Neuropathic pain following spinal cord injury (SCI) is notoriously difficult to treat and is a high priority for many in the SCI population. Resolving this issue requires animal models fidelic to the clinical situation in terms of injury mechanism and pain phenotype. This Review discusses the means by which neuropathic pain has been induced and measured in experimental SCI and compares these with human outcomes, showing that there is a substantial disconnection between experimental investigations and clinical findings in a number of features. Clinical injury level is predominantly cervical, whereas injury in the laboratory is modeled mainly at the thoracic cord. Neuropathic pain is primarily spontaneous or tonic in people with SCI (with a relatively smaller incidence of allodynia), but measures of evoked responses (to thermal and mechanical stimuli) are almost exclusively used in animals. There is even the question of whether pain per se has been under investigation in most experimental SCI studies rather than simply enhanced reflex activity with no affective component. This Review also summarizes some of the problems related to clinical assessment of neuropathic pain and how advanced imaging techniques may circumvent a lack of patient/clinician objectivity and discusses possible etiologies of neuropathic pain following SCI based on evidence from both clinical studies and animal models, with examples of cellular and molecular changes drawn from the entire neuraxis from primary afferent terminals to cortical sensory and affective centers. © 2016 Wiley Periodicals, Inc.
Methylprednisolone is a corticosteroid medication used in acute traumatic spinal cord injury (SCI) to tackle secondary injury cascades. Its use in acute SCI has been the subject of controversy for over 30 years. The second National Acute Spinal Cord Injury Study (NASCIS-2) demonstrated a small benefit of methylprednisolone, 1 though this conclusion was derived from a post hoc subgroup analysis. 2 Studies that followed did not reach the same conclusion and reported potential adverse effects of the drug. 3 However, the 2017 AOSpine guideline continues to recommend high-dose methylprednisolone within 8 hours postinjury, 4 based on a meta-analysis with rigid inclusion criteria. 5 This Journal Club article reports on a study from Liu et al., 6 who have attempted to resolve this controversy. The study provides an elegant example of meta-analytic methods and has important implications for neurologic clinical practice. Hypotheses and design Does acutely administered methylprednisolone improve neurologic recovery following traumatic SCI? To answer this important question, Liu et al. 6 performed a meta-analysis of clinical trials and observational studies. The use of a meta-analysis is important here as it synthesizes all available evidence and provides the highest possible strength of recommendation for its use in clinical management. Methods This meta-analysis followed the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines, which is an evidence-based minimum set of items for reporting in systematic reviews and meta-analyses. 7 A comprehensive literature search was performed of PubMed and the Cochrane Library, and articles were further restricted to those published in journals included in the Science Citation Index. In addition to traditional database searches, manual searches of the reference lists of all of the relevant studies, review articles, and conference abstracts were also conducted. Searching multiple databases is recommended when conducting metaanalyses in order to identify all the relevant articles. For instance, the Cochrane Handbook suggests the use of MEDLINE (accessible through PubMed) and the Cochrane Central Register of Controlled Trials. 8 Other commonly used databases include the Web of Science and Google Scholar. 9
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