Keywords Diabetic neuropathy Spinal cord Regional anesthesiaTo the Editor:I read with interest the clinical report entitled ‘‘Sub-clinical neuropathy in diabetic patients: a risk factor forbilateral lower limb neurological deficit following spinalanesthesia?’’ by S.D. Angadi and A. Garde, published inthe February 2012 issue of the Journal of Anesthesia.Although I agree with the authors about the fact that dia-betic patients may be at an increased risk of neurologicalinjury after regional anesthesia, I would like to make twocomments about this clinical report.First, in a previous report [1], I included the doublecrush hypothesis (DCH) as a possible factor (among sev-eral) to explain nerve insult after epidural anesthesia indiabetic patients. In 1973, Upton and McComas [2] laun-ched the following hypothesis: patients with carpal tunnelsyndrome or ulnar nerve neuropathy present not onlycompressive lesions at the wrist or elbow but also evidenceof damage at the level of the cervical roots of the samenerve. They called this the DCH.Later, in a retrospective study, Hebl et al. [3] applied theDCH to diabetic peripheral neuropathy (DPN). Theyreported that patients with pre-existing neural diabeticcompromise might be more susceptible to injury whenexposed to a secondary insult at another site, such astrauma, ischemia, and toxic compromise. Nevertheless,there is no evidence-based work in the literature to confirmthe hypothesis of Hebl et al. [3] regarding DPN. Further-more, diabetes is a generalized disease, and the vascularand metabolic mechanisms associated with DPN arecomplex and completely different from nerve entrapment.Despite the fact that the DCH has been accepted in manyexperimental and clinical reports, studies are needed toconfirm this hypothesis. In the literature, modern trendsshow that there is controversy about the DCH, and recentstudies seem to dismiss this interpretation of nerve injury[4]. Furthermore, a focal compression site on a nerveinfluences other regions on the same nerve according to alinear relationship. Thus, damage could be related to DCHat another site on the same nerve [4]. Accordingly, DCH isless likely to be involved as a damage mechanism afterneuraxial anesthesia in patients with DPN. Moreover,secondary neurologic damage after neuraxial anesthesia indiabetic patients could be explained by mechanical trauma,neuronal ischemia, or local anesthetic toxicity. Thus, theserisk factors can influence patient outcome, even though thecourse of spinal anesthesia appears uneventful [1, 4].Second, DPN is one of the most common forms ofneuropathy. There is some evidence that vascular dys-function (microangiopathy), driven by metabolic changes,is an important cause of DPN [1, 5]. Although these vas-cularand metabolic mechanisms have been proposed [1, 5],a complete understanding of its pathogenesis remainselusive [5]. All studies have focused mainly on DPN, andcentral nervous system involvement has been largelyoverlooked [5]. Selvarajah et al. [5] reported that centralnervous system involvement could be seen early in patientswith subclinical DPN. Using magnetic resonance imaging,they demonstrated that the cervical spinal cord index wassignificantly reduced in patients with clinical DPN.Moreover, they demonstrated that this spinal cordinvolvement is an early process which is present not only in