Data Bases • Custom Term Papers • Free Term Papers • Free Research Papers • Free Essays • Free Book Reports • Plagiarism? Links • Top 100 Term Paper Sites • Top 25 Essay Sites • Top 50 Essay Sites • Search 97,000 Papers @ DirectEssays.com • Search 101,000 Papers @ ExampleEssays.com • Search 90,000 Papers @ MegaEssays.com Free Essays • Term Paper Sites • Chuck III's Free Essays • Free College Essays • TermPaperSites.com • My Term Papers • Get Free Essays • Essay World • Planet Papers	Search Lots of Essays Back to Subjects - Psychology Schizophrenia A Cognitive Dysfunction Schizophrenia A Cognitive Dysfunction Running head: Cognitive dysfunction of the brain. Schizophrenia: A Cognitive Dysfunction? Schizophrenia is often a chronic relapsing psychotic disorder that disrupts normal thought, speech, and behavior. It is a cluster of severe prolonged mental disturbances that “...is by far the most chronic and disabling of the major mental disorders. This disease may be one disorder, or it may be many disorders, with different causes” (Andreasen & Schutlz, 1999). It is a disease that makes it difficult for a person to tell the difference between real and unreal experiences. In addition, “it enables the person to think logically, to have normal emotional responses to others, and to behave normally in social situations” (Andreasen, 1999). People with schizophrenia may have difficulty in remembering, talking, and behaving appropriately. Schizophrenia is a disease with a physical cause, like cancer or heart disease; therefore, it must not be confused with “split personality.” Since schizophrenia is such a complex disorder, there is some dispute as to what causes it. In order to understand the world of a schizophrenic, it is imperative to understand all possible causes, including cognitive dysfunction in the brain. Since there is no one distinct cause for the onset of schizophrenia, there is no known cure. In this review, several important studies dealing with the causes of this disease will be reviewed. However, it is Andreasen’s “Integrative Theory of Schizophrenia” that will be the main focus of the review. According to the statistics, about 1% of the population has schizophrenia. Although it “strikes men and women equally, the symptoms may appear later in women than in men, however it most commonly begins between the ages of 15 and 25” (Arango, Bartko, Gold, & Buchanan, 1999). People with schizophrenia suffer from several cognitive and emotional impairments, such as perception (hallucinations), inferential thinking (delusions), motivation (avolition), and thought and speech (alogia); which sometimes comes on suddenly. However, usually the illness develops slowly over months or even years. At first, the symptoms may not be noticed or may be confused with those of other conditions. “Schizophrenia is characterized by a constellation of distinctive and predictable symptoms. The symptoms that are generally associated with the disease are called positive “psychotic” symptoms, which denote the presence of grossly abnormal behavior. These abnormal behaviors include thought disorder, delusions, and hallucinations” (Frith, 1995). The positive symptoms of schizophrenia are among its most striking features and they are the most difficult to understand. Hearing voices talking to you, experiencing alien thoughts being inserted into your mind, and believing that alien forces are controlling your most trivial actions are as well outside the normal range of experience. In addition, such experiences are very rarely reported by neurological patients. In consequence, neuropsychological tests relevant to the cognitive processes underlying these symptoms have not yet been developed (Andreasen, 1999). Delusions are common among individuals with schizophrenia. These are false beliefs that appear obviously untrue to other people. An affected person “begins to believe that people are reading their minds or plotting against them, that others are secretly monitoring and threatening them, or that they can control their people’s thoughts” (Andreasen, 1999). Hallucinations can be heard, seen, or even felt; most often they take the form of voices heard only by the afflicted person. Among the most prevalent symptoms associated with schizophrenia are auditory hallucinations, which are not simply words. “The patient hears people talking to him or about him. The experience has all the qualities of real communication. The voices seems to emanate from someone with intentions and desires who is using words to influence the behavior and beliefs of the patients. Such voices may describe the person’s actions, warn him of danger or even tell him what to do” (Arango et al., 1999). One long-lasting explanation of this symptom has been that it is the patient’s own inner speech or thought that is experienced as a voice...during auditory hallucinations, muscle activity in tongue and throat can sometimes be detected and occasionally subvocal speech is sufficiently loud to be picked up by a microphone and made audible. In past cases, the contents of the subvocal speech correspond with what the patient reports the voice to be saying...inner speech play a major part in certain aspects of working memory...if hallucinations involve inner speech then their presence should interfere with the performance of working memory tasks...the inner speech required for a verbal working memory task is associated with a observed greater activity in Broca’s area (Joseph, 1999). The combination of these distinct symptoms usually contributes to the alienation from family members, friends, and society. People with schizophrenia often become increasingly isolated and withdrawn as they progressively lose touch with reality in certain important ways. Less obvious than the “positive symptoms” but equally serious are the deficit or “negative symptoms” that represent the absence of normal behavior. Many chronic schizophrenic patients display a cluster of negative features which all concern poverty of action, poverty of thought, poverty of speech, and poverty of movement. In the case of speech, the patient will answer questions with as few words as possible, but will not elaborate his answers or ever initiate a conversation. His behavior is stimulus driven: he can produce an action in response to an appropriate stimulus but does not initiate actions spontaneously. Thus, patients with negative features have a specific problem with willed actions-namely, those actions for which is necessary to make a deliberate an conscious choice between several equally plausible options (Andreasen, 1999). These negative symptoms include the lack of initiative and inability to relate to others that often results in the person withdrawing from society. “These symptoms also include emotional flatness or lack of expression, an inability to start and follow through with activities, speech that is brief and lacks content, and a lack of pleasure or interest in life. “Negative” does not, therefore, refer to a person’s attitude, but a lack of certain characteristics that should be there” (Andreasen, 1999). The last major symptom of schizophrenia is bizarre behavior. Patients may talk to themselves, walk backward, laugh suddenly without explanation, make funny faces, or masturbate in public. In rare cases, they maintain a rigid, bizarre pose for hours on end. Alternately, they may engage in constant random or repetitive movements. At this point in time, experts are still not sure exactly what causes these symptoms to arise. According to some experts, one possible cause of schizophrenia may be heredity or genetics. “Experts think that some people inherit a tendency to schizophrenia. In fact, the disorder tends to run in families, but only among blood lines” (Andreasen, 1999). People who have family members with schizophrenia may be more likely to get the disease themselves. If both biological parents have schizophrenia, then there is nearly 40% chance that their child will get it too. Researcher has also shown that this happens even if the child is adopted and raised by mentally healthy adults. “In people who have an identical twin with schizophrenia, the chance of schizophrenia developing is almost 50% (Lawrie, Whalley, Kestelman, Abukmeil, Bryne, Hodges, Rimmington, Best, Owens, & Johnston, 1999). It is also believed that events in a person’s environment trigger schizophrenia. Some studies have shown that influenza infection or improper nutrition during pregnancy and complications during birth may increase the risk that the baby will develop schizophrenia later in life. Many researchers believe schizophrenia is likely caused by a complex combination of gene and environmental factors. Certain people are born with a tendency to develop the disease, but the disease only appears if these people are exposed to unusual stresses or trauma. Nonetheless, most experts agree that symptoms are provoked by chemical disturbances of the brain function, but no mechanism is known. The view that mental disorders result from abnormalities of brain chemistry received the first experimental support during the 1940’s. Hallucinogens such as LSD , and later amphetamine and mescaline, were found to produce schizophrenia-like symptoms in healthy patients. Brain imaging techniques, such as magnetic resonance imaging (MRI) and positron-emission tomography (PET), have led researchers to discover specific structural abnormalities in the brains of people with schizophrenia (Lawrie et al., 1999). For example, people with chronic schizophrenia tend to have enlarged brain ventricles (cavities in the brain that contain cerebrospinal fluid). They also tend to have a smaller overall volume of brain tissue compared to mentally healthy people. Other people with schizophrenia show abnormally low activity in the frontal lobe of the brain, which governs abstract thought, planning, and judgement. There has also been evidence of other possible abnormalities in many other parts of the brain, including the temporal lobes, basal ganglia, thalamus, hippocampus, and superior temporal gyrus. These defects may partially explain the abnormal thoughts, perceptions, and behaviors that characterize schizophrenia. It was proposed that psychotic symptoms in schizophrenia are related to dopaminergic hyperactivity in the brain. Investigators have found an increase of radioligang binding to dopamine receptors in basal ganglia tissue among deceased schizophrenics. “The brain is made up of nerve cells, called neurons, and chemicals, called neurotransmitters. Thus, according to the “dopamine theory,” there is an imbalance of the neurotransmitter dopamine, which is thought to cause the symptoms of schizophrenia. This neurotransmitter is the primary brain chemical that appears to be involved in this disorder, and most medications used to treat schizophrenia target this neurotransmitter and its receptors in the brain” (Sedvall & Farde, 1995). Dopamine is one of several brain chemicals that allow nerve cells to send messages to each other and schizophrenics may either be very sensitive to or they may produce too much of this chemical, which causes interference between chemicals. Researchers believe that because of this interruption between neurotransmitters, the brain of a schizophrenic may not be able to process information correctly. For example, “a person without schizophrenia usually filters out unneeded information. However, a person with schizophrenia cannot always filter out this extra information because of interruption between neurotransmitters” (Sedvall, 1999). Other neurotransmitters and their receptors also may be affected in people with schizophrenia. Serotonin for example may also play a role in causing the symptoms of schizophrenia. Cognitive impairments have always been associated with schizophrenia. There is a wide range of impairments, and perhaps not surprising when the wide range of symptoms and signs that can be observed in schizophrenic patients are taken into consideration . Since these impairments are essential features of the disorder, many researchers have tried to find explanations for the dysfunction. One of the most significant studies that tried to explain the cognitive dysfunction of the brain in schizophrenics was done by Nancy Andreasen. In this study, Andreasen, Paradiso, & O’Leary (1998) explains the causes of schizophrenia in three phases, which makes up what is called “Cognitive Dysmetria.” According to Andreasen et al., schizophrenia was initially diagnosed as a brain disease, which was supported primarily through the use of neuroimaging techniques such as computerized tomography (CT). This neuroimaging technique consistently showed that patients had diffused nonspecific abnormalities such as prominent sulci or ventricular enlargement. The next phase that Andreasen et al. (1998) discusses drew on traditions of neurology and neuropsychology. These traditional methods attempted to localize the anatomic abnormalities and relate specific manifestations of the illness to specific brain regions. Some specific relationships that were hypothesized and partially verified include the prefrontal cortex and negative symptoms, the temporal lobes and auditory hallucinations, and the planum temporale and thought disorder. The third phase, which is fairly recent, draws on traditions of cognitive psychology, models of distributed parallel processing, and the study of neural circuitry. The emphasis of this phase is an attempt to understand schizophrenia as an abnormality in fundamental cognitive processes and distributed circuits. This phase shifts the development of the “Integrative Theory of Schizophrenia.” The integrative approach has several advantages: It attempts to explain the diversity of schizophrenic symptoms with a single theory or mechanism. It applies a “top-down” approach that permits the testing of abnormalities in multiple related regions, rather than a piecemeal “bottom-up” approach, which examines a single region and a single symptom at a time. It is also consistent with most current thinking in neuroscience, which maps circuits and assumes distributed parallel processing. The major disadvantage of the integrative approach is that it can quickly become quite complex and lead to multinodal models that are difficult to test in a single experiment. According to neuropsychologists, there is a system that coordinates the processing, prioritization, and expression of information. Andreasen et al. (1998) suggests that it is this system that has been disturbed in schizophrenics, therefore, making it more distributed and complex. The disturbance encompasses not just executive functions, but several forms of memory, attention, emotion, and motor activity within the brain. To express the diversity of the disturbance and to call attention to the subcotical components, Andreasen et al., referred to this as “cognitive dysmetria.” As a cognitive abnormality, dysmetria would express itself as difficulty in coordinating the processing, prioritization, retrieval, and expression of information. This type of fundamental deficit could express itself as any of the broad range of symptoms of schizophrenia: hallucinations, delusions, disorganized speech, disorganized behavior, and attentional impairment. No specific group of regions has yet emerged as the “schizophrenia circuit,” but a consensus is developing on some of the nodes that may be involved, and they are probably linked together in a cognitive network. These nodes include various subregions within the frontal cortex (orbital, dorsolateral, medial), the anterior cingulate gyrus, the thalumus, several temporal-lobe subregions, and the cerebellum. There are three nodes that Andreasen et al. (1998) elaborated on in her study: prefrontal, thalamic, and cerebellum. The prefrontal cortex has been extensively studied in schizophrenia using neuropathology. Andreasen et al. (1998) found that this particular area of the brain permits the generation of specifically human functions such as language and speech, which are frequently interrupted in schizophrenia. The thalamic area has many functions, which are being explored in basic neuroanatomical studies. However, it has been proposed that it serves as a generator. The thalamus is conventionally divided into relay and diffuse projections nuclei. “The relay nuclei project to sensory and motor cortical regions and receive projections from the same cortical areas. These recurrent connections may allow the thalamus to modulate sensory and motor input. The diffuse projection nuclei are believed to be part of a system that governs the level of arousal in the brain. Whatever its roles, the thalamus must have a fundamental and important function in human cognition because of its extensive connections to the rest of the brain“(Joseph, 1999). Research on thalamic abnormalities in schizophrenia patients has shown a significant decrease in size, but it is not reported due to the fact that the findings could be due to partial voluming with the enlarged ventricles. However, their has been reports of abnormal activation in the thalamus when schizophrenic patients are experiencing auditory hallucinations. The final area of the brain that has been research in schizophrenic patients is the cerebellum. The cerebellum is phylogenetically interesting, which suggests that it could perform cognitive as well as a motor functions in humans. This makes this particular area well suited to perform massive parallel processing because of the nature of its cellular array. “Output from the cerebellum passes through the thalamus before projecting on to various neocortical regions, including the prefrontal cortex. The entire system appears to be a reciprocally connected circuit with modular specificity. Cerebro-cerebellar connections have been established for motor, sensory, and limbic regions, as well as for parts of prefrontal and parietal association cornices” (Andreasen et al., 1998). Schizophrenic patients with abnormalities in this area of the brain, suffer from verbal associative learning, and visual spatial skills, agrammatic speech, impaired memory, impaired procedural learning, decreased general intelligence as measured by IQ tests, abnormalities in representation of temporal information, impaired cognitive planning, and impaired nonmotor, learning and error detection. This neuroanatomical model helped to explain the multiple and diverse symptoms of schizophrenia. In addition it showed expressed the idea that these diverse symptoms of schizophrenia reflects different abnormalities in connectivity in the circuitry that links prefrontal and thalamic regions. It also showed where cerebro-cerebellar connectivity may be disrupted. The concept of “cognitive dysmetria” was intended to highlight the importance of explaining the multiple symptoms of schizophrenia by identifying basic cognitive mechanisms. In conclusion, schizophrenia is a very disturbing dysfunction in the brain. This disorder puts the patient and their family members in a different world. However, it is very important to understand the symptoms and causes of schizophrenia in order to understand the world of a person suffering from this disorder. I really enjoyed researching this disorder, because it enlightened me about the world of a schizophrenic person. Bibliography: Bibliography Andreasen, N., & Schultz, S., (1999). Schizophrenia. The Lancer, 353(9162), 1425-1430. Andreasen, N., Paradiso, S., & O’Leary, D., (1998). “Cognitive Dysmetria” as an integrative theory of schizophrenia: A dysfunction in cortical-subcortical-cerebellum creativity? Schizophrenia Bulletin, 24(2), 203-218 Arango, C.; Bartko, J.; Gold, J.; & Buchanan, R., (1999). Prediction of neuropsychological performance by neurological signs in schizophrenia. The American Journal of Psychiatry, 156(9), 1349-1357 Frith, C., (1995). Functional imaging and cognitive abnormalities. The Lancer, 346(8975), 615-620 Joseph, R., (1999). Frontal lobe psychopathology: Mania, depression, confabulation, catatonic, preservation, obsessive compulsions, and schizophrenia. Psychiatry, 62(2), 138-172 Lawrie, S.; Whalley, H.; Kestelman, J.; Abukmeil, S.; Byrne, M.; Hodges, A.; Rimmington, E.; Best, J.; Owens, D.; & Johnstone, E., (1999). Magnetic resonance imaging of brain in people at high risk of developing schizophrenia. The Lancer, 353(9146), 30-33 Sedvall, G., & Farde, L., (1995). Chemical brain anatomy in schizophrenia. The Lancer, 346(8977), 743-749 Word Count: 2768
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