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PubMedDate not supplied

Effect of transcorneal electrical stimulation in patients with nonarteritic ischemic optic neuropathy or traumatic optic neuropathy.

PURPOSE: To determine whether transcorneal electrical stimulation (TES) can improve the visual function of patients with nonarteritic ischemic optic neuropathy (NAION) or traumatic optic neuropathy (TON). METHODS: Eight consecutive patients at the Osaka University Hospital were studied. TES (600-800 microA, 20 Hz, 30 min) was applied once each to three eyes with NAION and to five eyes with TON, using a contact lens-type stimulating electrode. The primary outcome measurement was the change in visual acuity at 1 to 3 months after TES. An improvement in visual acuity was defined as a change of > or =0.3 log (minimum angle of resolution) (logMAR) units. The side effects of TES were also investigated. RESULTS: After TES application, the visual acuity improved in two patients with NAION and in four patients with TON. Visual acuity did not worsen in any of the eyes. Only a mild superficial punctuate keratopathy was observed in all eyes immediately after TES, and it healed by the next day. CONCLUSIONS: Visual acuity can be improved after TES without major complications in some patients with NAION or TON. These results suggest that TES should be considered as a new treatment for eyes with optic neuropathy.

Adolescent↗
PubMed1985

Effects of sorbinil therapy in diabetic patients with painful peripheral neuropathy and autonomic neuropathy.

Clinical investigations with the aldose reductase inhibitor sorbinil in patients with peripheral neuropathy due to diabetes are described. After an improvement in motor and sensory nerve conduction velocities was demonstrated in asymptomatic diabetic patients taking sorbinil (compared with velocities during a placebo period), 11 patients with painful diabetic neuropathy were treated with sorbinil for three weeks without alterations in diabetic management or control. Therapy was placebo-controlled in a single-blind fashion in eight patients. Pain (assessed by or on a zero to 20 rating scale), which had been constant for many months before entry into the study and unresponsive to numerous medications, improved from a mean score of 16 to 8 and returned when the drug was discontinued. Objective improvement in sensation and strength were observed in some cases. Improvements in nerve conduction velocity and cardiac autonomic function were also documented. Cardiac autonomic neuropathy was studied in 36 patients in a double-blind, placebo-controlled, randomized, noncrossover trial. Patients received one 250-mg sorbinil tablet or one placebo tablet daily for six weeks, after a one-week baseline period. Glycemic control did not change during the study period, as indicated by unaltered glycohemoglobin levels. Response was assessed by expiration-inspiration ratios, obtained on electrocardiography during six cycles per minute respiration, and by resting minimal heart rate, both measures of vagal function. In the sorbinil-treated group, expiration-inspiration ratios improved from 1.074 +/- 0.012 to 1.096 +/- 0.020 (p less than 0.03). There was a slight decrease in the ratios in the placebo-treated group, from 1.112 +/- 0.023 to 1.105 +/- 0.023 (not significant). The difference between the Week 0 to Week 6 changes in each group was significant (p less than 0.01). Resting minimal heart rate decreased in the sorbinil-treated group from 76.4 +/- 2.3 to 66.8 +/- 2.8 +/- 2.4 beats per minute (p less than 0.001), with a mean change of 10 +/- 2. In the placebo-treated group, heart rate was unchanged (77.9 +/- 3.9 to 77.5 +/- 3.3 beats per minute). The two-sample t test of the within-group differences was also significant (p less than 0.001). The changes in both expiration-inspiration ratios and resting minimal heart rate are consistent with a sorbinil-related improvement in cardiac parasympathetic nerve function. Several isolated cases of apparent sorbinil-related improvements in autonomic symptoms have been observed.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMedDate not supplied

Clinical investigation of epalrestat, an aldose reductase inhibitor, on diabetic neuropathy in Japan: multicenter study. Diabetic Neuropathy Study Group in Japan.

A number of diabetic patients with diabetic neuropathy were treated with epalrestat, an aldose reductase inhibitor, since this drug was launched into the market in Japan. More than 5000 patients with diabetic neuropathy who were treated with epalrestat for 3-12 months were treated to analyze the efficacy and the adverse reactions of the drug in this study. The improvement rates of subjective symptoms (i.e., spontaneous pain, numbness, coldness, and hypoesthesia) was 75% (slightly improved or better) and those of nerve function tests (i.e., motor nerve conduction velocity, sensory nerve-conduction velocity, and vibration threshold) 36%. Adverse drug reactions were encountered in 129 cases (2.5%) out of 5249 patients, none of which were severe ones. Although data are limited, they strongly suggest that epalrestat is a highly effective and safe agent for the treatment of diabetic neuropathy.

Adult↗
PubMed2005

Validation of Michigan neuropathy screening instrument for diabetic peripheral neuropathy.

OBJECTIVE: The reliability and accuracy of the Michigan neuropathy screening instrument (MNSI) have been discussed recently. As a result of the difficulties of performing and analyzing nerve biopsy as a standard diagnostic test, electromyography and neuronography is used as the best alternative diagnostic procedure. The objective of this study was to determine the diagnostic performance of the test characteristics and cut-off point of MNSI scoring for the diagnosis of diabetic peripheral neuropathy. METHOD: Over a 2-year period, a cross-sectional study was conducted on 176 type 2 diabetic patients. An internist carried out the MNSI and the sum of scores varying from 0 to 1 for each abnormality as revealed in foot appearance, ulceration, ankle reflexes and vibratory perception has been recorded. A neurologist, who was blind to the MNSI scores, performed all neurophysiological studies. The test performance characteristics of the MNSI procedure were measured for different cut-off values. RESULTS: MNSI scores of 1.5, 2.0, 2.5 and 3.0 were assessed as cut-off values. Sensitivities were 79%, 65%, 50% and 35% and specificities were 65%, 83%, 91% and 94%, respectively. Positive predictive values increased and negative predictive values decreased for each score. Accuracies, likelihood ratios and post-test probabilities were measured. CONCLUSION: The accuracy of MNSI scoring makes it a useful screening test for diabetic neuropathy in taking a decision regarding which patients should be referred to a neurologist for electrophysiological studies. High specificity, likelihood ratios over 5 and a moderate to good post-test probability give a high diagnostic impact for MNSI scoring. We suggest a cut-off point of 2 for the MNSI procedure. However, electrophysiological studies should be considered when the patient has signs and symptoms other than those rated by the MNSI, suggesting peripheral nerve involvement, and also because the MNSI is still just a screening test.

Adult↗
PubMed2001

Hereditary neuropathy with liability to pressure palsies mimicking multifocal compression neuropathy.

Hereditary neuropathy with liability to pressure palsies (HNPP) is a recurrent disorder of the peripheral nervous system characterized by reversible episodes of sensorimotor deficits after neural compression injuries. Also known as tomaculous neuropathy, HNPP is further characterized ultrastructurally by multiple focal thickenings (tomacula) of peripheral myelin and has an autosomal dominant inheritance. The neuropathology of HNPP includes a partial deletion encoding the peripheral myelin protein 22 (PMP-22) gene on chromosome 17, resulting in underexpression of PMP-22. We describe multiple compression mononeuropathies in an individual with HNPP and report neuropathologic findings in 2 clinically asymptomatic family members. Diagnosis was confirmed using pulsed-field gel electrophoresis. We believe that this diagnosis is clinically underappreciated by hand surgeons and should be considered in the differential diagnosis of patients with atypical presentations of compression neuropathies.

Adult↗
PubMed2002

[Diabetes and assessment of working capability--neuropathy and autonomic neuropathy].

Up to now no obligatory guidelines for the assessment of working capability exist for patients with diabetes and peripheral and/or autonomic neuropathy. Precise investigations of clinical symptoms of an existing polyneuropathy are preconditions for this assessment. For the evaluation of the working capability a detailed analysis of working conditions and working place is necessary. Special attention is needed with respect to the prophylaxis of the diabetic foot. Cardiac autonomic neuropathy as well as the autonomic neuropathy of the gastro-intestinal tract are of importance for the assessment of working capability. In practice inadequate diagnostic procedures occur up to now and assessment of working capability is mostly not included into these diagnostic procedures. The processing of corresponding recommendations should be a common task of diabetologists and job physicians.

Diabetic Neuropathies↗
PubMed1998

Hereditary motor and sensory neuropathy--Lom, a novel demyelinating neuropathy associated with deafness in gypsies. Clinical, electrophysiological and nerve biopsy findings.

A previously unrecognized neuropathy was identified in Bulgarian gypsies, and was designated hereditary motor and sensory neuropathy-Lom (HMSNL) after the town where the initial cases were found. It was subsequently identified in other gypsy communities. The disorder, which is of autosomal recessive inheritance, was mapped to chromosome 8q24. It begins consistently in the first decade of life with gait disorder followed by upper limb weakness in the second decade and, in most subjects, by deafness which is most often first noticed in the third decade. Sensory loss affecting all modalities is present, both this and the motor involvement predominating distally in the limbs. Skeletal deformity, particularly foot deformity, is frequent. Severely reduced motor nerve conduction velocity indicates a demyelinating basis, which was confirmed by nerve biopsy. The three younger patients biopsied showed a hypertrophic 'onion bulb' neuropathy. The hypertrophic changes were not evident in the oldest individual biopsied and it is likely that they had regressed secondarily to axon loss. In the eight cases in which brainstem auditory evoked potentials could be recorded, the results suggested demyelination in the eighth cranial nerve and also abnormal conduction in the central auditory pathways in the brainstem. As no myelin genes are known to be located at chromosome 8q24, the disorder may involve a gene for a novel myelin protein or be due to an abnormality of axon-Schwann cell signalling.

Adolescent↗
PubMed2003

Clinical diagnosis of diabetic polyneuropathy with the diabetic neuropathy symptom and diabetic neuropathy examination scores.

OBJECTIVE: To evaluate the discriminative power of the Diabetic Neuropathy Symptom (DNS) and Diabetic Neuropathy Examination (DNE) scores for diagnosing diabetic polyneuropathy (PNP), as well as their relation with cardiovascular autonomic function testing (cAFT) and electro-diagnostic studies (EDS). RESEARCH DESIGN AND METHODS: Three groups (matched for age and sex) were selected: 24 diabetic patients with neuropathic foot ulcers (DU), 24 diabetic patients without clinical neuropathy or ulcers (DC), and 21 control subjects without diabetes (C). In all participants, the DNS and DNE scores were assessed and cAFT (heart rate variability [HRV], baroreflex sensitivity [BRS]), and EDS were performed (Nerve Conduction Sum [NCS] score; muscle fiber conduction velocity: fastest/slowest ratio [F/S ratio]). RESULTS: Both the DNS and the DNE scores discriminated between the DU and DC groups significantly (P < 0.001). The DNE score even discriminated between DC and C (P < 0.05). Spearman's correlation coefficients between both DNS and DNE scores and cAFT (HRV -0.42 and -0.44; BRS -0.30 and -0.29, respectively) and EDS (NCS 0.51 and 0.62; F/S ratio 0.44 and 0.62, respectively) were high. Odds ratios were calculated for both DNS and DNE scores with cAFT (HRV 4.4 and 5.7; BRS 20.7 and 14.2, respectively) and EDS (NCS 5.6 and 16.8; F/S ratio 7.2 and 18.8, respectively). CONCLUSIONS: The DNS and DNE scores are able to discriminate between patients with and without PNP and are strongly related to cAFT and EDS. This further confirms the strength of the DNS and DNE scores in diagnosing diabetic PNP in daily clinical practice.

Adult↗
PubMed1999

Assessment of gastric neuropathy using electrogastrography in asymptomatic diabetic patients. Correlation with cardiac autonomic neuropathy.

This study assessed gastric neuropathy in type 1 diabetes mellitus and its relationships with cardiac autonomic neuropathy. Fifty-four asymptomatic type 1 patients (43 +/- 12 years) and 15 healthy subjects participated in the study. Cutaneous electrogastrography (EGG) was recorded for 4 h before, during, and 4 h after the ingestion of a standard meal. EGG frequency was divided into three bands: bradygastria [< 2 cpm), normal (2-4 cpm) and tachygastria (4-10 cpm)]. Assessment of diabetic autonomic neuropathy was based on Ewing tests and time and frequency domain indexes, which were analyzed from 24-h continuous ECG recordings. Tachygastria was significantly more common in diabetic patients than in controls throughout the recording period (38 +/- 5 vs 23 +/- 11.8%, p < 0.001), before (37 +/- 6 vs 26.5 +/- 8.9%, p < 0.001), during (41 +/- 7.8 vs 23 +/- 10.5%, p < 0.001) and after the meal (37 +/- 6.9 vs 29 +/- 9.8%, p < 0.001). The percentage of dominant frequency in the normal range was significantly lower in diabetic patients than controls (49 +/- 6 vs 63.3 +/- 11.1%, p < 0.001). Tachygastria was correlated with duration of diabetes (r = 0.234, p < 0.05), but not with glycaemic control. Abnormalities in gastric myoelectrical activity were not correlated with Ewing tests or time and frequency domain indexes.

Adult↗
PubMedDate not supplied

[Hereditary neuropathy with liability to pressure palsies (tomaculous neuropathy). Clinical, electrophysical and molecular study of two affected families].

INTRODUCTION: Hereditary neuropathy with liability to pressure palsies (HNPP) is an autosomal-dominant disorder of peripheral myelin characterized by episodes of recurrent mononeuropathies usually involving nerves at common sites of entrapment and compression. Additional features include evidence of a diffuse demyelinating sensorimotor polyneuropathy on nerve conduction studies, focal myelin thickening (tomacula) on sural nerve biopsy, and a 1.5 Mb deletion on 17p11.2 encompassing the peripheral myelin protein 22 (PMP22) gene in most families. PATIENTS AND METHODS: Two girls, aged 10 and 12 years, presented with peroneal nerve palsy and peroneal nerve palsy plus tibial nerve palsy, respectively. In none case, a clear causal factor was recognizable. Neurophysiological studies: both cases showed diffuse sensory and motor nerve conduction velocity slowing and prolongation of distal motor latencies. In addition, features of focal entrapment neuropathy were obtained at proximal peroneal nerve level. Sural nerve biopsy: large axons demyelination, redundant myelin and intraaxonal looping (case 1) and tomaculas (case 2). Molecular genetics: 17p12-p11 deletion was demonstrated in both affected girls, the mother and two maternal uncles of case 1 and in the father, paternal grandfather and two paternal uncles of case 2. CONCLUSIONS: NHPP should be suspected in cases of peripheral neuropathy without clearly recognizable cause. Electrophysiological and molecular studies permit both delineation of the condition and identification of otherwise clinically normal family members.

Child↗
PubMed1984

[Diabetic neuropathies. IV. Autonomous neuropathy. Peripheral sympathetic innervation and the cardiovascular system].

The clinical conditions due to damage to the peripheral sympathetic nervous system during diabetic neuropathy mainly involve alterations to subcutaneous vasomotility , temperature body regulation and exudation, which may take form of hyper or hypoactivity. Gustatory exudation and local anhydrosis are described in detail as well as the connection with aggravating factors like long duration, poor balance and early onset of diabetes mellitus . Change in the relevant cardiovascular reflexes, commonly used in diagnosing diabetic neuropathy, are also analysed with a discussion of their physiopathological background and clinical significance. Finally the painless infarct, sudden death and abnormal response to hypoglycaemia, that are the common features of diabetic neuropathy, are also described.

Body Temperature Regulation↗
PubMed1995

African, Native American, and European mitochondrial DNAs in Cubans from Pinar del Rio Province and implications for the recent epidemic neuropathy in Cuba. Cuba Neuropathy Field Investigation Team.

Genetic predisposition, particularly specific mitochondrial DNA (mtDNA) backgrounds, has been proposed as a contributing factor in the expression of an epidemic of bilateral optic neuropathy that has affected residents of Cuba since 1991. To substantiate or refute the possibility that specific subsets of mtDNAs could participate in disease expression, we took advantage of the heterogeneous ethnic origin of the Cuban population and the recent identification of a number of mtDNA polymorphisms that appear to be specific for Africans, Native Americans, and Europeans. The screening of both carefully selected people with epidemic neuropathy and control subjects from the Pinar del Rio Province for these polymorphisms revealed that African, Native American, and European mtDNA haplotypes were equally represented among case and control subjects, and suggested that approximately 50% of Cuban mtDNAs originated from Europeans, 46% from Africans, and 4% from Native Americans. These findings demonstrate that mutations arising in specific mtDNAs are unlikely to play a role in the epidemic neuropathy and indicate that analysis of mtDNA haplotypes can be a valuable tool for assessing the relative maternal contribution of Africans, Native Americans, and Europeans in a mixed population.

Africa↗
PubMed1995

Vincristine neuropathy in type I and type II Charcot-Marie-Tooth disease (hereditary motor sensory neuropathy).

A patient with Ewing's sarcoma and demyelinating type Charcot-Marie-Tooth disease (CMT) developed severe neuropathy after receiving a total vincristine dose of 6 mg. Recovery was slow and incomplete. A second patient with axonal type CMT developed moderate neuropathy but tolerated extended vincristine administration and recovered quickly. Possible underlying neuropathy should be excluded before vincristine treatment is begun by careful examination including inspection of the feet, followed by electrophysiologic studies as indicated. In demyelinating CMT, vincristine should be avoided; in axonal form cautious use may be considered.

Adolescent↗
PubMed2001

Pyridoxine-induced neuropathy in rats: a sensory neuropathy that responds to 4-methylcatechol.

Sensory neuropathies are frequently associated with diabetes or with antimitotic treatments in humans suffering from cancer, and are in this case the most important limitation to the use of antimitotic drugs. For this reason, there is a need to establish and validate animal models of sensory neuropathies that could be routinely used, together with the already known models, for studying and evaluating the effects of putative neuroprotective compounds. In the present study, we prove by behavioral and electromyographical analyses that (a) it is possible to induce a nonlethal, exclusively sensory, reversible neuropathy by intoxicating rats with large amounts of pyridoxine, using a new schedule of intoxication; (b) 4-methylcatechol, a drug known to induce nerve growth factor synthesis, improves the clinical status of pyridoxine-intoxicated animals, shortens the duration of the disease, and restores the morphological integrity of the sensory fibers. Owing to its mode of installation and its clinical features, we propose that this model be used as an additional model for preclinical studies of neuroprotective drugs.

Animals↗
PubMed1997

Sensory neuropathies including painful and toxic neuropathies.

In most peripheral neuropathies, dysfunction of motor and sensory nerve fibres is present. However, in some of them either pattern may predominate or be exclusively present. In this review we describe the clinical characteristics of sensory neuropathies, with emphasis on their possible causes. Guidelines are given for the diagnostic approach in these patients and, where possible, suggestions are given for treatment, including symptomatic treatment of painful neuropathies.

Humans↗
PubMed1998

[Quantitative thermotest - investigations of thermal and nociceptive afferents in neuropathy. Is a multicentric approach useful to investigate rare painful neuropathies?].

Disturbances of small afferent nerve fibres play an important role in painful neuropathies. Quantitative thermotest offers a possibility to quantify these disturbances that can not be detected by conventional electrophysiology. It is a psychophysical method to investigate thermal and nociceptive afferents by determining thermal thresholds. Former experiences have shown that quantitative thermotest can be a helpful tool not only in daily routine but also for research work concerning pathophysiological mechanisms of neuropathy. Therefore a multicentric approach to investigate rare painful neuropathies seems to be useful.

English Abstract↗
PubMed1988

Guanethidine adrenergic neuropathy: an animal model of selective autonomic neuropathy.

Chronic administration of guanethidine to adult rats induces a selective autoimmune adrenergic neuropathy. Physiological and biochemical features of this disorder in the peripheral nervous system were explored in young adult Sprague-Dawley rats given daily intraperitoneal guanethidine monosulfate for 5 weeks. Control rats received daily saline injections. The guanethidine-treated animals gained less weight, had ptosis, and had a lower mean arterial blood pressure in the supine and upright tilted positions. Norepinephrine was depleted in the peroneal, sural, tibial, and vagal nerves, the nutrient artery to the tibial nerve and in the superior cervical sympathetic ganglion of the drug-treated animals. On light microscopy, there was an inflammatory cell infiltrate and neuron loss in the superior cervical ganglion. Caudal and sciatic-tibial nerve conduction values were well preserved in the guanethidine-treated animals as was the 'C' potential derived from unmyelinated vagal fibers recorded in an in vitro chamber. The 'C' potential recorded from the cervical sympathetic trunk, however, was reduced in amplitude correlating with the loss of norepinephrine content in the harvested contralateral superior cervical sympathetic ganglion. The findings further support the view that guanethidine produces a selective adrenergic neuropathy in the rat--providing a useful standard with which to gauge autonomic involvement in other models of neuropathy. In addition, loss of the cervical sympathetic 'C' potential suggests that this presumed preganglionic structure also contains postganglionic adrenergic fibers.

Animals↗
PubMedDate not supplied

Bedside neuropathy disability score compared to quantitative sensory testing for measurement of diabetic neuropathy in children, adolescents, and young adults with type 1 diabetes.

BACKGROUND: While regular yearly screening for diabetic retinopathy and nephropathy is well established in patients with diabetes mellitus, there are no standardized diagnostic tests for diabetic peripheral neuropathy (DPN). In the present study, we compared the bedside neuropathy disability score (NDS) with quantitative sensory testing (QST) for screening for DPN in youth with type 1 diabetes mellitus. METHODS: One hundred sixty-six patients aged 10 to 34 years (median 21 years) were evaluated for DPN by the NDS and QST. Quantitative sensory testing was also done in 43 healthy, age-matched controls. Diabetic peripheral neuropathy grade by both methods was correlated with disease-related variables. RESULTS: On QST, the diabetic group had significantly higher mean scores for vibration (P<.001) and warm sensation (P<.01) than controls, and lower scores for cold sensation (P<.05); however, there was a great degree of overlap. The NDS significantly correlated with the vibration threshold, but not with the warm and cold thresholds. The NDS significantly correlated with age at testing, diabetes duration, and long-term and current HbA1c levels (P<.001), and with the presence of microalbuminuria and diabetic retinopathy (P<.001). Analysis of the QST variables yielded significant correlations of vibration and warm sensation with age at testing (P<.001, P<.05, respectively) and of vibration with diabetes duration (P<.001) and retinopathy (P=.05); none of the quantitative tests correlated with glycemic control. CONCLUSIONS: The stronger association of the NDS with glycemic control and other microvascular complications compared to the perception thresholds, and its shorter time of performance and lack of costly equipment, may make the NDS the preferred method for measuring DPN in this population.

Adolescent↗