Effects of diabetes duration and glycemic control on free radicals in children with type 1 diabetes mellitus

Parameters of lipid peroxidation, protein oxidation, and antioxidant defense systems were measured in blood samples from 47 children with type 1 diabetes mellitus and from 51 healthy controls, matched for age and sex. In the diabetic children, chemiluminescent assay of plasma superoxide anion gave photoemission (counts x 10(3), mean +/- SD) of 674 +/- 412, which were significantly higher than those in the controls (452 +/- 185; p <0.05). Plasma vitamin A levels in the diabetic children (243 +/- 90 microg/dl) were also higher than those in the controls (207 +/- 59 microg/dl, p <0.05). In a subgroup of 24 diabetic children with blood HbA1C levels >or=8.5%, plasma lipoperoxide (LPO) and vitamin E levels were higher (p <0.05) than those in 23 diabetic children with blood HbA1C levels <8.5%. In a subgroup of 26 children with diabetes duration >or=5 yr, plasma LPO levels were higher (p <0.05) than those in 21 children with diabetes duration <5 yr. These findings confirm the presence of oxidant stress in children with type 1 diabetes mellitus and demonstrate that certain indices of oxidant stress are influenced by the duration of diabetes and by the efficacy of glycemic control. These observations suggest that supportive therapy aimed at oxidative stress may help to prevent clinical complications in children with type 1 diabetes mellitus.     

Influence of blood lead concentration on the nerve conduction velocity in patients with end-stage renal disease

Diseases of the peripheral nervous system are the most prevalent in patients with end-stage renal disease (ESRD). Although increased blood levels of lead in ESRD have been reported, the role of lead remains to be elucidated. The purpose of this study was to determine the connection of blood lead concentration with peripheral nerve conduction velocity. One hundred ninety-eight healthy subjects (control group) and 68 patients with ESRD undergoing hemodialysis (ESRD group) were enrolled. Nerve conduction was measured within two hours after hemodialysis. Orthodromic sensory nerve action potentials and compound muscle action potentials were recorded on the median, ulnar, and radial nerves. Hemoglobin-corrected blood lead was significantly higher in ESRD patients than in controls (9.1+/-2.8 microgram/dL vs. 5.9+/-2.3 microgram/dL, p<0.001). 32.4% of 68 ESRD patients with diabetes mellitus were significantly related to poorer motor and sensory nerve conduction velocity (p<0.001). However, blood lead was not a significant predictor of the nerve conduction velocity (p>0.05). Our result suggested that even though the blood lead levels were high in ESRD, they were not associated with the decline of peripheral nerve function. Diabetes mellitus is a primary independent risk of neuropathy in ESRD patients.     

Effect of body temperature changes on evoked potentials

Short-latency somatosensory (SSEPs) and brainstem auditory evoked potentials (BAEPs) were recorded in 12 patients with fever due to respiratory infection (age, 44.3 +/- 20.9 years, mean +/- SD) to clarify the effect of body temperature change on conduction in the central somatosensory and brainstem auditory pathways. Subjects were studied during episodes of fever (37.9 +/- 0.8 degrees C) and after their body temperature had decreased (36.6 +/- 0.3 degrees C). The central conduction time (CCT), which is the peak latency between N 13 and N 20, was significantly longer after body temperature had decreased than during fever. Likewise the interpeak latency between waves I and V (I-V IPL) was significantly prolonged following decrease in body temperature. These results suggest that increases in body temperature have an effect upon conduction in the central somatosensory and brainstem auditory pathways.     

Event-related potential in patients with diabetes mellitus]

The event-related potential (ERP) was recorded for 24 patients with diabetes mellitus (age 67.5 +/- 8.5 years, mean +/- SD) and 28 healthy controls (age 61.0 +/- 10.6 years) to elucidate the involvement of the central nervous system (CNS) in diabetes mellitus. ERP was recorded during auditory discriminative tasks. The latencies of N100, P200, N200 and P300 from the Pz region were measured. Patients with diabetes mellitus showed significant prolongation of N200 and P300 latencies compared with the normal subjects, while no significant differences in N100 and P200 latencies were found between the two groups. In six of 24 patients, the P300 latency delayed beyond the 2SD of the appropriate age-related value estimated from the normal regression line. The delay of the P300 latency was not related to either the duration of illness, therapeutic methods, or metabolic control. From the present results, it would appear that higher brain function is impaired even in diabetic patients not manifesting overt CNS signs and symptoms.     

Electrophysiological comparison between patients with Binswanger's encephalopathy and Alzheimer's disease

Short-latency somatosensory (SSEPs), brainstem auditory evoked potentials (BAEPs) and event-related potentials (ERPs) were studied in 7 patients with Binswanger's encephalopathy, 12 patients with Alzheimer's disease and 17 normal subjects. Patients with Binswanger's encephalopathy showed significantly prolonged central conduction time (CCT) and P300 latency, and prolonged tendency of I-V IPL compared to those of normal subjects. In particular, CCT showed significant prolongation compared to that of patients with Alzheimer's disease. In patients with Alzheimer's disease, I-V IPL and P300 latency were significantly prolonged compared to those of normals although there was no significant difference in CCT between Alzheimer's disease and normal subjects. These results indicate some difference between Binswanger's encephalopathy and Alzheimer's disease from the electrophysiological aspects although both of these entities are characterized by progressive mental deterioration.     

Are low magnesium levels in type 1 diabetes associated with electromyographical signs of polyneuropathy?

OBJECTIVE: Our aim was to study the relationship between the magnesium status in type 1 diabetic patients and disturbances in nerve conduction velocity. Furthermore we wanted to investigate whether repletion of magnesium depletion could improve the decreased nerve conduction velocity measurements. In a cross-sectional study, 154 type 1 diabetic patients were screened for their erythrocyte magnesium content and an electrophysiological measurement of the peripheral nervous system was carried out. In a subsequent intervention study, out of this screened population, 23 type 1 patients, with disturbed nerve conduction velocity measurements and low erythrocyte magnesium levels [< 2.3 mmol/L) were given oral magnesium supplements, during 1 year. Twenty type 1 patients with identical characteristics served as controls. In the cross-sectional study disturbed nerve conduction velocities were found in the older patients, in patients with a longer duration of diabetes and a worse metabolic control. EMG polyneuropathy signs were significantly more frequent in diabetic patients with low erythrocyte Mg. The intervention study demonstrated that under unchanged metabolic control, supplementation with magnesium could improve nerve conduction, especially in younger patients with a shorter duration of diabetes. Erythrocyte Mg was lower in type 1 diabetic patients with polyneuropathy. Mg supplementation increasing Mg RBC might (possibly?) improve nerve conduction measured by electromyography at least in younger patients with a short duration of diabetes and presenting early signs of the neurological complication.     

Residual C-peptide production in type I diabetes mellitus. A comparison of different methods of assessment and influence on glucose control

The aims of the present study were to compare various methods for assessment of residual insulin production and to evaluate its role in the metabolic regulation in insulin-dependent, type I diabetes mellitus. Glycosylated hemoglobin (HbA1) was used as a measure of the long-term glycemic control. Twenty-eight patients with type I diabetes mellitus with onset before the age of 30 and with a duration of less than 6 years were studied. C-peptide in plasma in the fasting state, after glucagon stimulation, and the 24-hour urinary excretion were measured. Fasting plasma C-peptide was detected in 61%, and 39% showed a significant rise after glucagon stimulation. The increment correlated negatively with HbA1 (rs = -0.57, p less than 0.001), as did the 24-hour urinary excretion (rs = -0.61, p less than 0.001). The 16 patients with urinary C-peptide values of at least 1 nmol had a mean HbA1 of 8.9 +/- 0.3%, as opposed to 11.6 +/- 0.5% for those excreting less (p less than 0.001). Measurement of the 24-hour urinary excretion of C-peptide provides a reliable method for evaluating residual insulin secretion.     

Conduction velocity of motor nerve and cervical sympathetic and vagus nerve in streptozotocin diabetic rats

We investigated the conduction velocity of motor and autonomic nerves, motor nerve to foot interosseous muscle and cervical vagus and sympathetic nerve, in streptozotocin diabetic rats (1-3 months duration of diabetes) and compared it with that of age-matched controls. In diabetic rats, the motor nerve conduction velocity was significantly reduced but the conduction velocity of cervical vagus and sympathetic nerves was not reduced.     

Oral zinc therapy in diabetic neuropathy

The present double blind randomized study was conducted on 50 subjects; 20 age and sex matched healthy controls (Group--I); 15 patients of diabetes mellitus with neuropathy who received placebo for 6 weeks (Group--IIA); and 15 patients of diabetes mellitus with neuropathy who were given supplemental zinc sulphate (660 mg) for 6 weeks (Group--IIB). Serum zinc level, fasting blood sugar (FBS) and post prandial blood sugar (PPBS) levels and motor nerve conduction velocity (MNCV) were estimated on day 0 and after 6 weeks in all subjects. Serum zinc levels were significantly low (p < 0.001) in group IIA and IIB as compared to healthy controls (Group--I) at baseline. After 6 weeks the change in pre and post therapy values of FBS, PPBS and MNCV (median and common peroneal nerve) were highly significant (P = < 0.001) for group IIB alone with insignificant change (P = > 0.05) in group IIA. No improvement (P = > 0.05) in autonomic dysfunction was observed in either groups. Therefore, oral zinc supplementation helps in achieving better glycemic control and improvement in severity of peripheral neuropathy as assessed by MNCV.     

The usefulness of the brainstem auditory evoked potential in the early diagnosis of cranial nerve neuropathy associated with diabetes mellitus

BACKGROUND: An evaluation of the extent and mechanism of damage of the central nervous system in diabetes mellitus is of high value in current neurological research. Electrophysiological abnormalities are frequently present is completely asymatomatic diabetes mellitus (DM) patients. Limited data is available in the use of brainstem auditory evoked potential (BAEP) in DM. AIM: Is to evaluate the efficacy of BAEP as a method useful in the diagnosis of subclinical damage of the central nervous system in DM. MATERIAL AND METHOD: 67 diabetes and 32 healthy controls - age and sex matched - were chosen. The diabetes were of type I and II and more than or less than 10 years duration. The BAEP was elicited by using auditory stimulus by using Dantec Evomatic 4000 evoked potential machine. The latency of component response recored as waves I, III and V, interpeak latency (IPLs) I - III, I - V, III - V and amplitude of waves V. RESULTS: The difference was highly significant in the increased latency of waves I, III and V, interpeak latency (IPLs) I - III, I - V, III - V and amplitude of waves V of each type of diabetes as compared to control. Comparison of the type and duration of diabetes between each other showed no significant difference. CONCLUSION: BAEP recording can represent an objective, clinically useful and non invasive procedure to stress the early impairment both of the auditory nerve and of brainstem function.     

Peripheral neuropathy in patients with diabetes mellitus presenting as Bell's palsy

The aim of this study is to evaluate the peripheral nerves in diabetes mellitus with or without peripheral facial paralysis (PFP). A total of 49 diabetic patients with PFP within the last year (23 females, mean age 60.3 +/- 9.3), and 83 diabetic patients without PFP (41 females, mean age 59.5 +/- 9.9) were enrolled. The neurological examination, eye-blinking response, needle EMG and electrophysiological parameters of peripheral nerves were evaluated. The neuropathic pain, other positive and negative sensory symptoms were statistically more frequent in controls than the PFP group, while no difference was noted in total neuropathy score. Sural sensorial nerve action potential amplitudes were same in both groups, but median nerve amplitudes were significantly lower in the PFP group. It is suggested that PFP is not a part of multifocal neuropathy in diabetes mellitus. However, at least some parts of the nerve conduction studies were involved, focal neuropathies were more frequent while sensory neuropathies with small nerve fiber involvement were less frequent in diabetes patients with PFP.     

Advanced glycation endproducts in nondiabetic patients with obstructive sleep apnea

SUBJECT OBJECTIVE: The formation and accumulation of advanced glycation endproducts (AGEs) has been implicated in the progression of age-related diseases such as diabetes mellitus and atherosclerosis. We hypothesize that AGE concentrations may be increased in subjects with obstructive sleep apnea (OSA), a condition associated with increased oxidative stress. METHODS: One hundred nineteen nondiabetic patients with OSA and 234 age-matched healthy controls and 134 patients with type 2 diabetes were recruited for participation in the study. Serum AGEs were assayed by competitive enzyme-linked immunosorbent assay using a polyclonal rabbit antisera raised against AGE-RNase. RESULTS: Serum AGEs were increased in OSA subjects, as compared with controls, but were less increased than the AGEs of patients with type 2 diabetes (control: 3.22 +/- 0.54 unit per mL; OSA: 3.68 +/- 0.39; diabetes mellitus: 4.11 +/- 0.99; analysis of variance p < .01). In the subjects with OSA, serum AGEs correlated with the duration of nocturnal desaturation (r = 0.21, p = .025) and plasma total 8-isoprostane concentration, a biochemical marker of oxidative stress (r = 0.22, p = .015), but not with fasting glucose level. On general linear model univariate analysis, the association between serum AGEs and 8-isoprostane was independent of age, sex, body mass index, smoking status, and glucose. CONCLUSION: Serum levels of AGEs were increased in nondiabetic subjects with OSA and were associated with the severity of OSA. Whether increased AGE formation contributes significantly to the high cardiovascular risk associated with OSA remains to be determined.     

2型糖尿病患者的肺弥散功能检测分析(英)

目的：检测2型糖尿病患者的肺通气和弥散功能，探讨肺脏是否为糖尿病慢性病变的靶器官。方法： 对107名2型糖尿病患者行肺通气及弥散功能检测，并与61名年龄、性别匹配的健康者比较。糖尿病患者需行糖化血红蛋白（HbA1c）、尿白蛋白排泄率（AER）检测、眼底检查以及神经传导速度检查，以评价血糖控制水平以及糖尿病微血管病变状况。结果： 2型糖尿病组肺通气功能与正常对照组相比，无显著差异。2型糖尿病组一氧化碳弥散量（DLCO）及单位肺泡容积的一氧化碳弥散量（DLCO/VA）较对照组明显降低（P<0.05）。DLCO、DLCO/VA与微血管病变积分呈负相关（r分别为-0.291、 -0.324，P<0.01）。此外，DLCO/VA还与年龄、病程呈负相关（r分别为-0.269、-0.236，P<0.05）。结论： 2型糖尿病患者虽然肺通气功能基本正常，但有弥散功能受损，提示肺脏可能也是糖尿病慢性病变的靶器官之一。     

甲钴胺治疗新诊断2型糖尿病周围神经病变疗效观察

目的：了解甲钴胺对2型糖尿病周围神经病变的治疗效果。方法：收集住院的新诊断为2型糖尿病患者44例,做神经传导速度检查,与正常人30例比较。用甲钴胺治疗2周,复查神经传导速度,并与治疗前比较。统计学分析与对照组比较用独立样本t检验,治疗前后比较用配对t检验。结果：新诊断2型糖尿病患者神经传导速度较对照组明显降低（P〈0.05或0.01）;经甲钴胺治疗2周后,2型糖尿病组神经传导速度较治疗前明显增加（P〈0.05或0.01）。结论：新诊断2型糖尿病患者已经出现周围神经传导速度下降,甲钴胺治疗可以使其有所改善。     

The cutaneous silent period in diabetes mellitus

The cutaneous silent period (CSP) may be useful as a method for the evaluation of smaller and unmyelinated fiber dysfunctions. CSP refers to the brief interruption in voluntary contraction that follows strong electrical stimulation of a cutaneous nerve. The aim the present study is to establish whether CSP can be instrumental in the determination of diabetic neuropathy. The nerve conduction studies and CSP evaluations were both used in patients with Diabetes Mellitus and control group. All patients were given clinical neurological examinations for the determination of small-fiber neuropathy (SFN). The CSP values for patients with SFN were compared with values of those without SFN. The nerve conduction velocities had changed unfavorably in diabetic patients. No median nerve CSP reponse could be obtained in two of the diabetic patients. CSP latency (84.6+/-14.0) in diabetics was longer than controls (76.2+/-13.1) (p=0.018). The duration of CSP was similar for the two groups (p=0.46). The CSP latency showed a correlation with routine nerve conduction studies. While the CSP latencies (86.7+/-15.8) of patients who were clinically diagnosed with SFN were similar to the latencies (81.3+/-10.4) of patients without SFN (p=0.606), the duration of CSP (44.6+/-13.7) in patients with SFN was shorter than the duration (55.3+/-12.2) in patients without SFN (p=0.012). These results indicate that even though the CSP does not provide any advantage over routine electrodiagnostic studies in determining diabetic neuropathy, still it may be a useful method for the early detection of diabetic SFN.     

H-reflex latency and sensory conduction in the assessment of neuropathy in patients of chronic obstructive lung disease.

H-reflex latency, proximal conduction velocity and distal proprioceptive conduction velocity were studied along with distal motor and sensory conduction in 38 patients of chronic obstructive lung disease grouped according to age and duration of the disease, as well as in 35 age-matched smoker controls and 14 non-smoker controls. The mean values of all the parameters studied in all the patient groups were significantly different from those of the non-smoker control group. Smoker controls also showed significant abnormality in all the parameters except motor conduction velocity. Among the patients, significant abnormality (mean +/- greater than 2 SD) was seen in 44.7% in motor conduction, 86.8% in sural nerve distal latency, 97% in Ia conduction velocity, 78.9% in H-reflex latency and 60.5% in proximal conduction velocity, as compared to the non-smoker control values. Among the old patients with more than 10 years of the disease, 62.5% had all the parameters significantly abnormal. More than one parameter was affected in 97.4% of the patients. The intra-group and inter-group differences in all the parameters studied, except motor conduction velocity, were statistically significant indicating that age, chronicity of the disease and smoking can produce nerve conduction defects independently and collectively. It is suggested that though all parameters studied are highly sensitive to neuropathies, proximal H-latency studies are best suited for grading conduction defects in patients of chronic obstructive lung disease, since in many patients sural nerve action potential (52.63%) and distal H-reflex response for Ia conduction studies (81.52%) could not be elicited.(ABSTRACT TRUNCATED AT 250 WORDS)     

Central hypoxaemia in rats provokes neurological defects similar to those seen in experimental diabetes mellitus: evidence for a partial role of endoneurial hypoxia in diabetic neuropathy.

Endoneurial hypoxia has been put forward as a factor contributing to diabetic neuropathy. The aim of this study was to determine whether alterations in motor nerve conduction velocity, Na+/K(+)-ATPase activity and substance P content of nerve and skin tissue, characteristic of the diabetic rat, could develop in non-diabetic animals subjected to a central hypoxaemia for five weeks. Compared to normoxic controls, five weeks of central hypoxaemia caused a fall in motor nerve conduction velocity of 30% (P less than 0.01), a decrease in sciatic nerve substance P content (68%; P less than 0.001) combined with elevated substance P content per unit area foot skin (44%; P less than 0.01). This pattern of change is qualitatively similar to that seen in diabetic rats. The Na+/K(+)-ATPase activity, however, was unaltered by the hypoxic environment. These findings support strongly a partial role for hypoxia in the pathogenesis of diabetic neuropathy.     

Early peripheral nerve abnormalities in impaired glucose tolerance

Increased prevalence of impaired glucose tolerance (IGT) has been recently detected in patients with painful sensory neuropathy. To determine whether nerve abnormalities are present in IGT we investigated IGT subjects without clinical neuropathy. Nerve conduction studies (NCS) were performed in 12 subjects with IGT without symptoms and signs of neuropathy. The results were compared with those obtained from 12 patients with type 2 diabetes (DM) without clinical neuropathy and 12 healthy controls. Sensory NCS of the sural nerve were performed on different segments, the distal-leg (10 cm proximal to the lateral malleolus) and the proximal-leg segment (10 cm more proximal). The distal conduction velocity of the sural nerve was increased in IGT subjects, compared both to healthy controls and DM patients. No difference was found among the groups with respect to the sensory conduction velocity of the sural nerve fibers in the proximal-leg segment. A reduction of both distal and proximal amplitudes of the sural nerve action potentials was detected in DM patients compared with IGT subjects and controls. The abnormal conduction velocity in the distal segment of the sural nerve, observed in IGT subjects without clinical neuropathy, suggests that the myelin dysfunction of the distal sensory fibers represents the earliest detectable nerve response to the hyperglycemia. The reduced amplitude of the sural nerve action potential in asymptomatic patients with DM arises from the axonal degeneration and represents a more advanced stage of nerve disease.     

Incidence of subclinical trigeminal and facial nerve involvement in diabetes mellitus.

We investigated the frequency of subclinical trigeminal and facial nerve involvement in 40 patients with diabetes mellitus and without clinical signs of cranial nerve lesions. 60% of the patients had distal symmetric sensory polyneuropathy which was confirmed by nerve conduction studies. Trigeminal and facial nerve functions were evaluated electrophysiologically using the blink-reflex R1 component (BlinkR-R1), masseter reflex (MassR), the first exteroceptive suppression of the masseter muscle (Mass-ES1), and distal motor latency of the facial nerve (DML VII). Latencies were significantly prolonged for the BlinkR-R1 (p < 0.0001), the Mass-ES1 (p < 0.05), and DML VII (p < 0.005) in diabetics compared with controls. No significant difference was found for the MassR. Prolonged latencies (> mean + 2.5 SD of age-matched controls) were demonstrated for the Mass-ES1 in 12.5%, BlinkR-R1 in 10%, DML VII in 6.2%, and MassR in 5% in individual of patients. Our findings indicate that trigeminal and facial nerve involvement is not infrequent in diabetics, although it is significantly less frequent than limb nerve involvement.     

Testing of the refractory period in sensory nerve fibres is the most sensitive method to assess beginning polyneuropathy in diabetics.

INTRODUCTION: In patients with diabetes mellitus (DM) without any clinical signs of polyneuropathy neurophysiological examinations intend to find early involvement of peripheral nerves. Conventionally, nerve conduction velocity (NCV) measurements of sensory nerves are performed. The purpose of this study is to investigate wether refractory period measurements may be more sensitive. METHODS: We compared 30 IDDM/NIDDM diabetics without clinical signs of neuropathy (25 male, 5 female, age 45-73 years, mean 64.3 years) with age-matched controls. Sensible nerve conduction velocity (NCV) of radialis and suralis nerves were performed at 37 degrees C as well as double stimulations. The interstimulus interval were decreased stepwise by 0.2 ms beginning with 4.6 ms to determine the end of the relative refractory period. RESULTS: Statistically significant differences of NCV and refractory period were found. The most profound differences between diabetics and normals were seen in refractory period of n. suralis. Regarding the 95% percentile as cut-off value of the normal range, pathological NCV of N. suralis were found in 4 patients. Pathological refractory period, however, were found in 9 patients. CONCLUSION: Refractory period measurements of N. suralis are more sensitive than conventional NCV assessment in detection of beginning dysfunction in peripheral nerves of patients with diabetes mellitus without clinical signs of polyneuropathy.