糖尿病周围神经病变的神经传导检查特点

目的 分析神经传导检查在糖尿病周围神经病变（DPN）中的特点,提高此方法诊断DPN的敏感性. 方法 对符合标准的213例患者的2283条神经行传统的神经传导、F波、H反射检查,并分析各条神经总的神经电生理检查情况. 结果 2283条神经进行常规神经传导检查结果显示,感觉神经传导速度（SCV）中,正中神经的异常率最高;运动神经传导速度（MCV）中,胫神经、正中神经异常率高;最长的胫神经运动神经神经传导异常率为47.45％,容易合并卡压的正中神经感觉神经传导异常率为46.83％,而腓肠神经感觉神经传导异常率最低（22.60％）.对有临床明确症状的21条神经进行神经传导检查,异常率可达76.19％.对感觉神经传导异常的尺神经进行运动神经传导检查,尺神经异常率为57.14％.常规神经传导检查,正中神经感觉神经传导异常率（46.83％）高于正中神经运动神经传导异常率（41.13％）.正中神经感觉神经传导异常者运动神经传导异常率为76.56％,正中神经运动神经传导异常者感觉神经传导异常率为89.63％.尺神经F波、胫神经H反射的异常率分别为25.83％、52.24％.结论 DPN具有长度依赖性、与临床表现一致、感觉重于运动、全长弥漫受累等特点,根据这些特点选择神经进行神经传导检查,可提高神经传导检查诊断DPN的敏感性.     

The electrophysiological findings of subclinical neuropathy in patients with recently diagnosed type 1 diabetes mellitus

To assess the prevalence of subclinical neuropathy within the first year of type 1 diabetes mellitus, 30 patients and 14 healthy subjects have been studied prospectively. The patients whose diabetes duration was longer than 1 year have been excluded from the study. Control group consisted of healthy volunteers. Subjective neuropathy symptoms, neurological examination, and electrophysiological findings were evaluated. All patients were clinically asymptomatic. At least two abnormal independent neurophysiological nerve parameters, which were required as the criterion of the peripheral nervous system subclinical involvement, were found as in 96.6% of diabetic patients in the first years. The percentages of abnormal electrophysiological parameters in different motor and sensory nerves were 86.7% in sural nerve, 83.3% in peroneal motor nerve, 73.3% in posterior tibial motor nerve, 66.7% in median motor nerve, 63.3% in ulnar motor nerve, 60% in median sensory nerve, and 46.7% in ulnar sensory nerve. While distal motor latency, F conduction time, and minimum F latency were the most frequent abnormal parameters in the upper extremity electrophysiological study; conduction velocity, minimum and mean F latencies, F conduction time were the most frequent abnormal parameters in the lower extremity. In all sensory nerve conduction studies, the most frequent abnormal parameter was the onset latency. In the autonomic sympathetic nerve electrophysiological study, plantar SSR latency was found significantly longer than the control group. In the lower extremity generally somatic motor fibres, sensory large fibres and sympathetic autonomic nerve fibres were found to be more affected. There is a correlation between HbA1c levels and nerve conduction velocity in posterior tibial and peroneal nerves. However, upper extremity nerve conduction dysfunction was not correlated with HbA1c value. Neither the duration of disease nor the age of the subject correlated with the nerve dysfunction.     

Nerve conduction velocity study of the upper limb in Raynaud's phenomenon

A prospective study of upper limb nerve conduction velocity was performed in 39 subjects (9 males, 30 females, mean age 46.8 years) with idiopathic Raynaud's phenomenon (RP) and 18 patients (3 males, 15 females, mean age 49.9 years) with RP secondary to systemic sclerosis (SS). Five subjects with idiopathic RP (13%) showed slowing of sensory conduction velocity (SCV) of the distal median nerve, associated with delayed distal motor latency (DML) of the same nerve in three patients, without clinical signs or symptoms of carpal tunnel syndrome (CTS). Three patients with secondary RP (17%) had reduction of SCV of the distal median nerve, associated with increased DML of the same nerve in one and with clinically silent slowing of SCV of the ulnar nerve in two (11%). Mean distal SCVs of the median nerve were significantly lower and mean DMLs were significantly higher in both groups with respect to a control group. Mean distal conduction of the ulnar nerve was significantly slower only in the group with secondary RP. No slowing was observed in the proximal part of any nerve. It seems likely that patients with idiopathic RP have slowing of conduction in the distal part of the median nerve, along the carpal tunnel. Since slowing does not occur in all parts of the nerves of the hand, it cannot be related to acral vasomotor disturbances, but to local or systemic factors. In contrast, patients with secondary RP had slowing of median and ulnar nerve conduction velocity, presumably related to subclinical distal peripheral neuropathy. A nerve conduction study of the hand could be useful in cases of suspected secondary origin of RP. In idiopathic RP, slowing of conduction may only affect the median nerve, whereas in secondary RP it may affect other nerves of the hand. Received: 13 October 1999 / Accepted: 6 March 2000     

The value of electromyographic studies in leprosy

In Dakar, during a definite period of time, all the new leprosy cases have been subjected to an electromyographic examination before treatment: a total of 37 patients and 518 examined nerves including all clinical forms: NCV: 33% of the examined nerves are found to be affected. The sensory nerves are frequently and early involved. In frequency order: sural (54%), posterior tibial (50%), sensory ulnar (35%), sensory median (29%), motor ulnar (28%), lateral popliteal (17%) and motor median (12%). The study of the SCV seems relatively more reliable than the sensory testing in the case of the ulnar and the median (75 comparisons): concordance in 69% of the cases; SCV only abnormal in 19%; sensory testing only abnormal in 12%. The EMG detection is superior to the motor testing and to the motor nerve conduction for the lateral popliteal (32 comparisons): 41% of concordant examination; 59% of differences among which 44% of anomalies revealed only by detection.     

Peripheral neuropathy in Behçet disease: an electroneurophysiological study

The aim of this study was to determine the peripheral nerve involvement electrophysiologically in Behçet patients without clinically evident neurological signs and symptoms. Sixty-three patients who fulfilled the International Study Group Classification Criteria for Behçet’s disease (BD) and 49 healthy control subjects were enrolled to the study. Conventional electrophysiological studies of peripheral nerves including F latencies were performed to all subjects. Thirty-one male and 32 female Behçet patients with a mean age of 33.6?±?11.1 years and (22 male and 27 female healthy control subjects with a mean age of 35.8?±?9.9 years were included to the study. All but four of the patients were active. In the BD group, electrophysiologically diagnosed neuropathy was detected in nine (14.28%) patients. One (1.58%) patient had sensorimotor polyneuropathy, one patient (1.58%) had sural and ulnar sensorimotor neuropathy, three (4.75%) patients had median and one patient (1.58%) had ulnar sensorimotor neuropathy. Sural nerve sensorial action potential was unobtainable in two (3.17%) patients and prolonged F latencies were observed in two (3.17%) patients. In the control group only one subject (2.4%) had low sural sensorial conduction velocity. The frequency of neuropathy was higher in the patients with BD when compared with the control subjects. Sensory nerves were affected more prominently than motor nerves. There was no relationship between the clinical and laboratory characteristics of the patients and the electrophysiologic findings. No significant difference was observed between the clinical parameters of the patients with and without electrophysiologically detected neuropathy, except the levels of disease duration (8.8?±?5.1 vs 5.28?±?4.3 years, respectively, p?相似文献   

Arthritis as presenting manifestation of pure neuritic leprosy--a rheumatologist's dilemma

OBJECTIVES: Leprosy classically presents with cutaneous and neurological manifestations. In diagnosed cases of leprosy, rheumatological involvement varies from 1% to 70%. A primary articular presentation without cutaneous manifestations is not yet known. Herein, we present our experience of five cases of leprosy that presented with predominant articular involvement in the absence of cutaneous manifestations. METHODS: The study was conducted in the Department of Clinical Immunology, Sanjay Gandhi Postgraduate Institute of Medical Sciences located in the state of Uttar Pradesh, one of the nine endemic states in India. Case records of patients with a definite diagnosis of leprosy were screened for the presenting manifestations, pattern of articular involvement, tenosynovitis, neurological signs and symptoms. Reports of nerve conduction study (NCS), nerve and synovial biopsy and other diagnostic tests were retrieved from laboratory records. Available radiographs were examined for evidence of juxta-articular osteopenia and erosions. RESULTS: Case records of 11,740 patients were screened, of which 28 had a diagnosis of leprosy. Twenty patients had presented with rheumatological complaints primarily. Five of the patients who presented with inflammatory arthritis with/without tenosynovitis (n = 4) and tenosynovitis alone (n = 1) had pure neuritic leprosy. All of these patients had thickened peripheral nerves and abnormal NCS. Sural nerve biopsy confirmed the diagnosis of leprosy in all these cases. CONCLUSION: A combination of tenosynovitis and thickened nerves in association with symmetric polyarthritis should raise a suspicion of leprosy even in the absence of cutaneous features.     

Cardiac autonomic neuropathy in patients with type 2 diabetes mellitus having peripheral neuropathy: A cross-sectional study

AimsThe aim was to see the frequency of CAN in type 2 diabetes mellitus patients with peripheral neuropathy, and its association with peripheral nerve conduction abnormalities.MethodsA cross-sectional study at BIRDEM was conducted in 62 patients with type 2 diabetes mellitus having electrophysiologically diagnosed peripheral neuropathy. CAN was detected by four clinical tests - heart rate response to deep breathing and valsalva maneuver, blood pressure response to standing and sustained handgrip.ResultThe study showed that all patients had CAN – 14.52% had early, 26.67% had definitive and 59.68% had severe CAN. Patients with severe CAN had significantly reduced nerve conduction velocity and amplitude of peripheral nerves (sural 4.36 ± 12.77 vs 9.65 ± 17.77 m/s, p = 0.009; 2.23 ± 1.89 vs 3.01 ± 2.76 mV, p = 0.001; peroneal 7 ± 4.23 vs 8.53 ± 5.99 mV, p = 0.047; tibial 0.008 ± 0.03 vs 0.026 ± 0.05 mV, p = 0.009) and higher serum triglyceride levels (221.17 ± 120.61 vs 197.76 ± 68.43 mg/dl, p = 0.033).ConclusionDiabetic patients with peripheral neuropathy have CAN, the severity of which increases with worsening neuropathy.     

Peripheral sensory nerve dysfunction in children and adolescents with Type 1 diabetes mellitus

The aim of the present study was to investigate peripheral sensory nerve function in diabetic children and adolescents without neurological symptoms. Ninety-two children and adolescents with Type 1 (insulin-dependent) diabetes mellitus (mean ± SD age: 14.2 ± 2.1 years, diabetes duration: 5.8 ± 3.0 years) and 80 healthy control subjects (age: 13.8 ± 2.2 years) matched for age, sex, body mass index, and height standard deviation score were involved in the study. Using a sine-wave transcutaneous stimulator, current perception threshold (CPT) testing at 2000, 250 and 5 Hz was performed on the left median and peroneal nerves. Diabetic children had increased CPT at 2000 Hz on both nerves as compared to the control group (median (interquartile range), median nerve: 2.43 (2.20–3.43) vs 1.80 (1.51–2.60) mA, p = 0.02; peroneal nerve: 3.51 (2.81–4.82) vs 2.70 (2.04–3.70) mA, p = 0.01). Twenty-one (23 %) of patients had CPT values higher than that of any healthy individual. Of these, elevated CPT was observed in 9 (9.8 %) patients on the median nerve, in 8 (8.7 %) patients on the peroneal nerve, and in 4 (4.3 %) patients on both median and peroneal nerves. Using multiple logistic regression analysis, worse long-term metabolic control and advanced puberty were independently predictive of peripheral sensory nerve dysfunction as the dependent variable (adjusted OR (95 % CI): 3.4 (1.2–6.2), p = 0.01, and 2.8 (1.1–5.6), p = 0.03, respectively). In conclusion, evidence of peripheral sensory nerve dysfunction is not rare in children and adolescents with diabetes and can be demonstrated by CPT testing in asymptomatic patients. Poor metabolic control is a risk factor for such subclinical neuropathy, and pubertal development may be involved in the pathogenesis of diabetic peripheral neuropathy. © 1998 John Wiley & Sons, Ltd.     

Peripheral and autonomic nerve function in 259 diabetic patients with peripheral neuropathy treated with ponalrestat (an aldose reductase inhibitor) or placebo for 18 months. United Kingdom/Scandinavian Ponalrestat Trial.

The potential of the aldose reductase inhibitor ponalrestat (600 mg daily) to ameliorate diabetic neuropathy was evaluated in 259 diabetes mellitus patients with peripheral neuropathy (defined by abnormal vibration perception threshold and abnormal peroneal motor conduction velocity) in a double-blind placebo-controlled clinical trial running for 18 months. Overall, no beneficial effect of ponalrestat on vibration perception thresholds, nerve conduction velocities, and nerve action potential amplitudes was detected. Because vibration perception thresholds and conduction velocities in median, peroneal, and sural nerves did not deteriorate in the placebo group, the potential of ponalrestat to prevent the expected deterioration in peripheral nerve function that occurs with an increased duration of diabetes was not tested. Patients with an abnormal heart rate reaction to standing (abnormal 30:15 ratio; n = 84) on ponalrestat did not deteriorate in this autonomic nerve function test as shown in those on placebo. In conclusion, ponalrestat did not improve peripheral nerve function in diabetes mellitus patients with signs of peripheral neuropathy, although it did ameliorate a deterioration in autonomic nerve function in diabetic patients with signs of autonomic neuropathy.     

Subclinical nerve dysfunction in children and adolescents with IDDM

Summary The purpose of this study was to investigate whether young insulin-dependent diabetic patients still develop peripheral nerve dysfunction when using modern multiple insulin injection therapy and to elucidate if this correlated with various disease parameters. Seventy-five patients, 7 to 20 years old with a duration of diabetes of more than 3 years, and 128 age-matched healthy control subjects underwent bilateral studies of median, peroneal, and sural nerves. Presence of diabetes lowered motor conduction velocity (p<0.0001), sensory conduction velocity (p<0.0001) and sensory nerve action potential (p<0.05) in all examined nerves. The mean change in conduction velocity induced by diabetes was –4.8 m/s in the peroneal nerve, –3.3 m/s in the median motor nerve, –2.6 m/s in the sural nerve and –2.4 m/s in the median sensory nerve. Fifty-seven percent of the patients had abnormal conduction (values outside 95% predictive interval) which was seen most often in the motor nerves, especially in the peroneal nerve (41%) followed by the median nerve (24%). In multiple regression analysis, long-term poor metabolic control and increased body length correlated with nerve dysfunction identified in most examined parameters. Three patients had signs or symptoms suggestive of neuropathy. It is concluded that despite modern multiple insulin injection therapy, with reasonably good metabolic control, nerve dysfunction is still common in children and adolescents with insulin-dependent diabetes mellitus. Risk factors are increased height and long-term poor metabolic control.Abbreviations IDDM Insulin-dependent diabetes mellitus - MIT multiple insulin injection therapy - MCV motor nerve conduction velocity - CMAP compound muscle action potential - DML distal motor latency - SCV sensory nerve conduction velocity - SNAP sensory nerve action potential     

Peripheral nerve abnormalities in newly-diagnosed diabetic children

Summary The prevalence of clinical and subclinical peripheral neuropathy was evaluated in 51 unselected children at the time of onset of type I diabetes. Twenty-eight patients were followed for one year in order to establish the influence of metabolic control on peripheral nerve function. Twenty-two % of the diabetic children showed nerve conduction abnormalities at the onset and 11.7% had clinical features of peripheral neuropathy. After one year of disease, these figures had changed to 14.3% and 7.1%. Five of 7 children with altered electrophysiological tests in the baseline assessment had had normalization of all parameters one year later. No correlations between insulin requirement and nerve conduction were found. The M value was significantly correlated only with median sensory conduction velocity (p<0.005). Significant correlations were demonstrated between HbA₁ concentration and both peroneal motor conduction velocity (p<0.025) and median sensory conduction velocity (p<0.005); these correlations were still present after one year of disease. In the first period of diabetic disease there is functional rather than structural damage of the nerves. The pathogenetic role of hyperglycemia is confirmed; however individual susceptibility to nerve dysfunction may play an important role in the nerve impairment in diabetes. This study was supported by the C.N.R. Project ‘Preventive and Rehabilitative Medicine’, Subproject ‘Degenerative Diseases of the Nervous System’; Project N. 84.02472.56.115.10324.     

Prevalence of peripheral neuropathy and associated risk factors in children with type 1 diabetes

AimTo detect the prevalence of diabetic polyneuropathy (DPN) in children with type 1 diabetes (T1D) and to identify associated the risk factors.MethodsThis cross-sectional study evaluated children aged between 2 and 16y with T1D for ≥2 y. Detailed neurological examination, neuropathy symptom score, and nerve conduction studies were done in all children to assess nerve dysfunction. Disease-related factors were evaluated for the prediction of neuropathy.ResultsSixty-six children (67% boys) were enrolled. The mean age at the time of diagnosis of T1D was 7.1 ± 2.6 years. The mean duration of diabetes was 4 ± 1.8 years. None of the patients had neuropathy on clinical examination or on the neuropathy symptom score. The prevalence of subclinical DPN was 18.2% (n = 12/66). The type of neuropathy was pure motor (n = 11, 91.6%) and mixed sensorimotor (n = 1, 8.3%). The common peroneal nerve was most commonly affected (n = 6, 50%), followed by the tibial (n = 4, 33.3%) nerve. The most common patterns of nerve involvement were mixed axonal and demyelination (n = 7, 58.3%), followed by axonal (n = 3, 25%) and demyelinating type (n = 2, 16.6%). Children with subclinical DPN had a significant reduction in velocity of tibial, common peroneal, median motor, and ulnar motor nerves; delayed latency in common peroneal, median motor, ulnar motor, and median sensory nerves compared to those without DPN (p value <0.05). A higher body mass index predicted the development of subclinical DPN (p value <0.05).ConclusionNearly one-fifth of children with T1D have subclinical neuropathy as early as two years of the disease. A higher body mass index is significantly associated with DPN. Electrophysiological studies should be performed regularly to screen for nerve dysfunction and its progression.     

Sj?gren Syndrome-Associated Small Fiber Neuropathy: Characterization From a Prospective Series of 40 Cases

We conducted the current study to analyze the clinical, immunologic, and neurophysiologic features of primary Sjögren syndrome (pSS)-associated sensory small fiber neuropathies (SFNs). Forty consecutive pSS patients with SFN were included. SFN was defined by the presence of suggestive sensory painful symptoms with normal nerve conduction studies and abnormal neurophysiologic tests for small nerve fibers or a low intraepidermal nerve fiber density at skin biopsy. Included patients were compared to 100 pSS patients without peripheral neuropathy.SFN patients were mainly female (92.5%). Age at pSS diagnosis was 55.3 ± 13.1 years, and at SFN diagnosis, 58.9 ± 11.8 years, with a median time to SFN diagnosis after symptom onset of 3.4 years. Clinical symptoms included burning pains (90%), numbness (87.5%), tingling (82.5%), pins and needles (72.5%), electric discharges (70%), and allodynia (55%). Dysautonomia included vasomotor symptoms (66%) and hyperhidrosis (47%). Abnormal neurophysiologic tests included laser evoked potentials (97.5%), thermal quantitative sensory testing (67.5%), and sympathetic skin reflex (40%). A skin biopsy revealed low intraepidermal nerve fiber density in 76% of the 17 tested patients.Compared to the 100 pSS patients without peripheral neuropathy, the 40 pSS-SFN patients were older at pSS diagnosis (55.3 ± 13.1 vs. 49.5 ± 14.9 yr; p = 0.03), and more often had xerostomia (97.5% vs. 81%; p = 0.01) and arthralgia (82.5% vs. 65.0%; p = 0.04). Immunologically, they were characterized by a lower prevalence of serum B-cell activation markers, that is, antinuclear antibodies (65% vs. 85%; p = 0.01), anti-SSA (42.5% vs. 71%; p = 0.002), and anti-SSB (17.5% vs. 39%; p = 0.017); rheumatoid factor (32.5% vs. 66%; p = 0.0005); and hypergammaglobulinemia (35% vs. 62%; p = 0.005).In conclusion, we report the main features of SFN in patients with pSS, the first such study to our knowledge. Our results show that patients with pSS-associated SFN are characterized by an older age at pSS diagnosis and a distinctive immunologic profile hallmarked by a lower frequency of serum B-cell activation markers.     

Exacerbation of chronic inflammatory demyelinating polyradiculoneuropathy during interferonbeta-1b therapy in a patient with childhood-onset multiple sclerosis

Interferonbeta-1b (IFNbeta-1b) is commonly used for relapsing-remitting multiple sclerosis (MS). We report a 23-year-old woman with childhood onset relapsing-remitting MS treated with IFNbeta-1b who developed overt chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) immediately after therapy. A baseline conduction study before IFNbeta-1b therapy revealed decreased motor conduction velocities and prolonged F wave latencies in several nerves, but there was no neurological sign indicating neuropathy. The existence of subclinical demyelinating neuropathy before IFNbeta-1b treatment was suggested, although the clinical criteria for CIDP were unfulfilled. Following two months of IFNbeta-1b therapy, numbness of her right upper and lower limbs progressively worsened and all tendon reflexes were depressed. Electrophysiologically, F waves were not evoked in any limbs except for the left ulnar and tibial nerves, which showed marked prolongation of F wave latencies. Moreover, subclinical hyperthyroidism developed in association with high titers of anti-thyroglobulin and antithyroid peroxydase antibodies, which were negative before IFNbeta-1b therapy. These findings indicated that peripheral demyelination worsened at the nerve roots after IFNbeta-1b therapy. In addition to the development of autoimmune thyroid disease, the patient now fulfilled the criteria for probable CIDP. Along with the results of a previous report demonstrating IFNbeta-induced CIDP development in patients with childhood MS, this case underscores IFNbeta as a potential risk factor for CIDP in patients with childhood onset MS.     

Near normoglycaemia improved nerve conduction and vibration sensation in diabetic neuropathy

Summary Twelve C-peptide deficient Type 1 (insulin-dependent) diabetic patients with abnormal peripheral nerve function were randomly assigned to continuation of conventional insulin therapy (CIT) or to continuous subcutaneous insulin infusion (CSII). There were no statistically significant differences at entry to the study between the two treatment groups in nerve function assessed by neurologic disability score, computer assisted sensation examination and measurements of amplitudes, distal latencies, F-wave latencies and somatosensory evoked potential latencies over the spine and conduction velocities of motor and sensory fibers of ulnar, median, peroneal, tibial, plantar and sural nerves. In addition, mean plasma glucose from 24 h profiles (12.5 vs 10.6 mmol/l, respectively) and HbA₁ (11.0 vs 11.6%, respectively) did not differ significantly between the two treatment groups at entry. Despite improved glycaemia from CSII in 5 patients (one dropped out of the study after 2 months) contrasted to CIT in 6 patients (5.3 vs 9.9 mmol/l, respectively, p=0.002) and HbA1 (8.5 vs 10.7%, respectively, p=0.002), there were no significant differences in measurements of peripheral nerve function after 4 months. After 8 months of improved glycaemia (4.4 vs 10.2 mmol/l, p=0.004) and improved HbA₁, (8.3 vs 10.5%, p=0.002), nerve conduction (p=0.03) and vibratory sensation threshold (p=0.002) were significantly better in patients treated with CSII than those who received CIT. The improvements in nerve function, although small, provide further evidence that some clinical endpoints of neuropathy are favorably influenced by improved control of glycaemia.     

No correlation between impairment of cerebrovascular reserve capacity and electrophysiologically assessed severity of neuropathy in noninsulin-dependent diabetes mellitus

INTRODUCTION: Microvascular abnormalities have an important role in the most frequent neurological complications of diabetes mellitus: neuropathy and cerebrovascular disorders. Severity of neuropathy as well as of cerebral microvascular damage can be quantitatively evaluated by instrumental methods like nerve conduction studies and transcranial Doppler. In the present study, we investigated whether a correlation exists between the severity of peripheral neuropathy and the impairment of cerebrovascular reserve capacity (CRC) in 20 patients with Type 2 diabetes mellitus. METHODS: CRC was measured by transcranial Doppler and defined as the maximal percentage increase in blood flow velocity in the middle cerebral artery within 20 min after an intravenous dose of 1000 mg of acetazolamide. Nerve conduction studies of the median, ulnar, peroneal, and sural nerves were performed. Severity of neuropathy was scored based on conduction velocities, amplitudes, and distal latencies. RESULTS: There was no correlation between the neuropathic score and CRC (R= .003, P= .99). Neither CRC nor the neuropathic score correlated significantly with age, duration of diabetes, and serum values of HbA(1c), glucose, insulin, von Willebrand factor, and alpha(2) - macroglobulin. Severity of neuropathy but not CRC correlated with microalbuminuria (R= .47, P= .038 and R= .14, P= .54). Improper treatment reflected by HbA(1c) >10% was associated with significantly more severe albuminuria, higher actual blood glucose level, higher von Willebrand factor activity, and marginally higher neuropathic score (21 vs. 13, P=.096), but was not associated with CRC (44% vs. 42%, P= .81). When duration of diabetes was dichotomized to 15 years and less or over 15 years, CRC was significantly smaller (35% vs. 50%, P= .036) and neuropathy was more severe in the subgroup with longer diabetes duration (19 vs. 11.5 points, P= .07). CONCLUSIONS: Although both CRC and peripheral nerve function are affected more severely in patients with long-lasting Type 2 diabetes mellitus, damage in the cerebrovascular system and in the long peripheral nerves occur independently. As in diabetes mellitus pathological changes in autonomic and large peripheral nerves develop simultaneously, decreased CRC in diabetic patients might be predominantly due to structural changes of resistance arteries or to metabolic than to neurogenic factors.     

Peripheral Neuropathy in Chronic Obstructııve Pulmonary Dıısease

ABSTRACT

The aim of this study was to evaluate the frequency and characteristics of peripheral nervous system involvement in chronic obstructive pulmonary disease and its relation with proinflammatory cytokines such as TNF-α, IL-6, IGF-1 and CRP. Forty chronic obstructive pulmonary disease patients with a mean age 62.8 ± 5.5 years and 33 healthy controls with a mean age of 61.8 ± 7.4 were included into this study. All subjects were evaluated with standard motor and sensory nerve conduction studies. Serum TNF-α, IL-6, CRP and IGF-1 were measured. The muscle strengths of three muscle groups (knee extensors, shoulder abductors and flexors) were assessed with a hand-held dynamometer. Peripheral neuropathy was detected at 15%% of chronic obstructive pulmonary disease patients. Ulnar motor and sensory nerves, left sural nerve distal latencies were found significantly prolonged than healthy volunteers (p == 0.011), peroneal nerve conduction velocities was found lower in patients than in healthy controls (p == 0.021), tibial nerve amplitudes was found lower in patients than healthy controls (p == 0.046). CRP and TNF-α were found significantly higher in chronic obstructive pulmonary disease patients and IGF-1 was found significantly lower in chronic obstructive pulmonary disease patients. There was no correlations between proinflammatory cytokines, CRP and electrophysiological findings. Left sural nerve's sensory nerve action potential amplitude was correlated positively with FEV₁%% (r == 0.425; p == 0.009). Muscle strength at the shoulder and knee were significantly reduced in patients with COPD when compared with controls. The frequency of neuropathy was higher in chronic obstructive pulmonary disease when compared with the healthy controls. Chronic obstructive pulmonary disease patients have subclinical peripheral nerve involvements.     

糖尿病周围神经病700例临床与神经电生理分析

目的探讨糖尿病周围神经病的临床和电生理特点,明确电生理检查的诊断价值。方法对700患者进行感觉和运动神经传导测定,240例患者进行针极肌电图测定。结果507例(724%)患者电生理检查异常,其中307例(606%)为多发性周围神经病,74例(146%)为腕管综合征;感觉神经传导异常程度重于运动神经,波幅的下降程度较传导速度减慢明显,下肢重于上肢(P<005)。仅有46%的患者针极肌电图异常而神经传导正常。结论糖尿病周围神经病的临床和电生理表现均以感觉神经受损为主;电生理检查有助于发现临床病变,但并非所有患者均能发现电生理异常;建议不将针极肌电图进行糖尿病周围神经病的筛查作为常规使用。     

Central motor conduction time in multiple sclerosis: an comparison of visual and somatosensory evoked potentials in relation to the type of disease course

The central motor conduction time (CMCT) was measured by electrical transcranial and spinal stimulation in 70 consecutively admitted patients with definite multiple sclerosis and 26 normal volunteers. The results of the patientgroup were compared with visual and somatosensory (median and tibial nerve) evoked potentials. The mean CMCT of the volunteers was 5.4 ms versus 11.1 ms in the patient group. In 55 of the 70 patients (79%) the CMCT was delayed (p less than 0.0001). VEP showed pathologic results in 67%, SEP of tibial nerve in 51%, SEP of median nerve in 41% of the patients. In 10 of the 70 cases (15%) only CMCT was pathologic. Especially in the first attack of the disease the CMCT (79% pathologic results) was superior in comparison to the evoked potentials (VEP and SEP together 43% pathologic findings). In our cases without clinical evidence of a pyramidal tract lesion a subclinical affection of this pathway could be determined in 69% by a pathologic CMCT. We regard this method therefore as a valuable tool in the early diagnosis of multiple sclerosis.     

Association of peripheral neuropathy with subclinical left ventricular dysfunction in patients with type 2 diabetes

ObjectivesThe impacts of diabetic peripheral neuropathy (DPN) on clinical manifestations of left ventricular (LV) function in patients suffering from type 2 diabetes mellitus (T2DM) and the preserved LV ejection fraction (LVEF) lack a full evaluation. This study was carried out to investigate the correlation of peripheral neuropathy with subclinical LV systolic dysfunction, accompanied by the exploration of the relevant clinical features of peripheral neuropathy in these patients.MethodsA retrospective analysis was conducted depending on the data of 101 consecutive inpatients with T2DM and preserved LVEF (all ≥ 50 %), without coronary artery disease and other histories of heart disease. All subjects received both a nerve conduction assessment and a speckle-tracking echocardiography examination. Global longitudinal strain (GLS) was conducted to assess the subclinical LV systolic function.ResultsForty-six (46 %) patients were diagnosed as DPN according to electrophysiological examination and clinical assessment. A significant difference was revealed in GLS between patients with and without DPN (16.5 ± 2.8 vs. 19.3 ± 3.4, p < 0.001). Multiple logistic regression analysis indicated GLS as one of the independent determinative factors for DPN (odds ratio, 0.68; P < 0.001). In addition, motor-sensory nerve conduction exhibited a significant positive correlation with GLS, which may not be revealed between the types of peripheral nerve damage.ConclusionsDespite the preserved LVEF, the subclinical LV myocardial dysfunction may have occurred in T2DM patients with DPN. Peripheral nerve conduction was significantly correlated with GLS. An early assessment of nerve conduction may exert a dual warning significance for the progression of subclinical LV dysfunction in asymptomatic patients with T2DM.