Schizophrenia: Risk Factors, Cognition and Structure

dementia praecox Risk Factors, Cognition and StructureJohn RogersSchizophrenia a canvas of happen factors, cognitive deficits, geomorphologic and function abnormalities. basisOccurring in about 1% of the worlds population, schizoid derangement is a disorder of abnormal cognition encompassing oddities in perception, thinking, attention, learning, inhibition, storage, manner relating to and others (Cunningham Peters, 2014). Traditionally, dementia praecox has been broken down into several subtypes depending on the symptomology expressed (e.g. paranoid, disorganized, schizo fall uponive, catatonic).The symptomology of the disease is subdivided into 2(prenominal) positive and negative classifications, as substantially as cognitive deficits. haughty symptoms implicated in the disease include delusion, hallucination, disorganized speech or clang associations, whereas negative symptoms include emotional flattening, a affableity, anhedonia or avolition (Butcher, 2010). This essa y has four-spot main aims. Firstly, while a definitive puddle of schizophrenia soundless eludes us, an abundance of look for has identified a wide array of biological and psychosocial risk factors and these aetiological factors exit be outlined.Secondly, cognitive deficits associated with the disorder will be outlined. This section will highlight the wide airing contour of cognitive deficits presented in patients and discuss some of the batteries of cognitive leavens developed in assessing the finish of these shortfalls.Subsequently the structural abnormalities associated with the disease will be briefly revised, along with some of the confines of structural studies. Additionally the essay aims explore whether schizophrenia is a advancing disorder or solely a disorder of neurodevelopment based on structural summary.Prior to concluding, the essay will review some findings from fMRI studies investigating the functional connectivity indoors the schizophrenic capitulum a nd how they relate to both the positive and negative symptoms presented in the sickness. Furthermore, the limitations of fMRI studies, natural out of a lack of precision of hemodynamic response measurements will be highlighted by analysing the results of an experiment examining activation during a working memory task. aetiologyThe aetiology of schizophrenia is complex and can non be reduced down to a single causal factor. This is evident when we consider the subtypes and indeed individual cases of the unhealthiness deviate massively in their presentation, responsiveness to treatment and illness escape (Moore, Kelleher Corvin, 2011).An abundance of look into into the cause of the disorder suggests that a combination of predispositional physiologic factors and a multitude of environmental risk factors result in foreland pathways underdeveloped abnormally.Schizophrenia is a polygenic disease and thus cannot be explained by one mutated gene. Eyles, Feldon Meyer (2012) get unde r ones skin identified 40 genes implicated in the development of the disease, signifying that it is a cocktail within a certain genotype that confers susceptibleness to the illness.A study by Tinari et al. (2004) found that the genotype for higher risk in the illness only resulted in schizophrenia when an individual grew up in a dysfunctional vs. heathy family, suggesting that while biology provides the tinder, environment produces the spark.The dopamine hypothesis has s tood out as the more proficient biological speculation to date in investigating the causes of schizophrenia. bandage originally thought to be a functional excess of dopamine, research has indicated that it is actually increased sensory receptor density and sensitivity, (particularly super-sensitivity at the D2 receptors Wong et al. 1986) that may contribute to susceptibility of the disease (Butcher, 2010). other successful biologically based studies into the aetiology of schizophrenia include the glutamate hypoth esis, ductless gland studies and twin hereditary studies ( feel Cunningham Peters for review, 2014). Although the aforementioned studies and approaches ar useful in intellect the illness, they all share a common limitation they each can the environmental and developmental factors that may contribute more to the oncoming of the illness than genetics (Bagby Juhasz, 2013).Cannabis use has been closely related to the onset of schizophrenia, with materialization males who use being at pregnantly greater risk of developing the illness (Zammit et al., 2002). Moreover, 75% of individuals presenting with first-episode psychosis use the drug regularly (Archie et al., 2007) although some swear the correlation with high usage rates is due to self-medication (Dsouza et al., 2005).Other well documented psychosocial risk factors include urban living, immigration, childhood experiences of trauma or neglect and immunological factors (for review see Cunningham and Peters, 2014)Cognitive def icitsAbout 60-80% of schizophrenic patients display cognitive deficits (Lewis, 2004) across a multitude of domains including attention, memory, processing speed, social cognition, reasoning and communicative learning (Keefe Harvey, 2012 special K et al. 2004).A study by Keefe et al., (2005) found that 98% of patients achieve more woefully on cognitive tests than would be predicted by their parents education level. Additionally, a parade of studies have shown that cognitive impairment can reach two measurement deviations below a goodly control mean (for review see Keefe Harvey, 2012).The MATRICS (measurement and treatment research in cognition in schizophrenia Green et al., 2004) project has developed a barrage of ten tests (MATRICS Consensus Cognitive battery MCCB) in order to access cognitive functioning across these domains (see fig. 1) build 1. Shows the severity and profile of cognitive impairment in patients using the MCCB (Keefe et al. 2011a)This spread of cognitive deficits manifest itself across numerous domains from social to financial and occupational. For example, poor attention or attentive vigilance may result in an individual being unable to come up instructions or revolve around on a task in an occupational setting, or follow individual or group conversations in a social setting.Furthermore, schizophrenic individuals experience deficits in social cognition that create further bother within these settings such as theory-of-mind task performance (Tan et al., 2005) and perception of negative emotions, fear and facial affect in others (Penn et al, 1997).Research suggests that some of the cognitive deficits implicated in schizophrenia may develop prior to the onset of the disorder. A study by Jones Rodgers (1994) identified 30 individuals with schizophrenia from a random sample of 5000 individuals born in 1946. All subjects had been tested for non-verbal, verbal and reading abilities, arithmetic, and vocabulary, at ages 8, 11 and 15. Th eir progressively low scores in relation to heathy peers indicated a risk factor for the disease.These results should be approached with caution as a dysfunctional home environment may also affect both the academic ability in children as well as contribute to the onset of the illness. Nevertheless, other research has found similar results suggesting the cognitive deficit in a young person is a significant risk factor (Caspi et al., 2003 Erlenmeyer-Kimling et al. 2000).Although the impact of antipsychotic medications on neurocogniton provides minimal benefits to patients (Keefe Harvey, 2012), modern research has shown that patients who receive psychosocial support preform significantly better on several cognitive tasks than those who do not, suggesting that such interventions may be serious to those suffering with the disorder (Dalagdi et al., 2014).Structural abnormalitiesAn abundance of research has aimed at identifying the structural deficits within schizophrenia. The closely well documented deficits associated with the disorder are compromised exsanguinous matter integrity (Kubicki et al., 2007) in addition to, a reduced color matter volume across a range of neuroanatomical flying fields including the precedent cingulate, frontlet and temporal lobes, hippocampus/amygdala and the thalamus (Shepard et al. 2002). Moreover, dorsolateral prefrontal cells have a simple dendritic organisation, indicating fewer synapses than a heathy individual (Kolb Whishaw, 2009)What remains a source of debate within the literature of the mind-set structure of schizophrenia is whether the disorder is progressive throughout the life-span or is strictly a neurodevelopmental disorder.While the lions share of the sMRI research posits that the illness progressively affects both grey and blanched matter (for meta-analysis see Olabi et al., 2011), others have suggested that the progressive structural abnormalities observed could more be a consequence of numerous mutually excl usive variables (e.g. low physical activity, smoking, stress, alcohol, cannabis, anti-psychotic medication Zipursky, Reilly Murray, 2012). Furthermore, Zipursky et al. (2012) argue in that respect is an absence of present of any toxic effect of psychosis on brain tissue.Zhang et al., (2014) used dissemination tensor imaging and a cross-sectional design in order to analyze whether schizophrenia produces progressive brain abnormalities. They found that schizophrenic patients showed lower fragmental anisotropy (diffusion in the cells) values in the corpus callosum and corona radiate, and that these values were negatively correlated with the age of the patient.These researchers used a cross-sectional design and a majority of drug-nave participants in an attempt to control for any medication effects, however, in doing this they open their results to scrutiny by drawing inferences about differences in two different brains.There are several limitations in structural studies in schizo phrenia. Firstly, its very difficult to measure the effect of anti-psychotics on the brain without a control group of drug nave patients. Given the debilitate nature of the illness, its difficult to find older patients that have not been medicated for long periods of time. Furthermore, if these patients are severely psychotic, it may prove impossible to test them, meaning some samples arent a true representation of the population.Secondly, in that location are causal problems in the structural studies. Consider, for example, an experiment using sMRI undertaken by Fornito et al., (2012). Their results showed schizophrenic patients have altered interregional connectivity and hypoactivation in the prefrontal cortex. What remains indecipherable is whether schizophrenic patients have these altered patterns of activation are a cause or are a consequence of the disorder. operating(a) abnormalitiesSchizophrenia is believed to be a disorder arising from disturbances in brain connectivity (Fornito et al., 2012) and that these disruptions prevent functionality in cognitive domains which often require communication between several distinct regions (Konrad Winterer, 2008).An analysis of resting functional connectivity of the disorder by Venkataraman et al. (2012) posits that patients display two distinct patterns when compared with healthy controls and that these patterns are correlated with the symptomology expressed. Abnormally increased connectivity between the median(a) parietal and frontal lobes was correlated with the presentation of positive symptoms, whereas decreased connectivity between medial parietal and temporal regions, and the temporal cortex, bilaterally corresponded with the presentation of negative symptoms (Venkataraman et al. 2012).Functional studies in schizophrenia typically use fMRI, which measures hemodynamic response related to changes in neural activity. While their usefulness in neuropsychology cannot be overstated, they are not without thei r limitations due to their precision.Consider for example the following experiment by Royer et al. (2009). This study found that even though schizophrenic individuals did not perform as well as the healthy groups in the working memory task (n-back), patients that did do well showed hyper-activation in the prefrontal and parietal lobes when compared to the control.Furthermore, fMRI showed increased activity in the superior frontal sulcus (self-awareness) and the posterior parietal cortex (planning of movement, attentional maintenance, response preparation/monitoring Royer et al. (2009)) during successful trails. here(predicate) we run into a problem due to the lack of precision in the fMRI. While we can now observe frontal-parietal over-activation, we cannot distinguish whether this suggests either or both (i) a compensatory mechanism allowing patients to perform well despite damage cognitive functioning or, (ii) over-activation in the parietal areas corresponds to the BA 40 area (s hort term memory), suggesting improved effort (Royer et al., 2009).ConclusionUltimately, schizophrenia is one of the most horrific examples of what can happen when the brain goes wrong. The disorder has a colossal social and financial burden on sufferers, family members and healthcare systems.While in that location is no single cause of the disease, at least that we know of, research has shown the disorder to have a wide variety of risk factors in both biological and psychosocial domains. Schizophrenia presents itself in a wide variety of moderately to severely debilitating cognitive deficits although very recent research has shown that psychosocial interventions may at least curve the extent of these shortfalls (Dalagdi et al., 2014), at least in individuals whose positive or negative symptoms are not too extreme.Structurally, schizophrenia can be observed as disorder of compromised white matter integrity (Kubicki et al., 2007), reduced grey matter within the frontal and temporal lobes, hippocampus/amygdala and the thalamus (Shepard et al., 2002) and simple dendritic organisation within the dorsolateral prefrontal cells.The jury is out on whether schizophrenia is a progressive or neurodevelopmental disorder and this is primarily due to the difficulty in lordly for variables such as the effects of anti-psychotic medications, stress, and long term institutionalisation may have on brain structure.The positive or negative symptoms expressed in schizophrenia are related to the functional abnormalities in connectivity between the miscellaneous brain regions (Venkataraman et al., 2012). While fMRI studies can provide us with blue-chip clues as to which brain regions are implicated in specific processes, there are issues with precision when comparing blood flow to activation is accurate areas.