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Aims To examine the natural history of chronic painful diabetic neuropathy (CPDN).
Methods A cross-sectional study of 350 people with diabetes was performed during 1998–1999 to assess the prevalence of CPDN in the community. Fifty-six patients with CPDN were identified and were followed up an average of 5 years later.
Results From the original cohort, 12 patients had died and 14 had moved away or were unable to participate in the follow-up study. Thus 30 patients with CPDN [21 male, mean (sd) age 68.6 years (9.4), mean (sd) duration of diabetes 15.4 years (8.7)] were re-assessed. Seven (23%) had been pain free for at least 12 months and 23 continued to report neuropathic pain of similar quality and severity [total McGill Pain Questionnaire Score median (interquartile range) at follow-up 22 (16–39) vs. 20 (16–33) at baseline, P = 0.3; mean (sd) visual analogue scale (VAS) score for pain over the preceding 24 h 5.3 cm (2.9) vs. 4.6 cm (2.5) at baseline, P = 0.1]. Only 65% had ever received treatment for CPDN despite 96% (22/23) reporting pain to their physician; 43.5% had received antidepressants, 17.4% anticonvulsants, 39% opiates and 30% had tried complementary therapies.
Conclusions The neuropathic pain of CPDN can resolve completely over time in a minority (23%). In those in whom painful neuropathic symptoms had persisted over 5 years, no significant improvement in pain intensity was observed. Despite the improvement in treatment modalities for chronic pain in recent years, patients with CPDN continue to be inadequately treated.
Re: Natural history of painful diabetic neuropathy
Small-fibre involvement in diabetic patients with neuropathic foot pain.
Vlckova-Moravcova E, Bednarik J, Belobradkova J, Sommer C. Diabet Med. 2008 Jun;25(6):692-9.
Quote:
AIMS: To assess small-fibre involvement in diabetic patients with neuropathic pain.
METHODS: Peripheral nerve function was assessed in 30 patients with Type 2 diabetes mellitus (T2DM, n = 24) or impaired glucose tolerance (IGT, n = 6), and clinical symptoms of neuropathic pain in the feet, using nerve conduction studies, autonomic tests, thermal quantitative sensory testing (T-QST) and quantification of intra- and subepidermal nerve fibre densities in skin punch biopsies.
RESULTS: Clinical signs of isolated small-fibre sensory involvement were present in 13 patients [pure small-fibre neuropathy (pSFN)], seven patients had isolated positive sensory symptoms without neurological deficits (pSFN-). Ten patients had concomitant electrophysiological and/or clinical signs of large-fibre sensory involvement [mixed-fibre neuropathy (MFN)]. Twenty-seven patients (90%) had both reduced skin innervation and abnormalities of the T-QST parameters. Two other patients displayed either abnormal skin innervation or T-QST, and only one patient had normal findings on both tests. The criteria of small-fibre neuropathy (SFN) were met in all 20 patients without large-fibre involvement. Small-fibre involvement was also present in the 10 MFN patients. Both T-QST and skin biopsy parameters revealed significant differences between these clinical subgroups, with increased severity of small-fibre involvement in the MFN group. Autonomic dysfunction was found in 43% of patients and did not correlate with either clinical, T-QST or skin biopsy data.
CONCLUSIONS: Although the exact mechanism of neuropathic pain in diabetic patients is not known, pain is almost invariably accompanied by small-fibre dysfunction and pathology irrespective of autonomic or large-fibre involvement.
Natural history of painful diabetic neuropathy
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