Causes and Symptoms of Schizophrenia - Research Paper Example

Causes and Symptoms of Schizophrenia Abstract Schizophrenia had been a public concern for the past several years owing to what it can do to the individual, family, and community in general. The aim of this research is to present some of the causes and symptoms of schizophrenia. Causes include genetic factor, perinatal complications, interaction of gene with the environment, and other studies contributing to the cause of the disease. Symptoms are also identified citing several studies as well. Books are used to back the research however previous researches are the main sources of information. Introduction Schizophrenia is viewed as a serious psychotic disorder characterized by disruptions in normal functioning with signs of withdrawal, emotional and affective disturbances, and loss of contact with reality. In psychological analysis, schizophrenia is termed as a disorder to represent those who have failed to establish the integrity of their ego processes necessary to resolve conflict between the id and the demanding superego. Historically, the disease had affected many in the past and unfortunately in some cultures, victims were considered weak or possessed by evil spirits. Thus, they were treated with harmful methods. The heterogeneity of schizophrenic manifestations also makes the disease mistakenly known to be other forms of psychotic disorder. However, with several studies the disease is better understood but its prevalence is still massive to date (Bhugra, 2005) affecting more than 24 millions globally. Although, previous studies linked the disease with low socioeconomic status, Bhugra revealed that both genders of any status are afflicted with a proportion of 4 is to1, 000. While studies on its prevalence contributes to a better diagnosis and treatment of schizophrenia, in depth discussion of its causes and symptoms provides a more rounded knowledge of the behavior of schizophrenics. Review of Related Literature Causes The role of genetic factor in schizophrenia has started with the extensive studies of Franz Kallman involving twins in which he found out that the disorder is likely to occur in another twin if it existed with the other. Such finding accounts for more than 85% among monozygotic twins. Several succeeding researches also had proven the same findings employing sophisticated analysis (Kolb, 1977). It is further posited that children with schizophrenia in their family are 15 percent at risk of the disease than those without cases of schizophrenia in their families. In other studies, children with schizoid parents who were given for adoption show a higher incidence of schizophrenia. The phenotyping resemblance was employed in these studies as an indirect method to know the relationship of genes with the disease. In another study involving European ancestry, abnormalities in chromosomes are seen to contribute to schizophrenia. Their animal model indicated that DISC 1 was identified to play a part in the translocation of chromosomes. Furthermore, a segment of the gene cathechol-O- methytransferase is also found to be absent in chromosome 22 believed to increase the risk of schizophrenia 20 times greater (Hamilton, 2008). The COMT gene is found to be responsible for the velo-cardio-facial syndrome experienced by schizophrenics. Surprisingly, this same study indicated that only a few play a part in the occurrence of schizophrenia despite large samples involved and comprehensive genotyping. Hamilton explained that despite the little role of genes in the occurrence of schizophrenia, it does not mean that it has no influence or contribution to schizophrenia in populations outside Europe. Hemming went on to conclude that more studies on both the molecular levels and the population have to be conducted. It is interesting to note also that the study of Fleming (2011) seemingly criticizes the previous studies on familial tendencies of schizophrenia pointing that there were flaws on the methodologies employed and in the statistical analysis. The appraisal of families and twins showed inconsistencies of the techniques used. In addition, Fleming added that the micro imaging method failed to reveal a clear genetic connection with schizophrenia. This criticism however does not indicate that the previous studies were wrong. Majority of the geneticists agree that a defect in genetic transmission, deletion or duplication explains the predisposition to schizophrenia. Another cause of schizophrenia is the perinatal complications during pregnancy. Infection, depression or stress, and urban birth are seen as the culprit triggering the disease during this period. In the study by Gilmore (2010), he found out that maternal depression significantly increases the likelihood of schizophrenia. Gilmore explained however that the maternal depression itself did not cause schizophrenia, its interplay with the unpleasant environment exposures combined with abnormalities in genes make it 9 times more likely for the fetus to develop schizophrenia. The reason behind is attributed to what the situation can do to the development of the brain. One of which is the reduction in hippocampal volume and neurogenesis as evident in their study on rhesus monkey. In human, stress interferes with the neurodevelopment and the functional circuits in the brain when the neurotransmitter dopamine is altered. An imbalance may cause the transmission of stimuli to and from the brain to be disturbed causing uncoordinated thinking and distorted perception. Pregnant mothers who are exposed to certain infections during pregnancy are found to be vulnerable to give birth to children who are likely to develop schizophrenia in their adolescent period. Similar to depression, the exposure of pregnant mothers with influenza virus and other viruses at any time of their pregnancy causes structural and functional abnormalities in the central nervous system of the fetus particularly the chemical substances involve in the transmission of messages. The imbalances in the mesocorticolimbic dopamine in the intrauterine life affect the child’s adult life (Jarskog et al, 2004) since the normal neuron development and their functioning is altered. Jarskog and company also discussed that infection has a direct effect on the generation of antibodies as it cross react with neuronal antigens. The mechanism of cytokines in response to fight the infection alters normal brain development. This reaction points to the biological predisposition of schizophrenia pointing now to the dopamine hypothesis. Along this line, biological predisposition such as chemical reactions and structures of the brain further explains the occurrence of the condition. It has been suggested that the accumulation of hallucinogenic substances exacerbate schizophrenia. Methionine believed to increase the level of S-adenosylmethionine favoring transmethylization also is found to have the same action (Kolb, 1977). In reviewing the literature of Os and McGuffin ( 2003), they presented an argument that schizophrenia is not a product of a single causative factor alone but rather a contribution of psychological and social environment. Any biological abnormality the individual may bring with birth is influenced with his transaction with parents and significant others. With this, the interaction within the family should be supportive in nature so that the child will unfold his potentials and develop his ego adequately which is needed to hurdle life’s events. Os and McGuffin (2003) reiterated that emotional family background and life events precipitate relapses. From some studies, schizophrenic patients have spent their childhood in seriously disturbed families in which conflicts, aggressiveness, absence of emotional support, and domineering attitude are evident. Furthermore, environment without adequate and proper stimulation for the child’s growth impedes the early development of attitude of security and trust upon which self control and independence unfolds. The regressive withdrawal of schizophrenic individuals into an infantile emotional behavior shows impairment in the early mother-infant relationship. Such defect may in turn results to the inability of the child to socialize. This finding suggests that the goal of treatment for schizophrenia includes the cognition of social environment to improve quality of life, social cognition, and social functioning (Tas et al, 2011). This is supported with similar study of Moll and Saeki (2009) where they found out that the improved social life of schizophrenia reduced their hospitalization. Symptoms Symptoms of schizophrenia develop in years which start from childhood or may appear in the adolescent period. Although, manifestation of symptoms depends on the type of schizophrenia, early signs and symptoms are anxiety, increasing tension, confusion, and social withdrawal. A sign of distractibility in conversation is also evident. The individual may converse to others with breaks in sentences and with inappropriate answers to conversation. He may also look away or may stare, or does not blink eyes when talking to others or displays trance like spell or microcatatonic periods. His sensitivities to sound are magnified because of uncertain auditory perceptions thus at times he feels frightened and confused. In addition, the individual is preoccupied with abstract thinking. It is somewhat surprising that a few patients in this acute phase may recognize they have abnormal mental thinking and willing to discuss it however may later lost such desire to understand the problem and is not interested anymore to talk about it (Kolb, 1977). One study discussed that a typical early symptom of schizophrenia is associated with the cognitive impairment during childhood and adolescence. The study of Welham and colleagues (2009) identified IQ score as a sign of impending schizophrenia later in one’s life. Individuals scoring low compared to their peers are likely to suffer from mental aberration. It was also noted that verbal, non verbal and mathematical poor performances together with deficit in attention, motor and executive functioning are all associated with schizophrenic attitude. As the disease progresses, disturbance of affect, attention, thinking, perception, emotional reaction, motor behavior and social relations become apparent. Disturbance of affect is characterized with the inability of the patient to regulate feelings and emotions which may later progress to indifference. Euphoria and depression is also present which is more severe than normal people. Another affect disturbance is the unrelated emotional expression manifested by inappropriate smiling, giggling or laughing. The patient may exhibit an emotion opposite of the experience or ideas presented. For instance, the patient may laugh and giggle as he speaks of death of his love ones or may be agitated when told of tragedy. Kolb (1977) explains this as the result of withdrawn affect from the consciousness. The patient displays attention deficit however it does not mean he is intellectually impaired. The narrowing of attention is the result of lost of interest in his external environment. One study corroborates with this concept. Everett and company (1989) revealed in their findings that patients show attention deficit when presented with a demanding task. In their study, the schizophrenics are observed to have trouble maintaining focus for a long time in the activity given them if it involves complex work compared with the control group. When it involves answering question, schizophrenics usually present a reply that is uninformative and trivial. Although, they show an understanding of the question, they provide an erroneous answer showing they are living in the world of fantasy. Another sign and symptom is the distortion of perception which is marked with deviation of sensory and perceptual behavior. The patient shows a shift of perception of significant members of the family such as the parents or to whom he relates with. Olfactory and gustatory hallucination frequently occurs as a form of adjustment to the environment. The patient tends to criticize and accuse others indicating an extension of hallucination to include auditory hallucinations. This disorganized ego is recognized as the cause of the projected images which the patient accepts as the reality. Hallucination is also accompanied with delusions in which the most common is the belief that God or other external forces are in control with the behavior and thoughts. As a result, the patients claim his life is in danger because someone is staging to kill him. At times, he may display delusion of grandeur reflected in his belief that he is the king of a certain country. The thought and communication of schizophrenia is also fragmented similar with those of the early onset. The patient talks in a dereistic type of verbigeration as a result of the loosened associated links. Flight of ideas which may later develop to incoherence, blocking, and scattering of thinking are all evident as the patient tries to communicate with others making the comprehension difficult for non schizoid to understand. Such form of expression of ideas is a result of the patient’s self meaning. Apart from this, a feeling of ambivalence is evident in which there is a shift of love and hate disposition. His social relations is also affected with his negativism as reflected in his rejection of food, refusal to do what is requested, and even refusal to void. Echolalias, the repetition of words uttered by somebody and ecopraxia, the repetition of movement are all a manifestation. Motor disturbances are also characterized with waxy flexibility disregarding physical discomforts it may cause the schizophrenic. Conclusion Behaviors displayed by schizophrenia is better understood when the many causes such as genes, perinatal complications, and environmental factors are all considered. These different causative factors in turn present various signs and symptoms. However, symptoms common to all schizophrenia involves disturbances in emotions, thoughts and communications, perceptions, motors and social relations. The understanding of these phenomena in the life of a schizoid not only provides a more effective treatment but more so perceiving early signs for early intervention. Reference Page Bhugra, D. (2005). The global prevalence of schizophrenia. Journal of Pmed. 2(2). Everett, J., et al. ( 1989). The selective attention deficit in schizophrenia: limited resource or cognitive? Journal of nervous and mental disease. Fleming,MP. & Martin, CR. (2011). Genes and schizophrenia: a pseudoscientific disenfranchisement of the individual. Journal of psychiatric and mental health nursing. Vol. 18. P. 469-478. Gilmore, J. (2010). Understanding what causes schizophrenia: A developmental perspective. American journal of psychiatry. 8-10. Hamilton, S. (2008). Schizophrenia candidate genes: Are we really coming up blank? American Journal of psychiatry. 165: 420-423. Jarskog, F. et al. (2004). Prenatal infection and risk for schizophrenia. Neuropsychopharmacology. Moll, MF., & Seaki, T. ( 2009). Social life of people with diagnosis of schizophrenia, attended at psychosocial care center. Rev. Lat. Am. Enfermagem. 17(6). Os, JV. & McGuffin, P. (2003). Can social environment causes schizophrenia? The British journal of psychiatry. 182: 291-292. Tas, C., et al. (2011). Impact of family involvement on social cognition training in clinically stable outpatients with schizophrenia. Psychiatry Res. Ahead of print. Welham, J., et al. (2009). The antecedents of schizophrenia: A review of birth cohort studies. PMCID. 35(3). 603-623. Read More