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Many varieties of neuropathy occur with diabetes mellitus (DM) from different underlying mechanisms, the most common being a symmetrical, length-dependent, sensorimotor polyneuropathy (DSPN). A less frequent diabetic neuropathy which can cause severe morbidity, diabetic lumbosacral radiculoplexus neuropathy (DLRPN), is a painful, rapidly evolving, asymmetric, lower-limb, paralytic neuropathy associated with weight loss1. The name DLRPN emphasizes the association of this syndrome with DM and its sites of involvement (roots, plexus and nerves). The natural history and underlying mechanisms of DLRPN have been debated with various names reflecting different views that include: diabetic myelopathy2, diabetic amyotrophy3, Bruns-Garland syndrome4, diabetic mononeuritis multiplex5, proximal diabetic neuropathy6, diabetic lumbosacral plexopathy7, diabetic polyradiculopathy8 and multifocal diabetic neuropathy9. Regardless, in most discussions of DLRPN, pain is usually present. In early clinical descriptions of DLRPN, Chokroverty and colleagues state that this syndrome can be symmetrical, slowly progressive and occasional painless10. They and others suggest that the pathological basis of DLPRN is probably metabolic derangement10–13. Others note that the disease is usually asymmetrical and painful, presenting as a “mononeuritis multiplex” due to ischemic injury5. Asbury incorporates both concepts proposing that the acute and asymmetrical cases are due to ischemic injury whereas the slower, more symmetrical cases result from metabolic derangement and that “proximal (motor) diabetic neuropathy” encompasses a spectrum of disorders6. Additional authors note that cases of purely proximal diabetic motor neuropathies exist, but are poorly defined14. Recent studies report ischemic injury from microvasculitis as the pathophysiological basis of typical, painful, DLPRN1, 15–19. In contrast, diabetic patients with lower limb motor syndromes without pain have received little attention. Amato and Barohn highlight that motor polyradiculoneuropathies without pain do occur in DM20. Although they consider this painless syndrome could be a type of DLRPN, they question whether such cases are chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) occurring in diabetic patients, an association also suggested by others21–24. Their discussion rekindles interest into how to best classify diabetic patients with a motor predominant painless neuropathy. However, there has been no systematic evaluation of the clinical, electrophysiological, and pathological features of this painless syndrome. Here, we study a cohort of diabetic patients with a lower limb and motor predominant neuropathy without pain and compare this group to a cohort of previously studied DLRPN patients1. In order to formally answer if painless diabetic motor neuropathy is a variant of DLPRN, diabetic CIDP, or another entity, we ask 1) What are the clinical features of this painless syndrome? 2) What are the laboratory and electrophysiological findings? 3) What are the pathological features? As we believe the classification should be primarily based on the underlying disease mechanism, we place the most emphasis on pathological findings in this group compared to nerve biopsies from DLRPN, DSPN and CIDP.