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Table 2 Examples of Contributions of fMRI to the understanding of CNS circuitry underlying Chronic Pain

From: Breaking down the barriers: fMRI applications in pain, analgesia and analgesics

STUDY FOCUS REFERENCE MAJOR FINDINGS COMMENT
Neuropathic Pain    
Mechanical Allodynia Peyron et al., 2004. [69] Activated regions mirror control network activated by brush, cold to the normal side. Regions activated include SI, SII and insula. Study tackles an issue of ongoing pain and the problems associated with ongoing background pain.
Back Pain vs. Postherpetic Neuropathy Apkarian et al., 2004. [34]   A potentially huge step forward in the use of fMRI to differentiate chronic pain subtypes.
Trigeminal Neuropathy Becerra et al., 2005 [33] Becerra et al., 2006 [70] V2 neuropathy patients evaluated in a repeat study for mechanical (brush) and thermal (cold and heat) stimuli. Mechanistic changes in CNS function to specific stimuli.
Chronic Back Pain Giesecke et al., 2004. [31] Heterotopic pressure stimulus applied to the thumb activates a number of brain regions. Generalized increase in pain sensitivity in chronic pain; pain >> in patients than controls for the same pressure stimulus. Equally painful stimuli produced similar brain activations.
Spinal Cord Injury (SCI) Nicotra et al., 2005 [71] Seven patients with SCI evaluated including painful stimuli (shock) in an aversive paradigm. Conditioning stimuli produces enhancement of activity in dorsal anterior cingulated, PAG and superior temporal gyrus to conditioning stimuli and attenuation in subgenual aCG, ventromedial prefrontal and posterior cingulated to threat of shock. The study is able to dissect apart possible changes in the brains of SCI patients, including central sensitization and alterations in affective components of the brain (subgenual aCG) that may be part of a disturbance of affective and autonomic processing.
Unpleasant Odor Villemure et al., 2005 [72] Single patient with neuropathic pain where pain increased when exposed to experimental odors in thalamus, amygdala, aCG and SI. This study may suggest subcortical mechanisms of aversion have a common neural circuitry.
Complex Regional Pain Syndrome    
Pediatric CRPS Lebel et al., 2005. [73] Pediatric group with relapsing CRPS of lower extremity. Changes to cold most predominant. Clinical models within particular groups of diagnosis may be used to determine the etiology of more chronic conditions e.g., adult CRPS.
Mechanical Allodynia in Adult CRPS Maihofner et al., 2005 [40] Twelve Patients. Pin-prick hyperalgesia activates a number of cortical regions (SI, SII, Insula, aCG, frontal cortex). Study focus is on cortical regions only and indicates significant changes in functioning in affected vs., unaffected. No control group.
Sympathetically Maintained Pain (SMP) Apkarian et al., 2001. [74] Evaluation of stimuli to painful site before and after sympathetic blockade. SMP associated with increased prefrontal, aCG activation and decrease in contralateral thalamus. Correlates of CNS function shown:ineffective blocks did not change cortical activityplacebo response same as effective block
Fibromyalgia    
Primary fibromyalgia (FM) Cook et al., 2004 [75] Fibromyalgia compared with control group. Fibromyalgia group more sensitive on psychophysical evaluation. Non-painful stimuli produced greater activation in a number of regions including prefrontal, SMA, insula and cingulated cortices. Pain produced greater activation in the contralateral insula in (FM) patients. Central changes with increased sensitivity/hyperalgesia are clearly manifest behaviorally and on fMRI. Such insights provide a new approach to understanding a heretofore ill- defined disease.
Catastrophizing Gracely et al., 2004 [6] Pressure stimulus applied to the thumb (i.e., heterotopic). SII activation >> in high catasrophizers; contralateral aCG and bilateral lentiform nucleus. This was independent of depression. Catastrophizing may contribute to the pain state by enhancing the emotional reaction to pain.
Visceral Pain    
Functional bowel disorder Kwan et al., 2005 [76] Healthy (11) vs. Patients (9) underwent painful rectal distention. Activation in the medial thalamus, hippocampus for pain. On line ratings of pain responses. – clear differences in emotional circuitry of medial thalamus and hippocampus.
Irritable Bowel Syndrome (IBS) with constipation vs. diarrhea Wilder-Smith et al., 2004 [77] Female healthy (10) and IBS (10; 5-constipated and 5-diarrhea) underwent rectal distention and painful heterotopic pain applied to activate DNIC. Significant differences in CNS regions (prefrontal cortex, amygdala, aCG, PAG, Hippocampus) between constipated and diarrhea groups and controls. Different responses in patient subtypes of IBS suggesting differences in endogenous modulatory systems.
Irritable Bowel Syndrome (IBS) Mertz et al., 2000 [78] Healthy (16) vs. patients with IBS (18), IBS patients have increased activation in aCG. Increased central sensitivity to the same type of stimulus.
Visceral and Cutaneous Hypersensitivity in Irritable Bowel Syndrome (IBS) Verne et al., 2003 [32] Rectal cutaneous pain produced increased activation in thalamus and SI, I, aCG, pCG and prefrontal cortex. The brain is adversely affected in chronic pain – both visceral and cutaneous hyperalgesia produced. These findings provide a window on how we may address treatments for these patients.
Irritable Bowel Syndrome (IBS) Bonaz et al., 2002. [79] Rectal pain produced in 11 female subjects with IBS. Activation in insula, amygdala and striatal regions. Greater activation in patients in the insula and frontal regions. Similar to other studies a more complex alteration in pain processing is present in this group of subjects. Issues of variability in patients are still a concern.
Chronic Inflammation    
Vulvar vestibulitis Pukall et al, 2005. [80] Allodynia measured in patients (14) and controls (14) age and contraceptive matched. Similar type of changes in patients with IBS, Fibromyalgia.