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At least 127 records · Page 7Linked to original sources
PubMed1986

Experimental chronic hypoxic neuropathy: relevance to diabetic neuropathy.

The cardinal electrophysiological abnormalities in experimental diabetic (EDN) and experimental galactose (EGN) neuropathy, models in which endoneurial hypoxia has been demonstrated, are a slowing in nerve conduction velocity (NCV) and a resistance to ischemic conduction block (RICB). These electrophysiological abnormalities are also present in human diabetic neuropathy, where microangiopathy has been demonstrated to be more severe than in EDN so that endoneurial hypoxia is also likely to be present. We examined the effects of endoneurial hypoxia per se on normal nerves. In rats subjected to chronic hypoxia (10% O2) for up to 10 wk, the two electrophysiological abnormalities had developed by 4 wk and were very similar in degree to those seen in EDN and EGN. These abnormalities occurred in the absence of hyperglycemia, nerve sorbitol accumulation, or myoinositol reduction. Resting O2 consumption was reduced, the percent increase in nerve lactate under anoxic stress was increased, and nerve free sugars were normal. Hexokinase and phosphofructokinase activities were not altered substantially when studied under conditions of O2 excess. These findings indicate that hypoxia per se will cause conduction slowing and suggest that the hypoxic nerve develops RICB because of a reduced energy requirement and an increased efficiency of anaerobic glycolysis, but without major changes in the activity of its controlling glycolytic enzymes.

Animals↗
PubMedDate not supplied

Cardiosympathetic neuropathy is independent of cardioparasympathetic neuropathy in patients with non-insulin-dependent diabetes mellitus.

The relationship between cardiosympathetic neuropathy and cardioparasympathetic neuropathy was investigated in 103 patients with non-insulin-dependent diabetes mellitus. Cardioparasympathetic nerve function was assessed by comparing electrocardiographically the expiratory and inspiratory R-R interval ratios, during a period of deep breathing, and the coefficients of variation of the R-R intervals. Cardiosympathetic nerve function was assessed by determining the uptake of [123I]metaiodobenzyl guanidine into the myocardium. The results indicate that there is no significant correlation between cardioparasympathetic and cardiosympathetic nerve function.

Body Mass Index↗
PubMed1985

Quantitative evaluation of diabetic autonomic neuropathy by using heart rate variations--determination of the normal range for the diagnosis of autonomic neuropathy.

Heart rate (HR) variations--in supine resting position, during deep breathing and on standing--were measured in 162 healthy subjects and 168 diabetics by use of an instantaneous-HR-change continuous recorder. As indices of HR variations, the standard deviation of the HR at rest (SD of HR), the mean difference between maximal and minimal HR during deep breathing (delta I-E) and the HR increase on standing (delta HR) were determined. In healthy subjects, the values for each test declined with age and the log-transformed data fitted the linear regression. The 90% confidence limits were calculated for the normal range and the values below normal range were defined as abnormal. In diabetics, the incidence of abnormal response were 19% in the SD of HR, 38% in the delta I-E and 22% in the delta HR. The delta I-E was the most sensitive index for the autonomic neuropathy. The delta HR was considered to be able to detect the different mechanisms of neural reflexes because of the poor correlation between the delta HR and the respiratory HR variations. The present studies suggested that delta I-E and delta HR should be measured at the same time to evaluate the autonomic neuropathy.

Adolescent↗
PubMed1997

Effects of treatment with the antioxidant alpha-lipoic acid on cardiac autonomic neuropathy in NIDDM patients. A 4-month randomized controlled multicenter trial (DEKAN Study). Deutsche Kardiale Autonome Neuropathie.

OBJECTIVE: To evaluate the efficacy and safety of oral treatment with the antioxidant alpha-lipoic acid (ALA) in NIDDM patients with cardiac autonomic neuropathy (CAN), assessed by heart rate variability (HRV). RESEARCH DESIGN AND METHODS: In a randomized, double-blind placebo-controlled multicenter trial (Deutsche Kardiale Autonome Neuropathie [DEKAN] Study), NIDDM patients with reduced HRV were randomly assigned to treatment with daily oral dose of 800 mg ALA (n = 39) or placebo (n = 34) for 4 months. Parameters of HRV at rest included the coefficient of variation (CV), root mean square successive difference (RMSSD), and spectral power in the low-frequency (LF; 0.05-0.15 Hz) and high-frequency (HF; 0.15-0.5 Hz) bands. In addition, cardiovascular autonomic symptoms were assessed. RESULTS: Seventeen patients dropped out of the study (ALA n = 10; placebo n = 7). Mean blood pressure and HbA1 levels did not differ between the groups at baseline and during the study, but heart rate at baseline was higher in the group treated with ALA (P < 0.05). RMSSD increased from baseline to 4 months by 1.5 ms (-37.6 to 77.1) [median (minimum-maximum)] in the group given ALA and decreased by -0.1 ms (-19.2 to 32.8) in the placebo group (P < 0.05 for ALA vs. placebo). Power spectrum in the LF band increased by 0.06 bpm2 (-0. 09 to 0.62) in ALA, whereas it declined by -0.01 bpm2 (-0.48 to 1.86) in placebo (P < 0.05 for ALA vs. placebo). Furthermore, there was a trend toward a favorable effect of ALA versus placebo for the CV and HF band power spectrum (P = 0.097 and P = 0.094 for ALA vs. placebo). The changes in cardiovascular autonomic symptoms did not differ significantly between the groups during the period studied. No differences between the groups were noted regarding the rates of adverse events. CONCLUSIONS: These findings suggest that treatment with ALA using a well-tolerated oral dose of 800 mg/day for 4 months may slightly improve CAN in NIDDM patients.

Autonomic Nervous System Diseases↗
PubMed1995

Hereditary neuropathy with liability to pressure palsies and inherited brachial plexus neuropathy--two genetically distinct disorders.

OBJECTIVE: To determine whether hereditary neuropathy with liability to pressure palsies (HNPP) and inherited brachial plexus neuropathy (IBPN) are genetically distinct disorders and to evaluate the usefulness of fluorescence in situ hybridization (FISH) for diagnosing HNPP in individual patients. DESIGN: We studied representative metaphases from patients with HNPP and IBPN with use of FISH and a DNA probe. MATERIAL AND METHODS: With use of FISH, 14 persons from 4 unrelated families with HNPP and 7 members from 3 unrelated families with IBPN were studied. We used a DNA probe that hybridizes to chromosome 17p11.2 in an area thought to be deleted in HNPP. RESULTS: Each participant in this study who had HNPP showed deletion of this chromosome site. Each of the 10 control subjects and 7 patients with IBPN showed normal fluorescent signals on both number 17 chromosomes. CONCLUSION: These results demonstrate that HNPP and IBPN are genetically different. FISH with this probe is a sensitive and specific method for detecting the chromosomal deletion in individual patients without the use of family studies or linkage analysis.

Brachial Plexus Neuritis↗
PubMed2000

Hereditary motor and sensory neuropathy associated with auditory neuropathy in a Gypsy family.

In a Slovene Gypsy family of 19 subjects from four generations three patients with clinical characteristics compatible with hereditary motor and sensory neuropathy - Lom (HMSNL). were found They had severe distal and milder proximal muscle atrophy and weakness with areflexia of myotatic jerks. Two had facial weakness at the time when already wheelchair bound. All sensory modalities were affected distally in the limbs. Sluggish pupillary responses to light and convergence were found. They had skeletal abnormalities. One patient had polydactily on the hand. Nerve conduction studies were compatible with demyelinative polyneuropathy. Nerve biopsy showed mainly axonal loss without hypertrophic changes. Auditory neuropathy was diagnosed in all of them. None of the patients had duplication of 17p1.2-12 or point mutations in the Protein zero. Peripheral myelin protein and Connexin32 genes. Similar disorder that mapped to 8q24 was previously described in some Bulgarian and Italian Gypsy families. Members of our family may suffer from the same hereditary disease and may carry the same ancestor mutation, which was in the past spread in European Gypsy populations.

Adolescent↗
PubMed1996

Is early diabetic neuropathy a disorder of the dorsal root ganglion? A hypothesis and critique of some current ideas on the etiology of diabetic neuropathy.

Investigations into the etiology of diabetic polyneuropathy have largely concentrated on the mixed peripheral nerve trunk. Although a number of workers have suggested that reductions in mixed nerve blood flow account for early diabetic polyneuropathy, experimental results remain controversial and are not fully sustained by human studies. Later disease is unquestionably associated with microangiopathy. Patients with diabetic neuropathy may have exclusive and severe sensory and autonomic involvement without obvious motor disease. The prominent sensory involvement in early diabetic polyneuropathy may suggest that the disease particularly targets dorsal root ganglia. Dorsal root ganglia (DRG) have features that might suggest they would be vulnerable to changes known to occur in diabetes, i.e. microangiopathy, excessive polyol flux and protein glycosylation. Autonomic ganglia may also be targeted early in the disease. The interest in using growth factors to treat diabetic neuropathy is at least partly based on the hypothesis that these agents might provide important trophic support for DRG neurons.

Diabetic Neuropathies↗
PubMed1989

Hereditary motor and sensory neuropathy type II followed in the next two generations by a clinically distal motor neuropathy.

Four members in 3 generations of a family are reported, who suffered from dominantly inherited hereditary motor and sensory neuropathy Type II. The diagnosis was not made in the first patient, seen at the age of 11 years, because she had no sensory symptoms. The presence of partial denervation in the EMG led to a mistaken diagnosis of distal chronic spinal muscular atrophy. Examination of her mother 11 years later and of her uncle after a further 6 years clearly established the correct diagnosis. Electrophysiological findings in all patients supported the diagnosis of hereditary motor and sensory neuropathy Type II.

Child↗
PubMedDate not supplied

Evaluation of the vagal-sympathetic interaction in diabetics with autonomic neuropathy through power spectrum density analysis of the heart rate. A critical revision of the natural history of diabetic autonomic neuropathy is possible.

In this paper we apply spectral analysis methods to heart rate variability to assess the autonomic nervous system activity in normal subjects and in patients affected by different degrees of diabetic autonomic neuropathy. The current opinion, based on different clinical tests, is that parasympathetic impairment occurs earlier in autonomic dysfunctions. However, the use of power spectrum density analysis based on a single parameter (heart rate) suggests a simultaneous involvement of parasympathetic and sympathetic pathways leading to the conclusion that perhaps the natural history of diabetic autonomic neuropathy should be substantially rewritten.

Autonomic Nervous System Diseases↗
PubMed1984

[Diabetic neuropathy. II. Autonomic neuropathy. The gastrointestinal system].

Autonomic diabetic neuropathy of the alimentary canal takes several basic forms: a) oesophagopathy , b) gastroparesis, c) enteropathy, d) bile duct disorders. In many cases three are no subjective symptoms. In other the onset of the clinical condition may take acute and dangerous forms as in gastropathy. In still other cases e.g. enteropathy, the neuropathy may develop in bizarre and unexpected ways which are highly damaging to the patient's quality of life though in most cases they are not fatal. Bile disorders involving minimal motility after stimulus, as in denervation and reduced sensitivity to pain are particularly significant. Diabetics are more likely to suffer from calculosis (59.6% of cases), with septic complications (20% in diabetics compared to 7.8% in non-diabetics) or cholestasis (20% in diabetics v. 15.8% in non-diabetics). These figures indicate that all diabetics and especially the elderly should be subjected to careful examination to identify any bile disorders.

Cholelithiasis↗
PubMed1996

Hereditary neuropathy with liability to pressure palsies: distinguishing clinical and electrophysiological features among patients with multiple entrapment neuropathy.

Hereditary neuropathy with liability to pressure palsies is caused by deletion of the PMP-22 gene. As its relatively mild symptoms may escape detection by clinical examination alone, we screened the gene in patients with multiple entrapment neuropathy (MEN) that had been diagnosed by nerve conduction studies (NCS). Two of the eight patients with MEN had deletion of the gene. The characteristic features that distinguished them from the other MEN patients were predominantly sensory deficits associated with mild weakness and subclinical polyneuropathy as detected by NCS.

Adolescent↗
PubMed1998

Multifocal motor neuropathy with conduction block misdiagnosed as multiple entrapment neuropathies.

We describe a 58-year-old male with a few years history of multifocal weakness in the upper limbs with minimal to absent sensory complaints. He was diagnosed as having multiple compressive neuropathies, which required repeated decompressive surgeries. Electrodiagnostic studies prior to diagnosis were limited to a few nerves, evaluating only distal segments. Because of delay in making the diagnosis, his condition progressed, and possibly because of the unnecessary surgeries, he developed atrophy in some muscles, which resulted in significant motor disability. He was later diagnosed as having multifocal motor neuropathy with conduction block and has partially responded to intravenous immunoglobulin therapy.

Atrophy↗
PubMed1980

Pure axonal neuropathy: nerve xenografts and clinicopathological study of a family with peripheral neuropathy, hereditary ataxia, focal necrotizing encephalopathy, and spongy degeneration of brain.

Three family members had the unusual combination of severe peripheral neuropathy, atypical hereditary ataxia, spongy degeneration of cerbral hemispheres, and cerebellar and brainstem foci of necrotizing encephalopathy, proved pathologically in one autopsied case. A sural nerve from a patient, devoid of myelinated fibers, was transplanted into thymectomized, lethally irradiated, and bone marrow reconstituted adult mice. A normal number of myelinated fibers was present in the grafts eleven weeks later. Eighteen weeks after grafting, mice were reconstituted with syngeneic thymus to return immunocompetence. Schwann cells in the graft were rejected and axons became totally denuded of myelin after thymus reconstitution. The peripheral neuropathy is thus due to axonal disease since human Schwann cells were capable of normally myelinating regenerating mouse axons. A puzzling feature after rejection was the absence of myelin debris containing macrophages in the grafts. It is suggested that part of the rejection process in this model is mediated by antibody rather than by cellular mechanisms.

Adolescent↗
PubMed1991

Paraneoplastic vasculitic neuropathy: a treatable neuropathy.

Paraneoplastic vasculitic neuropathy has been recently described. We report the first case of this disorder which responded both clinically and electrophysiologically to cyclophosphamide treatment. A 54-year-old woman with a history of metastatic endometrial carcinoma in remission had asymmetrical polyneuropathy, electrophysiological findings consistent with a diffuse axonal neuropathy, high sedimentation rate and spinal fluid protein, and microvasculitis with axonal degeneration on nerve biopsy. The patient was treated with 150 mg of cyclophosphamide daily with gradual clinical and electrophysiological improvement.

Action Potentials↗
PubMed1998

Light chain deposition disease neuropathy resembling amyloid neuropathy in a multiple myeloma patient.

A 65-year-old man with IgG lambda multiple myeloma developed severe polyneuropathy with prominent thermal-pain sensory impairment and autonomic failure. Although the clinical presentation suggested amyloid neuropathy, nerve biopsy showed the immunohistochemical and ultrastructural features typical of light chain deposition disease (LCDD). A precise morphologic and clinical description of LCDD neuropathy is given for the first time in the present report.

Aged↗
PubMed2004

[Regional anaesthesia for labor adn delivery in a parturient with neuropathy with liability to pressure palsy (tomaculous neuropathy)].

Tomaculous neuropathy (or hereditary neuropathy with liability to pressure palsy [HNLPP]) is a rare and hereditary disease which incidence has probably been underestimated. It is characterised by demyelination resulting in numbness and weakness after nerve pressure, injury or stretch. Despite a well-documented genetic pathophysiologic mechanism, implications for anaesthesia in patients with HNLPP are only speculative and the use of regional anaesthesia is debatable. We report here the case of a patient with HNLPP who was followed during two consecutive pregnancies in the same hospital and for whom an expert of the SOS-RA hotline service was consulted before each delivery. For the first delivery, epidural analgesia was performed for labour pain control but a caesarean section was necessary because of failure to progress (0.0625% bupivacaine with 0.2 microg/ml sufentanil for labour then 2% lidocaine with adrenaline for surgery). Two years later, the patient was again seen for a preanaesthetic visit because elective Caesarean section was planned. Spinal anaesthesia using hyperbaric bupivacaine and sufentanil was used. Both deliveries were uneventful and there were no neurologic complaints in the postpartum periods.

Adult↗
PubMed2004

Auditory neuropathy in hyperbilirubinemia: is there a correlation between serum bilirubin, neuron-specific enolase levels and auditory neuropathy?

This study evaluated whether a correlation exists between increased serum bilirubin and neuron-specific enolase (NSE) assays (a biochemical index of neuronal damage) and auditory neuropathy. Nineteen term neonates without hemolysis whose serum bilirubin levels were above 20 mg/dl and 27 healthy term newborns with bilirubin levels <13 mg/dl were included in the study. Auditory brainstem responses (ABRs) and transient evoked otoacoustic emissions (TEOAEs) of patients with hyperbilirubinemia were obtained before discharge. This preliminary study did not show any correlation between the serum NSE and bilirubin values. However, infants who had auditory neuropathy had significantly higher NSE levels, and thus these patients, being in the high-risk group, need close follow-up.

Auditory Diseases, Central↗