The journal of pain : official journal of the American Pain Society
-
Current fear-anxiety-avoidance models of chronic pain emphasize pain-related fear and anxiety as potential precursors for disabling chronic pain; however, anxiety and fear are often used interchangeably when discussing pain. Fear is a present-oriented emotive state associated with an imminent threat (eg, a patient about to receive an injection), whereas anxiety is a more general, future-oriented emotive state, that occurs in anticipation of threats without requiring an objective stimulus (eg, the possibility of receiving an injection). Theoretical and empirical evidence suggests pain-related fear and anxiety represent distinct cognitive constructs. Moreover, pain-related anxiety has been posited as a manifestation of anxiety sensitivity, which has implications for several theoretical models as well as treatment. The Fear of Pain Questionnaire and the Pain Anxiety Symptoms Scale-20 are popular measures, often used comparably, that were designed to measure pain-related fear and anxiety, respectively. These measures, along with the Anxiety Sensitivity Index, were administered to an undergraduate sample (N = 268; 66% women). Results of confirmatory factor analyses suggest each measure represents a related, but distinct, construct. Furthermore, correlations with anxiety sensitivity suggest that pain-related anxiety may be better conceptualized as a fundamental fear. Implications and directions for future research are discussed. ⋯ Fear-anxiety-avoidance models of chronic pain posit pain-related fear and anxiety as diatheses for disabling chronic pain. This research suggests theoretical and clinical distinctions between pain-related fear and anxiety. Moreover, pain-related anxiety appears more complex than a manifestation of anxiety sensitivity; pain-related anxiety may be better conceptualized as a fundamental fear.
-
Inflammatory cytokines contribute to lumbar radiculopathy. Regulation of cytokines for transient cervical injuries, with or without longer-lasting inflammation, remains to be defined. The C7 root in the rat underwent compression (10gf), chromic gut suture exposure (chr), or their combination (10gf+chr). Ipsilateral C7 spinal cord and dorsal root ganglia (DRG) were harvested at 1 hour after injury for real-time PCR analysis of IL-1beta, IL-6, and TNF-alpha. Cytokine mRNA increased after all 3 injuries. TNF-alpha mRNA in the DRG was significantly increased over sham after 10gf+chr (P = .026). Spinal IL-1beta was significantly increased over sham after 10gf and 10gf+chr (P < .024); IL-6 was significantly increased after 10gf+chr (P < .024). In separate studies, the soluble TNF-alpha receptor was administered at injury and again at 6 hours in all injury paradigms. Allodynia was assessed and tissue samples were harvested for cytokine PCR. Allodynia significantly decreased with receptor administration for 10gf and 10gf+chr (P < .005). Treatment also significantly decreased IL-1beta and TNF-alpha mRNA in the DRG for 10gf+chr (P < .028) at day 1. Results indicate an acute, robust cytokine response in cervical nerve root injury with varying patterns, dependent on injury type, and that early increases in TNF-alpha mRNA in the DRG may drive pain-related signaling for transient cervical injuries. ⋯ Inflammatory cytokine mRNA in the DRG and spinal cord are defined after painful cervical nerve root injury. Studies describe a role for TNF-alpha in mediating behavioral sensitivity and inflammatory cytokines in transient painful radiculopathy. Results outline an early response of inflammatory cytokine upregulation in cervical pain.