Diagnosis Of Peripheral Neuropathy Research Articles

Sobre el diagnóstico de las neuropatías periféricas: estudio clínico y neurofisiológico

The diagnosis of peripheral neuropathy is based on clinical and neurophysiological features. This study aims to establish the diagnostic validity of different symptoms and clinical signs, as well as its correlation with electroneurography (ENG), to determine its sensitivity (SE), specificity (SP), positive (PLR) and negative likelihood ratio (NLR) for every peripheral neuropathies type. A sample of 108 patients with clinical suspicion of peripheral neuropathy (pain, paresthesias, loss of strength, areflexia) was studied. ENG (nerve conduction velocity and response amplitude values in 208 nerves [Median and Posterior Tibial]) was used to confirm the diagnosis, classifying the sample in axonal group (A), demyelinating (D) and normal (N). It was made descriptive statistics of this sample, studies of SE, SP, PLR and NLR of symptoms, and association (contingency tables [Chi square] and Odds Ratio) between symptoms and clinical features. The patients with paresthesias, loss of strength or pathologic reflexes have larger motor latency (p< 0.01). Those with paresthesias, areflexia or pain have fewer sensitive conduction velocity (p< 0.05). Symptoms's value for sensory damage's diagnosis is (SE= 0.92, SP= 0.48, PLR= 1.78, NLR= 0.14). For motor damage (SE= 0.72, SP= 0.68, PLR= 2.25, NLR= 0.41). For axonal damage (SE= 0.83, SP= 0.44, PLR= 1.49, NLR= 0.37). And for demyelinating damage (SE= 0.92, SP= 0.44, PLR= 1.66, NLR= 0.16). The symptoms's combination is much more sensitive and has fewer NLR than each isolated symptom in all neuropathic damage's types. Paresthesias's presence is more indicative of sensory damage and loss of strength of motor damage. Pain is the only symptom that can aim for axonal damage than demyelinating.

Diagnostic work-up in peripheral neuropathy: an analysis of 171 cases

This study was set up to evaluate retrospectively the efficacy of a standard diagnostic procedure, including non-invasive and invasive (spinal tap, nerve/muscle biopsy) investigations, in the diagnosis of peripheral neuropathy....

Automated morphometric analysis in peripheral neuropathies

We describe a three-step algorithm for the morphometric analysis of color images of nerve specimens, currently used in the diagnosis of peripheral neuropathies. The algorithm first segments the images by applying a clustering method in the color space. It then identifies and eliminates irrelevant regions and, in the final step, calculates the diagnostic parameters required for clinical analysis. The results obtained on 25 images are reported and compared with corresponding measurements made by neurologists.

Hoffman-Tinel Sign: The Realities

The Hoffman-Tinel sign, although originally described by Paul Hoffman, is commonly referred to as the Tinel sign. It is one of the most commonly used tests in the clinical evaluation of periperhal nerves. The sign is used in the diagnosis of compression neuropathies, such as carpal and cubital tunnel syndromes, but it is also useful in the diagnosis of a variety of neurological maladies. Despite controversy, the Hoffman-Tinel sign remains important in the diagnosis of peripheral neuropathies and for the evaluation of the regenerating nerve after injury.

Recognizing peripheral neuropathy

PREVIEWNearly every day, primary care physicians see patients complaining of numbness, pain, weakness, or dizziness. Peripheral neuropathy is often the cause of these and additional symptoms, and systemic disease may be at the root of all the problems. In this article, Dr Morgenlander gives an overview of how to use physical findings, patients' descriptions of their symptoms, and the family and medical history to confirm a diagnosis of peripheral neuropathy and narrow the search for an underlying cause.

Biopsy Diagnosis of Peripheral Neuropathy

Biopsy Diagnosis of Peripheral Neuropathy

Biopsy Diagnosis of Peripheral Neuropathy

Biopsy Diagnosis of Peripheral Neuropathy

Biopsy Diagnosis of Peripheral Neuropathy, 1995. By Gyl Midroni and Juan M. Bilbao. Published by Butterworth-Heinemann. 477 pages. $C208.00

Biopsy Diagnosis of Peripheral Neuropathy, 1995. By Gyl Midroni and Juan M. Bilbao. Published by Butterworth-Heinemann. 477 pages. $C208.00

Biopsy Diagnosis of Peripheral Neuropathy

Biopsy Diagnosis of Peripheral Neuropathy

BOOK REVIEW

Book Review in this ArticlesBiopsy Diagnosis of Peripheral Neuropathy by Gyl Midroni and Juan M. Bilbao

Magnetic resonance neurography of the median nerve.

A magnetic resonance imaging sequence, combining fat and flow suppression with T2 weighting, has been used to produce high conspicuity images of the median nerve within the carpal tunnel. Standard maximum intensity projection techniques were then used to produce three-dimensional (3D) reconstructions of the nerve. Comparison of 3D projections with the wrist in a neutral position and wrist flexed at 45 degrees depicted changes in the shape and course of the median nerve through the carpal tunnel of normal volunteers. In some cases of carpal tunnel syndrome evidence of a localized compression was observed. A 3D image of a nerve may help in the diagnosis of peripheral neuropathy and be an aid to surgery of or near major nerves.

Relationships between Biomarkers of Exposure and Neurological Effects in a Group of Workers Exposed to Acrylamide

A study was performed among 41 workers heavily exposed to a mixture of acrylamide and acrylonitrile in the city of Xinxiang, Henan province, People′s Republic of China. The workers underwent a complete medical and neurological examination and provided blood and urine for the determination of several biomarkers of exposure. Among the exposed workers, signs and symptoms indicating peripheral neuropathy were found with statistically significant increased frequencies compared to a group of controls from the same city. Based on neuropathic signs and symptoms and quantifiable indicators of peripheral nervous dysfunction, such as vibration thresholds and electroneuromyography measurements, a neurotoxicity index (NIn) specific for acrylamide-induced peripheral neuropathy was designed. The NIn, which adequately predicted the clinical diagnosis of peripheral neuropathy, was significantly correlated with the levels of mercapturic acids in 24-hr urine, hemoglobin adducts of acrylamide, accumulated in vivo doses of acrylamide, employment time, and vibration sensitivity. The NIn was correlated also with hemoglobin adducts of acrylonitrile, which was explained primarily by a correlation between acrylamide and acrylonitrile exposure in this workshop. However, it was not significantly correlated with momentary measures of exposure such as concentrations of acrylamide in the air or in the plasma of exposed workers. This study is the first in which adduct monitoring has been applied to the same group of individuals in which adverse health effects have been observed. The results seem to indicate that hemoglobin adducts are useful as predictors of acrylamide-induced peripheral neuropathy and that measurements of vibration thresholds are useful for identifying early neurotoxic effects in workplaces with hazardous exposures to acrylamide.

Leigh Syndrome: Pyruvate Dehydrogenase Defect. A Case With Peripheral Neuropathy

Pyruvate dehydrogenase deficiency is one of the most common causes of encephalopathy associated with lactic acidosis and is known to account for congenital lactic acidosis, recurrent ataxia, and infantile Leigh syndrome. Hitherto, however, peripheral neuropathy has not been regarded as a presenting symptom of pyruvate dehydrogenase deficiency. Here, we report on a boy who presented peripheral neuropathy with severe limb hypotonia, absent deep-tendon reflexes, and reduced motor nerve conduction velocities at 8 months of age. Persistent hyperpyruvicemia with normal lactate/pyruvate molar ratios in plasma were highly suggestive of a pyruvate dehydrogenase deficiency, and the determination of pyruvate dehydrogenase activity in circulating lymphocytes led to the diagnosis of pyruvate decarboxylase (PDH-E1) deficiency in the proband. Based on this observation, we suggest that pyruvate dehydrogenase deficiency should be considered in the diagnosis of peripheral neuropathy in infancy, especially when associated with persistent hyperpyruvicemia, normal lactate/pyruvate molar ratios in plasma, and recurrent episodes of drowsiness and hypotonia of unknown origin.

Clinical utilization and complications of sural nerve biopsy

Surgeons frequently perform sural nerve biopsy as part of the work-up of patients with peripheral neuropathy. The indications for the procedure, therapeutic value, and complications associated with the procedure have received little attention in the surgical literature. A retrospective chart review of 60 patients with the suspected diagnosis of peripheral neuropathy undergoing sural nerve biopsy was performed. Vasculitis was suspected in 29 (48%) patients undergoing biopsy. This diagnosis was confirmed in 6 of the 29 patients and resulted in the alteration of therapy in 31% of patients with this suspected diagnosis. In 27 (45%) patients, the etiology of their peripheral neuropathy was unknown. Twelve (44%) patients in this group had sural nerve pathology; however, no change in therapy was required. Ten patients in our series had associated malignant tumors; some of these patients were diagnosed after referral for sural nerve biopsy. Twenty-five (42%) patients remained undiagnosed after biopsy. Nerve conduction studies were performed in 14 (22%) patients. Thirteen patients with abnormal lower extremity nerve conduction studies had 6 normal and 7 abnormal biopsy results. The one patient with a normal study had a normal nerve biopsy result. There were six (10%) patients with wound infections, seven (12%) patients with delayed wound healing, and three (5%) patients with new onset of chronic pain in the distribution of the sural nerve, for an overall complication rate of 27%. There was no correlation between the preoperative use of antibiotics, type of local anesthetic used, or length of nerve excised and complication rate. We conclude that the complication rate after sural nerve biopsy is significant. Strict criteria should be employed in selecting patients for sural nerve biopsy including a careful neurologic history and physical examination, nerve conduction studies, appropriate work-up for vasculitis if suspected, and implementation of a search for malignancy if this is not apparent. If the diagnosis is still in question, then sural nerve biopsy would seem appropriate, especially in patients with suspected vasculitis.

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The present study was undertaken to evaluate the influence of clinical examination and complementary tests on the diagnosis of peripheral neuropathies. Most of the patients (81.8%) were submitted to laboratory tests, 47.4% were submitted to electromyography, and 22.5% to biopsy. A syndromic diagnosis was made in 99.0% of the patients, topographic diagnosis in 98.6%, and etiological diagnosis in 73.2%. An average of 4.8 tests per patient were requested and 36 of the 93 different tests always gave normal results. The importance of the findings is discussed.

Reliability of a digital electroneurometer for the determination of motor latency of the median nerve

Measurement of distal motor latencies of the median nerve are often part of electrodiagnostic studies used to verify a diagnosis of peripheral neuropathy. Since electrodiagnostic studies are time consuming, expensive, and impractical for large-scale screening of at-risk individuals, a portable digital electroneurometer was developed for measuring motor latencies as a screening tool for early detection of nerve compression syndromes, including carpal tunnel syndrome. The purpose of this study was to determine the intertester and intratester reliability of a digital electroneurometer in subjects with (n=12) and without (n=20) clinical signs of carpal tunnel syndrome. This study addressed only the reliability and not the validity of this device. Using a repeated measures design, three evaluators performed two distal motor latency tests on the median nerve of each of the subjects. Pearson product-moment correlations for intratester reliability ranged from 0.94 to 0.99, and the intraclass correlation coefficient for intertester reliability was 0.96. Two examiners obtained statistically larger latency values on the second test, although these differences are judged to be clinically insignificant. Use of an electroneurometer may expand motor latency testing to a wider variety of settings.

Automated Morphometric Study of Human Peripheral Nerves by Image Analysis

In this paper we describe a program using the image analyzer SAMBA, which allows an automatic analysis of silver stained semithin nerve sections. The operator can interactively delimit the contour of the fascicle to be analysed by means of a digitizing tablet connected to the system which generates a mask of the region. Segmentation of the fibre images is conducted as a function of brightness threshold defined by the operator. Fibre clusters are automatically separated using morphological procedures like dilatation. Morphometric parameters such as the external and axonal diameters, myelin sheath thickness and circularity are measured. We are now testing this method on normal and pathological human superficial peroneal nerves. Preliminary results are promising and the development of adequate statistical analysis of morphometric data will provide us with a new tool for the diagnosis of peripheral neuropathies.

Aide au diagnostic electrophysiologique de la neuropathie peripherique diabetique

The electrophysiological diagnosis of peripheral neuropathy in diabetics becomes increasingly difficult with the increase in number of parameters measured. We have examined 102 subjects: 60 diabetics, 32 control subjects and 10 with impaired glucose tolerance. From the 37 recorded parameters during 8 examinations, a linear discriminant analysis allowed us to separate the 19 diabetics with clinical neuropathy and the control subjects with only 5 parameters, with a good concordance (96%): the motor conduction velocities (MCV) of the peroneal and median nerves, the amplitude of the action potential (AP) of the sural nerve, the Hmax/Mmax ratio and the M latency of the Hoffman reflex. These parameters, weighted with a coefficient, constitute a score of discrimination. This score has been tested by the Jackknife method on the same sample (94% of well-classified patients), then validated on the other patients. Thus we propose a method to aid the diagnosis of diabetic peripheral neuropathy, without the arbitrary character of the classical single parameter method, and allowing easy repetition.

Central-peripheral delayed neuropathy caused by diisopropyl phosphorofluoridate (DFP): Segregation of peripheral nerve and spinal cord effects using biochemical, clinical, and morphological criteria

Systemic injection of diisopropyl phosphorofluoridate (DFP; 1 mg/kg, sc) causes delayed neuropathy in hens. This effect is associated with a high level of organophosphorylation of neuropathy target esterase (NTE) followed by an intramolecular rearrangement called “aging.” Phenylmethanesulfonyl fluoride (PMSF) also attacks the active center of NTE but “aging” cannot occur. This compound does not cause neuropathy and protects against a subsequent challenge systemic dose of DFP. Intraarterial injection of DFP (0.185 mg/kg) into only one leg of hens caused a high NTE inhibition (>80%) in the sciatic nerve of the injected leg, but not in other parts of the nervous system (37% average). A unilateral neuropathy with typical histopathological lesions developed in the injected leg. PMSF (0.55 mg/kg) injected into each sciatic artery caused 47% inhibition of sciatic nerve NTE but only 17–22% inhibition of NTE elsewhere; it did not produce clinical or histopathological lesions. When these hens were challenged with DFP (1 mg/kg, sc), high inhibition of residual-free NTE (>85%) occurred throughout the nervous system and clinical signs of a syndrome different from the classical delayed neuropathy developed: this spinal cord type of ataxia was associated with histopathological lesions in the spinal cord but not in peripheral nerve. PMSF (1 mg/kg) injected into only one sciatic artery caused selective protective inhibition of sciatic nerve NTE of that leg. After systemic challenge by DFP, clinical effects expressed were a combination of spinal cord ataxia plus unilateral peripheral neuropathy. The challenge dose of DFP (1 mg/kg, sc) was insufficient to produce clear histopathological lesions in unprotected peripheral nerves although spinal lesions were found in these hens. Thus clinical evaluation of the peripheral nervous system by means of walking tests and a simple test of “leg retraction” reflexes was more sensitive and specific in diagnosis of peripheral neuropathy than was the histopathology.

The density of myelinated fibres is related to the fascicle diameter in human superficial peroneal nerve: Statistical study of 41 normal samples

The density of myelinated fibres in the superficial peroneal nerve was studied in 41 samples from 24 control human subjects. Photographic montages of the whole nerve fascicle were made from semithin and ultrathin transverse sections and used for a statistical analysis of sampling procedures, range of variations and relations between density and other variables. The results indicate that the spatial distribution of myelinated fibres within a nerve is often non-uniform. Therefore, it was not possible to define a statistically valid sampling system. The study of relations between variables shows the lack of any correlation between density and age and a considerable variation in the density. In contrast, there is a strong positive linear correlation between the surface area of the nerve fascicle and its content of myelinated fibres. That is, the fibre density of a given normal nerve is related to its diameter and can be predicted within a narrow range of error. We propose the term “derived density” for this value, and its application as a tool in the diagnosis of peripheral neuropathies is now being studied.