First of all, we don't know yet what (if anything) will come out of Congress this summer. But even assuming that some form of EBM (evidenced based medicine?) studies are required for coverage, I can't agree that no EBM studies currently exist for CRPS.

Consider, "Evidence of focal small-fiber axonal degeneration in complex regional pain syndrome-I (reflex sympathetic dystrophy)," Oaklander AL, Rissmiller JG, Gelman LB, Zheng L, Chang Y, Gott R, Pain, 2006; 120: 235-243, free full text at http://www.rsds.org/2/library/articl..._pain_2006.pdf, the abstract of which follows:

CRPS-I consists of post-traumatic limb pain and autonomic abnormalities that continue despite apparent healing of inciting injuries. The cause of symptoms is unknown and objective findings are few, making diagnosis and treatment controversial, and research difficult. We tested the hypotheses that CRPS-I is caused by persistent minimal distal nerve injury (MDNI), specifically distal degeneration of small-diameter axons. These subserve pain and autonomic function. We studied 18 adults with IASP-defined CRPS-I affecting their arms or legs. We studied three sites on subjects’ CRPS-affected and matching contralateral limb; the CRPS-affected site, and nearby unaffected ipsilateral and matching contralateral control sites. We performed quantitative mechanical and thermal sensory testing (QST) followed by quantitation of epidermal neurite densities within PGP9.5-immunolabeled skin biopsies. Seven adults with chronic leg pain, edema, disuse, and prior surgeries from trauma or osteoarthritis provided symptom-matched controls. CRPS-I subjects had representative histories and symptoms. Medical procedures were unexpectedly frequently associated with CRPS onset. QST revealed mechanical allodynia (P < 0.03) and heat-pain hyperalgesia (P < 0.04) at the CRPS-affected site. Axonal densities were highly correlated between subjects’ ipsilateral and contralateral control sites (r = 0.97), but were diminished at the CRPS-affected sites of 17/18 subjects, on average by 29% (P < 0.001). Overall, control subjects had no painful-site neurite reductions (P = 1.00), suggesting that pain, disuse, or prior surgeries alone do not explain CRPS-associated neurite losses. These results support the hypothesis that CRPS-I is specifically associated with post-traumatic focal MDNI affecting nociceptive small-fibers. This type of nerve injury will remain undetected in most clinical settings. [Emphasis added.]

OR

"The Brain in Chronic CRPS Pain: Abnormal Gray-White Matter Interactions in Emotional and Autonomic Regions," Paul Y. Geha, Marwan N. Baliki, R. Norman Harden, William R. Bauer, Todd B. Parrish, and A. Vania Apkarian, Neuron 60, 570–581, November 26, 2008, free full text at http://www.apkarianlab.northwestern....S_Neuron08.pdf and in particular, the first two paragraphs of the "discussion" portion of the article at pp. 574-575:

DISCUSSION

The main outcome of the current study is the observation that CRPS patients exhibit regional gray matter atrophy in a single cluster encompassing right VMPFC [ventromedial prefrontal cortex], AI [anterior insula], and NAc [nucleus accumbens], localized decreased white matter anisotropy, and changes in branching and connectivity of white matter tracts linked to these site-specific gray and white matter abnormalities. Unlike results from chronic back pain and fibromyalgia (Apkarian et al., 2004b; Kuchinad et al., 2007), whole-brain gray matter and ventricular size were similar between CRPS and control subjects. Aging effects on whole-brain gray matter volume were similar but smaller than those seen in fibromyalgia (Kuchinad et al., 2007), suggesting a smaller impact of the condition on whole-brain gray matter parameters. Notably, the relationship between brain white matter skeletal FA and brain gray matter volume seems completely disrupted in CRPS, implying reorganization of white matter tracks in a manner that no longer conforms to the relationship seen in healthy subjects. Because this is a disruption at the whole-brain level, it entails either diffuse disruption of gray to white matter relationships or multiple distinct abnormalities with compensatory remodeling of the brain in CRPS.

Role of Right AI in CRPS Symptoms

Regional gray matter density comparison indicated atrophy within a single cluster for the whole group of CRPS. The same brain region or portions of the same cluster exhibited atrophy even after subdividing the group by age or by laterality of CRPS pain. Hence, the atrophy spanning AI, VMPFC, and NAc seems a robust result in CRPS and is right hemisphere dominant. Moreover, this atrophy was related to the two fundamental clinical characteristics of CRPS, duration and intensity, which impacted the density of this cluster above and beyond normal aging. When the cluster was subdivided into separate anatomical regions, the right AI correlated with duration of CRPS pain. The insula is the brain structure most often observed activated in acute pain tasks (Apkarian et al., 2005). In CRPS patients, bilateral AI activity correlates with ratings of touch-induced pain (allodynia) and pin-prick hyperalgesia (Maihofner et al., 2005, 2006). Moreover, recent human brain imaging studies, consistent with the older literature regarding the role of the insula as a viscerosensory cortex (Craig, 2002; Saper, 2002), highlight the role of the right AI in the representation of autonomic and visceral responses Critchley, 2005). Patients with pure autonomic failure due to peripheral disruption of autonomic responses exhibit reduced right AI activity (Critchley et al., 2001) and atrophy in right AI (Critchley et al., 2003a). In healthy subjects, neural activity in right AI predicts subjects’ accuracy in heartbeat detection, while local gray matter volume, at coordinates closely approximating the center of the cluster we observed atrophied in our CRPS patients, correlates with subjective ratings of visceral awareness (Critchley et al., 2004). Furthermore, by comparing brain activity and autonomic responses in a fear conditioning task between healthy subjects and pure autonomic failure patients, Critchley and colleagues conclude that the right AI is involved in emotional representations, ‘‘wherein ‘feelings’ are the integration of both the mapping of internal arousal and conscious awareness of emotional stimuli’’ (Critchley et al., 2002). Given that CRPS patients are presumed to be in a constant negative emotional state and exhibit multiple signs of abnormal autonomic function, atrophy of right AI in CRPS corroborates the above studies and suggests that central anatomical abnormalities may explain fundamental symptoms of CRPS. [Emphasis added.]

Call me crazy, but I think these qualify as Evidence Based Medicine, albeit medicine requiring the backup of a tertiary medical center. But if that's what's required to make a firm diagnosis, then treating CRPS will require more and not less expensive medicine, if EBM standards are to be employed, because, after a long, long time they now exist. Put another way, it may be time to drop the "Syndrome" from CRPS.

Mike