We report the features of non-length dependent small fiber neuropathy (SFN) and compare them to those with distal length-dependent SFN. In a series of 224 consecutive neuropathy patients, we evaluated 44 patients with SFN diagnosed in the presence of both symptoms and signs. Eleven were classified as non-length dependent SFN. Disease associations were Sjögren's syndrome (two patients), impaired glucose tolerance, rheumatoid arthritis, hepatitis C virus, Crohn's disease, and idiopathic (five patients). In the 33 patients with distal SFN, the age of onset was significantly older and more had impaired glucose metabolism (16/33). In both groups, pain was mainly characterized as burning, but patients with non-length dependent SFN more often reported an "itchy" quality and allodynia to light touch.

of a levodopa-nonresponsive PD patient who failed to improve after pallidotomy also failed to improve after DBS STN. 10 Our patients were all levodopa-responsive and, aside from a single patient, improved after their pallidotomy.There are several reasons why postpallidotomy STN DBS may result in less robust motor improvement. First, there is an obvious referral bias toward patients who were not satisfied after their pallidotomy, either for objective or subjective reasons. This may represent a more aggressive disease process or more atypical course. The pre-and postpallidotomy off drug UPDRS scores, however, were similar in this group of pallidotomy DBS patients compared to our pallidotomy population in general (n ϭ 89). 1 Dyskinesia scores were also similar. Second, electrophysiological recordings, on which we greatly rely for placement, can be altered in the STN following GPi ablation, possibly resulting in suboptimal placement. 11 Random suboptimal placement is possible in either group. Third, there could be redundant physiological effects that would mitigate against subsequent improvement after the second procedure. A single study that simultaneously implanted GPi and STN DBS found that combined stimulation was no more effective than STN stimulation alone. 12 Fourth, we present a relatively small number of patients and the results could be different with a larger sample.Overall, the small corpus of literature on the efficacy and safety of postpallidotomy STN DBS is mixed. We recommend prudence when considering DBS in this population. REFERENCES

As the occurrence of restless legs syndrome (RLS) in diabetes is controversial, the aim of this study was to assess the prevalence of RLS in a cohort of patients with diabetic neuropathy and to analyze the features of the associated neuropathy. We investigated the occurrence of RLS diagnosed in accordance with the criteria of the International Restless Legs Syndrome Study Group in a cohort of patients with polyneuropathy and mononeuropathy multiplex associated with diabetes mellitus (DM), or impaired glucose tolerance (IGT), or impaired fasting glucose (IFG) in a retrospective study. RLS was present in 33/99 patients with neuropathy associated with DM/IGT/IFG (84 with distal polyneuropathy and 15 with multiple mononeuropathy). Comparing patients with or without RLS, small fiber sensory neuropathy was more common in the RLS patients (15/33 vs. 15/66), as were symptoms of burning feet (10/33 vs. 6/66). In several patients, RLS was responsive to neuropathic pain medications. The frequent occurrence of RLS in association with thermal dysesthesias may reflect the involvement of small sensory fibers in the form of hyperexcitable C fibers or A-delta fiber deafferentation. We suggest that RLS may be triggered by abnormal sensory inputs from small fibers, especially involved in neuropathy associated with DM/IGT/IFG. Our data show that RLS is a relevant feature of diabetic neuropathy, as a frequent and potentially treatable manifestation of small fiber involvement in the course of DM and IGT/IFG.

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RLS is frequent in painful polyneuropathy and is significantly associated with decreased small fiber input, thus nociceptive deafferentation may represent a factor interacting with RLS "generators," possibly at spinal level. We suggest that overactivity of the spinal structures implicated in RLS may be triggered by nociceptive deafferentation in a subgroup of patients with painful polyneuropathy. Our findings, prompting a mechanistic characterization of RLS associated with painful polyneuropathy, have to be confirmed in a prospective study.