In the first two parts of this imaging series we looked at the brain imaging techniques that we currently have at our disposal and their utility in exploring alterations in brain structure at the methodological and neurochemical levels. In this, the last article of the imaging series, we explore the value of neuroimaging as a means of understanding changes in brain function due to psychological and pharmacological challenges. Finally, we introduce an exciting new approach of resting-state functional connectivity as a tool that will allow one to explore intrinsic circuits of the brain.
For more than 100 years, psychiatry has sought to understand how changes in the brain result in thoughts, subjective experiences and ultimately psychiatric disorders. The idea that brain activity was relevant to the human mental state goes back millennia (if we accept the evidence of trepanning in cave-dwellers). In the late 1800s, William James, one of the founding fathers of psychology, developed a means of estimating brain blood flow using the "human circulation balance" on which a person was stabilised in the horizontal plane. When they were then given a task such as mental arithmetic the head end of the "human circulation balance", as developed by Angelo Mosso, began to lower towards the ground, indicating increased blood flow in the brain resulting from mental effort. The modern MR techniques of arterial spin labeling (ASL) and functional magnetic resonance imaging (fMRI), which will be discussed further in this article as they pertain to some disease states, work on the same principles: if a part of the brain is engaged in effort then increases in blood flow can be imaged.
Prior to the advent of other imaging techniques, including fMRI, studies examining cortical blood flow were conducted using PET imaging either with F-deoxyglucose or O-water tracers. The resultant images, however, did not have as good time resolution as fMRI but O-water – if used in a block design such as presenting a series of anxiety-provoking stimuli contrasted against a safety signal – could also identify brain circuits underpinning fear, anxiety and alterations in mood. Figure 1 shows one such study comparing anxiety circuits in patients with conditioned anxiety with those of patients with social anxiety disorder1. You can see that there is a large overlap in the regions involved in the two groups with classic anxiety-related areas, including the insula and anterior cingulate cortex which show increased activity. However, the patient group showed activity in two regions that were not activated those with conditioned anxiety. We believe these are relevant to the specific anxiety cognitions of social anxiety patients as the prefrontal region and the temporal region are involved in affective response planning and body position awareness, both of which are central to social anxiety disorder.