Height is an independent risk factor for neuropathy in diabetic men.

Height may increase the risk of diabetic polyneuropathy, but previous studies are inconclusive. Our purposes were to further examine the hypothesis that height (HT) is an independent risk factor for diabetic polyneuropathy and to determine which electrophysiologic measures are influenced by HT in diabetic subjects. We studied 170 Japanese American men (ages 43-73 years, mean 61) including: 69 diabetic men (mean HT 166 cm), 54 normal men (mean HT 167 cm), and 47 men with impaired glucose tolerance (IGT) (mean HT 164 cm), measuring 28 nerve conduction study (NCS) parameters. We used data from normal men in developing regression models to adjust NCS parameters for HT, age, and temperature. Factor analysis was employed to reduce the 28 NCS parameters to five physiologically meaningful factors, one of which, a factor representing median and peroneal sensory amplitudes, was significantly correlated with HT (r = -0.38, P = 0.0011) in diabetic men; taller subjects having smaller sensory nerve amplitudes. No significant correlation was found between this factor and body mass index. This factor had no correlation with HT in normal or IGT men. Our data do not confirm previous reports of associations between HT and slowed motor conduction velocities in diabetic subjects. This study does, however, support the hypothesis that HT is an independent risk factor for sensory polyneuropathy in diabetic subjects.

Dermatomal somatosensory evoked potentials: cervical, thoracic, and lumbosacral levels.

Somatosensory evoked potentials were recorded at the scalp to stimulation of the skin at C4, C5, C6, C7, C8, T2, T4, T6, T8, T10, T12, L2, L3, L4, L5, and S1 dermatomes and of the tibial nerve. Stimulation and recording techniques are described. Data were obtained from 41 normal subjects, 25 of which had all 16 dermatomes studied. Wave form descriptions include both typical and atypical presentations. Descriptive statistics for latency, amplitude, left to right comparisons, and level to level comparisons are given. Scalp response latencies for distal extremity dermatomes were well correlated with height but not with vertebral column length, whereas latencies for thoracic dermatomes were not well correlated with either height or vertebral column length. Since scalp response amplitude data were not normally distributed, they were logarithmically transformed and minimum and maximum limits for 1 S.D., 2 S.D., and 3 S.D. derived. Left/right amplitude ratios were similarly treated. Level to level comparisons were achieved with a Z score concordance analysis, which showed that the response values at one level can be used to predict the response values at another level.

Influences of height and gender on normal nerve conduction studies.

Our purpose was to examine the effects of gender on nerve conduction results in healthy subjects. Fifty-four men, mean age 60.2 years and mean height 167cm, were compared with 62 women, mean age 62.2 years and mean height 153cm. We studied median, ulnar, sural, peroneal, and tibial nerves. Analyzing the raw data, women had significantly faster conduction velocities than men for all nerves except median motor (p < 0.05) three of four sensory amplitudes were larger in women and two of four motor amplitudes were larger in men (p < 0.05). After adjustment of the data for height, most statistically significant differences in conduction velocity disappeared, although differences in amplitude persisted. We conclude that most gender differences in nerve conduction velocity can be largely explained by height, whereas amplitude differences persist despite correction for height, temperature, and age.

Factor analysis. A methodology for data reduction in nerve conduction studies.

Analyzing multiple nerve conduction study parameters individually is statistically problematic. The goal of this study was to develop a useful factor analysis scheme for assessment of nerve conduction study abnormalities in diabetic neuropathy. Hypotheses were: (1) factor analysis produces a few physiologically meaningful factors, (2) there are associations between factors and markers of diabetic severity and (3) clinical impressions are related to factor scores. We studied 165 Japanese-American men: 52 nondiabetic, 66 diabetic and 47 with impaired glucose tolerance. One author (W.C.S.) obtained 28 nerve conduction study parameters in all subjects and factor analysis extracted five factors from these parameters. These factors were related to conduction velocities (factor 1), distal ulnar function (factor 2), sensory amplitudes (factor 3), distal median function (factor 4) and distal peroneal function (factor 5); together, they explain 57% of the variability in the total data. Diabetic factor scores were significantly (P less than 0.05) below that of the controls and correlations with fasting blood sugar were significant at the P less than or equal to 0.001 level. Use of this technique promises to permit sensible analysis of large amounts of data in clinical studies of diabetic and other types of polyneuropathy.

Further studies on the electrodiagnosis of diabetic peripheral polyneuropathy using discriminant function analysis.

Discriminant function analysis can be useful when applied to multiple nerve conduction parameters for diabetic and nondiabetic subjects to reveal the essential dimension along which key neuropathic differences occur between these groups. In this study, 19 electrophysiologic parameters were used in a stepwise discriminant function analysis to reveal a highly significant dimension of intergroup differences between 67 diabetic and 75 normal adult Japanese-American males. The classification functions thereby derived are more sensitive and specific than those reported previously for this population. Furthermore, when 72 additional subjects with impaired glucose tolerance were examined, they showed considerable overlap with the normal and separation from the diabetic groups, respectively. Their intermediate position between normal and diabetics in the key discriminant dimension indicates that essential neuropathic change is, at most, incipient in this latter group.