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At least 19 recordsLinked to original sources
PubMed1990

Impairment of cardiorespiratory reflexes and its association with distal somatic neuropathy in diabetic patients free from clinical symptoms of autonomic neuropathy.

Signs of autonomic cardiac neuropathy and its association with distal somatic neuropathy were investigated in 36 type 1 and 28 type 2 diabetic patients free from clinical symptoms of autonomic neuropathy. Using bedside tests (deep-breathing, Valsalva manoeuvre and lying-to-standing) definitive cardiac autonomic neuropathy was found in 28 patients (44%), early cardiac autonomic neuropathy was observed in 19 patients (30%) while 17 patients (26%) showed no alterations. The values of motor nerve conduction velocity in peroneal nerves (41.8 +/- 0.7 m/s, mean +/- SEM) were significantly (p less than 0.01) lower in patients with definitive cardiac autonomic neuropathy than those (45.8 +/- 1.1 m/s) of patients without any signs of cardiac autonomic neuropathy. These latter values were, however, significantly (p less than 0.001) lower than those (53.7 +/- 0.7 m/s) of control subjects (n = 50). Signs of early or definitive cardiac autonomic neuropathy were recorded in 31 of 35 diabetic patients with distal somatic neuropathy assessed by measurement of motor nerve conduction velocity in peroneal nerves. It was concluded that abnormal results of noninvasive tests for autonomic neuropathy, i.e. alterations in cardiorespiratory reflexes indicating parasympathetic impairment of cardiac innervation could be often found in diabetic patients without clinical signs of autonomic neuropathy. These alterations could be frequently observed in diabetic patients with distal symmetrical somatic neuropathy.

Adult↗
PubMed1990

[Correlations between cardiorespiratory reflex impairment and distal neuropathy in diabetics free of clinical symptoms of autonomic neuropathy].

Signs of autonomic cardiac neuropathy and its association with distal symmetrical polyneuropathy were investigated in adult diabetic patients free from clinical symptoms of autonomic neuropathy. Cardiorespiratory reflexes were assessed by non-invasive tests (deep-breathing, Valsalva manoeuvre and lying-to-standing) evaluating parasympathetic function of cardiac innervation. Measurement of motor nerve conduction velocity in both peroneal nerves and neurological physical examination were carried out for assessment of distal somatic neuropathy. Among 64 diabetics, definitive signs of cardiac autonomic neuropathy were found in 28 patients (44%), early signs of cardiac autonomic neuropathy were observed in 19 patients (30%) while no alterations were documented in 17 patients (26%). The values of motor nerve conduction velocity in peroneal nerves (41.8 +/- 0.7 m/s) were significantly (p less than 0.01) lower in patients with definitive cardiac autonomic neuropathy (n = 28) than those (45.8 +/- 1.1 m/s) of patients without any signs of cardiac autonomic neuropathy (n = 17). These latter values were, however, significantly (p less than 0.001) lower than those (53.7 +/- 0.7 m/s) of control subjects (n = 50). Abnormal results of non-invasive tests for autonomic neuropathy, i.e. alterations of cardiorespiratory reflexes indicating parasympathetic impairment in cardiac innervation could be often found in diabetics without clinical signs of autonomic neuropathy. These alterations could be frequently observed in diabetics with distal symmetrical neuropathy as well as in diabetic patients with one or more late specific complications.

Autonomic Nervous System Diseases↗
PubMedDate not supplied

The epidemiology of diabetic neuropathy. Diabetic Cardiovascular Autonomic Neuropathy Multicenter Study Group.

Although neuropathy has long been recognized as a complication of diabetes, the impact of this condition has not been adequately established. The prevalence of diabetic neuropathy is virtually unknown because the published studies differ considerably with regard to definition, method of assessment, and patient selection. Furthermore, the determination of prevalence has been hampered by the fact that there is no generally accepted classification of the variety of manifestations of diabetic neuropathy. The introduction of new sensitive diagnostic methods aids in the detection of less severe stages of neuropathy, as compared with clinically based assessment, and renders the disease more prevalent. The prevalence of diabetic neuropathy in the few reported population-based studies was approximately 30%. We have evaluated the prevalence of cardiovascular autonomic neuropathy in a group of approximately 1000 diabetic patients randomly included from 21 hospitals in Germany, Austria, and Switzerland. The results of this study and those of a prospective study on the natural history of neural dysfunction during the first 5 years after diagnosis of type 1 diabetes will be presented.

Adolescent↗
PubMed1988

Histopathological heterogeneity of neuropathy in insulin-dependent and non-insulin-dependent diabetes, and demonstration of axo-glial dysjunction in human diabetic neuropathy.

Altered sorbitol and myo-inositol metabolism, (Na,K)-ATPase function, electrochemical sodium gradients, axonal swelling, and distortion and disruption of the node of Ranvier ("axo-glial dysjunction") directly implicate hyperglycemia in the pathogenesis of neuropathy in diabetic rats, but the relevance of this sequence to clinical neuropathy in heterogeneous groups of diabetic patients remains to be established. Fascicular sural nerve morphometry in 11 patients with neuropathy complicating insulin-dependent diabetes revealed a pattern of interrelated structural changes strikingly similar to that of the diabetic rat when compared to age-matched controls. 17 older non-insulin-dependent diabetic patients with comparable duration and severity of hyperglycemia and severity of neuropathy, displayed similar nerve fiber loss, paranodal demyelination, paranodal remyelination and segmental demyelination compared to age-matched controls, but axo-glial dysjunction was replaced by Wallerian degeneration as the primary manifestation of fiber damage, and fiber loss occurred in a spatial pattern consistent with an ischemic component. The mechanistic model developed from the diabetic rat does indeed appear to apply to human diabetic neuropathy, but superimposed hormonal, metabolic, vascular, and/or age-related effects alter the morphologic expression of the neuropathy in non-insulin dependent diabetes.

Age Factors↗
PubMed1976

Studies on drug-induced neuropathies. III. Motor nerve deficit in cats with experimental acrylamide neuropathy.

To assess motor nerve and motor nerve terminal function in acrylamide neuropathy, cats were given i.m. injections of acrylamide (15 mg/kg) daily for 10 days to induce a peripheral neuropathy. Tests of function were performed on the day of the 10th injection (day 0) and 7, 21 and 35 days thereafter. In untreated animals tetanic conditioning evoked stimulus-bound repetition (SBR) in 85% of soleus alpha-motoneurones. Following administration of acrylamide, the percent of axons elaborating SBR were: day 0 -- 79%, day 7 -- 71%, day 21 -- 31%, day 35 -- 22%. The response of soleus muscle to SBR is normally a post-tetanic potentiation (PTP) of contractile tension which is proportional to the tetanic conditioning frequency; during the development of the neuropathy, PTP in response to all tetanic frequencies progressively declined, concomitant with and as a result of the declining incidence of SBR. These data indicate that initial functional alterations in motor nerves during acrylamide neuropathy occurs at the level of the nerve terminal, preceding alterations in conduction velocities in the axons. However, the motor nerve deficit is not adequate, in either time to onset or severity, to account for the clinical manifestations of the neuropathy. The possible contribution to clinical signs of the neuropathy made by lesions to other peripheral nerves is discussed.

Acrylamides↗
PubMed1992

[Carcinomatous autonomic neuropathy and the autoantibodies in paraneoplastic neuropathy].

Carcinomatous autonomic neuropathy is a syndrome of autonomic dysfunction associated with malignant neoplasm. It is most often associated with small-cell lung cancer. Auto-immune mechanism is suspected to underlie this syndrome. Among the symptoms of autonomic dysfunction, intestinal pseudo-obstruction is most frequently seen. The autonomic dysfunction often precedes the discovery of the cancer. Several autoantibodies have been reported in paraneoplastic neuropathies. Anti-Hu antibody, which was originally reported in paraneoplastic sensory neuronopathy, has also been detected in some cases with autonomic failure. Anticarbohydrate antibody activity has been frequently shown in IgM M-proteins associated with peripheral neuropathies. These include anti-MAG, Po, and sulphated glucuronyl glycolipids in demyelinating neuropathy and anti-GM1 in motor dominant neuropathy or motor neuron disease. Further investigation should reveal more glycoconjugate antigens as targets of possible auto-immune attack in paraneoplastic neuropathies.

Autoimmune Diseases↗
PubMedDate not supplied

Measuring subclinical neuropathy: does it relate to clinical neuropathy? Pittsburgh epidemiology of diabetes complications study-V.

We report results from 120 (25- to 34-year-old) participants in a neuropathy substudy of subjects with insulin-dependent diabetes mellitus (IDDM) taking part in a cohort follow-up study. Diabetic neuropathy was evaluated by quantitative sensory testing, nerve conduction studies, and clinical examination. Mean quantitative sensory thresholds differed significantly by clinical category of abnormal sensation and ankle reflex activity. Mean sural and peroneal amplitudes and conduction velocities were also significantly lower for subjects classified as having abnormal ankle reflex activity. Modeling potential correlates in logistic analyses showed glycemic control, triglyceride levels, and hypertension status to be independently associated with clinically overt neuropathy. Similar lipid and hemodynamic parameters were associated with abnormality by any single assessment method used to define neuropathy. Although follow-up is needed to resolve the best assessment methods for determining neuropathy, these results suggest that good glycemic control as well as control of blood pressure and lipids is advisible.

Adult↗
PubMed1990

Hereditary motor and sensory neuropathy type 1 (HMSN1) associated with cranial neuropathy: an autopsy case report.

A family with hereditary motor and sensory neuropathy type 1 (HMSN1) is reported. Three patients suffered only pupillary abnormality, two patients showed Adie's syndrome and peripheral neuropathy, and one had cranial neuropathy. Adie's syndrome and severe peripheral neuropathy. Autopsy of the latter revealed reduction of myelinated nerve fibers in the trigeminal, facial and hypoglossal nerves. There was extensive degeneration of the posterior column of the spinal cord. At the anterior horns, loss of motor neurons was observed, particularly at the lumbar level. The anterior and posterior roots showed loss of myelinated fibers. HMSN1 is only rarely associated with cranial neuropathy, and this is probably the first autopsy-proved case.

Adie Syndrome↗
PubMed1991

The Rochester Diabetic Neuropathy Study: design, criteria for types of neuropathy, selection bias, and reproducibility of neuropathic tests.

A cross-sectional survey and subsequent longitudinal study among diabetic residents of Rochester, MN--The Rochester Diabetic Neuropathy Study (RDNS)--is population-based and uses quantitative, validated, and unique end points to detect, classify, and stage neuropathy. Nondiabetic persons, drawn from the same population, serve as controls. For patients 10 to 70 years old, the RDNS cohort is representative of diabetics living in Rochester, MN. We assessed reproducibility of tests used to characterize and quantitate severity of neuropathy in 20 diabetic subjects without neuropathy and with varying severities of neuropathy. Using intraclass correlation coefficient (rI) as a measure of test reproducibility, we found high rI (usually 0.9 or better) with small confidence intervals for the Neurologic Disability Score (NDS); weakness subset of NDS (W-NDS); vibratory and cooling detection thresholds (using computer-assisted sensory examination [CASE] IV); compound muscle action potentials; sensory nerve action potentials; and motor nerve conduction velocities. There was good agreement among three trained observers for NDS and the W-NDS.

Action Potentials↗
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↗
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↗
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↗
PubMed1988

Factors in development of diabetic neuropathy. Baseline analysis of neuropathy in feasibility phase of Diabetes Control and Complications Trial (DCCT). The DCCT Research Group.

The Diabetes Control and Complications Trial (DCCT) is a multicenter randomized clinical trial studying the effect of intensive insulin therapy on the early vascular and neurological complications of insulin-dependent diabetes mellitus (IDDM). During the feasibility phase of the DCCT, baseline neurological histories, physical examinations, and laboratory measurements of somatic and autonomic nerve function were obtained in 278 well-characterized IDDM subjects. Subjects were free of advanced complications, including the presence of peripheral or autonomic neuropathy sufficiently severe to require treatment. Analyses of the cross-sectional data reveal that clinically detectable peripheral neuropathy was present in 39% of the subjects. The presence of clinical neuropathy correlated with greater age, longer duration of IDDM, and male gender. The somatic and autonomic test results confirm the relationship between age, diabetes duration, and male gender and diabetic neuropathy. These results support an effect of age and gender on the development of diabetic complications.

Adolescent↗
PubMed1985

[Metabolic neuropathies. I. Diabetic neuropathies].

This is a review article on diabetic neuropathy. The different patterns of diabetic neuropathies, including focal and multifocal, distal symmetrical and autonomic neuropathy are exposed. Length dependent degeneration of fibers is suggested by the pattern of sensory loss and by morphological findings. The various hypotheses on the mechanisms of the neuropathy, including the possible role played by ischemia and by the accumulation of sorbitol in Schwann's cells, are reviewed. The therapeutic implications of the clinical, pathological and biochemical abnormalities are discussed.

Cranial Nerve Diseases↗
PubMed1986

[11 cases of neuropathy induced by almitrine, of which one had optic neuropathy].

The only etiologic factor retained in 11 patients with sensory or sensory-motor neuropathy was almitrine therapy. In one patient there was in addition an optic neuropathy. The reduction in visual acuity in this patient coincided with the onset of the sensory-motor neuropathy of lower limbs after treatment with 100 mg/day of almitrine over a 2-year period. No other metabolic, inflammatory, toxic, vascular or immunologic cause was found. There was a moderate chronic respiratory insufficiency. Visual recuperation started one month after the arrest of almitrine treatment and was satisfactory 7 months later. The other 10 patients had neuropathy of limbs without visual disorders. Neuromuscular biopsy in one case showed lesions to be of the axonal type.

Aged↗