Imaging Modalities and Their Findings in Patients With Complex Regional Pain Syndrome: A Review

Abstract

Complex regional pain syndrome (CRPS) is a systemic or regional pain pathology associated with the nondermatomal or dermatomal distribution of excruciating intolerable pain, which might be triggered by an insignificant or weak stimulus or sometimes without any. Its symptoms encompass neurological, musculoskeletal, dermatological, and vascular realms. It is usually preceded by an episode of nerve injury or intervention set in numerous circumstances ranging from trauma to surgeries to chronic diseases. CRPS has been shrouded in a veil of mystery and was called a psychological phenomenon without any proper organic basis when it was described by Ambroise Pare initially. This led to disproportionately fewer research investments into this disease. Given the great advancement of diagnostic modalities since its inception, researchers and physicians have been trying to identify the physiological basis for it and have succeeded. Numerous pathophysiological pathways have been involved in this disease, but all of them point toward the possibility of improper pain processing at various levels of the pain pathway along with brain plasticity leading to aberrant neuronal circuitry between different segments of the sensory cortex, basal ganglia, prefrontal cortex, and insula. This paper explores the various studies done to evaluate the role of different imaging modalities, ranging from three-phase bone scintigraphy (TPBS) to diffusion traction imaging (DTI).

Keywords: chronic pain; crps; diagnosis; fmri; imaging.

Figure 1. Role of neuronal inflammation in complex regional pain syndrome.

Figure credits: Adarsh Vardhan Tangella. CGRP, calcitonin gene-related peptide; IL-1beta, interleukin 1 beta; PGE2, prostaglandin E2; NGF, nerve growth factor; TNF alpha, tumor necrosis factor alpha

Figure 2. Mechanism of bone resorption and impaired mineralization in CRPS.

Image credit: Adarsh Vardhan Tangella. CRPS, complex regional pain syndrome; RANKL, receptor activator of nuclear factor kappa-Β ligand