Pain Catastrophizing, Self-reported Disability, and Temporal Summation of Pain Predict Self-reported Pain in Low Back Pain Patients 12 Weeks After General Practitioner Consultation: A Prospective Cohort Study.

OBJECTIVES: Patients with low back pain (LBP) often demonstrate pain sensitization, high degree of pain catastrophizing, and psychological distress. This study investigated whether pain sensitization mechanisms, the Pain Catastrophizing Scale (PCS), and Start Back Screening Tool were associated with pain in recurrent LBP patients 12 weeks after consulting their general practitioner (GP). MATERIALS AND METHODS: In 45 LBP patients, pressure pain thresholds, temporal summation of pain (TSP), conditioned pain modulation (CPM), the Roland Morris Disability Questionnaire (RMDQ), and the PCS were assessed before consultation. Patients were classified into low to medium or high risk of poor prognosis on the basis of the Start Back Screening Tool. Worst pain within the last 24 hours was assessed on a visual analogue scale (VAS) at inclusion and 12 weeks after GP consultation. RESULTS: VAS scores were reduced after 12 weeks in the low-to-medium (N=30, P<0.05), but not the high-risk group (N=15, P=0.40). RMDQ was reduced after 12 weeks (P<0.001), but with no difference between the groups. PCS was reduced in the low-to-medium and the high-risk group (P<0.05). TSP was significantly higher at follow-up in the high-risk group compared with the low-to-medium-risk group (P<0.05). A linear regression model explained 54.9% of the variance in VAS scores at follow-up utilizing baseline assessments of TSP, RMDQ, and PCS. DISCUSSION: This study indicate that patients with LBP and high self-reported disability, high pain catastrophizing, and facilitated TSP assessed when consulting the GP might predictive poor pain progression 12 weeks after the consultation.

Astrocytic expression of ZIP14 (SLC39A14) is part of the inflammatory reaction in chronic neurodegeneration with iron overload.

Neurodegeneration is associated with inflammation and mismanaged iron homeostasis, leading to increased concentration of non-transferrin-bound iron (NTBI) in the brain. NTBI can be taken up by cells expressing Zrt-, Irt-like protein-14 (ZIP14), which is regulated by iron overload and pro-inflammatory cytokines, for example, interleukin-1ß (IL-1ß) and IL-6. Here, we focus on the astrocytic involvement and regulation of ZIP14 in an experimental model of chronic neurodegeneration with inflammation and iron overload. Rats were unilaterally injected with ibotenic acid in striatum resulting in excitotoxicity-induced neuronal loss in substantia nigra pars reticulata (SNpr). ZIP14 expression was measured in SNpr using immunohistochemistry, western blotting, and RT-qPCR. Cultures of primary astrocytes were examined for Zip14 mRNA expression after stimulation with ferric ammonium citrate (FAC), IL-6, or IL-1ß. To study the involvement of ZIP14 in astrocytic iron uptake, uptake of 59 Fe was investigated after treatment with IL-1ß and siRNA-mediated ZIP14 knockdown. In the lesioned SNpr, reactive astrocytes, but not microglia, revealed increased ZIP14 expression with a main confinement to cell bodies and cellular processes. In astrocyte cultures, FAC and IL-1ß stimulation increased Zip14 expression and IL-1ß stimulation increased uptake of 59 Fe. Increased 59 Fe uptake was also observed after siRNA-mediated ZIP14 knockdown suggesting that lowering of ZIP14 impaired the balance between astrocytic uptake and export of iron. We conclude that astrocytes increase ZIP14 expression in response to inflammation and iron exposure and that ZIP14 seems pertinent for iron uptake in astrocytes and plays a role for a balanced astrocytic iron homeostasis.