Abstract
Chronic pain affects 50% of adults with sickle cell disease (SCD). Although central sensitization is thought to contribute to the pathogenesis of this chronic pain, no studies have examined differences in functional connectivity of the brain between patients with SCD with and without chronic pain. We performed an observational cohort study using resting-state functional MRI (rsfMRI) of the brain on adults with SCD with and without chronic pain. We tested the hypothesis that, compared to those without chronic pain, those with chronic pain would have differences in functional connectivity between the periaqueductal grey (PAG) and other regions of the brain. Twenty-two adults with SCD, 15 with chronic pain and 7 without chronic pain, as well as 10 African-American controls, underwent rsfMRI of the brain. When SCD patients with chronic pain were compared to those without chronic pain, significant differences in connectivity were noted between the PAG and 9 regions of the brain, including several in the default mode network, a network involved in introspection that has been implicated in other chronic pain syndromes. Changes in functional connectivity between patients with SCD with and without chronic pain suggest a mechanism for chronic pain that involves neuro-plastic changes to the brain.
Highlights
Chronic pain is prevalent in adults with sickle cell disease (SCD) [1]
When patients with SCD without chronic pain were compared to controls, the only differences in connectivity that were found were between the periaqueductal grey (PAG) and the occipital gyrus, and the PAG and the superior frontal gyrus (Fig 2)
Patients with SCD showed few differences in connectivity between the PAG, a region of the brain involved in pain modulation, and other regions; even fewer differences were found when controls were compared to the subset of SCD patients who did not have chronic pain
Summary
Chronic pain is prevalent in adults with sickle cell disease (SCD) [1]. Thirty percent of patients experience daily pain, and 50% meet criteria for a chronic pain syndrome [1]. It is logical to assume that vaso-occlusion-induced tissue damage (avascular necrosis, leg ulcers) is the cause of this chronic pain [2,3], many patients have widespread pain, or lack an anatomic correlate for their pain, and exhibit hyperalgesia and/or allodynia, signs of peripheral and central sensitization [4,5,6]. It has been hypothesized that factors inherent to SCD, such as tissue. Resting state fMRI of chronic pain in adults with SCD data collection and analysis, decision to publish, or preparation of the manuscript
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