Wenzel HG, Vasseljen O, Mykletun A, Nilsen TI. Pre-injury health-related factors in relation to self-reported whiplash: longitudinal data from the HUNT study, Norway. Eur. Spine J. doi:10.1007/s00586-012-2186-2 (2012) (Epub ahead of print).
Whiplash-associated disorders are common and associated with high healthcare costs. In this large longitudinal study of over 40,000 individuals in Norway, predictors for reporting a whiplash trauma were examined. The study demonstrated that impaired self-reported health before injury was strongly associated with subsequent reporting of a whiplash trauma. The association was even stronger with the reporting of a whiplash trauma in conjunction with neck pain. This finding has implications for the understanding of mechanisms and treatment of whiplash-associated disorders as it may indicate that preinjury health affects the outcome of a whiplash trauma.
– Written by Nanna B Finnerup
Mijnhout GS, Kollen BJ, Alkhalaf A, Kleefstra N, Bilo HJ. Alpha lipoic acid for symptomatic peripheral neuropathy in patients with diabetes: a meta-analysis of randomized controlled trials. Int. J. Endocrinol. 2012, 456279 (2012).
In this systematic review, intravenous α-lipoic acid 600 mg/day over 3 weeks was found to have a clinically relevant effect in neuropathic pain in diabetic polyneuropathy (grade of recommendation A). The effect of orally administered α-lipoic acid was also statistically significant but lower, and it was described as unclear if the improvements seen after 3–5 weeks at a dosage of >600 mg/day was clinically relevant. In total, four randomized controlled trials were included in the review. As none of the trials were designed for neuropathic pain assessment, further trials are warranted.
– Written by Nanna B Finnerup
Alexander GM, Peterlin BL, Perreault MJ, Grothusen JD, Schwartzman RJ. Changes in plasma cytokines and their soluble receptors in complex regional pain syndrome. J. Pain 13, 10–20 (2012).
The identification of biomarkers of disease has real promise in the definition of diseases and disease subgroups, and could play a major role in the design of clinical trials. Of course, such biomarkers may also shed light on the pathophysiological mechanisms of disease. Complex regional pain syndrome is often a severe and disabling condition; preliminary reports have indicated that the pathophysiology may involve neuroinflammation and activation of the immune system. This study involved 148 patients with complex regional pain syndrome and 60 age- and gender-matched controls. Each subject had a thorough clinical evaluation, determination of thermal detection thresholds, thermal pain tolerance, finger tap rate, skin temperature and blood sampling for cytokines, chemokines and their soluble receptors. Although the normal subjects were significantly different from the patients with complex regional pain syndrome as a group in respect to the chemical analyses of blood samples, a distinct subgroup of 36% of the patients with elevated TNF-α, as well as other analytes, had chemical abnormalities that correlated with their disease severity and duration. Medications that the patients were taking did not seem to influence the levels of cytokines or chemokines, or their receptors. This study suggests that patients with similar clinical appearances may have differing underlying mechanisms. Response to therapy could be determined by the underlying mechanisms and not the diagnostic rubric applied to the patient.
– Written by John D Loeser
Marshall TM, Herman DS, Largent-Milnes TM et al. Activation of descending pain-facilitatory pathways from the rostral ventromedial medulla by cholecystokinin elicits release of prostaglandin-E2 in the spinal cord. Pain 153, 86–94 (2012).
Ligation of the L5/L6 spinal nerves in rats increased levels of cholecystokinin (CCK) twofold in the rostral ventromedial medulla (RVM). Injection of CCK into the RVM led to hypersensitivity to tactile stimulation in the hindpaw and an increase in cerebrospinal fluid prostaglandin E2. Intraspinal naproxen reduced the response to RVM CCK. Furthermore, RVM CCK increased spinal 5-hydroxyindole acetic acid (5-HIAA), a metabolite of 5-hydroxytryptamine (5-HT). These findings suggest that chronic nerve injury can lead to activation of descending facilitatory mechanisms, which can lead to hyperalgesia, and that the mechanism for this sensory change is related to the release of prostaglandin E2 and 5-HT in the spinal cord.
– Written by John D Loeser
Sviggum HP, Jacob AK, Arendt KW, Mauermann ML, Horlocker TT, Hebl JR. Neurologic complications after chlorhexidine antisepsis for spinal anesthesia. Reg. Anesth. Pain Med. 37, 139–144 (2012).
Chlorhexidine gluconate (CHG) is a rapid and effective topical agent commonly used for surgical skin antisepsis. It lacks US FDA approval for neuraxial procedures secondary to a lack of safety evidence in this regard. A retrospective review of medical records of adult patients undergoing spinal anesthesia over a 4-year period was undertaken. Of 11,095 patients receiving 12,465 spinal anesthetics, 57 cases (0.46%) were assessed to have neurologic complications (new or progressive numbness, paresthesias, hypesthesias, dysesthesias or weakness within 1 week of the spinal anesthetic). A considerable majority (80.7%) of this group achieved complete neurologic recovery. This overall incidence of peripheral and neuraxial nerve injuries was similar to other published literature. Of the 57 cases, only five (0.04%) were considered to have a possible relation to the spinal anesthetic. None of these showed any evidence of association with CHG neurotoxicity (arachnoiditis, aseptic meningitis or lumbar plexopathy). Although previous animal studies have shown evidence of neurotoxicity with direct application of CHG to neural structures, the complication rate of 0.04% demonstrated in this study is similar to that of other studies in which spinal anesthesia was performed regardless of topical skin antisepsis was employed. The authors conclude that at this time the advantages of using CHG for skin antisepsis appear to exceed potential risks.
– Written by Michael Erdek
Finlayson RJ, Gupta G, Alhujairi M, Dugani S, Tran de QH. Cervical medial branch block: a novel technique using ultrasound guidance. Reg. Anesth. Pain Med. 37, 219–223 (2012).
The authors endeavored to investigate the use of ultrasound (US) as an alternative to fluoroscopy for diagnostic block of the third occipital nerve and the C3–C6 medial branches. The study was completed in two phases. Phase I attempted to assess the reliability of using US for correct needle placement at the articular pillar target sites in 20 patients. US scanning took place in the transverse plane and, after needle placement, a lateral radiograph was performed subsequently to confirm needle position. Phase II involved the injection of 0.3 cm3 of contrast material after the initial needle placement, monitored under real-time US visualization in 50 patients. Subsequent fluoroscopic examinations were performed to assess contrast spread. In Phase I, all needle tips were found to be positioned on the articular pillar, with 80.9% being on the center of the pillar. In Phase II, the targeted level was covered by contrast material in >94% of blocks, while spread of contrast to a contiguous nontargeted level occurred in 13.5% of blocks. The C6 level required the greatest number of needle passes and also had the highest incidence of needle tip placement outside the center of the articular pillar. Importantly, in approximately 8% of blocks, a blood vessel was found with US to be directly overlying the articular pillar target site. The authors conclude that the 95% success rate achieved with US guidance is similar to that seen with fluoroscopic needle placement, while US affords the potential benefits of convenience, decreased radiation exposure to the patient and the operator, and the ability to visualize blood vessels potentially overlying target sites.
– Written by Michael Erdek
Financial & competing interests disclosure
NB Finnerup receives research funding from the Europain Investigational Medicines Initiative, which is a public–private partnership between the pharmaceutical industry and the EU. NB Finnerup has also received research funding from Grünenthal, served as a consultant for Astellas, Grünenthal and Pfizer, and has received honorarium from Norpharma. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
No writing assistance was utilized in the production of this manuscript.