TABLE OF CONTENTS
1.Schizophrenia – the background
1.1.Introduction and Definitions
1.2.History of Schizophrenia
2.Causes of Schizophrenia
5.1.In Early Childhood
7.Other Conditions (Schizophrenia-like)
8.Medication and Schizophrenia
9.Therapy and Schizophrenia
10.Hospitalization as an Option
12.Appendices (Diagnostic Criteria)
12.1.Appendix A – Paranoid Type
12.2.Appendix B – Disorganized Type
12.3.Appendix C – Catatonic Type
12.4.Appendix D – Residual Type
1. Schizophrenia – the background
1.1 Introduction and Definitions
Adolescent schizophrenia is a largely misunderstood, under-studied area of schizophrenia. Adolescence is a period of development marked at the beginning by the onset of puberty and at the end by the attainment of physiological or psychological maturity (Dictionary of Psychology). Schizophrenia may be defined as a general label for a number of psychotic disorders with various cognitive, emotional and behavioural manifestations and is a term that originated with Eugen Bleuler in 1911 as a replacement for the term Dementia Praecox.
The above definition may seem a little too academic, but the term literally refers to a ‘splitting in the mind’; a dissociation between emotions and cognition. Schizophrenia is a severe brain disease that results in a person losing touch with reality. The disease is accompanied by hallucinations, delusions, disorganized speech and behaviour, among others. These are just a few of the accompanying symptoms but together they affect social interactions and thought processes and have serious impact on the functioning of the sufferer.
We do not know exactly what causes schizophrenia, but it affects 1 in 100 people and is one of the most serious mental disorders (Furnham, 2008). The lifetime prevalence of schizophrenia in the United States of America is about 1 percent. The age of onset for schizophrenia occurs earlier in males than females, with the age group 16-25 years of age having the highest prevalence rates (Castle & Murray, 1993). Although the disease usually appears in late adolescence or early adulthood, seemingly without warning, it is a gradual disease that develops over many years (Gur & Johnson, 2006). Schizophrenia is very rare before age 11 but symptoms can appear as early as the mid- to late teens and are usually seen before age twenty; with most cases developing between age fifteen and twenty-five (Haycock, 2009). As such, a diagnosis is seldom made before age 18 (early-onset schizophrenia) and after age 50.
While the symptoms of schizophrenia may cause psychotic behaviour, most are not particularly violent and will not strike out at other. As little as 4% of violent acts are committed by people with schizophrenia and homicides by those who suffer with the disease is approximately 1 in 3000 cases. We admittedly still know very little about schizophrenia and are unable to prevent its occurrence but with early detection and intervention the sufferer can have a better quality of life.
1.2 History of Schizophrenia
It is agreed that we do not know how long schizophrenia has been around but mental illnesses have evidence in tablets, carvings and writings of the ancient world. While these inscriptions give a hint of its existence, they are too vague to give recognition for the symptoms and features of schizophrenia.
A number of researchers will concede that schizophrenia may have been around in the late Middle Ages. In the sixteenth century, Shakespeare’s plays acknowledge mental illness but Torrey believes that the first ‘true’ description of schizophrenia only materialized in the early nineteenth century.
As early as 1809, a superintendent of a British hospital, John Haslam, outlined a description of the symptoms of schizophrenia in Observations on Madness and Melancholy. During the course of 1801-1809, a French physician, Philippe Pinel described many cases of schizophrenia in his patients. In 1834, a Russian author Nikolai Gogol provided an early, yet complete description of schizophrenia in his short story Diary of a Madman. A French psychiatrist, Benedict-Augustin Morel, coined the Latin term dementia praecox (1852) which meant early or premature loss of mind to describe schizophrenia. Paranoid psychosis was first described in 1868; disorganized schizophrenia in 1869 and catatonic schizophrenia in 1872. In 1896, Emil Kraepelin unified the distinct categories of schizophrenia (hebephrenic, catatonic and paranoid) under the name dementia praecox.
In the twentieth century, Eugen Bleuler (1911), replaced Kraepelin’s term of ‘dementia praecox’ with ‘schizophrenia’. The choice of term was focused on the thought processes rather than on the outcome of the illness. Bleuler realized that the disease caused a ‘splitting of the mind’ from the reality around them. This splitting of the mind caused the misconception of a split personality. Bleuler believed that schizophrenia consisted of more than one disease and the disease could be traced to damage to specific areas of the brain.
Early theorists proposed that psychopathology (especially schizophrenia) was the result of inconsistency in family communications (Bateson, Jackson, Haley, & Weakland, 1956). In recent years, biological factors have been associated with depression, suicide and certain forms of schizophrenia (Sue, Sue & Sue, 1997). The specifics of causal factors in the development of schizophrenia will be discussed in detail later in this paper.
1.3 Early Treatment
Although schizophrenia as a disorder materialized in the nineteenth and early twentieth century, doctors were unable to treat it. Three early methods of treatment are discussed below:
Insulin Coma Therapy was developed by a Polish psychiatrist and neurophysiologist Manfred Joshua Sakel in the 1930s. Inducing an insulin coma in his patients, he discovered that the lowering of the blood sugar levels depleted the brain and body of energy. Deprived of energy, the brain shuts down, causing convulsions and eventually coma. Sakel saw improvement in the symptoms of his patients with schizophrenia in 90% of cases. Eventually, other doctors in the field discovered that this form of therapy had little effect in the long term and it was discontinued when tranquilizer type drugs entered the market.
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Lobotomy as a procedure for the elimination of schizophrenia was popularized in the 1940s and early 1950s by the neurologist Walter Freeman. This psychosurgical procedure was pioneered by Moniz and Lima; it involved the cutting of the nerve connections between the area of the brain above the eye (the prefrontal cortex) and the rest of the brain. Freeman used an ice pick-like instrument in his variation of the lobotomy (the transorbital lobotomy) that simplified the procedure. The ice pick pierced the thin bone behind the eye socket and was pushed into the brain; back and forth movements severed the connections. Although this was a fast procedure (lasting only a few minutes) it was a medical fad. A staggering 18 000 lobotomies were conducted in the US alone before doctors realized that it did more harm than good. Although psychotic patients were pacified, it left them apathetic, emotionally stunted and unable to concentrate. In effect, the lobotomy caused severe brain damage to the patient and was discontinued in 1951.
Drug therapy and deinstitutionalization began with the introduction of antipsychotic and other mental health medication. In 1955, state mental institutions in the US housed approximately 560 000 patients; by the year 2000 this number has dropped by some 90%. The introduction of drug therapy and public policy has produced an improvement in the understanding of schizophrenia and thus a decline in long-term hospitalization of patients. In 1951, French psychiatrists Jean Delay and Pierre Deniker discovered that chlorpromazine (Thorazine) was extremely effective in treating schizophrenia (Sue, Sue & Sue, 1997). In addition, the Community Health Act of 1963 assisted in the move to rehabilitate patients and deinstitutionalize them (Haycock, 2009).
2. Causes of Schizophrenia
While we acknowledge that relatively little is known about the causes of schizophrenia, current research into the disease focuses on brain abnormalities, genetics and environment factors (Gur & Johnson, 2006). The disease may have a viral cause but is most certainly precipitated by stress.
2.1 Brain Abnormalities
The most accepted hypothesis among researchers is that schizophrenia is a brain disease. A reduction in metabolic activity in the frontal cortex of people who have been diagnosed with schizophrenia has been noted. The central nervous system uses neurotransmitters to carry information in chemical form across the synapse. Injury to the brain and disease can disrupt the process by which neurons send messages to one another. The neurotransmitter dopamine has been associated with schizophrenia, although serotonin, glutamate and others may be impaired in different brain regions of the limbic structures, ganglia, prefrontal cortex, temporal lobes and the cerebellum (Haycock, 2009). Tyrosine hydroxylase, a chemical related to dopamine has been found in large quantities in schizophrenics, implying that excess tyrosine may create an excess of dopamine. There are a number of different dopaminergic receptors that are metabotropic, with D1 and D2 receptors having a direct link to schizophrenia. In addition, a higher level of norepinephrine has been found in the brain of schizophrenics, and some researchers suspect that an excess of serotonin may be present in the brain (Gur & Johnson, 2006).
Banich (2004) notes that both microsomatagnosia (the sensation that parts of the body are too big) and macrosomatagmosia (the sensation that parts of the body are too small) can occur with schizophrenics. Schizophrenia has been associated with temporal lobe dysfunction, as the temporal lobe aids in creating a mental map of the body. These temporal regions dysfunction has been associated with the delusions that schizophrenics experience.
While an excess of dopamine has been implicated in the development of schizophrenia (Cooper, Bloom & Roth, 1986), some believe that schizophrenia can ‘cause’ the secretion of excess amounts of dopamine. It is important to note also that other researchers believe that there is no biological marker for schizophrenia at all (Szymanski, Kane & Lieberman, 1991). However, in contradiction, it is estimated that anywhere from 20 to 65 percent of schizophrenics show some sign of neurological abnormalities (Buchsbaum, 1990).
Is there any evidence that schizophrenia runs in families? Since 1980, 11 major family studies have shown that the risk for schizophrenia in first-degree relatives is higher than the general population (Gur & Johnson, 2006). Parents, siblings and children of schizophrenics are twelve times more likely (5.9%) to develop the disease than the general population. Biological relatives and depressed adoptees are more likely to share the same disorder than adopted relatives (Loehln, Willerman & Horn, 1988).