophrenia is a universal condition and an ancient one. Typical cases are evident in the medical writings of ancient Greece and Rome, and the condition occurs today in every human society. While the content of delusions and hallucinations varies from culture to culture, the form of the illness is similar everywhere. Two World Health Organization studies, applying a standardized diagnostic approach, have identified characteristic cases of schizophrenia in developed and developing world countries from around the globe ( World Health Organization 1979, Jablensky et al. 1992). One of these studies (Jablensky et al. 1992) demonstrated that the rate of occurrence of new cases (the incidence) is similar in every country studied from India to Ireland—around one per 10,000 adults each year. However, since both death and recovery rates for people with psychosis are higher in the Third World, the point prevalence of schizophrenia (the number of cases existing at any point in time) is lower in the Third World—around 3 per 1,000 of the adult population compared to 6 per 1,000 in the developed world ( Warner and de Girolamo 1995). The risk of developing the illness at some time in one’s life (the lifetime prevalence) is a little higher—around one percent of the developed world population. See Mental Illness, Epidemiology of.

3. Conceptual Framework

The bio-psychosocial model of illness clarifies how different factors shape schizophrenia. The model posits that the predisposition to developing an illness, its onset, and its course are each influenced by biological, psychological, and sociocultural factors. A variety of factors can affect the different phases of schizophrenia, many being environmental. Some, such as genetics, gender, and synaptic pruning are innate. Biological, psychological and social factors are involved to some extent in most phases of schizophrenia. In general, however, the research suggests that the factors responsible for the predisposition to developing an illness are more likely to be biological, that psychological factors are often important in triggering the onset, and that the course and outcome are particularly likely to be influenced by sociocultural factors.

4. The Course And Outcome Of Schizophrenia

Wide variation occurs in the course of schizophrenia. In some cases the onset of illness is gradual, extending over months or years; in others it begins suddenly. Some have episodes of illness lasting weeks or months with full remission of symptoms between each episode; others have a fluctuating course in which symptoms are continuous; others again have little variation over the course of years. Swiss psychiatrist, Luc Ciompi, studied the onset, course, and outcome of illness in people with schizophrenia, following them into old age (Ciompi 1980). He found that the onset of the illness was either acute (less than six months from first symptoms to full-blown psychosis) or insidious in roughly equal numbers of cases; the course was episodic or continuous in approximately equal numbers of patients; and the outcome was moderate to severe disability in half the cases and mild disability or full recovery in the other half.

Despite popular and professional belief, schizophrenia does not have a progressive, downhill course with universally poor outcome. In fact, schizophrenia usually becomes less severe as the sufferer grows older. A review of outcome studies conducted in Europe and North America throughout the twentieth century reveals that, over the course of months or years, 20 to 25 percent of people with schizophrenia recover completely from the illness—all their psychotic symptoms disappear and they return to their previous level of functioning. Another 20 percent continue to have some symptoms, but are able to lead satisfying and productive lives ( Warner 1994). In the developing countries, recovery rates are even better. The two World Health Organization studies mentioned above ( World Health Organization 1979, Jablensky et al. 1992) have shown that good outcome occurs in about twice as many patients diagnosed with schizophrenia in the developing world as in the developed world. The reason for the better outcome in the Third World is not completely understood, but it may be that many people with mental illness in developing world villages are better accepted, less stigmatized, and more likely to find work in a subsistence agricultural economy ( Warner 1994).

5. Factors Affecting The Course Of Schizophrenia

Age of onset: The later in life the illness begins, the milder it proves to be. Onset of schizophrenia before the age of 14 is rare, but when it does begin this early it is associated with a severe course of illness. Onset after the age of 40 is also rare, and is associated with a milder course.

Gender: Women usually develop their first symptoms of schizophrenia later than men and the course of their illness tends to be less severe. The reason for these differences is not clear, but may be related to the protective effect of female hormones on brain development and function.

Stressful life events: Stress can trigger episodes of schizophrenia. People with schizophrenia are more likely to report a stressful life event preceding an episode of illness than during a period of remission. Similarly, stressful events are more likely to occur prior to an episode of schizophrenia than in the same time period for people drawn from the general population (Rabkin 1982). Life stress is also more common before the first episode of schizophrenia and so, although stress does not cause the illness, it may well influence the timing of onset.

The research indicates that the life events occurring before episodes of schizophrenia are milder and less objectively troublesome than those before episodes of other disorders such as depression (Beck and Worthen 1972), suggesting that people with schizophrenia are exquisitely sensitive to stress.

Domestic stress: The robust results of the ‘expressed emotion’ (EE) research, conducted in several countries in the developed and developing worlds, reveal that people with schizophrenia living with relatives who are critical or over-involved (referred to in the research as high EE) have a higher relapse rate than those living with relatives who are less critical or intrusive (low EE) (Leff and Vaughn 1985, Parker and Hadzi-Pavlovic 1990). A meta-analysis of 26 EE studies of schizophrenia conducted in 11 countries indicates that the relapse rate over a two-year follow-up period was more than twice as high, at 66 percent, for patients in families which included a high EE relative than in low EE households (29 percent) (Kavanagh 1992). Other studies have shown that relatives who are less critical and over-involved exert a positive therapeutic effect on the person with schizophrenia, their presence leading to a reduction in the patient’s level of arousal (Sturgeon et al. 1981). There is no indication that the more critical and over-involved relatives are abnormal by everyday Western standards; low EE family members may be unusually low-key and permissive (Angermeyer 1983).

Several studies have shown that family psychoeducational interventions can lead to a change in the level of criticism and over-involvement among relatives of people with schizophrenia and so reduce the relapse rate (Falloon et al. 1982, Berkowitz et al. 1981). Effective family interventions provide three basic ingredients: (a) education about the illness; (b) help in developing problem-solving mechanisms; and (c) practical and emotional support (McFarlane 1983, Falloon et al. 1982, Leff and Vaughn 1985).

Substance use: Drug and alcohol abuse is more common among people with serious mental illness. Unemployment, social isolation, and alienation may contribute to these high rates. Several studies have shown that people with serious mental illness who abuse substances have a worse course of illness (Drake and Wallach 1989) but other researchers have found psychopathology to be no worse or, sometimes, lower among people with mental illness who use substances (Zisook et al. 1992, Buckley et al. 1994). One reason for this discrepancy may lie in the common finding that substance users are also more likely to be noncompliant with treatment (Drake and Wallach 1989); the poor course of illness, when it is observed, may be a result of this noncompliance rather than a direct consequence of substance use.

6. Causes Of Schizophrenia

There is no single organic defect or infectious agent which causes schizophrenia, but a variety of factors increase the risk of developing the illness, including genetic factors and obstetric complications.

Genetic factors. Relatives of people with schizophrenia have a greater risk of developing the illness, the risk being progressively higher among those who are more genetically similar to the person with schizophrenia (see Fig. 1). For a second-degree relative the lifetime risk is about two percent (twice the risk for someone in the general population); for a first-degree relative is about ten percent, and for an identical twin (genetically identical to the person with schizophrenia) the risk is close to 50 percent (Gottesman 1991).

Schizophrenia Research Paper Figure 1

Studies of people adopted in infancy reveal that the increased risk of schizophrenia among the relatives of people with the illness is due to inheritance rather than environment. The children of people with schizophrenia have the same increased prevalence of the illness whether they are raised by their biological parent with schizophrenia or by adoptive parents (Gottesman 1991, Warner and de Girolamo 1995).

There is evidence implicating several genes in causing schizophrenia ( Wang et al. 1995, Freedman et al. 1997), and it is likely that more than one is responsible, either through an interactive effect or by producing different variants of the disorder. See Mental Illness, Genetics of.

Obstetric complications. A review and meta-analysis of studies conducted prior to mid-1994 on the effect of obstetric complications in schizophrenia, reveals that complications before and around the time of birth appear to double the risk of developing the illness (Geddes and Lawrie 1995). In a more recent metaanalysis of a different sample of studies, the same researchers found the risk to be increased by a factor of 1.4.

Since these analyses were published, more recent studies have shown variable results. Data gathered at the time of birth from very large cohorts of children born in Finland and Sweden in the 1960s and 1970s indicate that various obstetric complications double or triple the risk of developing schizophrenia (Hultman et al. 1999, Dalman et al. 1999, Jones et al. 1998). An American study shows that the risk of schizophrenia is more than four times greater in those who experience oxygen deprivation before or at the time of birth, and that such complications increase the risk of schizophrenia much more than other psychoses like bipolar disorder (Zornberg et al. 2000). Recent Scottish research, on the other hand, found the effect of obstetric complications to be less than in prior studies (Kendell et al. 2000). Other recent research suggests that only early-onset (before age 30) cases of schizophrenia are associated with obstetric complications (Byrne et al. 2000, Cannon et al. 2000).

Obstetric complications are a statistically important risk because they are so common. In the general population, they occur in up to 40 percent of births (the precise rate of occurrence depending on how they are defined) (McNeil 1988, Geddes and Lawrie 1995). The authors of the meta-analyses cited above estimate that complications of pregnancy and delivery may increase the prevalence of schizophrenia by 20 percent (Geddes and Lawrie 1995).

The obstetric complications most closely associated with the increased risk of developing schizophrenia are those that induce fetal oxygen deprivation, particularly prolonged labor (McNeil 1988), and placental complications (Jones et al. 1998, Hultman et al. 1999, Dalman et al. 1999). Early delivery is also more common for those who go on to develop schizophrenia, and infants who suffer perinatal brain damage are at a much-increased risk of subsequent schizophrenia (Jones et al. 1998). Trauma at the time of labor and delivery, and especially prolonged labor, is associated with an increase in structural brain abnormalities—cerebral atrophy and small hippocampi— which occur frequently in schizophrenia (McNeil et al. 2000).

Viruses. The risk of intrauterine brain damage is increased if a pregnant woman contracts a viral illness. We know that more people with schizophrenia are born in the late winter or spring than at other times of year, and that this birth bulge sometimes increases after epidemics of viral illnesses like influenza, measles, and chickenpox. Maternal viral infections, however, probably account for only a small part of the increased risk for schizophrenia ( Warner and de Girolamo 1995).

7. Myths About The Causes Of Schizophrenia

Parenting: Contrary to the beliefs of professionals prior to the 1970s and to the impression still promoted by the popular media, there is no evidence, even after decades of research, that family or parenting problems cause schizophrenia. As early as 1948, psychoanalysts proposed that mothers fostered schizophrenia in their offspring through cold and distant parenting. Other theorists blamed parental schisms, and confusing patterns of communication within the family (Lidz et al. 1965, Laing and Esterton 1970). The double-bind theory, put forward by anthropologist Gregory Bateson, argued that schizophrenia is promoted by contradictory parental messages from which the child is unable to escape (Bateson et al. 1956). While enjoying broad public recognition, such theories have seldom been adequately tested, and none of the research satisfactorily resolves the question of whether differences found in the families of people with schizophrenia are the cause or the effect of psychological abnormalities in the disturbed family member (Hirsch and Leff 1975). Millions of family members of people with schizophrenia have suffered needless shame, guilt, and stigma because of this widespread misconception.

Drug abuse: Drug abuse does not cause schizophrenia, though it is possible, but by no means certain, that it can trigger the onset of the illness. Hallucinogenic drugs like LSD can induce short episodes of psychosis and heavy use of marijuana and stimulant drugs like cocaine and amphetamines may precipitate brief, toxic psychoses with features similar to schizophrenia (Bowers 1987), but there is no evidence that these drugs cause a long-lasting illness like schizophrenia. In the 1950s and 1960s, LSD was used as an experimental drug in psychiatry in Britain and America, but the proportion of these volunteers and patients who developed a long-lasting psychosis was scarcely greater than in the general population (Cohen 1960, Malleson 1971). A Swedish study found that army conscripts who used marijuana heavily were six times more likely to develop schizophrenia later in life (Andreasson et al. 1987), but this may well have been because those people who were destined to develop schizophrenia were more likely to use marijuana as a way to cope with the premorbid symptoms of the illness. Schizophrenia is preceded by a long period of prodromal symptoms, and a German study has demonstrated that the onset of drug and alcohol abuse in people with schizophrenia usually follows the very first negative symptom of schizophrenia (such as social withdrawal) but precedes the first positive symptom (such as hallucinations). The authors conclude that substance use is an avenue to the relief of the earliest symptoms of the illness, but is not a cause (Hambrecht and Hafner 1995).

8. The Brain In Schizophrenia

Physical changes in the brain have been identified in some people with schizophrenia. The analysis of brain tissue after death has revealed a number of structural abnormalities, and new brain-imaging techniques have revealed changes in both the structure and function of the brain during life. Techniques such as magnetic resonance imaging (MRI) reveal changes in the size of different parts of the brain, especially the temporal lobes. The fluid-filled spaces (the ventricles) in the interior of the temporal lobes are often enlarged and the temporal lobe tissue diminished. The greater the observed changes the greater the severity of the person’s thought disorder and auditory hallucinations (Suddath et al. 1990).

Some imaging techniques, such as positron emission tomography (PET), measure the actual functioning of the brain and provide a similar picture of abnormality. PET scanning reveals hyperactivity in the temporal lobes, particularly in the hippocampus, a part of the temporal lobe concerned with episodic memory (Tamminga et al. 1992). Another type of functional imaging, electrophysiological brain recording using EEG tracings, shows that most people with schizophrenia seem to be excessively responsive to repeated environmental stimuli and more limited in their ability to blot out irrelevant information (Freedman et al. 1997). In line with this finding, those parts of the brain that are supposed to screen out irrelevant stimuli, such as the frontal lobe, show decreased activity on PET scan (Tamminga et al. 1992).

Tying in with this sensory screening difficulty, postmortem brain tissue examination has revealed problems in a certain type of brain cell—the inhibitory interneuron. These neurons damp down the action of the principal nerve cells, preventing them from responding to too many inputs. Thus, they prevent the brain from being overwhelmed by too much sensory information from the environment. The chemical messengers or neurotransmitters ( primarily gammaamino butyric acid or GABA) released by these interneurons are diminished in the brains of people with schizophrenia (Benes et al. 1991, Akbarian et al. 1993) suggesting that there is less inhibition of brain overload.

Abnormality in the functioning of these interneurons appears to produce changes in the brain cells that release the neurotransmitter dopamine. The role of dopamine has long been of interest to schizophrenia researchers, because drugs like amphetamines that increase dopamine’s effects can cause psychoses that resemble schizophrenia, and drugs that block or decrease dopamine’s effect are useful for the treatment of psychoses (Meltzer and Stahl 1976). Dopamine increases the sensitivity of brain cells to stimuli. Ordinarily, this heightened awareness is useful in increasing a person’s awareness during times of stress or danger, but, for a person with schizophrenia, the addition of the effect of dopamine to an already hyperactive brain state may tip the person into psychosis.

These findings suggest that in schizophrenia there is a deficit in the regulation of brain activity by interneurons, so that the brain over-responds to environmental signals and lacks the ability to screen out unwanted stimuli. This problem is made worse by a decrease in the size of the temporal lobes, which ordinarily process sensory inputs, making it more difficult for the person to respond appropriately to new stimuli.

9. Why Does Schizophrenia Begin After Puberty?

Schizophrenia researchers have long been puzzled about why the illness normally begins in adolescence when important risk factors, such as genetic loading and neonatal brain damage, are present from birth or sooner. Recent research attempts to address the question.

Normal brain development leads to the loss of 30–40 percent of the connections (synapses) between brain cells during the developmental period from early life to adolescence (Huttenlocher 1979). Brain cells themselves do not diminish in number during this period, only their connectivity. It appears that we may need a high degree of connectivity between brain cells in infancy to enhance our ability to learn language rapidly (toddlers learn as many as twelve new words a day). The loss of neurons during later childhood and adolescence, however, improves our ‘working memory’ and our efficiency to process complex linguistic information (McGlashan and Hoffman 2000).

For people with schizophrenia, this normally useful process of synaptic pruning is excessive, leaving fewer synapses in the frontal lobes and medial temporal cortex (Feinberg 1983). In consequence, there are deficits in the interaction between these two areas of the brain in schizophrenia, which reduce the adequacy of working memory ( Weinberger et al. 1992). One intriguing computer modeling exercise suggests that decreasing synaptic connections and eroding working memory in this way not only leads to abnormalities in the ability to recognize meaning when stimuli are ambiguous but also to the development of auditory hallucinations (Hoffman and McGlashan 1997).

It is possible, therefore, that this natural and adaptive process of synaptic elimination in childhood, if carried too far, could lead to the development of schizophrenia (Feinberg 1983). If true, this would help explain why schizophrenia persists among humans despite its obvious functional disadvantages and its association with reduced fertility. The genes for synaptic pruning may help us refine our capacity to comprehend speech and other complex stimuli, but, when complicated by environmental assaults resulting in brain injury, the result could be symptoms of psychosis. As yet, this formulation is speculative.

10. Effective Interventions In Schizophrenia

There is more agreement now about what is important in the treatment of schizophrenia than ever before. In establishing the World Psychiatric Association global project designed to combat the stigma and discrimi- nation resulting from schizophrenia ( Warner 2000), prominent psychiatrists from around the world recently agreed on the following principles:

People with schizophrenia can be treated effectively in a variety of settings. These days the use of hospitals is mainly reserved for those in an acute relapse. Outside of the hospital, a range of alternative treatment settings have been devised which provide supervision and support and are less alienating and coercive than the hospital ( Warner 1995).

Family involvement can improve the effectiveness of treatment. A solid body of research has demonstrated that relapse in schizophrenia is much less frequent when families are provided with support and education about schizophrenia.

Medications are an important part of treatment but they are only part of the answer. They can reduce or eliminate positive symptoms but they have a negligible effect on negative symptoms. Fortunately, modern, novel antipsychotic medications, introduced in the past few years, can provide benefits while causing less severe side effects than the standard antipsychotic drugs which were introduced in the mid-1950s.

Treatment should include social rehabilitation. People with schizophrenia usually need help to improve their functioning in the community. This can include training in basic living skills; assistance with a host of day-to-day tasks; and job training, job placement, and work support. The psychosocial clubhouse is one effective model for providing many of these forms of assistance (Mosher and Burti 1989). The assertive community treatment model has proven effective in preventing relapse and hospital admission (Stein and Test 1980).

Work helps people recover from schizophrenia. Productive activity is basic to a person’s sense of identity and worth. The availability of work in a subsistence economy may be one of the main reasons that outcome from schizophrenia is so much better in Third World villages ( Warner 1994). Given training and support, most people with schizophrenia can work, as has been demonstrated by several north Italian employment programs ( Warner 1994). However, due to problems such as work disincentives in disability pension schemes, high general unemployment and inadequate vocational rehabilitation services, the employment of people with schizophrenia in Britain and the United States has routinely been as low as 15 percent in recent years ( Warner 2000).

People with schizophrenia can get worse if treated punitively or confined unnecessarily. Extended hospital stays are rarely necessary if good community treatment is available. Jails or prisons are not appropriate places of care. Yet, around the world, large numbers of people with schizophrenia are housed in prison cells, usually charged with minor crimes, largely because of the lack of adequate community treatment. People with schizophrenia and their family members should help plan and even deliver treatment. Consumers of mental health services can be successfully employed in treatment programs, and when they help train treatment staff, professional attitudes and patient outcome both improve (Sherman and Porter 1991, Warner 2000).

People’s responses towards someone with schizophrenia influence the person’s course of illness and quality of life. Negative attitudes can push people with schizophrenia and their families into hiding the illness and drive them away from help. If people with schizophrenia are shunned and feared they cannot be genuine members of their own community. They become isolated and victims of discrimination in employment, accommodation, and education ( Warner 2000). The recent US Surgeon General’s report on mental illness cited stigma as one of the most important obstacles to effective treatment (US Department of Health and Human Services 1999).

Bibliography:

  1. Akbarian S, Vinuela A, Kim J J, Potkin S G, Bunney W E J, Jones E G 1993 Distorted distribution of nicotinamideadenine dinucleotide phosphate-diaphorase neurons in temporal lobe of schizophrenics implies anomalous cortical development. Archives of General Psychiatry 50: 178–87
  2. Andreasson S, Allebeck P, Engstrom A, Rydberg U 1987 Cannabis and schizophrenia: A longitudinal study of Swedish conscripts. Lancet 1987(2): 1483–86
  3. Angermeyer M C 1983 ‘Normal deviance’: Changing norms under abnormal circumstances. Presented at the Seventh World Congress of Psychiatry, Vienna
  4. Bateson G, Jackson D, Haley J 1956 Towards a theory of schizophrenia. Behavioral Science 1: 251–64
  5. Beck J, Worthen K 1972 Precipitating stress, crisis theory, and hospitalization in schizophrenia and depression. Archives of General Psychiatry 26: 123–9
  6. Benes F M, McSparran I, Bird E D, San Giovani J P, Vincent S L 1991 Deficits in small interneurons in prefrontal and cingulate cortices of schizophrenic and schizoaffective patients. Archives of General Psychiatry 48: 996–1001
  7. Berkowitz R, Kuipers L, Eberlein-Fries R, Leff J D 1981 Lowering expressed emotion in relatives of schizophrenics. New Directions in Mental Health Services 12: 27–48
  8. Bowers M B 1987 The role of drugs in the production of schizophreniform psychoses and related disorders. In: Meltzer H Y (ed.) Psychopharmacology: The Third Generation of Progress. Raven Press, New York
  9. Buckley P, Thompson P, Way L, Meltzer H Y 1994 Substance abuse among patients with treatment-resistant schizophrenia: Characteristics and implications for clozapine therapy. American Journal of Psychiatry 151: 385–9
  10. Byrne M, Browne R, Mulryan N, Scully A, Morris M, Kinsella A, McNeil T, Walsh D, O’Callaghan E 2000 Labour and delivery complications and schizophrenia: Case-control study using contemporaneous labour ward records. British Journal of Psychiatry 176: 531–6
  11. Cannon T D, Rosso I M, Hollister J M, Bearden C E, Sanchez L E, Hadley T 2000 A prospective cohort study of genetic and perinatal influences in the etiology of schizophrenia. Schizophrenia Bulletin 26: 351–66
  12. Ciompi L 1980 Catamnestic long-term study on the course of life and aging of schizophrenics. Schizophrenia Bulletin 6: 606–18
  13. Cohen S 1960 Lysergic acid diethylamide: Side effects and complications. Journal of Nervous and Mental Disease 130: 30–40
  14. Dalman C, Allebeck P, Cullberg J, Grunewald C, Koster M 1999 Obstetric complications and the risk of schizophrenia. Archives of General Psychiatry 56: 234–40
  15. Drake R E, Wallach M A 1989 Substance abuse among the chronically mentally ill. Hospital and Community Psychiatry 40: 1041–6
  16. Falloon I R H, Boyd J L, McGill C W, Razani J, Moss H B, Gilderman A M 1982 Family management in the prevention of exacerbations of schizophrenia: A controlled study. New England Journal of Medicine 306: 1437–40
  17. Feinberg I 1983 Schizophrenia: Caused by a fault in programmed synaptic elimination during adolescence? Journal of Psychiatric Research 17: 319–34
  18. Freedman R, Coon H, Myles-Worsley M, Orr-Urtreger A, Olincy A, Davis A, Polymeropoulos M, Holik J, Hopkins J, Hoff M, Rosenthal J, Waldo M C, Reimherr F, Wender P, Yaw J, Young D A, Breese C R, Adams C, Patterson D, Adler L E, Kruglyak L, Leonard S, Byerley W 1997 Linkage of a neurophysiological deficit in schizophrenia to a chromosome 15 locus. Proceedings of the National Academy of Sciences of the USA 94: 587–92
  19. Geddes J R, Lawrie S M 1995 Obstetric complications and schizophrenia. British Journal of Psychiatry 167: 786–93
  20. Gottesman I 1991 Schizophrenia Genesis: The Origins of Madness. Freeman, New York
  21. Hambrecht M, Hafner H 1995 Substance abuse or schizophrenia: Which comes first? Presented at the World Psychiatric Association Section of Epidemiology and Community Psychiatry Symposium, New York
  22. Hirsch S, Leff J 1975 Abnormality in Parents of Schizophrenics. Oxford University Press, London
  23. Hoffman R E, McGlashan T H 1997 Synaptic elimination, neurodevelopment, and the mechanism of hallucinated ‘voices’ in schizophrenia. American Journal of Psychiatry 154: 1683–9
  24. Hultman C M, Sparen P, Takei N, Murray R M, Cnattingius S 1999 Prenatal and perinatal risk factors for schizophrenia, affective psychosis, and reactive psychosis of early onset: Case control study. British Medical Journal 318: 421–6
  25. Huttenlocher P R 1979 Synaptic density in the human frontal cortex–developmental changes and effects of aging. Brain Research 163: 195–205
  26. Jablensky A, Sartorius N, Ernberg G, Anker M, Korten A, Cooper J E, Day R, Bertelsen A 1992 Schizophrenia: Manifestations, incidence and course in different cultures: A World Health Organization ten-country study. Psychological Medicine Monograph Supplement 20
  27. Jones P B, Rantakallio P, Hartikainen A-L, Isohanni M, Sipila P 1998 Schizophrenia as a long-term outcome of pregnancy, delivery, and perinatal complications: A 28-year follow-up of the 1996 north Finland general population birth cohort. American Journal of Psychiatry 155: 355–64
  28. Kavanagh D J 1992 Recent developments in expressed emotion and schizophrenia. British Journal of Psychiatry 160: 601–20
  29. Kendell R E, McInneny K, Juszczak E, Bain M 2000 Obstetric complications and schizophrenia: Two case-control studies based on structured obstetric records. British Journal of Psychiatry 176: 516–22
  30. Laing R D, Esterton A 1970 Sanity, Madness and the Family: Families of Schizophrenics. Penguin Books, Baltimore
  31. Leff J, Vaughn C 1985 Expressed Emotion in Families. Guilford Press, New York
  32. Lidz T, Fleck S, Cornelison A 1965 Schizophrenia and the Family. International Universities Press, New York
  33. MacGlashan T H, Hoffman R E 2000 Schizophrenia as a disorder of developmentally reduced synaptic connectivity. Archives of General Psychiatry 57: 637–48
  34. Malleson N 1971 Acute adverse reactions to LSD in clinical and experimental use in the United Kingdom. British Journal of Psychiatry 118: 229–30
  35. McFarlane W R (ed.) 1983 Family Therapy in Schizophrenia. Guilford Press, New York
  36. McNeil T F 1988 Obstetric factors and perinatal injuries. In: Tsuang M T, Simpson J C (eds.) Handbook of Schizophrenia: Nosology, Epidemiology and Genetics. Elsevier Science, New York
  37. Meltzer H Y, Stahl S M 1976 The dopamine hypothesis of schizophrenia: A review. Schizophrenia Bulletin 2: 19–76
  38. Mosher L, Burti L 1989 Community Mental Health: Principles and Practice. Norton, New York
  39. Parker G, Hadzi-Pavlovic D 1990 Expressed emotion as a predictor of schizophrenic relapse: An analysis of aggregated data. Psychological Medicine 20: 961–5
  40. Rabkin J G 1982 Stress and psychiatric disorders. In: Goldberger L, Breznitz S (eds.) Handbook of Stress: Theoretical and Clinical Aspects. Free Press, New York, pp. 566–84
  41. Sherman P S, Porter M A 1991 Mental health consumers as case management aides. Hospital and Community Psychiatry 42: 494–8
  42. Stein L I, Test M A 1980 Alternative to mental hospital treatment: I. Conceptual model, treatment program, and clinical evaluation. Archives of General Psychiatry 37: 392–7
  43. Sturgeon D, Kuipers L, Berkowitz R, Turpin G, Leff J 1981 Psychophysiological responses of schizophrenic patients to high and low expressed emotion relatives. British Journal of Psychiatry 138: 40–5
  44. Suddath R L, Christison G W, Torrey E F, Casanova M F, Weinberger D R 1990 Anatomical abnormalities in the brains of monozygotic twins discordant for schizophrenia. New England Journal of Medicine 322: 789–94
  45. Tamminga C A, Thaker G K, Buchanan R, Kirkpatrick B, Alphs L D, Chase T N, Carpenter W T 1992 Limbic system abnormalities identified in schizophrenia using positron emission tomography with fluorodeoxyglucose and neocortical alterations with deficit syndrome. Archives of General Psychiatry 49: 522–30
  46. US Department of Health and Human Services 1999 Mental Health: A Report of the Surgeon General. US Department of Health and Human Services, Substance Abuse and Mental Health Services Administration, Center for Mental Health Services, National Institutes of Health, National Institute of Mental Health, Rockville, MD
  47. Wang S, Sun C, Walczak C A, Ziegle J S, Kipps B R, Goldin L R, Diehl S R 1995 Evidence for a susceptibility locus for schizophrenia on chromosome 6pterp22. Nature Genetics 10: 41–6
  48. Warner R 1994 Recovery from Schizophrenia: Psychiatry and Political Economy. Routledge, New York
  49. Warner R (ed.) 1995 Alternatives to the Hospital for Acute Psychiatric Care. American Psychiatric Press, Washington, DC
  50. Warner R 2000 The Environment of Schizophrenia: Innovations in Practice, Policy and Communications. Routledge, London
  51. Warner R, de Girolamo G 1995 Epidemiology of Mental Problems and Psychosocial Problems: Schizophrenia. World Health Organization, Geneva, Switzerland
  52. Weinberger D R, Berman K F, Suddath R, Torrey E F 1992 Evidence of a dysfunction of a prefrontal-limbic network in schizophrenia: A magnetic resonance imaging and regional cerebral blood flow study of discordant monozygotic twins. American Journal of Psychiatry 149: 890–7
  53. World Health Organization 1979 Schizophrenia: An International Follow-up Study. Wiley, Chichester, UK
  54. Zisook S, Heaton R, Moranville J, Kuck J, Jernigan T, Braff D 1992 Past substance abuse and clinical course of schizophrenia. American Journal of Psychiatry 149: 552–3
  55. Zornberg G L, Buka S L, Tsuang M T 2000 Hypoxia-ischemia-related fetal neonatal complications and risk of schizophrenia and other nonaffective psychoses: A 19-year longitudinal study. American Journal of Psychiatry 157: 196–202
Neuroscience of Schizophrenia Research Paper
Schemas, Frames, And Scripts In Cognitive Psychology Research Paper

ORDER HIGH QUALITY CUSTOM PAPER


Always on-time

Plagiarism-Free

100% Confidentiality
Special offer! Get discount 10% for the first order. Promo code: cd1a428655