Schizophrenia

Schizophrenia Schizophrenia is a particular type of psychosis, schizophrenia is perhaps one of the most debilitating of the severe mental illnesses. It is a chronic and disabling brain disorder that has affected people throughout history. About 1 percent of Americans have this mental illness (http://www.medicinenet.com/schizophrenia/article.htm). People with Schizophrenia aren’t able to make sense of hat they are saying. They can sit or stand in the same place without moving for hours. People with this illness seem normal until they try to express themselves. For a long time, schizophrenia was seen as a 'functional disorder’ with some doctors calling it a sociological phenomenon - i.e. patients with schizophrenia are normal people driven insane by the insane world (Gelder, 1989). But the efficiency of anti-psychotic drugs and recent advances in biological research has shown otherwise than the research done in the 1970s. Scientific advances in neuroscience, molecular biology, genetics and brain imaging over the years have provided credible evidence for the biological bases underlying schizophrenia. There have been many theories of possible causes. For instance, many years of family studies indicate that schizophrenia might be inherited and schizophrenia runs in some families. A person can inherit a tendency to develop the illness, especially if the mother or father has this disorder. The risk for inheriting schizophrenia is 10 percent in those who have an immediate family member with the illness. There is a 40 percent if the illness affect’s either parents or an identical twin. However, around 60 percent of people that have schizophrenia have no close relatives with the illness. Even with all that information scientists still do not know how many genes are involved or how the genetic predisposition is transmitted. Researchers also believe that people with schizophrenia are very sensitive to a brain chemical called dopamine, or they produce too much that the brain can’t handle it. Dopamine is neurotransmitter that allows nerve cells in the brain to send messages to one another. An imbalance of this chemical can affect the way a person's brain reacts and therefore causing mental illnesses such as schizophrenia. Technology now has allowed researchers to study the brain structure and it’s function in people with schizophrenia. They say many individuals with this disorder have subtle abnormalities in their brain structure. These abnormalities include a slight enlargement of the ventricles in the brain, and a slightly smaller size of some areas of the brain. But this is not true in all people with schizophrenia. Such abnormalities also have been identified in people who do not have schizophrenia so it is somewhat inconclusive. Developmental neurobiologists on the other hand suggest that schizophrenia may be a result of the neurons forming inappropriate connections during a fetus’s development. Seeing as there are so many possible explanations for the cause of schizophrenia, it is not surprise that researchers have a difficult time finding out what really causes schizophrenia. Schizophrenia like behaviors have been historically documented throughout the world, but its present categorization has been achieved fairly recently. In 1878 Kraepelin pulled various concepts together into one disease, that he termed dementia praecox or schizophrenia as it is called today. The disorder is characterized by delusions or hallucinations, looseness of associations, disturbances in the person’s sense of self, and bizarre or offensive behavior. It typically develops in the late teens or early twenties and majority of people with schizophrenia continue to suffer chronically or episodically throughout their lives (Kendell & Zealley, 1993). Although the cause of schizophrenia is inconclusive, it is shown that it has a tendency to run in families. But recently scientists have been able to investigate and identify the role genes play in the etiology (the study of causation, or origination) of this disorder. The first family studies of this disorder were done as early as 1916. Since then there has been over 50 scientific studies done that indicate that a person with a family member suffering from schizophrenia are at greater risk of contracting the disorder, a much higher percentage than a person with no family history of a family member with this disorder. The overall risk of developing schizophrenia in the general population has been indicated at around 1% to 2%. However, the approximate lifetime risks to first-degree relatives were estimated to be 6% for parents, 9% for siblings, 13% for offspring with one schizophrenic parent and 46% for offspring with two schizophrenic parents (Gottesman, 1993). Current research has utilized more-rigorous techniques and narrowed the diagnostic criteria, employing many different observations such as neurological and clinical trials. These observations produced lower risk estimates than those reported by Gottesman during his research. For example, Tsuang et al. (1999) reported an overall risk to first-degree relatives of schizophrenics to be 3.2%. Since the 1980s, with brain imaging techniques and other developments in neuroscience, it became apparent that the brains of people suffering from schizophrenia are different (both structurally and functionally) from those who do not have the disease. Yet the brains of normal individuals might also have different brain structures but not meaning they have schizophrenia. Like I had mention before, this fact is inconclusive to a certain point but yet still indicating that the brain structure of individuals with schizophrenia is very different. Prior to the availability of CT scans and MRI’s which has allowed to observe the brain structure in living subjects, many neuropathological studies have found constant abnormalities in the brains of deceased persons with schizophrenia. Evidence from neuroimaging studies has identified the two main differences between the brains of normal people and schizophrenic patients. First, there is a very noticable enlargement of the ventricles and cortical sulci in many patients with schizophrenia, it was shown more common among men than women. It is only evident at the onset of the illness, and does not progress over the course of it. However, this type of abnormality in the person’s brain is also similar in other disorders such as Parkinson and Bipolar Disorder. This suggests that it is more of an indicator, that some form of the abnormality is present, rather than a specific marker for a particular illness (Van Horn & McManus, 1992). The second major difference is the apparent hypofrontality, which is the reduced blood flow in the frontal regions of the brain in schizophrenic patients. This indicates impaired functioning of that area. The lack of blood flow can cause a reduction in the size of the brain itself. MRI studies (Soares & Mann, 1997; Lawrie & Abukmeil, 1998) have been consistent in finding loss of temporal lobe volume and loss of temporal lobe gray matter in schizophrenia sufferers. The areas which were found to be most affected are the limbic forebrain, (especially the amygdala and the hippocampus), and the basal ganglia (including the caudate, nucleus accumbens, and olfactory tubercle). Freedman et al., (1995) found that skull volume is reduced in persons with schizophrenia by 3.5%. Since brain growth drives skull growth, these findings suggest that the process causing schizophrenia takes place prior to the completion of brain growth (approximately age 18) (Elkis, et al. 1995). Studies by Fish et al., (1992) and Marcus et al., (1993) demonstrated the presence of some neurological impairments in the infants of schizophrenic parents. This strongly suggests that the process leading to schizophrenia is an error in development before birth rather than a developmental error occurring prior to birth, rather than a degenerative or destructive process. Given that suggestion, scientists believe that schizophrenia may be a developmental disorder. Resulting from neurons not being formed right during fetal growth. These developmental mistakes will go unnoticed until they reach puberty, when changes in the brain that occur normally during this critical stage of maturation and start interacting adversely with the malformed connections. This research has spurred efforts to identify prenatal factors including infections in utero that may affect development (Murray, et al., 1992). Some of the first bits of evidence to support this thesis came in 1988 from the study done by Mednick et al, of children given birth by women who were pregnant during the severe flu epidemic in Helsinki, Finland in 1957. It was also shown that the children of mothers who had contracted the flu during their second trimester of pregnancy had a greater chance of developing schizophrenia as adults. In spite of all the above evidence, it is necessary to take into account environmental and social factors, which may contribute to the psychological well being of an individual. Factors such as family stress, poor social interactions, infections or viruses, starvation or trauma at an early age may all be contributors to the development of schizophrenia later in one’s life. There have been many studies indicating such possibilities. For instance, there was a higher rate of schizophrenia among children in the Netherlands when their mothers were pregnant during the winter of 1944 to 1945, when the Nazi’s blockaded Dutch cities. This suggests that malnutrition may have played a role in those children developing schizophrenia (Gelder, et al. 1989). Also in McCreadie’s (1997; 2002) research, it has been suggested that the lack of the fatty acids such as DHA in breast milk which are also absent in pre packaged baby milk can increases the risk of the neurodevelopmental form of schizophrenia in the individual’s who are predisposed to the illness by genetic factors. Taking into account all of the above possibilities, Mirsky and Duncan (1986) both proposed to incorporate the psychological and biological findings into a singular form of schizophrenia. According to their finding based on their research, schizophrenia is a more biologically predisposed condition but it may not become a full blown mental disorder without it being influenced by the persons environment and/or stressors stressors. With all the information given above, here are is list of symptoms one may experience if you have schizophrenia. There are positive symptoms which are psychotic behaviors not seen in a person without schizophrenia. A person with positive symptoms can often "lose touch" with reality as these symptoms can come and go. The symptoms can be severe or hardly noticeable depending if the person is receiving treatment or not for their schizophrenia. The most common symptom is hallucination. They are things a person sees, hears, smells, or feels that no one else can. Voices are the most common type of hallucination in schizophrenic patients. The voices talk to the person about his or her behavior, have them do things they normally wont do and even warn them of pending danger. Sometimes the voices even talk to each other. People with schizophrenia may hear voices for a prolonged period of time before anyone actually realizes it. Other hallucinations also include seeing people that are not there as well as objects, smelling odors that no one else can smell and feeling things that aren’t there, for example feeling people or things touching them when they really aren’t there. Delusions are false beliefs that are not part of the person's culture. The person believes delusions even after other people tell them that they are not real or have any logic to them; they also have bizarre delusions at times. Some may also believe that people on television are directing special messages also known as subliminal messages to them and even that radio stations are broadcasting their inner thoughts. Schizophrenic people also believe they are someone else, and most commonly they believe they are famous people. They may have paranoid delusions and think that other people around them are trying to kill them or they family. These beliefs are called "delusions of persecution." Thought disorders are dysfunctional ways of thinking. A form of thought disorder is called "disorganized thinking." Its when a person has problem organizing their thought or have them logically connect in any way and they may even talk in a way that is hard to understand. Another form of this disorder is called "thought blocking." Its when a person suddenly stops speaking in the middle of a sentence and when asked why, the person may say that it felt as if the thought had been taken out their head. They may even make up words that don’t exist but makes complete sense to them. Finally we have movement disorders, its when a person may appear to have random body movements. A person with a movement disorder may repeat certain motions over and over again without even realizing that they do it sometimes. In a much more severe reaction a person may become catatonic. Catatonia is a state in which a person does not move for hours as if the person was a statue. Although this is rare today, it was much more severe when there was no known treatment foe schizophrenia. There are also negative symptoms, which are associated with disruptions to the person’s normal emotions and behaviors. These symptoms are harder to recognize since they are very similar to the symptom of depression. A few examples of these symptoms are, a lack of speech even when forced to talk, a lack of ability to begin and sustain planned activities, losing pleasure in everyday life and last is the Flat affect. Flat affect is when a person's face does not move or talk in a very low or faint voice. And lastly are cognitive symptoms. These symptoms are very subtle and like negative symptoms, cognitive symptoms are also somewhat difficult to recognize. Most of the time they are only detected by certain tests. This makes them have a poor ability to understand information and use it to make simple decisions, they have trouble paying attention and problems with their memory. These symptoms make it hard for the person to lead a normal life. With the evidence above it strongly suggests that there are several biological bases for schizophrenia. Genetic studies have provided possibly the most influential and important contribution to the understanding of schizophrenia. However, the current status of research on genes and schizophrenia has not yet specified the genes that cause schizophrenia. The disease can be caused by so many factors that it its extremely hard to pin point what really causes schizophrenia and its understanding needs more development. Basic knowledge about brain chemistry and its link to schizophrenia is also expanding rapidly. It is clear today with the firm findings of reduced frequency, duration, and severity of psychotic episodes in persons treated with anti-psychotic medication that dopamine has a major role to play in schizophrenia like disorders. Even with all the research that has been done over time, it’s not known whether the change in the dopamine activity happens before or after the onset of this disorder. If it occurs after, than overactive dopamine is just another symptom in a long list of symptoms associated with schizophrenia (Jones & Pilowsky, 2002). It may well be that schizophrenia is not a single disorder at all, but rather that it represents a common syndrome of behaviors and findings of mental status with multiple causes. Understanding all these causes and affects will be crucial for the care of patients suffering from schizophrenia. Although the doctors can not cure it, they can at the least alleviate the suffering that this disease brings on the patient, their family and loved ones. References Elkis, H., Friedman, L., & Wise, A. (1995). Meta-analyses of studies of ventricular enlargement and cortical sulcal prominence in mood disorders. Comparisons with controls or patients with schizophrenia. Faraone, S. V., Tsuang, D. & Tsuang, M. T. (1999). Genetics of Mental Disorders: A Guide for Students, Clinicians, and Researchers. Guilford, New York, USA. Fish, B., Marcus, J., Hans, S. L., Auerbach, J. G., & Perdue, S. (1992). Infants at risk for schizophrenia: Sequelae of a genetic neurointegrative defect. Freedman, R. (1995). Evidence in postmortem brain tissue for decreased numbers of hippocampal nicotinic receptors in schizophrenia. Gelder, M., Gath, D., & Mayou, R. (1989). 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