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Objective: The aim of the study was to demonstrate abnormalities of motor conduction of the tibial nerve across the tarsal tunnel in type 2 diabetes. Design: One hundred twenty-four consecutive patients (mean age = 66.6 yrs, 62.1% male) with distal symmetric diabetic polyneuropathy clinically diagnosed were prospectively enrolled. Nerve conduction studies of deep peroneal, tibial, superficial peroneal, medial plantar, and sural nerves and standard needle electromyography in the lower limbs were performed. Demographic, anthropometric, and clinical findings were collected. Results : Motor conduction velocity of the tibial nerve across tarsal tunnel was slowed in 60.5% of patients; another 4% showed conduction block across tarsal tunnel without reduction of motor conduction velocity. Overall percentage of abnormalities across tarsal tunnel (64.5%) exceeds that of the sensory conduction velocities of proximal sural and superficial peroneal nerves. Abnormal tibial motor conduction velocity across tarsal tunnel represents the most common abnormality among all motor nerve conduction study parameters and significantly correlates with hemoglobin level, diabetic neuropathic index score, and diabetic complications frequency. Conclusions : Tibial conduction abnormalities across tarsal tunnel are the most sensitive motor parameter in distal symmetric diabetic polyneuropathy, second only to conduction abnormalities of sensory/mixed distal nerves of the feet. The use of nerve conduction studies across tarsal tunnel of the tibial nerve may be useful in the electrophysiological protocol to confirm the diagnosis of distal symmetric diabetic polyneuropathy. [ABSTRACT FROM AUTHOR]

Objective: To compare the prevalence of diabetes in a consecutive sample of patients with ulnar neuropathy at the elbow (UNE) with that in patients with carpal tunnel syndrome (CTS) and to assess differences in demographic, clinical, and electrophysiologic findings between diabetic, idiopathic, and posttraumatic UNE., Design: Six thousand eight hundred seventy-one and 434 consecutive patients diagnosed with CTS and UNE, respectively, were admitted to an outpatient electromyography service between 1995 and 2006. Twenty-six UNE and 452 CTS patients also had diabetes., Results: Prevalence of diabetes in UNE was 6.0% and did not differ from that in CTS (6.6%); there were more male diabetic UNE patients (61.5%) than diabetic CTS patients (35.8%). There was no difference in occupation, duration of symptoms, association with CTS, polyneuropathy, and many neurographic findings of the ulnar, median, and radial nerves between diabetic and idiopathic or posttraumatic UNE patients when UNE groups were matched by sex and age, except for differences in sensory action potential amplitudes of diabetics vs. the other two groups., Conclusions: The prevalence of diabetes is the same in UNE and CTS patients. The patients with UNE and diabetes are clinically and electrophysiologically indistinguishable from other groups of UNE patients, except for a reduction in sensory action potential amplitudes in the diabetic UNE group, presumably owing to diabetic polyneuropathy. Subjects with UNE and diabetes could therefore be treated in the same way as patients with idiopathic forms.

Background and Purpose: Endothelium-derived NO is formed from L-arginine by endothelial NO synthase (eNOS) encoded by the NOS 3 gene on chromosome 7. Because several studies have indicated that NO plays a key role in the development of the atherosclerotic process, we investigated whether common variants in the eNOS gene are associated with an increased risk of plaque on carotid arteries., Methods: We studied 375 subjects attending the hypertension center of our institution to be screened for arterial hypertension. The examined subjects were classified according to the presence of carotid plaques (intima-media thickness >/=1.5 mm), and 2 intronic (CA and 27-bp repeats) polymorphisms and 1 exonic (Glu298Asp) polymorphism of the eNOS gene were explored., Results: Only the Glu298Asp polymorphism of eNOS was associated with the presence of carotid plaques (P:<0.05). In particular, there was an excess of homozygotes for the Asp298 variant among subjects with carotid plaques, whereas the number of subjects who had the Glu298 allele in exon 7 of the eNOS gene was equally distributed in both study groups. Interestingly, the risk of having carotid plaques was increased approximately 3 times in subjects who were homozygotic for the Asp298 variant compared with subjects who were homozygotic for the Glu298 variant and was independent of the other common risk factors (age, blood pressure, and smoking)., Conclusions: Homozygosity for Asp298, a common variant of the eNOS gene, is an independent risk factor for carotid atherosclerosis in this study population.