A technician then takes infrared images of both the patients affected and unaffected limbs, as well as reference images of other parts of the patients body, including his or her face, upper back, and lower back. After capturing a set of baseline images, some labs further require the patient to undergo cold-water autonomic-functional-stress-testing to evaluate the function of their autonomic nervous systems peripheral vasoconstrictor reflex. This is performed by placing a patients unaffected limb in a cold water bath (approximately 20 °C) for five minutes while collecting images. In a normal, intact, functioning autonomic nervous system, a patients affected extremity will become colder. Conversely, warming of an affected extremity may indicate a disruption of the bodys normal thermoregulatory vasoconstrictor function, which may sometimes indicate underlying CRPS. Radiography
Scintigraphy, plain radiographs, and magnetic resonance imaging  may all be useful diagnostically. Patchy osteoporosis (post-traumatic osteoporosis), which may be due to disuse of the affected extremity, can be detected through X-ray imagery as early as two weeks after the onset of CRPS. A bone scan of the affected limb may detect these changes even sooner and can almost confirm the disease. Bone densitometry can also be used to detect changes in bone mineral density. It can also be used to monitor the results of treatment since bone densitometry parameters improve with treatment. Ultrasound
Ultrasound-based osteodensitometry (ultrasonometry) may be potential future radiation-free technique to identify reduced bone mineral density in CRPS. Additionally, this method promises to quantify the bone architecture in the periphery of affected limbs.
Because immunological functions can modulate CNS physiology, a variety of immune processes have also been hypothesized to contribute to the initial development and maintenance of peripheral and central sensitization. Furthermore, trauma-related cytokine release, exaggerated neurogenic inflammation, sympathetic afferent coupling, adrenoreceptor pathology, glial cell activation, cortical reorganisation, and oxidative damage (e.g., by free radicals) are all factors which have been implicated in the pathophysiology of CRPS. In addition, autoantibodies are present in a wide number of CRPS patients and IgG has been recognized as one of the causes of hypersensitivity that stimulates A and C nociceptors, attributing to the inflammation.The mechanisms leading to reduced bone mineral density (up to overt osteoporosis) are still unknown. Potential explanations include a dysbalance of the activities of sympathetic and parasympathetic autonomic nervous system and mild secondary hyperparathyroidism. However, the trigger of secondary hyperparathyroidism has not yet been identified.In summary, the pathophysiology of complex regional pain syndrome has not yet been defined;  CRPS, with its variable manifestations, could be the result of multiple pathophysiological processes. Diagnosis
Diagnosis is primarily based on clinical findings. The original diagnostic criteria for CRPS adopted by the International Association for the Study of Pain (IASP) in 1994 have now been superseded in both clinical practice and research by the "Budapest Criteria" which were created in 2003 and have been found to be more sensitive and specific. They have since been adopted by the IASP.