Prof. A. Vania Apkarian is probably the leading neuroscientist specializing in pain today, at least in the U.S., his lab at Northwestern may be the place, and quite possibly the best overall article out there right now is the following, which has made freely available on the website of Abkarian's "Pain & Passions" Lab at Northwestern:

"The Brain in Chronic CRPS Pain: Abnormal Gray-White Matter Interactions in Emotional and Autonomic Regions," Paul Y. Geha,1 Marwan N. Baliki,1 R. Norman Harden,2 William R. Bauer,6 Todd B. Parrish,3 and A. Vania Apkarian1,4,5,*, Neuron 60, 570–581, November 26, 2008

1Department of Physiology
2Rehabilitation Institute
3Department of Radiology
4Department of Anesthesia
5Department of Surgery
Northwestern University, Feinberg School of Medicine, Chicago, IL 60611, USA
6Department of Neuroscience, University of Toledo, 3000 Arlington Avenue, Toledo OH 43614-2598, USA
*Correspondence: a-apkarian@northwestern.edu
DOI 10.1016/j.neuron.2008.08.022

SUMMARY

Chronic complex regional pain syndrome (CRPS) is a debilitating pain condition accompanied by autonomic abnormalities. We investigated gray matter morphometry and white matter anisotropy in CRPS patients and matched controls. Patients exhibited a disrupted relationship between white matter anisotropy and whole-brain gray matter volume; gray matter atrophy in a single cluster encompassing right insula, right ventromedial prefrontal cortex (VMPFC), and right nucleus accumbens; and a decrease in fractional anisotropy in the left cingulum-callosal bundle. Reorganization of white matter connectivity in these regionswas characterized by branching pattern alterations, as well as increased (VMPFC to insula) and decreased (VMPFC to basal ganglion) connectivity. While regional atrophy differentially related to pain intensity and duration, the strength of connectivity between specific atrophied regions related to anxiety. These abnormalities encompass emotional, autonomic, and pain perception regions, implying that they likely play a critical role in the global clinical picture of CRPS. [Emphasis added.]

PMID: 19038215 [PubMed - indexed for MEDLINE] PMCID: PMC2637446 [Available on 2009/11/26] http://www.ncbi.nlm.nih.gov/pubmed/1...ubmed_RVDocSum

And here's the corresponding text from pp. 575 - 577:

Role of VMPFC in CRPS in Relation to Emotional Decision-Making

Atrophy in the right VMPFC was correlated with the interaction of duration and intensity of CRPS pain, which functionally segregates the atrophy in this region from right AI [anterior insula] and suggests a more global impact, or ‘‘emotional load,’’ of CRPS on the VMPFC. Atrophy within this region was our primary hypothesis because CRPS patients perform poorly on the emotional decision-making task (Apkarian et al., 2004a), which has been shown to critically depend on an intact VMPFC (Bechara et al., 2000). In fact, even when CRPS pain is transiently reduced, performance on this task does not improve and CRPS patients do not show evidence of learning the task (Apkarian et al., 2004a). In contrast, chronic back pain patients who exhibit atrophy in the thalamus and dorsolateral prefrontal cortex (DLPFC) (Apkarian et al., 2004b), although also abnormal on this task, exhibit clear signs of learning and improved performance over time. Emotional decision-making critically depends on the ability to evaluate options in terms of potential reward or punishment; such decisions require proper capturing and evaluation of sensory cues, including bodily autonomic responses. It is thus not surprising that autonomic regulation and monitoring involve many of the same cortical regions implicated in emotional decision-making, especially ACC, VMPFC, and AI. Therefore differential atrophy of gray matter and abnormal connectivity of associated white matter tracks involving ACC, VMPFC, and AI in CRPS, in contrast to atrophy of DLPFC in chronic back pain, must underlie their differential responses on emotional decision-making, especially given the fact that CRPS is associated with autonomic abnormalities and chronic back pain is not.

Neurons within the VMPFC encode the emotional value of sensory stimuli (Kringelbach, 2005; Rolls, 2000). Moreover, patients with VMPFC lesions exhibit diminished emotional responses and social emotions (Anderson et al., 1999), as well as poorly regulated anger and frustration tolerance (Koenigs and Tranel, 2007). A recent study showed also abnormal utilitarian judgments on moral dilemmas that pit considerations of aggregate welfare against emotionally aversive behaviors (Koenigs et al., 2007). Parts of the region are activated during anticipation of pain (Porro et al., 2002), anticipation of placebo (Wager et al., 2004), when acute pain is enhanced (Lorenz et al., 2002), and especially when spontaneous pain of chronic back pain is high and sustained (Baliki et al., 2006, 2008). Importantly, this region projects to the hypothalamus and brainstem areas that link autonomic bodily processes with emotional responses (Ongur and Price, 2000). It also projects to the periaqueductal gray, thereby modulating spinal cord responses to nociceptive inputs (An et al., 1998). Therefore, the VMPFC region together with AI may be directly involved in determining characteristics of CRPS pain and associated autonomic abnormalities. We also demonstrated that the strength of white matter connectivity between VMPFC and NAc was related to the heightened anxiety generally seen in such patients. This is consistent with studies on mood and anxiety disorders emphasizing the role of hyperactivity in Brodmann area 25, part of VMPFC, in the pathophysiology of depression and its response to treatment (Ressler and Mayberg, 2007). Deep brain stimulation in the same white matter bundles we mapped here between NAc and VMPFC leads to decreased brain activity in VMPFC and remission of symptoms in treatment-resistant depression (Mayberg et al., 2005).

http://www.apkarianlab.northwestern....S_Neuron08.pdf (It's tough going, but the illustrations and schematic diagrams - which can't be copied here -are easier to follow than the text.)