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At least 55 records · Page 3Linked to original sources
PubMed1997

Approaches to improve epidemiological studies of diabetic neuropathy: insights from the Rochester Diabetic Neuropathy Study.

The quality of the epidemiological data on diabetic neuropathies remains poor for a variety of reasons. They include variability in 1) ascertainment of diabetes, 2) the clinical varieties of diabetic patients studied, 3) characterization of neurological dysfunction, 4) abnormal limits for neurological examinations and tests, 5) minimal criteria for neuropathy, 6) correct attribution of nondiabetic neurological disease, 7) correct attribution of type of neuropathy, 8) estimating neuropathy from use of multiple tests, and 9) estimating severity of polyneuropathy. We have tried to remedy these short-comings in the Rochester Diabetic Neuropathy Study (RDNS). It was not possible to adequately characterize and quantitate diabetic polyneuropathies using only one or two clinical or test abnormalities. To estimate severity of diabetic polyneuropathy, the results of the neurological examination and abnormalities of nerve conduction, quantitative sensory tests, and quantitative autonomic tests were combined into a composite score. One begins by scoring a standard test of neurological deficits (impairments) of the lower limbs (NIS[LL]) and adds to this transformed numbers for percentile abnormality of seven good functional tests. This NIS(LL)+7 tests score appears to provide a much more comprehensive and stable numeric score by which to diagnose and grade severity of diabetic polyneuropathy than does the use of individual clinical or test results. This test score should be useful as a measure of change in diabetic polyneuropathy for purposes of medical practice, epidemiology studies, and controlled clinical trials. The staging approach that we introduced previously continues to provide an important measure of overall severity of diabetic polyneuropathy, taking into account both symptoms and impairments.

Cross-Sectional Studies↗
PubMed1984

[Diabetic neuropathy. I). Peripheral neuropathy].

This is the first of a series of reports on diabetic neuropathy. Peripheral or somatic diabetic neuropathy is discussed with reference to its major symptoms: central, peripheral and amyotrophic mononeuropathies, symmetrical and asymmetrical polyneuropathies, peripheral arthropathy and finally diabetic cachexia. The various theories on the pathogenesis of peripheral neuropathy are presented. Finally data on 173 type I and II diabetics are presented. These patients, treated in outpatients departments, were paired by sex, weight and age with an equal number of non-diabetic subjects. The results of the survey largely confirm report in the literature. The importance of continuous medical surveillance for the identification and hence prevention of diabetic neuropathy is emphasized. This is particularly necessary since we have still much to learn about the natural history of the disease and for the moment the therapeutic approaches to the various neuropathies concerned are both tentative and symptomatic.

Adult↗
PubMed1983

Amyloid neuropathy in multiple myeloma and other plasma cell dyscrasias. A hypothesis of the pathogenesis of amyloid neuropathies.

The development of amyloid neuropathy is an uncommon complication of multiple myeloma. The clinical, electrophysiological and pathological features of 3 such patients are described. The small fiber neuropathy in these 3 cases was similar to that in patients with primary amyloidosis and with the Andrade-type of familial neuropathy, and differed from the large fiber neuropathy which more commonly develops in patients with multiple myeloma. We advance the hypothesis that the absence of the blood-nerve barrier in the dorsal root and sympathetic ganglia allows the access of amyloidogenic proteins to these ganglia, and that these ganglia are the primary site of damage to the peripheral nervous system in the amyloid neuropathies.

Adult↗
PubMed1994

An epidemic in Cuba of optic neuropathy, sensorineural deafness, peripheral sensory neuropathy and dorsolateral myeloneuropathy.

An epidemic outbreak of peripheral neuropathy affected Cuba in 1992-93 resulting in 50,862 cases (national cumulative incidence rate (CIR) 461.4 per 100,000). Clinical forms included retrobulbar optic neuropathy, sensory and dysautonomic peripheral neuropathy, dorsolateral myeloneuropathy, sensorineural deafness, dysphonia and dysphagia, spastic paraparesis, and mixed forms. For epidemiological purposes, cases were classified as optic forms (CIR 242.39) or peripheral forms (CIR 219.25). Increased risk was found among smokers (odds ratio (OR) 4.9), those with history of missing meals (OR 4.7) resulting in lower intake of animal protein, fat, and foods that contain B-vitamins, combined drinking and smoking (OR 3.5), weight loss (OR 2.8), excessive sugar consumption (OR 2.7) and heavy drinking (OR 2.3). Optic neuropathy was characterized by decreased vision, bilateral and symmetric central or cecocentral scotomata, and loss of color vision due to selective lesion of the maculopapillary bundles. Peripheral neuropathy was a distal axonopathy lesion affecting predominantly large myelinated axons. Deafness produced selective high frequency (4-8 kHz) hearing loss. Myelopathy lesions combined dorsal column deficits and pyramidal involvement of lower limbs with spastic bladder. Clinical features were those of Strachan syndrome and beriberi. Intensive search for neurotoxic agents, in particular organophosphorus esters, chronic cyanide, and trichloroethylene intoxication, yielded negative results. Treatment of patients with B-group vitamins and folate produced rewarding results. Most patients improved significantly and less than 0.1% of them remained with sequelae; there were no fatal cases. Supplementation of multivitamins to the entire Cuban population resulted in curbing of the epidemic. Overt malnutrition was not present, but a deficit of micronutrients, in particular thiamine, cobalamine, folate and sulfur amino acids appears to have been a primary determinant of this epidemic.

Adolescent↗
PubMed1997

An epidemic of optic neuropathy in Tanzania: characterization of the visual disorder and associated peripheral neuropathy.

An epidemic of subacute bilateral visual failure has affected large numbers of teenagers and young adult Africans in coastal Tanzania since 1988. Previous work had indicated that many patients had sensory symptoms, but the nature of the neurological involvement was uncertain. The primary objective of this study was to characterize the accompanying neurological disorder. Furthermore, the nature of the visual loss was uncertain from previous reports as both retinopathy and optic neuropathy had been suggested. Full ophthalmic and neurological examinations were carried out at the Muhimbili University Hospital in Dar es Salaam. Nerve conduction studies, pattern electro-retinograms and cortical visually evoked responses and colour contrast sensitivity tests were carried out. Thirty eight young Africans and 12 controls were included in the study. The characteristic fundus picture was symmetrical temporal optic atrophy, and thinning of the caeco-central nerve fibre layer. Fluorescein angiography was normal. The electrophysiological and colour contrast sensitivity tests confirmed optic neuropathy in the majority of cases but primary retinal involvement was indicated in some. Neurological examination and nerve conduction measurements showed evidence of a peripheral neuropathy in 47% of the patients. The peripheral neuropathy is likely to have involved large fibres (from the nerve conduction studies) but the symptoms suggest small fibre loss also. 42% had developed hearing loss. Urinary thiocyanate levels were uniformly low. Serum was negative for antibodies to HTLV-1. DNA analysis from three cases was negative for three known mutations associated with Leber's hereditary optic atrophy (11778, 3460 and 14484). This entity, occurring predominantly in a young age group, does not correspond closely to other tropical neurological syndromes previously described from East Africa although it is clinically very similar to Strachan's syndrome (originally described in the Caribbean and more recently in prisoners of war) and also to an epidemic of optic and peripheral neuropathy that has recently occurred in Cuba. The aetiology has not yet been determined. A micronutrient deficiency is likely but has not been established.

Adolescent↗
PubMed1993

Axonal neurofilamentous accumulations: a comparison between human and canine giant axonal neuropathy and 2,5-HD neuropathy.

The neuropathy produced by the hexacarbon 2,5-hexanedione (2,5-HD) resembles human and canine inherited giant axonal neuropathy (GAN) in the presence of giant axonal swellings that contain accumulations of neurofilaments. The accumulations are both paranodal and internodal in GAN and 2,5-HD induced neuropathy. Detailed morphometry on the neurofilaments reveals that the changes in human and canine GAN are closely similar and differ from those of 2,5-HD neuropathy, suggesting that the mechanisms underlying the formation of the axonal neurofilamentous accumulations differ between the two conditions. In both human and canine GAN, the neurofilaments are more closely spaced and are of greater diameter than in 2,5-HD neuropathy. The changes in the NF in GAN may be the consequence of flattening of the side-arms of the neurofilaments against the axis of the filaments.

Animals↗
PubMed1995

Impairment, disability, or handicap in peripheral neuropathy: analysis of the use of outcome measures in clinical trials in patients with peripheral neuropathies.

Outcome measures can be classified into measures of impairment, disability, and handicap. To investigate the biological effect of treatment, measures of impairment are appropriate. Studies investigating whether patients benefit from treatment in terms of improvement of functional health, however, require disability or handicap measures. In a review of the medical literature between 1978 and 1993, 73 controlled intervention studies in patients with peripheral neuropathies were found. Disability or handicap measures were used in two of 54 studies in patients with diabetic neuropathy, in two of six studies in patients with chronic inflammatory demyelinating polyneuropathy, in none of five studies in a mixed group of patients, and in all eight studies in patients with Guillain-Barré syndrome. The limited use of disability and handicap measures in patients with diabetic and mixed neuropathies can be explained by the experimental nature of most studies. In four of six studies, however, in patients with chronic inflammatory demyelinating polyneuropathy or neuropathy associated with monoclonal gammopathy that were designed to assess effectiveness of treatment, the choice of outcome measures was not appropriate. It is concluded that in the design of intervention studies in patients with peripheral neuropathy more attention should be paid to a proper choice of suitable outcome measures to assess the effectiveness of treatment.

Activities of Daily Living↗
PubMed2002

P-ANCA vasculitic neuropathy with 12-year latency between onset of neuropathy and systemic symptoms.

BACKGROUND: The differential diagnosis of chronic progressive multifocal asymmetric neuropathies is challenging. Vasculitic neuropathies, multifocal forms of chronic inflammatory demyelinating polyneuropathy, multifocal motor neuropathies, and asymmetric lower motor neuron disorders are important considerations. CASE PRESENTATION: We report a patient with an unusually long 12-year course of nonsystemic vasculitic neuropathy prior to the development of systemic manifestations. CONCLUSION: We discuss some of the difficulties involved in the diagnosis of chronic progressive multifocal asymmetric neuropathies.

Antibodies, Antineutrophil Cytoplasmic↗
PubMed1989

Spanish toxic oil syndrome neuropathy in three patients with hereditary motor and sensory neuropathy type I.

We describe three patients with hereditary motor and sensory neuropathy type I coming from a family who suffered from Spanish toxic oil syndrome with neuromuscular manifestations. Their clinical course neither differed from other kin only affected with the inherited neuropathy nor from other patients with Spanish toxic oil syndrome studied by us. These findings suggest that patients with hereditary motor and sensory neuropathy do not exhibit a special susceptibility to vasculitic neuropathy associated with Spanish toxic oil syndrome.

Adolescent↗
PubMed1996

Focal posterior interosseous neuropathy in the presence of hereditary motor and sensory neuropathy, type I.

A 30-year-old male with hereditary motor and sensory neuropathy, type I (HMSN I), presented with asymmetric weakness of finger extension and radial deviation with left wrist extension, previously felt to be a manifestation of the peripheral neuropathy. Nerve conduction studies confirmed HMSN I; however, needle EMG revealed marked, ongoing axonal loss in muscles innervated by the left posterior interosseous nerve (PIN) only. At surgery there was focal fusiform swelling in the PIN at exit from the supinator muscle, compatible with localized hypertrophic neuropathy, which has not been reported before in HMSN I. A concomitant focal mononeuropathy should be considered in cases of hereditary neuropathy with marked asymmetry of weakness.

Adult↗
PubMed2002

Future treatments for diabetic neuropathy: clues from experimental neuropathy.

Neuropathy remains a major complication of diabetes and there is no approved treatment that prevents its progression or alleviates the associated symptoms. Animal models of diabetic neuropathy are hampered by their short life span, which precludes the development of overt structural pathology, and they are best viewed as exhibiting early metabolic, neurochemical, and functional indices of nerve disorders that may predict progression to overt diabetic neuropathy. In this context, diabetic animals have use in both establishing potential etiologic mechanisms and for screening novel therapeutic agents. Treatment strategies are evolving in concert with a developing understanding of how hyperglycemia causes nerve dysfunction and recent or ongoing clinical trials are investigating this rational approach to drug design. It is only by the successful demonstration of clinical efficacy of a compound developed by this approach that the use of animal models of diabetic neuropathy can be validated.

Analgesics↗
PubMed1992

Congenital sensory neuropathy with anhidrosis (hereditary sensory neuropathy type IV).

Hereditary sensory neuropathies comprise a group of rare childhood diseases which are classified into four types. We present a Greek boy 11 years old with hereditary sensory neuropathy type IV (congenital sensory neuropathy with anhidrosis) whom we have followed up and studied during the last seven years. Our patient presented for the first time with recurrent hyperthermic episodes without sweating, and lack of pain sensation from the first months of life. Insensitivity to pain and thermal stimuli had resulted in burns on the extremities and self-mutilation of the tongue, lips and fingertips. When he was five and seven years old respectively he had two painless fractures of the ankles which led to insoluble orthopedic problems. He also suffered from mental retardation, which was obvious from his first years of life. Sweat gland investigations showed significant hypohidrosis or anhidrosis although the sweat glands were normal microscopically. Hereditary sensory neuropathy type IV, although rare, is important for dermatologists because it must be differentiated from other anhidrotic syndromes, and in view of the poor prognosis of the condition.

Child, Preschool↗
PubMed1978

A quantitative electrophysiological study of uraemic neuropathy. Diabetic and renal neuropathies compared.

The numbers of functioning motor units and the parameters of the electrically evoked motor unit potentials in the extensor digitorum brevis muscles of 30 patients on chronic haemodialysis for renal failure were obtained using recently introduced quantitative electrophysiological techniques. Measurements of the distal motor latencies and motor nerve conduction velocities in the lateral popliteal nerves of the same patients are also presented. The results support the presence of a "dying back" type of neuropathy in uraemia, with a preferential involvement of the fastest conducting motor axons. Collateral reinnervation and compensatory increase in size of surviving motor units is relatively impaired in uraemic neuropathy in comparison with a similar study on diabetic neuropathy. The significance of paranodal and segmental demyelination in producing abnormalities of conduction velocity in these neuropathies is discussed.

Action Potentials↗
PubMed1986

Neuropathy Symptom Profile in health, motor neuron disease, diabetic neuropathy, and amyloidosis.

We developed a true-or-false questionnaire with several hundred questions about symptoms encountered in peripheral neuropathy, to be scored by optical reader and computer. Responses were grouped into scales called "Neuropathy," "Weakness," "Sensory," "Autonomic," and subsets of these. Profiles in health were estimated for each scale based on responses from 300 healthy subjects 15 to 65 years old. The sensitivity and specificity of the scales were tested in patients with motor neuron disease, amyloidosis, or diabetes, with or without neuropathy. The questionnaire was useful in detecting neuropathy and staging severity, and in recognizing patterns that may have diagnostic implications.

Adolescent↗
PubMed1995

Hypertrophic neuropathy with complete conduction block-- hereditary motor and sensory neuropathy type III.

Hypertrophic neuropathy is a non-specific consequence of repeated demyelination and remyelination, encountered in a wide range of inherited and acquired disorders. We report an 11-year-old boy with HMSN III, a kind of hypertrophic neuropathy, with clinical, electrophysiologic and pathologic data. The electrophysiologic studies show complete conduction block in the upper and lower extremities with severe abnormal spontaneous activities. The pathologic findings of sural nerve reveal prominent hypomyelination, onion bulb formation, and severe endoneurial collagenization. Complete conduction block with the preservation of fair to good grade muscle strength is an unusual finding in hypertrophic neuropathy and other peripheral neuropathies, in general.

Child↗
PubMedDate not supplied

Diabetic neuropathy, the great masquerader: truncal neuropathy manifesting as abdominal pseudohernia.

OBJECTIVE: To describe a patient with diabetic truncal neuropathy and suggest a helpful diagnostic approach to this entity. METHODS: We present a case report, with a focus on physical, computed tomographic, and electromyographic findings. RESULTS: Because of an extensive differential diagnosis, diabetic truncal neuropathy is a rarely recognized and often misdiagnosed condition in patients with diabetes mellitus. In a 55-year-old man with a 13-year history of diabetes but no retinopathy, vasculopathy, or nephropathy, pain and a visible bulge in the left lower abdominal quadrant prompted radiographic assessment of the abdomen. A computed tomographic scan of the abdomen disclosed no mass but a weakening of the abdominal musculature suggestive of a pseudohernia. Subsequent electromyography showed evidence of polyradicular neuropathy. The patient was given treatment for pain control, and the pseudohernia resolved within 1 year. CONCLUSION: In patients with diabetes who have a painful abdominal mass, the potential presence of a diabetic truncal neuropathy should be considered.

Acetaminophen↗
PubMedDate not supplied

[The genetics of type 1 Charcot-Marie-Tooth disease, the hereditary focal neuropathies and the hereditary distal motor neuropathies].

INTRODUCTION: Charcot-Marie-Tooth disease (CMTD) or hereditary motor and sensory neuropathy shows great genetic heterogeneity. The type 1 (CMT-1) or demyelinating form and the type 2 (CMT-2) or neuronal form are two clinically and genetically distinct forms. DEVELOPMENT: Apart from the above mentioned motor and sensory forms, there is another type of neuropathy in which the clinical and neurophysiological involvement is exclusively motor and is known as distal spinal atrophy or hereditary distal motor neuropathy (HDMN), which is a syndrome to be included among the CMTD. The CMT-1 is the most prevalent form and the best understood from the genetic point of view. At least four genes have been reported to be involved: the gene for 22 kDa peripheral myelin protein (PMP-22), situated on the 17p11.2 chromosome (locus CMT-1A); the gene for myelin 0 protein situated on chromosome 1q23 (locus CMT-1B); the gene for conexine 32 (Cx32), found on chromosome Xq13 (locus CMT-X) and the gene EGR2 found on chromosome 10q21.1-q22.1. The genes PMP-22 and PO are related to autosomal dominant forms, the gene Cx32 is transmitted linked to chromosome X and transmission of gene EGR2 has been shown in both autosomal dominant and autosomal recessive forms. In the demyelinating forms with autosomal recessive inheritance, positive linkage has been found on four different loci: 8q21.1 (CMT-4A), 11q23 (CMT-4B), 5q23-33 (CMT-4C) and 8q24 in a form related to deafness (CMT-Lom). Two loci have been identified for the autosomal dominant forms of the HDMN. A large family initially and predominantly of the upper limbs is mapped on chromosome 7p (HDMN-V) and another with the classical phenotype mapped on chromosome 12q24. In the familial neuropathy with liability to pressure palsies in most families, deletion of the locus CMT-1A was found, and in rare cases mutation precisely of the PMP-22 gene. In familial amyotrophic neuralgia, genetic molecular analysis has shown linkage with markers on the chromosome 17q24-25.

Charcot-Marie-Tooth Disease↗
PubMedDate not supplied

Sensory-motor chronic neuropathy in two siblings: atypical presentation of tomaculous neuropathy.

Two siblings, born from a consanguineous marriage, in which tomaculous neuropathy (TN), diagnosed after nerve biopsy, presented as a chronic sensory-motor neuropathy. The clinical manifestations include also in both patients thyroid multinodular struma and in one case myopathic-like features. We believe that TN must be suspected not only in hereditary neuropathy with liability to pressure palsies, but also in any case with chronic sensory-motor neuropathy.

Adolescent↗