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PubMed1993

Painful neuropathy and foot ulceration in diabetic patients.

OBJECTIVE: To examine the prevalence of painful symptoms in neuropathic patients with or without foot ulceration. It has been suggested that there are two clinical presentations of sensory diabetic neuropathy with little overlap: painful (acute or chronic) and painless with recurrent foot ulceration. RESEARCH DESIGN AND METHODS: We examined three groups of diabetic patients matched for age and duration of diabetes--24 without neuropathy on clinical grounds (mean age 56.1 yr [range 38-76 yr], diabetes duration 12.6 yr [0.4-40 yr]), 30 with neuropathy (mean age 55.3 yr [range 21-73 yr], diabetes duration 17.3 yr [range 0.2-61 yr]), and 40 with neuropathic foot ulceration (mean age 58.1 yr [range 41-72 yr], diabetes duration 18.5 yr [range 1-46 yr])--and compared them with 20 healthy subjects (mean age 50 yr [range 37-69 yr]). For evaluation of neuropathy, the neuropathy symptom score, neuropathy disability score, and vibration perception threshold were measured. RESULTS: No difference existed between the neuropathic and foot ulcer groups in the neuropathy symptom score (4.2 +/- 3.9 [mean +/- SD] vs. 2.5 +/- 2.1, NS) and neuropathy disability score (15.1 +/- 5.7 vs. 16.8 +/- 6.1, NS), but the vibration perception threshold was lower in the neuropathic group (30.1 +/- 13.4 vs. 40.5 +/- 13.8 V, P < 0.001). Painful symptoms (neuropathy symptom score > 3), either in the past or during the time the study was conducted, had been experienced by none of the control subjects, 7 (29%) of the nonneuropathic group, 18 (60%) of the neuropathic group, and 17 (43%) of the foot ulcer group (NS for the last two groups), and were present at the time of examination in 13 (43%) of the neuropathic group and in 13 (33%) of the foot ulcer group (NS in all groups). Duration of symptoms was < 12 mo in 12 (40%) neuropathic and 15 (38%) foot ulcer patients (NS). CONCLUSIONS: We conclude that painful symptoms are frequent in diabetic neuropathy, irrespective of the presence or absence of foot ulceration and that these symptoms can occur at any stage of the disease. These results suggest that there is a spectrum of neuropathic syndromes from the painful to the patients with foot ulceration, and that much overlap exists.

Adult↗
PubMed1994

Risk factors for distal symmetric neuropathy in NIDDM. The San Luis Valley Diabetes Study.

OBJECTIVE: To investigate risk factors for distal symmetric (sensory) neuropathy among prevalent cases of non-insulin-dependent diabetes mellitus (NIDDM) in a population-based study in southern Colorado. RESEARCH DESIGN AND METHODS: Prevalent neuropathy was identified in 77 of 277 people with NIDDM by a standardized history and neurologic examination. Fifteen known or suspected risk factors for neuropathy were determined without knowledge of neuropathy status. RESULTS: Older age at examination, longer duration of diabetes, higher glycohemoglobin percentage, lower fasting C-peptide, insulin use, and presence of retinopathy and nephropathy (microalbumin > or = 200 micrograms/ml) were all significantly associated with neuropathy. Sex, ethnicity (Hispanic versus non-Hispanic white), height, systolic blood pressure, peripheral vascular disease, cigarette and alcohol use, and serum lipid levels were not significantly associated with neuropathy. In a multivariate logistic model, increasing age (odds ratio [OR] = 1.3, 95% confidence interval [CI] = 1.1-1.6), longer duration of diabetes (OR = 1.3, CI = 1.0-1.6), increased glycohemoglobin percentage (OR = 1.5, CI = 1.1-2.1), and insulin use (OR = 2.8, CI = 1.3-6.1) were associated with neuropathy. Retinopathy (OR = 3.0, CI = 1.2-7.7), but not nephropathy, was important when added to this model. CONCLUSIONS: Worse glycemic control and insulin use were independently associated with neuropathy in people with NIDDM. Whether insulin use represents another marker for severity of the metabolic disturbance or is an independent risk factor for neuropathy requires further study. We could not confirm associations of neuropathy with height, with nephropathy, or with retinopathy, independent of duration of diabetes.

Adult↗
PubMed1994

A practical two-step quantitative clinical and electrophysiological assessment for the diagnosis and staging of diabetic neuropathy.

OBJECTIVE: Early diagnosis of distal symmetric sensorimotor polyneuropathy, a common complication of diabetes, may decrease patient morbidity by allowing for potential therapeutic interventions. We have designed an outpatient program to facilitate diagnosis of diabetic neuropathy. RESEARCH DESIGN AND METHODS: Patients are initially administered a brief questionnaire and screening examination, designated the Michigan Neuropathy Screening Instrument (MNSI). Diabetic neuropathy is confirmed in patients with a positive assessment by a quantitative neurological examination coupled with nerve conduction studies, designated the Michigan Diabetic Neuropathy Score (MDNS). In this study, 56 outpatients with confirmed type I or II diabetes were administered the standardized quantitative components required to diagnose and stage diabetic neuropathy according to the San Antonio Consensus Statement (1) and the Mayo Clinic protocol (2). These same patients were then assessed with the MNSI and the MDNS. RESULTS: Of 29 patients with a clinical MNSI score > 2, 28 had neuropathy. Twenty-eight patients with an MDNS of > or = 7 had neuropathy, while 21 non-neuropathic patients had a score < or = 6. Of 35 patients with diabetic neuropathy, 34 had > or = 2 abnormal nerve conductions. Twenty-one normal patients and one patient with neuropathy had < or = 1 abnormal nerve conduction. CONCLUSIONS: The results indicate that the MNSI is a good screening tool for diabetic neuropathy and that the MDNS coupled with nerve conductions provides a simple means to confirm this diagnosis.

Adult↗
PubMed1994

Postural instability in patients with diabetic sensory neuropathy.

OBJECTIVE: Recent survey evidence suggests that sensory ataxia due to diabetic neuropathy may be a more frequent and serious problem than is commonly recognized. This view is further supported by research that confirms the major contribution of the somatosensory system to the control of posture. We therefore sought to determine the effects of significant diabetic distal symmetrical polyneuropathy on the control of posture. RESEARCH DESIGN AND METHODS: Fifty-one subjects, divided into three groups, participated in this study. Seventeen had diabetes and significant sensory neuropathy, 17 had diabetes and no neuropathy, and 17 had neither diabetes nor neuropathy. The subjects were matched across groups, and stringent exclusion criteria were applied. Postural stability during quiet standing was measured using a force platform. In addition to electrophysiological and quantitative sensory tests of neuropathy, a number of physical and functional characteristics were measured for all subjects. RESULTS: Postural instability was found to be significantly associated with sensory neuropathy, but not with diabetes per se. Patients with sensory neuropathy demonstrated between 66 and 117% more instability than did control subjects (depending on the testing condition). Based on multiple linear regression analyses, the most significant correlates of instability were the quantitative sensory measures of neuropathy and age. CONCLUSIONS: The loss of sensory perception secondary to diabetic distal symmetrical sensory neuropathy has a markedly detrimental effect on postural stability. The deficit is greatest when visual or vestibular cues are absent or degraded. Patients with neuropathy need to be informed of the postural consequences of this condition to limit the potential morbidity caused by falls.

Aging↗
PubMed1997

Risk factors for diabetic peripheral sensory neuropathy. Results of the Seattle Prospective Diabetic Foot Study.

OBJECTIVE: To identify risk factors for diabetic lower-extremity peripheral sensory neuropathy prospectively in a cohort of U.S. veterans with diabetes. RESEARCH DESIGN AND METHODS: General medicine clinic outpatients with diabetes were followed prospectively for the development of insensitivity to the 5.07 monofilament on the foot. RESULTS: Of 775 subjects, 388 (50%) had neuropathy at baseline. Of the 387 subjects without neuropathy at baseline, 288 were followed up, and of these, 58 (20%) developed neuropathy. Multivariate logistic regression modeling of prevalent neuropathy controlling for sex and race revealed independent and significant associations with age, duration of diabetes, glycohemoglobin level, height, history of lower-extremity ulceration, callus, and edema; an independent and inverse correlation was noted with ankle-arm index. Risk factors for incident neuropathy in multivariate logistic regression included age, baseline glycohemoglobin level, height, history of ulcer, and CAGE screening instrument alcohol score; current smoking and albumin level were inversely associated with risk. CONCLUSIONS: Poorer glycemic control increases the risk of neuropathy and is amenable to intervention. Height and age directly increase risk of neuropathy and may help identify patients at risk. A proportion of neuropathy in diabetic veterans is probably due to or worsened by alcohol ingestion. Neuropathy was less common in current smokers than subjects not currently smoking.

Age Factors↗
PubMed2006

Neuropathy among the diabetes control and complications trial cohort 8 years after trial completion.

OBJECTIVE: To evaluate the impact of prior intensive diabetes therapy on neuropathy among former Diabetes Control and Complications Trial (DCCT) participants. RESEARCH DESIGN AND METHODS: At the conclusion of the DCCT, subjects in the intensive group were encouraged to maintain intensive therapy, and subjects in the conventional group were encouraged to begin intensive therapy. Thereafter, we annually assessed neuropathy as part of the Epidemiology of Diabetes Intervention and Complications (EDIC) study. Neuropathy was defined using the Michigan Neuropathy Screening Instrument (MNSI). We recorded potential adverse consequences of neuropathy. RESULTS: At the first EDIC examination, 1,257 subjects participated in the neuropathy assessment. Consistent with DCCT results, the former intensive group showed a lower prevalence of neuropathy than the conventional group based on positive questionnaire (1.8 vs. 4.7%; P = 0.003) or examination (17.8 vs. 28.0%; P < 0.0001) results. Despite similar levels of glycemic control, symptoms and signs of neuropathy remained less prevalent among the former intensive group compared with the conventional group. At the beginning of the EDIC study, prior intensive therapy reduced the odds of having symptoms and signs of neuropathy using MNSI criteria by 64% (P = 0.0044) and 45% (P < 0.0001), respectively, with similar odds reductions observed for both neuropathic symptoms (51%, P < 0.0001) and neuropathic signs (43%, P < 0.0001) across 8 years of EDIC follow-up. CONCLUSIONS: The benefits of 6.5 years of intensive therapy on neuropathy status extended for at least 8 years beyond the end of the DCCT, similar to the findings described for diabetic retinopathy and nephropathy.

Diabetes Mellitus, Type 1↗
PubMed2000

Can diabetic neuropathy be prevented by angiotensin-converting enzyme inhibitors?

The incidence of diabetes and its complications is increasing to staggering proportions. Presently the WHO estimates an overall prevalence of 130 million, but by 2025 there will be 300 million individuals with diabetes mellitus. The incidence of diabetic neuropathy approaches 50% in most diabetic populations; there is no treatment, and its consequences in the form of foot ulceration and amputation are financially punishing for health care providers. Attempts to develop treatments have faltered for want of an understanding of the aetiology of diabetic neuropathy. As a consequence, 1999 saw the demise of two further compounds: recombinant growth factor by Roche-Genentech and the aldose reductase inhibitor zopolrestat, by Pfizer, both had reached phase III clinical trials. They joined an impressive list of at least 30 other compounds which have reached phase III clinical trials and failed to establish efficacy. The need to establish a viable treatment for human diabetic neuropathy is absolutely paramount. To provide a rational answer as to whether angiotensin-converting enzyme (ACE) inhibitors can prevent human diabetic neuropathy, two major issues need addressing: 1) Does vascular dysfunction cause human diabetic neuropathy? 2) Can ACE inhibitors ameliorate diabetic vascular dysfunction and hence neuropathy? Epidemiological studies support a strong association between neuropathy, retinopathy and nephropathy. Microangiopathy is deemed as the root cause of both nephropathy, and retinopathy and mounting evidence provides support for a vascular basis of diabetic neuropathy. ACE inhibitors appear to correct many of the abnormalities associated with the vascular dysfunction found in diabetes. Thus effective ACE inhibition impacts very positively on cardiovascular outcomes in patients with ischaemic heart disease, particularly in diabetic patients. ACE inhibition also prevents the development and progression of incipient and established diabetic nephropathy and delays progression of background retinopathy. Quinapril improves measures of diabetic autonomic neuropathy. Our recent study has demonstrated a significant improvement in peripheral neuropathy following 12 months of treatment with the ACE inhibitor trandolapril.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2000

Compressive neuropathies of the ulnar nerve at the elbow and wrist.

Compressive neuropathy of the ulnar nerve in the upper limb is a common problem that frequently results in severe disabilities. At the elbow, Lundborg concluded that the nerve was "asking for trouble" because of its anatomic course through confined spaces and posterior to the axis of elbow flexion. Normally, the ulnar nerve is subjected to stretch and compression forces that are moderated by its ability to glide in its anatomic path around the elbow. When normal excursion is restricted, irritation ensues. This results in a cycle of perineural scarring, further loss of excursion, and progressive nerve damage. Initial treatment for the acute and subacute neuropathy at the elbow is nonsurgical. Rest and avoiding pressure on the nerve may suffice, but if symptoms persist, splint immobilization of the elbow and wrist is warranted. For chronic neuropathy associated with muscle weakness, or neuropathy that does not respond to conservative measures, surgery is usually necessary. A variety of surgical procedures have been described in the medical literature, and deciding on the most effective procedure can be difficult considering the excellent results claimed by proponents for each. Unfortunately, there is a paucity of information based on prospective randomized clinical studies comparing the different surgical methods. Dellon attempted to provide some guidelines by reviewing the data in 50 articles dealing with nonsurgical and surgical treatment of ulnar neuropathies at the elbow. In order to provide uniform data, he re-interpreted the data in these articles using his own system for staging nerve compression. He reported that treatment was most successful for mild neuropathies, a conclusion few would challenge. Excellent results were also achieved in 50% of patients with mild neuropathies that were treated nonsurgically and in more than 90% treated by surgery, regardless of the procedure. For moderate neuropathies, nonsurgical treatment was generally unsuccessful, as were decompressions in situ. Medial epicondylectomies were effective in only 50% of cases and they had the highest recurrence rate. Regarding ulnar nerve transpositions, each method has its proponents, usually based on the training and experience of the surgeon. Subcutaneous transposition is the least complicated. It is an effective procedure, particularly in the elderly and in patients who have a thick layer of adipose tissue in their arms. It is the procedure of choice for repositioning the nerve during surgical reductions of acute fractures, arthroplasties of the elbow, and secondary neurorrhaphies. Intramuscular and submuscular transpositions are more complicated procedures. Although proponents of intramuscular transposition report favorable results, the procedure can result in severe postoperative perineural scarring. Submuscular transposition has a high degree of success and is generally accepted to be the preferred procedure when prior surgery has been unsuccessful. I also prefer it as the primary procedure for most chronic neuropathies that require surgery. Compressive neuropathies of the ulnar nerve in the canal of Guyon are less common, but they can also result in significant disabilities. Compression can occur in 1 of 3 zones. Zone 1 is in the most proximal portion of the canal, where the nerve is a single structure consisting of motor and sensory fascicles, and zones 2 and 3 are distal where the ulnar nerve has divided into motor and sensory branches. The clinical picture correlates with the zone in which compression occurs.

Cubital Tunnel Syndrome↗
PubMed2000

Diabetic autonomic neuropathy.

OBJECTIVE: The diabetic autonomic neuropathy is a poorly studied subject in our medical literature. This study is aimed at investigating the presence of diabetic autonomic neuropathy in a group of Sudanese diabetic patients and its relationship to factors like glycemic control, duration of diabetes and presence of peripheral neuropathy. METHODS: During one year we examined 120 diabetic patients and an age-matched control group of 42 by applying a battery of 5 cardiovascular autonomic tests, beside a full history and clinical examination. The patients were also tested for glycemic control and presence of peripheral neuropathy. RESULTS: Diabetic autonomic neuropathy was diagnosed in 48 patients (40%) of a mean age of 48.411 + 12.50 years, type 1/2 diabetes was 10/38, mean duration of diabetes 16.2 + 7.3 years, 41 with poor glycemic control (81%) and peripheral neuropathy was present in 32 patients (66%). We found a significant association between diabetic autonomic neuropathy and prolonged duration of diabetes (P<0.001), poor glycemic control (0.01>P>0.001) and presence of peripheral neuropathy (0.02>P>0.01). CONCLUSION: Diabetic autonomic neuropathy (both asymptomatic and symptomatic) is a common problem among our diabetic patients. It is significantly associated with prolonged duration, poor control of diabetes and presence of peripheral neuropathy. We need to augment the awareness of diabetes care providers to the occurrence, and peculiar features and tests of this syndrome.

Adult↗
PubMedDate not supplied

Hypothesis: low Na/K-ATPase activity in the red cell membrane, a potential marker of the predisposition to diabetic neuropathy.

OBJECTIVES: The development of diabetic complications does not depend entirely on diabetes duration and control. Predisposing and aggravating factors, either constitutional or environmental, seem to play a role. We have previously observed that polyneuropathy is more frequent, of earlier onset, and more severe among North African insulin-dependent diabetic patients than among Europeans matched for sex, duration and control of diabetes. The Na/K-ATPase activity displays sex and ethnic differences and a dysfunction of this enzyme is probably involved in the pathogenesis of diabetic neuropathy. We have therefore postulated that the predisposition of some diabetic patients to develop a polyneuropathy could be related to a low Na/K-ATPase activity. DESIGN: Red cell membrane Na/K-ATPase activity was studied in European men presenting with insulin-dependent diabetes mellitus for more than 15 years. 10 patients with neuropathy were matched to 10 patients void of neuropathy on duration of diabetes and HbA1c values. Thirteen healthy European men and 13 North African men born and living in France were also studied. RESULTS: Na/K-ATPase activity was lower in patients with neuropathy (200 +/- 31 vs 289 +/- 42 nmol Pi.mg protein-1.h-1 mean +/- SD; p less than 0.05). When compared to that of 13 European healthy men, Na/K-ATPase activity was lower in the whole group of diabetic patients but appeared to be in the normal range for patients without neuropathy and decreased in those with neuropathy. The 13 North African healthy men had lower values than the European healthy men (227 +/- 46 vs 298 +/- 60 nmol Pi.mg protein -1.h-1, p less than 0.05). CONCLUSION: Red cell membrane Na/K-ATPase activity is low in insulin dependent patients with neuropathy compared to those without neuropathy. This finding probably reflects a constitutional difference. This association could be explained if red cell and nerve membrane Na/K-ATPase abnormalities behave similarly according to glycaemic control in diabetic subjects. It is suggested that the predisposition to neuropathy of North African insulin-dependent diabetic patients may be related to lower Na/K-ATPase activity. A high level of activity of this enzyme may protect from diabetic neuropathy. This enzyme activity could be a marker of predisposition towards diabetic polyneuropathy.

Adult↗
PubMed2003

The prevalence of diabetic peripheral neuropathy in an outpatient setting.

This study was undertaken to clinically estimate the prevalence of diabetic peripheral neuropathy amongst patients attending an outpatient clinic and to evaluate their risk factors for developing peripheral neuropathy. It was a cross-sectional study of 134 diabetes mellitus patients who attended the Primary Care Clinic, University Hospital, Kuala Lumpur. The patients were interviewed for their demographic data, past and present medical/surgical history, social history, personal habits and symptoms of peripheral neuropathy. Foot examination and clinical neurological tests were conducted and the presence of peripheral neuropathy was assessed. The main outcome measures were the Neuropathy Symptom Score and the Neuropathy Disability Score. The prevalence of diabetic peripheral neuropathy was found to be 50.7%. Peripheral neuropathy was related to the age of the patient and the duration of diabetes but did not seem to be significantly related to diabetic control. To conclude, there was a high prevalence of peripheral neuropathy amongst the diabetics in this study. These patients developed peripheral neuropathy at a younger age and shorter duration of diabetes compared to a similar study that was done in the UK.

Adolescent↗
PubMed1996

[Functional, organic and histologic changes in the stomach in diabetic patients in relation to the presence of diabetic neuropathy].

Functional, organic and histological gastric changes were investigated in relation to the presence of autonomic neuropathy in 105 noninsulin-dependent diabetics (20 with autonomic neuropathy, 35 with peripheral neuropathy, 30 with both peripheral and autonomic neuropathy and 20 without neuropathy) and 40 control persons. The diagnosis of autonomic neuropathy was assessed by parasympathetic test of cardiovascular reflexes and peripheral neuropathy by classical neurological examination and EMG (Electromyogram). All subjects were examined by radiologic and endoscopic methods with gastric biopsy specimens for histologic and immunocytochemical analysis. The results of investigation showed that functional abnormalities, hiatus hernia (55%) and pylorospasm (50%) occur more frequently in patients with autonomic neuropathy. Gastritis, duodenal ulcer (5%) and polyps (25%) are significantly more frequent. Atrophic gastritis type A (20%) was more frequent in diabetics with autonomic neuropathy than in other diabetics, as well as other types of gastritis. Immunocytochemical analysis showed the presence of rare, pale ECL (Extensor Caudae Lateralis) cells in corpus and pale, hypogranulated G cells in antrum and hyperplasia and metaplasia of EC (Embryonal carcinoma) cells in antrum of the stomach. Functional, organic and histologic changes in patients with diabetic autonomic neuropathy suggest that the systemic investigation of the Gut is very important in such patients.

Diabetes Mellitus, Type 2↗
PubMed1997

A randomized, multicenter, double-blind, placebo-controlled, dose-finding study of ORG 2766 in the prevention or delay of cisplatin-induced neuropathies in women with ovarian cancer.

OBJECTIVE: The objective was to evaluate the efficacy of Org 2766 (a hexapeptide analogue of ACTH) in the prevention or delay of cisplatin-induced neuropathy during chemotherapy in women with ovarian cancer as measured by vibration perception threshold (VPT). METHODS: In this randomized, multicenter, double-blind, placebo-controlled study, 196 women with ovarian cancer were treated with cisplatin 75-100 mg/m2, cyclophosphamide 600-1000 mg/m2 plus placebo or two dose levels of Org 2766. The cisplatin-induced neuropathies were monitored by determining the VPT with the Vibratron II. VPT was determined for both the most sensitive great toe and the index finger on a monthly basis during treatment and months 1, 2, and 3 postchemotherapy. Once the blind was broken, it was found that 174 women (59 in placebo, 58 in 2 mg, and 57 in 4 mg) had enough data to allow evaluation. RESULTS: Over the course of follow-up, the VPT was found to increase. This is consistent with the development of cisplatin-induced peripheral neuropathies. The baseline VPT for the index finger was less than that of the great toe (0.65 vs 2.13), but the percentage change in VPT was the same for both (percentage increase in VPT of about 350%). When the VPTs are compared according to the dose of Org 2766 given, there appears to be no difference in the rate of change or degree of neuropathies that developed in these women receiving cisplatin and cyclophosphamide. CONCLUSIONS: The development of cisplatin-induced neuropathies is confirmed by measurement of the VPT. The rate of development of neuropathies seems to accelerate after the sixth course of cisplatin. When the development of neuropathies is evaluated on the basis of Org 2766 dosage, it is found that there is no difference in the rate or degree of neuropathies seen. Instead of providing protection from and delay of onset of peripheral neuropathies caused by cisplatin, these results suggest that the administration of Org 2766 appears to cause an increase in the rate of change and degree of neuropathies (P > 0.05).

Adrenocorticotropic Hormone↗
PubMed1995

Pudendal neuropathy in evacuatory disorders.

PURPOSE: Aims of the present study were to assess frequency of pudendal neuropathy in patients with constipation and fecal incontinence, to determine its correlation with clinical variables, anal electromyographic assessment, and anal manometric pressures, and to determine usefulness of the pudendal nerve terminal motor latency assessment in evaluation of these evacuatory disorders. METHODS: From 1988 to 1993, 395 patients (constipated, 172; incontinent, 223) underwent pudendal nerve terminal motor latency, electromyography, and anal manometry. Pudendal neuropathy was defined as a pudendal nerve terminal motor latency greater than 2.2 ms. RESULTS: Patients were a mean age of 60.7 (range, 17-88) years. Overall incidence of pudendal neuropathy was 31.4 percent (constipated, 23.8 percent; incontinent, 37.2 percent; P < 0.05). Incidence of pudendal neuropathy dramatically increased after 70 years of age in both groups (22 percent vs. 44 percent; P < 0.05). Moreover, subjects with pudendal neuropathy were older than those without pudendal neuropathy (mean age, 67 vs. 57 years; P < 0.05). The presence of pudendal neuropathy was associated with decreased motor unit potentials recruitment in patients with incontinence (P < 0.01). Patients with and without pudendal neuropathy had a similar mean squeezing pressure in both groups. CONCLUSION: Pudendal neuropathy is an age-related phenomenon. Although pudendal neuropathy is associated with abnormal anal electromyographic findings in patients with incontinence, no association with anal manometric pressures was found. Pudendal nerve terminal motor latency assessment is a useful tool in the evaluation of patients with fecal incontinence, but its role in the assessment of constipated patients remains unknown.

Adolescent↗
PubMed2001

Changes of gastric emptying rate and gastrin levels are early indicators of autonomic neuropathy in type II diabetic patients.

The authors investigated the effect of a balanced meal on gastric emptying rate and gastrin plasma concentrations in patients with type II diabetes and autonomic neuropathy, in diabetic patients without autonomic neuropathy, and in healthy subjects (controls). Before food the gastrin plasma concentrations were higher in patients with diabetes with autonomic neuropathy. After food, gastric emptying rate was slower in patients with diabetes with autonomic neuropathy, whereas gastrin plasma concentrations increased in 30 minutes in all groups but to a greater extent in patients with diabetes with autonomic neuropathy. Sixty minutes after food, there was a significant decrease in gastrin plasma concentrations in patients with diabetes with autonomic neuropathy, compared with the other two groups. These data suggest that in patients with type II diabetes with autonomic neuropathy, food causes slower gastric emptying and different plasma gastrin level responses from those in patients with type II diabetes without autonomic neuropathy and controls. There are therefore differences in the responses to food ingestion between these groups because of vagal denervation induced by autonomic neuropathy. These tests should be reserved for patients with symptoms suggestive of disturbed gastric emptying, or for patients with autonomic neuropathy without symptoms of gastroparesis.

Aged↗
PubMed2005

Is there a relationship between somatic and autonomic neuropathies in chronic alcoholics?

We investigated the relationship between somatic and autonomic neuropathy in 40 chronic alcoholics. Electromyographic and neurographic studies of upper and lower limbs and a battery of six cardiovascular reflex tests were carried out. A score for somatic or autonomic neuropathy was calculated. All parameters were investigated for possible relationship with total life dose (TLD) of alcohol intake. Somatic neuropathy was detected in 25 patients (62.5%) and autonomic neuropathy in 13 patients (32.5%). Nineteen patients (47.5%) presented only a somatic neuropathy, six patients (15%) had only an autonomic neuropathy, and seven (17.5%) had a combined somatic and autonomic neuropathy. TLD was significantly higher in the group of patients with combined neuropathy than in the group with isolated somatic neuropathy. There was no significant correlation between laboratory parameters of somatic and autonomic neuropathy. Our findings do not support the existence of a parallel involvement of peripheral somatic and autonomic cardiovascular nerve fibers in chronic alcoholism.

Adult↗
PubMed2006

Idiopathic neuropathy, prediabetes and the metabolic syndrome.

Peripheral neuropathy is a common problem encountered by neurologists and primary care physicians. While there are many causes for peripheral neuropathy, none can be identified in a large percentage of patients ("idiopathic neuropathy"). Despite its high prevalence, idiopathic neuropathy is poorly studied and understood. There is evolving evidence that impaired glucose tolerance (prediabetes) is associated with idiopathic neuropathy. Preliminary data from a multicenter study of diet and exercise in prediabetes (the Impaired Glucose Tolerance Neuropathy Study) suggests a diet and exercise counseling regimen based on the Diabetes Prevention Program results in improved metabolic measures and small fiber function. Prediabetes is part of the Metabolic Syndrome, which also includes hypertension, hyperlipidemia and obesity. Individual aspects of the Metabolic Syndrome influence risk and progression of diabetic neuropathy and may play a causative role in neuropathy both for those with prediabetes, and those with otherwise idiopathic neuropathy. Thus, a multifactorial treatment approach to individual components of Metabolic Syndrome may slow prediabetic neuropathy progression or result in improvement.

Blood Glucose↗
PubMed2003

"Auditory neuropathy": physiologic and pathologic evidence calls for more diagnostic specificity.

The term "auditory neuropathy" is being used in a rapidly increasing number of papers in the audiology/otolaryngology literature for a variety of individuals (mostly children) who fulfill the following criteria: (1) understanding of speech worse than predicted from the degree of hearing loss on their behavioral audiograms; (2) recordable otoacoustic emissions and/or cochlear microphonic; together with (3) absent or atypical auditory brain stem responses. Because of the general lack of anatomic foundation for the label "auditory neuropathy" as currently used, we review the anatomy of the auditory pathway, the definition of neuropathy and its demyelinating, axonal, and mixed variants. We submit that the diagnostic term "auditory neuropathy" is anatomically inappropriate unless patients have documented evidence for selective involvement of either the spiral ganglion cells or their axons, or of the 8th nerve as a whole. In view of biologic differences between peripheral nerves and white matter tracts in the brain, the term "auditory neuropathy" is inappropriate for pathologies affecting the central auditory pathway in the brainstem and brain selectively. Published reports of patients with "auditory neuropathy" indicate that they are extremely heterogeneous in underlying medical diagnosis, age, severity, test results, and that only a small number have undergone the detailed investigations that would enable a more precise diagnosis of the locus of their pathologies. The electrophysiology of peripheral neuropathies and the deficits expected with pathologies affecting the hair cells, spiral ganglion cells and their axons (auditory neuropathy sensu stricto), and brain stem relays are reviewed. In order to serve patients adequately, including potential candidates for cochlear implants, and to increase knowledge of auditory pathologies, we make a plea for more comprehensive evaluation of patients who fulfill the currently used audiologic criteria for "auditory neuropathy" in an effort to pinpoint the site of their pathologies. We suggest that the term auditory neuropathy be limited to cases in which the locus of pathology is limited to the spiral ganglion cells, their processes, or the 8th nerve, and that the term neural hearing loss be considered for pathologies that affect all higher levels of the auditory pathway, from the brainstem to the auditory cortex.

Audiology↗