Schizophrenia is one of the most common psychoses in the world, every year there is approximate one present of the world's population affecting by this disease. Generally, schizophrenia is defined as a chronic mental disorder, which has both a positive and negative symptoms. The positive symptoms include thought disorder, hallucinations and delusion while the negative symptoms are known as the absence of normal behaviors which can not only be found in schizophrenia but also other neurological disorders (Carlson, 1994). There are no exact reasons for schizophrenia yet and no any current cure for this most common psychosis. However, two main explanations of schizophrenia are widely used, that are the biological explanation and environmental explanation. The biological explanation mainly focuses on the impacts of genes, brain damage and dopamine while environmental explanation may investigate the influence of stress or social isolation on schizophrenia. This essay will analyse the evidences that kinds of biological dysfunction are the courses of schizophrenia depression. This essay first gives a brief introduction of schizophrenia followed by the discussion of the impacts of genes on schizophrenia. It will then go on to take a look at the dopamine hypothesis. The final part of this essay will focus on the relation between brain damage and schizophrenia.
Schizophrenia caused by biological factors is strongly supported as it can be heritable (Carlson, 1994). The linkage between gene factors and schizophrenia can be researched by twin studies and adoption studies. The very first adoption study was carried out by Kety, et al. (1968). They investigated a group of schizophrenic people, who had been adopted when they were children. The incidence of schizophrenia in the family which had schizophrenic adoptees was similar with the general population which is about 2%. However, the incidence in the schizophrenic adoptees' biological family (parents and siblings) was comparatively high (13%). The founding indicates that the patients became schizophrenia is not because they are growing up in a schizophrenia family but for the heritable reason. Later in 1987, a national wide adopting study was carried out in Finland by Tienari, et al. They looked at a total of 247 adopting families, which contains 112 adoptees that had schizophrenia mother and 135 adoptees that had normal mothers. All the offspring of both schizophrenic and normal were adopted during the first four years of their life. They found that the incidence of schizophrenia in two groups was quiet different. There were 7% of the offspring became schizophrenia whose biological mothers were schizophrenia while only 1.5% of the adoptees became schizophrenia with normal mother. This supported the hypothesis that possible genetic dysfunction contribute to schizophrenia.
To achieve more support for the influence of genetic factors on schizophrenia, researchers looked at twin studies which show the similar results with adoption studies. Twin studies generally investigate the twins who have been rarely apart (to avoid the environmental influence) and the difference between the monozygotic and dizygotic twins. Gottesman and Schields (1982) found that the concordance rate of schizophrenia in monozygotic twins (MZ) who share one hundred percent genes is approximately four times higher than dizygotic twins (DZ) who only have a fifty percentage gene shared. To support this result, Kendler (1983) reviewed nine twin studies, which contained 401 MZ and 478 DZ. Similar result gained, the concordance rates for MZ was 53% while for DZ is 15% (Tsuang et,al. 1991). Another systematic two-stage genome scan for schizophrenia is carried out later in 1999 by Cardno, et al. they suggested that the concordance rate is 40% for MZ and only 5% for DZ. All these studies provides strong evidence that schizophrenia has a genetic basis by showing the concordance rate of MZ is much higher than DZ. Nowadays the debate over whether schizophrenia has a genetic basis is no longer a controversy. The issue really draws attention which and where the "schizophrenic genes are. Several studies state that there are two possible locations for the "schizophrenic genes. The abnormalities of the long arm of chromosome 5 were found in a schizophrenic men as well as his uncle by Bassett et al (1988). They both have three pairs of this long arm rather than two, which is normal. This location has been supported later by using DNA markers to investigation in five Iceland families and two England families, which all have some schizophrenic members (Sherrington et al. 1988). Another location is on the pseudoautosomal region of the X chromosome which means the region that on the short arm of the X chromosome and change genetic material with the short arm of the Y chromosome (Carlson, 1994). The found that the schizophrenic children in the same family are more likely having the same sex if the schizophrenia history is on father's side indicates the "schizophrenic genes is located on the pseudoautosomal region (Crow, DeLisi & Johnstone, 1989; Gorwood et al. 1992). However schizophrenia is generally regarded caused by a series of genes rather than a specific one.
For the two symptoms of schizophrenia, there are some particular biological causes for each. The positive symptom, which includes the unique thought disorder, delusions and hallucination, is regarded be caused by "the overactivity of dopaminergic neurons (Carlson, 1994, page 545). By using Chlorpromazine on the schizophrenic patients in 1952, the dramatic effects of the antipsychotic drugs have been found. The using of antipsychotic drugs changed the way in which the schizophrenic patients treated before. They not only tranquilizing the patients but also reduce sort of positive symptoms, such as hallucinations and delusions (Carlson, 1994). Further more the common property of all the antipsychotic drugs using to reduce the positive symptoms of the schizophrenia was found by Creese et al. in 1976. That is they all block dopamine receptors. More specifically, the efficiency of a drug to reduce the positive symptoms of schizophrenia is heavily depended on its capability to block D2 dopamine receptors. Additionally, the drugs that produce the positive symptoms of schizophrenia can also be the evidence of the dopamine hypothesis. These drugs include amphetamine, cocaine, methylphenidate and L-DOPA, which all act as dopamine agonists and the symptoms caused by this drugs can be released by using antipsychotic ( Carlson,1994). However elation and euphoria are not the whole parts of positive symptoms of schizophrenia, thought disorder and paranoid delusions are also included. The disorder thought may be caused by the "indiscriminate activity of the dopaminergic synapses in the nucleus accumbens (Carlson, 1994, page 548) and the paranoid delusions may be caused by the overactivity of the dopaminergitic input to the amygdala (Fibiger, 1991).
Compared with the positive symptoms which are unique to schizophrenia, the negative symptoms such as flatted emotional response, poverty of speech and social withdrawal, are similar to symptoms that are caused by brain damage. The appearance of many neurological symptoms on the schizophrenic patients suggests the relation between brain damage and schizophrenia. For example, the schizophrenic patients always have catatonia, facial dyskinesias as well as eye movement dysfunction (Carlson, 1994). Brain image techniques have helped to find many evidences of the brain damage as a cause of schizophrenia. In 1982, CT scans gained by Weinberger and Wyatt, which have compared eighty chronic schizophrenia patients and sixty-six normal persons. They scanned the lateral ventricles and found that the schizophrenic patients' ventricles size were more than twice bigger than the normal subjects'. The proper reason for the bigger ventricles may be the loss of brain issue, and it supports that schizophrenia is associated with brain damage.
Another test which called Wisconsin Card Sort Test (WCST) is also used to investigate the relation between the damage to the dorsolateral prefrontal cortex and schizophrenia. In the WCST, four cards that have different patterns varied in numbers, color and shapes. The participants need to rank the cards in one of the differences. After the participants ranking the cards appropriately, the investigators change the ranking criterion. It was found that people with damage to the dorsolateral prefrontal cortex can do normally in the learning phase but have great difficult after the criterion changed. Weinberger, Berman and Zec (1986) states that the schizophrenic patients did not show an increased blood flow in the lateral prefrontal cortex during the processing of a computerized. Two scans of regional cerebral blood flow have made while both of the normal subjects and the schizophrenic patients doing the computerized WCST. The results showed that only the normal subjects shows the activation of the lateral prefrontal cortex while doing the test by showing the increased blood flow in the scan maps. Later in 1991, another study done by Rubin et al. supports these results. They found a decreased blood flow in the prefrontal cortex of the schizophrenic patients when they were doing the WCST. In addition, the discordance of schizophrenia in monozygotic twins can also be explained by brain damage. In 1990, Suddath et al. examined the MRI scans of MZ who were discordant for schizophrenia and found that the sibling, who is schizophrenic patient, has larger lateral and third ventricles, smaller anterior hippocampus and fewer gray matter in the left temporal lobe. Further more, in 1992, Weinberger et al. took MRI and PET scans of MZ who discordant for schizophrenia when they doing the WCST. They found that the schizophrenic sibling shows lower metabolic activating in the dorsolateral prefrontal and has smaller hippocampus formations.
In this essay, the evidences that kinds of biological dysfunction are the courses of schizophrenia depression have been discussed. The genetic basis in schizophrenia has been described by family, adopting and twins studies to suggest that the dysfunction of some genes may cause schizophrenia. The dopamine hypothesis has been introduced as a cause of the positive symptoms of schizophrenia. Finally the negative symptoms of schizophrenia have been explained by brain damage, to conclude, biological dysfunctions is one of the most important and powerful causes of schizophrenia. Nevertheless there are other explanations of schizophrenia cannot be ignored, such as the environmental explanation, cognitive explanation as well as psychological explanation.