Central sensitization in chronic low back pain: A narrative review

Central sensitization (CS) is a proposed physiological phenomenon in which central nervous system neurons become hyperexcitable, resulting in hypersensitivity to both noxious and non-noxious stimuli. The term central sensitivity syndrome (CSS) describes a group of medically indistinct (or nonspecific) disorders, such as fibromyalgia, chronic fatigue syndrome, and irritable bowel syndrome, for which CS may be a common etiology. In a previous study, the Central Sensitization Inventory (CSI) was introduced as a screening instrument for clinicians to help identify patients with a CSS. It was found to have high reliability and validity (test-retest reliability = .82; Cronbach's alpha = .88). The present study investigated a cohort of 121 patients who were referred to a multidisciplinary pain center, which specializes in the assessment and treatment of complex pain and psychophysiological disorders, including CSSs. A large percentage of patients (n = 89, 74%) met clinical criteria for one or more CSSs, and CSI scores were positively correlated with the number of diagnosed CSSs. A receiver operating characteristic analysis determined that a CSI score of 40 out of 100 best distinguished between the CSS patient group and a nonpatient comparison sample (N = 129) (area under the curve = .86, sensitivity = 81%, specificity = 75%). The CSI is a new self-report screening instrument to help identify patients with CSSs, including fibromyalgia. The present study investigated CSI scores in a heterogeneous pain population with a large percentage of CSSs, and a normative nonclinical sample to determine a clinically relevant cutoff value. Copyright © 2013 American Pain Society. Published by Elsevier Inc. All rights reserved.

To evaluate the evidence for the effectiveness of neuroscience education (NE) for pain, disability, anxiety, and stress in chronic musculoskeletal (MSK) pain. Systematic searches were conducted on Biomed Central, BMJ.com, CINAHL, the Cochrane Library, NLM Central Gateway, OVID, ProQuest (Digital Dissertations), PsycInfo, PubMed/Medline, ScienceDirect, and Web of Science. Secondary searching (PEARLing) was undertaken, whereby reference lists of the selected articles were reviewed for additional references not identified in the primary search. All experimental studies including randomized controlled trials (RCTs), nonrandomized clinical trials, and case series evaluating the effect of NE on pain, disability, anxiety, and stress for chronic MSK pain were considered for inclusion. Additional limitations: studies published in English, published within the last 10 years, and patients older than 18 years. No limitations were set on specific outcome measures of pain, disability, anxiety, and stress. Data were extracted using the participants, interventions, comparison, and outcomes (PICO) approach. Methodological quality was assessed by 2 reviewers using the Critical Review Form-Quantitative Studies. This review includes 8 studies comprising 6 high-quality RCTs, 1 pseudo-RCT, and 1 comparative study involving 401 subjects. Most articles were of good quality, with no studies rated as poor or fair. Heterogeneity across the studies with respect to participants, interventions evaluated, and outcome measures used prevented meta-analyses. Narrative synthesis of results, based on effect size, established compelling evidence that NE may be effective in reducing pain ratings, increasing function, addressing catastrophization, and improving movement in chronic MSK pain. For chronic MSK pain disorders, there is compelling evidence that an educational strategy addressing neurophysiology and neurobiology of pain can have a positive effect on pain, disability, catastrophization, and physical performance. Copyright © 2011 American Congress of Rehabilitation Medicine. Published by Elsevier Inc. All rights reserved.

For many individuals with chronic low back pain (CLBP), there is no identifiable cause. In other idiopathic chronic pain conditions, sensory testing and functional magnetic resonance imaging (fMRI) have identified the occurrence of generalized increased pain sensitivity, hyperalgesia, and altered brain processing, suggesting central augmentation of pain processing in such conditions. We compared the results of both of these methods as applied to patients with idiopathic CLBP (n = 11), patients with widespread pain (fibromyalgia; n = 16), and healthy control subjects (n = 11). Patients with CLBP had low back pain persisting for at least 12 months that was unexplained by MRI/radiographic changes. Experimental pain testing was performed at a neutral site (thumbnail) to assess the pressure-pain threshold in all subjects. For fMRI studies, stimuli of equal pressure (2 kg) and of equal subjective pain intensity (slightly intense pain) were applied to this same site. Despite low numbers of tender points in the CLBP group, experimental pain testing revealed hyperalgesia in this group as well as in the fibromyalgia group; the pressure required to produce slightly intense pain was significantly higher in the controls (5.6 kg) than in the patients with CLBP (3.9 kg) (P = 0.03) or the patients with fibromyalgia (3.5 kg) (P = 0.006). When equal amounts of pressure were applied to the 3 groups, fMRI detected 5 common regions of neuronal activation in pain-related cortical areas in the CLBP and fibromyalgia groups (in the contralateral primary and secondary [S2] somatosensory cortices, inferior parietal lobule, cerebellum, and ipsilateral S2). This same stimulus resulted in only a single activation in controls (in the contralateral S2 somatosensory cortex). When subjects in the 3 groups received stimuli that evoked subjectively equal pain, fMRI revealed common neuronal activations in all 3 groups. At equal levels of pressure, patients with CLBP or fibromyalgia experienced significantly more pain and showed more extensive, common patterns of neuronal activation in pain-related cortical areas. When stimuli that elicited equally painful responses were applied (requiring significantly lower pressure in both patient groups as compared with the control group), neuronal activations were similar among the 3 groups. These findings are consistent with the occurrence of augmented central pain processing in patients with idiopathic CLBP.