White Matter Psychology Essay

Outline and evaluate one or more biological explanations of schizophrenia (8 marks AO1/16 marks AO1)

Gray matter, an important constituent of central nervous system includes regions of the brain involved in sensory perception that includes vision, hearing, memory, emotions, speech, executive functions like decision making and self-control. Gray matter has been a focus of clinical attention and research as it has been consistently involved in studies to better understand brain pathology, pathophysiology and neurobiology in schizophrenia and bipolar disorder. Many meta-analytical reviews in structural neuroimaging studies have persistently shown abnormalities in schizophrenia and bipolar disorder.

Expert’s reason that unevenness in the complicated interconnected chemical responses of the brain connecting the neurotransmitters dopamine and glutamate, and maybe others, performs a part in schizophrenia. Neurotransmitters are elements that permit brain cells to interconnect with each other. Experts are acquiring more about brain chemistry and its connection to schizophrenia. Similarly, in small methods the brains of people with schizophrenia appear diverse than those of healthful people. For instance, fluid-filled holes at the middle of the brain, called ventricles, are greater in certain people with schizophrenia. The brains of people with the disorder similarly manage to have less grey matter, and certain

Today, scientists at the University of Iowa are studying abroad how people suffering from the mental disorder, schizophrenia, may have less brain tissue than those who do not have the disorder. Schizophrenia deeply affects the brain and causes individuals to lose touch with reality and have unorganized thoughts, troubled perceptions and unsuitable emotions and actions. “Schizo” means split and “phrenia” means mind, however this does not mean that this is a split mind or personality disorder, like most people commonly mistake this as. In order to understand this disorder, we need to take a look at the actual condition and how it is defined, apart from other disorders, speculated causes, such as genes from

Schizophrenia is a brain disease. Many studies have been conducted regarding the brain localization of schizophrenia. One study established that schizophrenia is characterized by significant loss in the grey matter of the brain. The loss was detected to be up to 25% in some areas and the damage was seen to begin at the parietal (outer) regions of the brain then spreading to the rest of the regions of the brain over a period of about five years ADDIN EN.CITE Rajagopalan1998923(Rajagopalan, MacBeth, & Varma, 1998)92392317Rajagopalan, MMacBeth, RVarma, SLXXY chromosome anomaly and schizophreniaAmerican Journal Medical GeneticsAmerican Journal Medical Genetics64-65811998( HYPERLINK l "_ENREF_9" o "Rajagopalan, 1998 #923" Rajagopalan, MacBeth, & Varma, 1998). Another study showed that patients who had the worst loss of brain tissue also exhibited the worst symptoms of schizophrenia such as hallucinations, psychotic and bizarre thoughts, hearing voices, depression and delusion ADDIN EN.CITE Conklin2002797(Conklin & Iacono, 2002)79779717Conklin, Heather M.Iacono, William G.Schizophrenia: A Neurodevelopmental PerspectiveCurrent Directions in Psychological ScienceCurrent Directions in Psychological Science33-371112002Sage Publications, Inc. on behalf of Association for Psychological Science09637214http://www.jstor.org/stable/20182759( HYPERLINK l "_ENREF_2" o "Conklin, 2002 #797" Conklin & Iacono, 2002).

For the past fifty years treatment of schizophrenia has been marked by its basis on the dopamine hypothesis for schizophrenia. However, this model for the disease and its subsequent treatment have left many patients without relief or help in dealing with this disease which has lead to a search for a better model. The dopamine model lacks the recognition of a whole range of symptoms associated with the disease and therefore can not be an accurate basis for treatment. More recently, there has been a shift to the glutamate hypothesis which has been shown to more accurately characterize the wide range of symptoms experienced by patients living with this disorder as well as the possibility in improvements for drug treatments.

Schizophrenia is a complex and highly debilitating mental illness that we are currently unable to treat in any way that guarantees success or return to previous function. It affects around 1% of the population and is associated with a thirteen-fold increase in the likelihood of suicide, so its effective control is paramount (Gogos et al., 2015). There have been several hypotheses as to the cause of schizophrenia. Many link genetic and environmental factors, and dysregulations of neurotransmitters dopamine, glutamate, and serotonin (Egbujo, Sinclair, & Hahn, 2016). The dopamine hypothesis currently suggests that hyperactive dopamine transmission in the basal ganglia leads to psychosis and underactive dopamine transmission in the prefrontal

Schizophrenia is a disease that has plagued societies around the world for centuries, although it was not given its formal name until 1911. It is characterized by the presence of positive and negative symptoms. Positive symptoms are so named because of the presence of altered behaviors, such as delusions, hallucinations (usually auditory), extreme emotions, excited motor activity, and incoherent thoughts and speech. (1,2) In contrast, negative symptoms are described as a lack of behaviors, such as emotion, speech, social interaction, and action. (1,2) These symptoms are by no means concrete. Not all schizophrenic patients will exhibit all or even a majority of these symptoms, and there is some

Currently there are no cures for schizophrenia, but the symptoms are helped by taking antipsychotic medication. The symptoms experienced by those with schizophrenia are grouped in to three categories: negative symptoms, positive symptoms, and cognitive symptoms (Regier 1993, p.92). The positive symptoms include, hallucinations, delusions, unusual or dysfunctional ways of thinking, agitated body movements. Negative symptoms include, flat affect, reduced pleasure in everyday life, difficulty sustaining tasks, and reduced speech. Cognitive symptoms include, disruption in executive functioning and working memory, as well as reduced ability to concentrate. The etiology of schizophrenia is still debated by psychologists and neuroscientists, but factors such as neuroanatomy, and environmental influences are believed to play a key role. A genetic predisposition to schizophrenia has been established by researchers, but it remains unclear what causes the phenotype to be expressed. The most agreed upon cause of schizophrenia refers to the diathesis-stress model, which explains schizophrenia as a response to an individual’s allostatic load becoming too much for the brain to cope with. Another popular explanation amongst neuroscientists is the dopamine

This paper defines schizophrenia from a biological and psychological perspective and also provides treatment to help combat symptoms of schizophrenia. This paper has three important contributions. First, by defining and expanding on schizophrenia from a biological perspective, I can identify the nature related predispositions. After expanding from a biological approach, secondly, I will analyze schizophrenia from a psychological aspect by determining if there is any environment or nurturing externals that can result to schizophrenia. Lastly, I will provide treatment details and also reveal early signs to schizophrenia. This paper is important because schizophrenia is an epic mental disease and it is crucially important to bring awareness to the public of how we can limit the illness. It is unclear whether schizophrenia have only a biological background or psychological background, but what was discovered is that both contribute to schizophrenia. Positive and negative treatment can be combatted undergoing pharmaceutical and psychotherapy,

Dopamine is a neurotransmitter associated with attention. Schizophrenics seem to have an increased number of D2 dopamine receptors on receiving neurons. This theory is support by the fact that Phenothiazines bind with D2 receptors and reduce positive symptoms. Another piece of supporting evidence is that Parkinson’s disease drug L-dopa, increase the level of dopamine and causes schizophrenic like symptoms in some people. However excess dopamine can only explain some types of schizophrenia, usually positive rather than negative.

Biological theorists believe that individuals may have a genetic predisposition for the schizophrenia if a close family member has been diagnosed with the disorder. Stress during adolescent years seems to provoke the disorder among individuals who have a family history of the disorder. In addition, this theory suggests biochemical abnormalities related to the dopamine neurotransmitters may also contribute to the illness as the brains neurotransmission of the dopamine is too frequent in occurrence (Comer, 2005). CAT and MRI scans have also indicated that abnormal brain structuring may also play a role in the development of schizophrenia due to a common occurrence of enlarged ventricles within schizophrenia sufferers (Comer, 2005). Various parts of the brain may not develop for function properly which seems lead to Type II schizophrenia. Studies have also pointed towards the idea that exposure to certain viruses before birth may lead to the eventual development of schizophrenia (Comer, 2005).

Over the years, experiments have produced evidence to suggest that dopamine plays a role in the development of Schizophrenia (Howes, McCutcheon, & Stone, 2015). Dopamine is a neurotransmitter that is produced in the substantia nigra and ventral tegmental regions of the brain. The belief that dopamine was involved in Schizophrenia arose after multiple studies performed with compounds produced an increase in extracellular concentrations of dopamine (Lieberman, Kane, & Alvir, 1987). The patients that were administered these compounds had similar symptoms to those observed from patients who were diagnosed with Schizophrenia (Lieberman et al., 1987).

In the research presented by Howes and Kapur (2009), they have pointed out a possible concern to invalidate the dopamine hypothesis in schizophrenia as current PET studies did not holding a firm position in measure the dopamine level, they were more to a postulation of a generated estimation from the data. Furthermore, Howes and Kapur (2009) also stressed that the role of dopamine could be circumvented by using the antipsychotic drugs which effectively to the psychotic symptoms but neutral to the dopamine system, thus the role of dopamine will be less critical in schizophrenia. This is because most of the recent antipsychotic researches only prove that dopamine merely contributed in providing a solution in alleviating the psychosis-liked-symptoms but those symptoms are not the symptoms only existed in schizophrenia.

The Dopamine Hypothesis theorizes that the symptoms portrayed in Schizophrenia is can be explained by abnormal function of dopamine in the brain. There have been three versions of the Dopamine Hypothesis. The first version of the hypothesis focuses on the dopamine receptors. Antipsychotic drugs that impact the metabolization and reabsorption of dopamine where found to be effective in treating the symptoms. It was theorized that if the symptoms of a Schizophrenic episode can be treated by the use of dopamine