Non-invasive brain imaging in human subjects To date, fMRI has revealed key brain areas (e.g., cingulate, insula, somatosensory, and motor cortices, the thalamus and basal ganglia) activated during the experience of pain, as shown in Fig. 3, (Peyron et al., 2000; Tracey et al., 2002a). This technique has also highlighted additional regions, such as the hippocampus (Ploghaus et al., 2001), which will contribute to states of anxiety that in turn exacerbate pain sensation. By the same token, other areas, such as the periaqueductal gray (PAG),
Fig. 3. PAG matter activation in response to noxious thermal stimulation. The right panel shows that activation in this region is increased when subjects do not attend to the noxious thermal stimulus and that this increased activation is concomitant with a decreased perceived pain intensity.
if activated, contribute to pain alleviation, seen at the behavioral level as the shift in attention used by some as an effective non-invasive strategy (see above). This mindset of distraction is characterized not just by an activated PAG, but by a decreased activity in the circuitry otherwise related to pain (Tracey et al., 2002b; Kupers et al., this volume).
Invasive (optical) imaging in non-human brains To date, our laboratory has succeeded in completing a pilot set of experiments to examine the effects of anesthetics on the spatiotemporal patterns of neuronal assembly formation in the cortex and hippocampus in vitro, using the mammalian brain slice model. Indeed, we found that in response to electrical paired-pulse stimulation, two anesthetics (thiopental and propofol) reduced the spatial spread and diminished the amplitude of neuronal assemblies, despite the two chemicals having diverse chemical structures. It has been reported previously that these two anesthetics induce the release of an amino acid neurotransmitter, g-aminobutyric acid (GABA), which leads to the activation of chloride channels. Interestingly, another compound used to treat neuropathic pain, gabapentin, is very similar in structure to GABA; however, it is not an anesthetic and it does not produce the same effects, following repeated stimulation, as do the two anesthetics (Fig. 4). These data suggest that loss of awareness with anesthesia does not depend on any one transmitter, such as GABA, but on some higher-order property of neuronal organization, such as macro assembly formations, and most importantly, their duration. Indeed, given that anesthesia itself is well known to be graded in stages (i.e., not all or none) (Rang and Dale, 1991), it would be appropriate for its neural correlate to be correspondingly analogue too (Fiset, this volume, Alkire, this volume). A current monitor for depth of anesthesia relies on a number of collated parameters from a patients EEG trace, which provides a numerical output, the Bispectral index (BIS) (Pomfrett, 1999). If a measure of neuronal ''assemblage'' (see the
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