This systematic review synthesizes literature describing prevalence, characteristics and prognosis of low back-related leg pain (LBLP) patients with neuropathic pain in primary care and/or similar settings. Inclusion and exclusion criteria were developed and used by independent reviewers to screen citations for eligibility. The initial search yielded 24,948 citations; after screening 12 studies were included. Neuropathic pain was identified by case ascertainment tools (n=5), by clinical history with examination (n=4), and by LBLP samples assumed neuropathic (n=3). Neuropathic pain prevalence varied from 19% to 80%. There was consistent evidence for higher back-related disability (n=3), poorer health-related quality of life (n=2) and some evidence for more severe depression (n=2), anxiety (n=3) and pain intensity (n=4) in patients with neuropathic pain. Results were less consistent when cases were identified through clinical history plus examination than those identified using case ascertainment tools. Prognosis (n=1) of LBLP patients with neuropathic pain was worse compared to those without, in all outcomes (leg pain intensity, leg and back-related disability, self-reported general health) except back pain intensity. No studies described prognostic factors. This systematic review highlights the evidence gap in neuropathic pain in LBLP in primary care, especially with respect to prognosis. PerspectivePatients with low back-related leg pain may have neuropathic pain. This systematic review emphasises the paucity of evidence describing the characteristics and prognosis of neuropathic pain in this patient population. Future research investigating prognosis of these M A N U S C R I P T A C C E P T E D ACCEPTED MANUSCRIPT3 patients with neuropathic pain is likely to contribute to better understanding and management. Key wordsLow back pain; leg pain; primary care; neuropathic pain; epidemiology M A N U S C R I P T A C C E P T E DACCEPTED MANUSCRIPT 4 IntroductionNeuropathic pain presents as one of the most challenging pain syndromes to identify and treat 52 . Patients with underlying neuropathic pain (considered to be pain caused by injury or disease to the somatosensory system 55 ) commonly self-report neuropathic characteristics such as prickling and/or burning sensations, and heat and pressure induced pain. The International Association for the Study of Pain (IASP) developed a grading system to assist researchers and clinicians to identify cases of neuropathic pain 55 . The grading system proposes that a patient presenting with pain, and with a plausible clinical history together with relevant neurological examination findings, meets the criteria for a working hypothesis of possible neuropathic pain 55 . With the addition of appropriate findings from diagnostic tests, a patient can meet the criteria for probable neuropathic pain. When clinical examination is not possible in epidemiological research, (for example, Torrance et al 54 andVanDenKerfhof et al 60 ) neuropathic case ascertainment tools use self-...

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Objectives: Little is known about the epidemiology of neuropathic pain in primary care patients consulting with low back-related leg pain. We aimed to describe prevalence, characteristics, and clinical course of low back-related leg pain patients with and without neuropathic pain, consulting with their family doctor in the United Kingdom. Materials and Methods: This was a prospective cohort study. Data were collected using a standardized baseline clinical examination and self-report questionnaires at baseline, 4, 12, and 36 months. We identified cases of neuropathic pain using 3 definitions: 2 based on clinical diagnosis (sciatica, with and without evidence of nerve root compression on magnetic resonance imaging), one on the self-report version of Leeds Assessment for Neurological Symptoms and Signs. Differences between patients with and without neuropathic pain were analyzed comparing each definition. Clinical course (mean pain intensity measured as the highest of leg or back pain intensity: mean of 3 Numerical Rating Scales, each 0 to 10) was investigated using linear mixed models over 36 months. Results: Prevalence of neuropathic pain varied from 48% to 74% according to definition used. At baseline, patients with neuropathic pain had more severe leg pain intensity, lower pain self-efficacy, more patients had sensory loss than those without. Distinct profiles were apparent depending on neuropathic pain definition. Mean pain intensity reduced after 4 months (6.1 to 3.9 [sciatica]), most rapidly in cases defined by clinical diagnosis. Discussion: This research provides new information on the clinical course of neuropathic pain and a better understanding of neuropathic pain in low back-related leg pain patients consulting in primary care.

Chronic constriction injury (CCI) of the sciatic nerve results in persistent mechanical hyperalgesia together with Fos protein expression in the lumbar spinal cord. We have examined the relationship between mechanical hyperalgesia and Fos expression within the lumbar spinal cord on days 14, 35 and 55 after either CCI or sham operation. To determine the role of NMDA receptor mechanisms in the maintenance of hyperalgesia and Fos expression, the NMDA antagonist MK-801 (0.3 mg kg-1 s.c.) was administered daily on days 28 to 34 after operation. CCI animals developed unilateral hind limb hyperalgesia that persisted unchanged from days 14 to 55 of the study. MK-801 treatment reduced hyperalgesia by 57% (p=0.02) on day 35 in CCI animals but did influence hyperalgesia at day 55. In the spinal cord, Fos positive cells were present bilaterally throughout laminae 3-10 at all time points examined in both CCI and sham group animals. Fos counts ipsilateral to the side of injury in laminae 3-10 correlated significantly with hyperalgesia scores in the CCI but not sham animals. MK-801 treatment resulted in a suppression of Fos expression in ipsilateral laminae 3-4 (p=0.0017) and laminae 5-10 (p=0.0026) of CCI animals on day 35. Fos expression in sham group animals was not inhibited by MK-801 treatment at day 35. These results indicate that Fos expression is maintained by differing mechanisms following nerve injury or sham operation. The functional consequences of Fos expression following nerve injury and sham operation are discussed.