Physiological Psychology and Ocd

Topics: Psychology, Brain, Cerebral cortex Pages: 5 (1445 words) Published: September 19, 2013
Physiological Psychology, what is it and why is it important?

Physiological Psychology is as described by Kalat (1998) as the study of the physiological, evolutionary, and developmental mechanisms of behaviour and experience. It is devoted to the study of brain functioning, how Neurons and Glia convey messages to one another and other parts of the body for it to function and work accordingly. Future studies of physiological psychology will help predict behavioural patterns in society and how brain functions can be “rewritten” through cognitive therapies .e.g. alcoholism, drug addictions.

Kalat (1998) further goes onto explain that a Biological psychologist (physiological psychologist) try to answer four types of questions about any given behaviour, how it relates to the physiology of the brain (what parts of the brain are active) and other organs, how it develops within the individual, how did the capacity for this behaviour evolve and why did this behaviour evolve.

Without the physiological understanding of how brain process work in relation to behaviour it is difficult to correctly diagnose a behaviour pattern and its cause.

Kalat (1998) describes that “having a little anxiety can be useful”, however OCD is a condition in which there is excessive anxiety.

OCD can be explained to a patient in simple physiological terms explaining the behaviour of the brain, for example:

OCD patients often have a broken mechanism (being a synapse interaction) in their brain that would usually stop a thought once you have it. In an OCD patient it does not (stop the thought) – so the thought is allowed to revolve. This seems in description that it would sound more like a broken record than OCD really does, but that isn’t what really happens.

OCD can be genetic but is most certainly physiological in nature. Without an understanding of brain functioning and how these neurons interact, how can psychologists work to alleviate the symptoms of the disorder?

Research into the biological causes and effects of OCD has revealed a link between OCD and insufficient levels of the brain chemical, serotonin. Serotonin is one of the brain's chemical messengers that transmit signals between brain cells. Serotonin plays a role in the regulation of mood, aggression, impulse control, sleep, appetite, body temperature and pain. For example persons with unregulated serotonin lead to destructive antisocial behaviour patterns, which society commonly experiences on a growing scale.

All of the medicines used to treat OCD raise the levels of serotonin available to transmit messages. Without physiological psychological research into the effects that these medicines have on the brain society would lack the knowledge and understanding of how to diagnose and appropriately treat disorders such as OCD.

Modern brain imaging techniques have allowed researchers to study the activity of specific areas of the brain. Such studies have shown that people with OCD have more than usual activity in three areas of the brain. These are:

The caudate nucleus, specific brain cells in the basal ganglia, located deep in the centre of the brain this area of the brain acts as a filter for thoughts coming in from other areas. The caudate nucleus is also considered to be important in managing habitual and repetitive behaviours.

When OCD is successfully treated with drugs or therapy, the activity in this area of the brain usually decreases. This shows that both drugs and a change in "thinking" can alter the physical functioning of the brain.

The prefrontal orbital cortex, located in the front area of the brain the level of activity in the prefrontal orbital cortex is believed to affect appropriate social behaviour. Lowered activity or damage in this region is linked to feeling uninhibited, making bad judgments and feeling a lack of guilt. More activity may therefore cause more worry about social concerns. Such concerns include: being meticulous, neat...

References: Kalat 1998 Biological Psychology
Molecular Psychiatry Molecular Psychiatry 14, 197-205 (February 2009) | doi:10.1038/sj.mp.400213
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