Biopsychosocial Model for the Mind

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Schizophrenia and Biopsychosocial Models:
Brain Localization, Genetics and Environment

Many theories have been put forth for the development of schizophrenia. The genetic model relies on the fact that an excellent causal predictor of the disease is having a close relative with the same diagnosis. Environmental factors such as drug use or trauma also have their followers. All sorts of chemical and cognitive models have also been adopted as causes, or at least as means of making better sense out of the genetic or environmental causes. Most of the problem seems to occur in the frontal lobes and hippocampus.

In general, current research suggests that a combination of genetic and environmental ingredients cause schizophrenia together. There is also a strong suggestion that there might be a distortion in certain DNA chains that affect the neural development of the brain. The nature of DNA networks relative to the development of neurons is also another popular theory (Harrison and Owen, 2003). If there is a duplication of certain DNA chains or networks, there can be a competition among them that leads to confusion in function, and even the elimination of one or the other. There is also a suggestion, based on some empirical evidence, that any increase in gray matter in different parts of the brain can lead to psychosis, including symptoms like schizophrenia (Hoffman, 2001).

The whole purpose of the Biopsychosocial model is to synthesize some of the above approaches. In other words, that the onset of illness like schizophrenia are caused by a combination of behavioral, genetic, social and biological causes. In some cases, things like trauma, social stress and high levels of emotional intensity among families are a cause for schizophrenia, or at least, cause for relapse after initial treatments (Stein, 2007).

Cognition

A variation of this is the cognitive model, proposed by Garety et al (2001) that posited a "snowball effect" of schizophrenia. In this model, initial vulnerabilities can lead to greater sensitivity to trauma or other stresses like extreme poverty or other health problems. Once these traumas exist, they can trigger a sort of cognitive distortion that alters the way reality is perceived. Preexisting negative self evaluations lead to events being perceived in a way having nothing to do with their reality (also see Hergenhahn, 2009, esp page 245). This, in turn, begins a cycle of hallucinations that are the gateway to full-blown schizophrenic symptoms. The point is that cognitive distortions such as jumping to conclusions, catastrophic thoughts or believes that are regularly contradicted by evidence recur and persist even in the face of treatment. The cognitive model can make sense out of these.

Others, such as Goldberg et al (2003), have stressed cognitive problems of a structural nature leading to a diagnosis of schizophrenia. In most cases, problems with attention, decision making and memory are all major correlates (if not causes) of the disease.

Genetics

The genetic factors in schizophrenia are substantial. In a recent paper, several networks of genes have been identified as regularly occurring among those with the disease. These concern networks dealing with axon guidance, synapse function and neuron mobility. These are developed early in the fetal stage of development. Axon guidance is significant because it deals with how neurons are brought to their proper destination in the brain. A mutation in this affects the "accuracy" in the development and placement of neurons. Neuronic cell mobility affects the development of synapses, and has everything to do with where these cells are positioned at an early stage in human life. This strongly suggests ...