Introduction and Impact of the New Diagnostic Criteria

A recurring theme throughout this text has been the absence of any mechanistic basis to substantiate the various pathophysiologies underlying CRPS types 1 & 2. Nevertheless, the Budapest criteria are having a significant influence on clinical practice by improving recognition of the subtle changes that may present in acute onset CRPS and help to distinguish this syndrome from other inflammatory/neuropathic pain syndromes. Identifying later stages or chronic CRPS is less intimidating, the signs are usually well defined with motor/MFPS and possible trophic changes; the pain is invariably mixed neuropathic/nociceptive and allodynia/hyperalgesia either superficial or deep can be severe. By retaining at least one sign in each of the four categories, sensory, vasomotor, sudomotor and motor/trophic of the Budapest criteria has improved the specificity to the point that the differential diagnosis from other conditions that present with similar signs and symptoms is now easier. While no less than five diagnostic criteria have been considered over the past 25 years (Veldman, Bruehl, Orlando Workshop—precursor to the Budapest Workshop—and Ott, Maihöfner CRPS prediction score {CPS}), validation of the Budapest criteria that yielded a sensitivity of .819 and a specificity of .679 provided the impetus for their international adoption. The improved specificity excludes those diseases that have similar clinical features in their differential diagnosis (Ott and Maihöfner 2018). Probably the most significant modification of the Budapest criteria were the results of the validation study (Harden et al. 2010). Unique to these results was the description of two decision rules that increased the usefulness of the criteria, namely, one rule for clinical diagnosis and a second rule to be applied for clinical research. These latter criteria increased the degree of specificity to 0.94 thereby markedly improving the integrity of research data, an example of which are measurements comparing autonomic dysfunction from other signs of neuropathic pain and therefore more likely supporting the diagnosis of CRPS. The authors, Harden et al. did point out a particular limitation of their validation study results which was the inclusion of a very heterogeneous neuropathic pain control group rather than making a comparison between CRPS patients and a much more homogeneous non-CRPS pain patient group that sustained a similar injury. Such criticism was most likely offset by the fact that the heterogeneous control group avoided any bias related to the perhaps unique clinical features associated with a single non-CRPS condition. In spite of the foregoing limitation and the fact study sites were multiple and international, the data support the merit of the Budapest criteria over the original IASP diagnostic criteria as being an instrument that has improved the fidelity of CRPS diagnosis.