The sural sensory/radial motor amplitude ratio for the diagnosis of peripheral neuropathy in type 2 diabetic patients.

BACKGROUND AND AIM: The diagnosis of peripheral diabetic neuropathy is based on clinical examination. Nerve conduction study (NCS) enables earlier diagnosis, but it is demanding and requires specialised personnel. In an attempt to simplify the procedure, this study aimed to identify a new electrophysiological index, which might correlate with results obtained on standardised NCS in patients with long-standing type 2 diabetes. PATIENTS AND METHODS: Medical records of type 2 diabetic patients evaluated for neuropathy by NCS were reviewed retrospectively. This analysis included 104 patients (50 men, 54 women) with a mean age of 67.1±5.5 years and mean diabetes duration of 13.1±2.7 years. NCS was performed on radial, ulnar, sural, and peroneal nerves. Neuropathy was defined as impaired NCS. Ratios of neurophysiological parameters from these nerves were calculated and each of them was compared with diagnosis of neuropathy. RESULTS: The sural sensory/radial motor amplitude ratio had the best combination of sensitivity (85%) and specificity (71%) for neuropathy. It also remained the strongest independent predictor of neuropathy in multivariate regression analysis: low levels of this ratio yielded an odds ratio of 7.7 for neuropathy. CONCLUSIONS: The sural sensory/radial motor amplitude ratio has a high sensitivity and a moderately high specificity for the diagnosis of neuropathy, low levels being associated with a nearly eightfold increase in the risk for neuropathy. These results encourage further evaluation of this and other electrophysiological indices to enable wider availability of NCS.

Apolipoprotein E and first-ever ischaemic stroke in Greek hospitalized patients.

The association between apolipoprotein E (ApoE) polymorphism and stroke is still controversial. This study investigated the potential association between ApoE genotypes and stroke subtypes, and risk factors for ischaemic stroke in Greek patients hospitalized with their first-ever ischaemic stroke. One hundred patients (70 men and 30 women; mean age +/- SD 60.7 +/-9.8 years) were included in the study. The control group comprised 96 age- and sex-matched healthy volunteers. Cerebral infarction was classified as atherothrombotic, cardioembolic or lacunar small-vessel stroke. The three common ApoE alleles (E2, E3 and E4) were determined using the semi-nested polymerase chain reaction. No significant difference in the ApoE alleles was found between patients and controls. Similarly, there was no significant association between ApoE alleles and stroke subtypes, common risk factors for ischaemic stroke and neck vessel stenosis. Although the sample size was small, these results do not support a role for ApoE polymorphism in the pathogenesis of ischaemic stroke.

Use of the new indicator test (Neuropad) for the assessment of the staged severity of neuropathy in type 2 diabetic patients.

UNLABELLED: The new indicator test for sudomotor function (Neuropad) has been shown to represent a highly sensitive and reproducible tool for the diagnosis of diabetic peripheral neuropathy. This study aimed to examine the utility of the indicator test in the assessment of the staged severity of neuropathy in patients with type 2 diabetes mellitus. The study included 120 type 2 diabetic patients (58 men) with a mean age of 67.3+/-5.9 years and a mean diabetes duration of 13.1+/-3.2 years. Neuropathy was diagnosed and staged by clinical examination and nerve conduction study, according to the Michigan classification system. Patients were also examined with the indicator test, applied on the plantar aspect of the feet. Time until complete colour change of the test was recorded and stratified into deciles according to the spread of measurements in the study population. Neuropathy was staged as class 0 in 37 patients, class 1 in 44 patients, class 2 in 28 patients and class 3 in 11 patients. Time until complete colour change was 436.5+/-62.9, 740+/-88.1, 1192.5+/-161 and 1817.3+/-127.4 seconds in patients staged as class 0, 1, 2 and 3 respectively (p=0.001). Use of a threshold lower than 530 seconds until complete colour change had 97% sensitivity and 100% specificity for diagnosis of class 0 neuropathy. Use of a threshold lower than 1000 seconds until complete colour change had 100% sensitivity and 97% specificity for class 1 neuropathy. A threshold lower than 1440 seconds had 93% sensitivity and 100% specificity for class 2 neuropathy. A threshold above 1440 seconds had 100% sensitivity and 99% specificity for class 3 neuropathy. A highly significant (Kendall's tau-b=0.848, p=0.001) correlation was shown between time until complete colour change of the test and Michigan class of neuropathy. CONCLUSIONS: It appears that the indicator test contributes substantially to the assessment of the staged severity of neuropathy in patients with type 2 diabetes mellitus. There is excellent agreement between the indicator test and the Michigan classification system. These results suggest a role for the indicator test in the assessment of diabetic neuropathy.

Evaluation of a new indicator test for sudomotor function (Neuropad) in the diagnosis of peripheral neuropathy in type 2 diabetic patients.

UNLABELLED: Sudomotor neuropathy is associated with reduction of plantar sweating and contributes to the pathogenesis of diabetic foot ulcers. The aim of the present study was to evaluate the new indicator test for sudomotor function (Neuropad) in the diagnosis of peripheral neuropathy among type 2 diabetic patients. This study included 104 type 2 diabetic patients (51 men) with a mean age of 64.2+/-5.6 years and a mean diabetes duration of 12.8+/-3.7 years. Peripheral neuropathy was diagnosed by means of the Diabetic Neuropathy Index (DNI). Sudomotor neuropathy was assessed by means of colour change in the indicator test. Peripheral neuropathy was diagnosed in 71 patients (68.3 %). Sudomotor neuropathy was diagnosed in 67 patients (94.4 %) with peripheral neuropathy and in 10 patients (30.3 %) without peripheral neuropathy (p=0.0001). Compared with DNI, sensitivity of the indicator test for diagnosing peripheral neuropathy was 94.4 % and specificity was 69.7 %. Overall prevalence of neuropathy was higher using the indicator test (77 patients, 74.0 %) than using the DNI (71 patients, 68.3 %). Time until complete colour change of the indicator test was 23.8+/-6.7 min in patients with peripheral neuropathy and 7.7+/-1.2 min in patients without peripheral neuropathy (p=0.001). Among patients with peripheral neuropathy, time until complete colour change of the indicator test was 14.2+/-1.9 min in those with a DNI value between 2.5 and 4.5, while it was 32.8+/-2.6 min in those with a DNI value between 5 and 8 (p=0.003). CONCLUSIONS: Use of the new indicator test has a very high sensitivity in detection of diabetic peripheral neuropathy. Sudomotor dysfunction can be demonstrated in a considerable part of patients with normal clinical examination. Time until complete colour change of the indicator test is associated with severity of peripheral neuropathy.

Partial depletion and multiple deletions of muscle mtDNA in familial MNGIE syndrome.

OBJECTIVE: To describe the unique combination of partial depletion and multiple deletions of mitochondrial DNA (mtDNA) on muscle DNA analysis of three siblings with mitochondrial neurogastrointestinal encephalomyopathy (MNGIE). BACKGROUND: MNGIE is a relatively homogeneous autosomal recessive disorder characterized by gastrointestinal dysmobility, ophthalmoparesis, peripheral neuropathy, mitochondrial myopathy, and altered white matter signal at brain imaging. Muscle multiple mtDNA deletions have been found in about half of the described cases. METHODS: We studied three affected siblings (two were monozygotic twins) born to nonconsanguineous parents. Muscle mtDNA was investigated by quantitative Southern and Slot blot techniques and by PCR analysis. Morphologic confirmation in the muscle tissue was achieved by using in situ hybridization with a mtDNA probe complementary to an undeleted region and by DNA immunohistochemistry. RESULTS: All three patients showed ragged red (RRF) and cytochrome c oxidase-negative fibers, as well as partial deficiency of complexes I and IV. Southern and Slot blot analyses showed mtDNA depletion in all patients. Multiple mtDNA deletions were also detected by PCR analysis. In situ hybridization demonstrated an overall signal weaker than controls, with a relatively higher signal in RRF. Antibodies against DNA showed a decreased cytoplasmic network. CONCLUSIONS: The muscle histopathology and respiratory chain enzyme defects may be accounted for by the decreased mtDNA amount and by the presence of mtDNA deleted molecules; however, relative levels of mtDNA seem to correlate with life span in these patients. The combination of partial depletion and multiple deletions of mtDNA might indicate the derangement of a common genetic mechanism controlling mtDNA copy number and integrity.