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Review
. 2004 Aug;53(8):1198-206.
doi: 10.1136/gut.2003.035642.

Brain imaging and functional gastrointestinal disorders: has it helped our understanding?

A R Hobson  1 , Q Aziz
Affiliations
Review

Brain imaging and functional gastrointestinal disorders: has it helped our understanding?

A R Hobson et al. Gut. 2004 Aug.
No abstract available

PubMed Disclaimer

Figures

Figure 1
Figure 1
Schematic diagram of the ascending pathways, subcortical structures, and cerebral cortical structures involved in processing pain. PAG, periaqueductal gray; PB, parabrachial nucleus of the dorsolateral pons; VMpo, ventromedial part of the posterior nuclear complex; MDvc, ventrocaudal part of the medial dorsal nucleus; VPL, ventroposterior lateral nucleus; ACC, anterior cingulate cortex; PCC, posterior cingulate cortex; HT, hypothalamus; S1, S2, first and second somatosensory cortical areas, respectively; PPC, posterior parietal complex; SMA, supplementary motor area; AMYG, amygdala; PF, prefrontal cortex; M1, motor cortex. All of these regions have been activated in studies of gastrointestinal pain. Adapted with permission from Price and colleagues.
Figure 2
Figure 2
Group mean positron emission tomography data showing z score maps for the non-painful sensation-baseline (top panel), pain-baseline (middle panel), and pain-non-painful sensation (bottom panel) contrasts. Bilateral activation of the insular and primary somatosensory and motor cortices can be seen separately in both images depicted in the top panel (non-painful) whereas stronger activation of the same areas can be seen in the middle panel (painful). Furthermore, activation of the anterior cingulate gyrus is also observed in the second image of the middle panel. The main areas of interest in the scans showing the pain definite sensation contrast are the right anterior insular cortex and the anterior cingulate gyrus, which can best be seen in the bottom panel. Adapted with permission from Aziz and colleagues.
Figure 3
Figure 3
(A) Images showing a comparison of cortical activity in response to rectal stimulation in a group of healthy subjects and patients with irritable bowel syndrome (IBS). It can be seen that greater activation of the anterior cingulate cortex (ACG) is observed in healthy subjects when compared with IBS. Adapted with permission from Silverman and colleagues. (B) Images showing a comparison of cortical activity in response to rectal stimulation in another group of healthy subjects and patients with IBS. It can be seen that greater activation of the ACG is observed this time in IBS patients when compared with healthy subjects. Adapted with permission from Mertz and colleagues.
Figure 4
Figure 4
Three cortical evoked potential (CEP) responses obtained from one female subject in response to electrical stimulation of the oesophagus, sigmoid colon, and rectum. It can be seen that the fact that the sigmoid is distal to the oesophagus is reflected by the increase in latency of the P1 component of the sigmoid response, due to the increased distance the afferent signal has to travel. However, it can also be noted that the rectal P1 response occurs earlier than both the oesophageal and sigmoid responses. This reflects the presence of faster conducting afferent fibres in the rectum, which is consistent with its role in maintaining continence.
Figure 5
Figure 5
Effect of increasing rectal stimulation intensities on the subsequent cortical evoked potential (CEP) response. It can be seen that as the intensity rises from sensory threshold through to pain, there is an associated increase in the amplitude of the CEP response and a decrease in the latency of each CEP component. This provides an objective neurophysiological correlate of subjective pain reports.
Figure 6
Figure 6
A normal cortical evoked potential (CEP) (top panel) and an oesophageal evoked potential (OEP) in two patients with non-cardiac chest pain (NCCP). Patient A demonstrated oesophageal hypersensitivity and this was associated with enhanced early and late CEP components. This profile is consistent with patient A having sensitised oesophageal afferents. Patient B demonstrated oesophageal hypersensitivity and this was associated with reduced amplitude and delayed latency of the first three CEP components. This is indicative of over reporting (that is, normal afferent transmission of a reduced stimulus intensity). However, there was a small enhancement of the late (500 ms) CEP component, which is likely to be associated with secondary pain processing. This patient does not have sensitised oesophageal afferents and is hypervigilant of oesophageal stimuli.
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