GAD and major depression disorder share the same genetic origin since the incidences of unipolar disorders have been found to be more frequent comorbid with GAD than bipolar disorders. Secondly, the fact that treatment of GAD and depression symptoms is usually the same, thus a support of high possibility of a common neurobiological dysfunction. Despite these supportive premises, the really exact neurological mechanisms have not yet been fully agreed upon by a scholarly community. As Shane, Jasiukaitis and Green, (2003), they puts it, there are other certain methods that can be applied to examine the neurological mechanisms. These methods that are applied are: single positron emission computed tomography and positron emission tomography have enabled metabolic activity and cerebral blood flow in various regions of the brain. And that is why they are utilized in examining the neurological mechanism.
Research observations indicate a possibility of hyperactive brain circuits occurring in Generalized Anxiety Disorder, whereas underactive brain is more likely to be associated with depression. This conclusion originates from the sense that: when at rest GAD patients do not show the differences in normal controls and baseline cerebral blood flow. While in contrast, depression disorders patients at rest usually show reduced cerebral blood flow in the frontal and temporal and parietal areas of the brain. Furthermore, GAD patient’s shows higher regional glucose metabolism during a passive in the cerebellum, thalamus, temporal and occipital, frontal lobes. Whereas there is evident increase in activities in the basal ganglia in GAD patients as opposed to those affected with depression.
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