OBJECTIVE To assess, in the general diabetic population, 1) the prevalence of painful neuropathic symptoms; 2) the relationship between symptoms and clinical severity of neuropathy; and 3) the role of diabetes type, sex, and ethnicity in painful neuropathy. RESEARCH DESIGN AND METHODS Observational study of a large cohort of diabetic patients receiving community-based health care in northwest England (n = 15,692). Painful diabetic neuropathy (PDN) was assessed using neuropathy symptom score (NSS) and neuropathy disability score (NDS). RESULTS Prevalence of painful symptoms (NSS ≥5) and PDN (NSS ≥5 and NDS ≥3) was 34 and 21%, respectively. Painful symptoms occurred in 26% of patients without neuropathy (NDS ≤2) and 60% of patients with severe neuropathy (NDS >8). Adjusted risk of painful neuropathic symptoms in type 2 diabetes was double that of type 1 diabetes (odds ratio [OR] = 2.1 [95% CI 1.7–2.4], P < 0.001) and not affected by severity of neuropathy, insulin use, foot deformities, smoking, or alcohol. Women had 50% increased adjusted risk of painful symptoms compared with men (OR = 1.5 [1.4–1.6], P < 0.0001). Despite less neuropathy in South Asians (14%) than Europeans (22%) and African Caribbeans (21%) (P < 0.0001), painful symptoms were greater in South Asians (38 vs. 34 vs. 32%, P < 0.0001). South Asians without neuropathy maintained a 50% increased risk of painful neuropathy symptoms compared with other ethnic groups (P < 0.0001). CONCLUSIONS One-third of all community-based diabetic patients have painful neuropathy symptoms, regardless of their neuropathic deficit. PDN was more prevalent in patients with type 2 diabetes, women, and people of South Asian origin. This highlights a significant morbidity due to painful neuropathy and identifies key groups who warrant screening for PDN.

The epidemiology and natural history of diabetic neuropathy (DN) remain poorly defined, partly because of poor patient selection and the variable criteria for what constitutes a diagnosis of DN. These aspects, as well as the pathogenesis of DN, will be covered in detail in this review. Studies have confirmed the major contribution of prolonged hyperglycemia in the etiopathogenesis of neuropathy and neuropathic pain (7–9,10), and this and other putative mechanisms will be discussed.

A 58-year-old man with type 2 diabetes mellitus has an asymptomatic plantar ulcer on the left foot that remains unhealed after four months. The ulcer measures 2 by 1 cm and is surrounded by callus under the first metatarsal head. Neurologic examination reveals loss of sensation of touch, pinprick, and vibration below the midcalf level bilaterally and the absence of ankle reflexes; the foot pulses are normal. How should this patient be evaluated and treated?