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Results for “Polyneuropathies”

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At least 91 records · Page 5Linked to original sources

PubMed2001

Sural nerve T cells in demyelinating polyneuropathy associated with monoclonal gammopathy.

The clinical presentation of polyneuropathy associated with monoclonal gammopathy is heterogeneous. As T cells in sural nerve biopsy specimens may represent a marker of inflammation, we analyzed whether the presence of sural nerve T cells in patients with demyelinating polyneuropathy associated with monoclonal gammopathy may help to define a specific clinical entity. Using immunohistochemical analysis we investigated the number and distribution of sural nerve T cells in 18 patients with polyneuropathy associated with IgM monoclonal gammopathy (including 14 with antibodies to the myelin-associated glycoprotein) and 7 with IgG monoclonal gammopathy, and compared them with sural nerves of 23 patients with chronic inflammatory demyelinating polyneuropathy (CIDP), 15 patients with chronic idiopathic axonal polyneuropathy (CIAP), and 10 normal controls. Six patients with polyneuropathy associated with monoclonal gammopathy had increased T cell densities compared with CIAP patients and normal controls. No differences were found in distribution or phenotype of the T cells. T cell densities in patients with IgM monoclonal gammopathy were significantly lower than in patients with IgG monoclonal gammopathy or with CIDP. Increased sural nerve T cells were significantly associated with a subset of patients who had a more progressive disease course and more pronounced weakness. Increased sural nerve T cells were found significantly more often in patients with a monoclonal gammopathy of the IgG isotype, which was frequently associated with hematological malignancy.

Adult↗

PubMed2000

Screening for HIV-associated distal-symmetric polyneuropathy in CDC-classification stages 1, 2, and 3.

OBJECTIVES: A total of 670 patients were screened for distal symmetric HIV-associated polyneuropathy during CDC stages 1-3 and its correlation to immunological deterioration. MATERIAL AND METHODS: Clinical examinations of 670 patients admitted to the neurological outpatient clinic at the Department of Neurology, University of Munster. Neurophysiological investigations were performed on the sural and peroneal nerve for detection of axonal and myelin lesion. RESULTS: Clinical examination proved progressive clinical signs and symptoms indicating distal symmetric polyneuropathy from CDC 1 (32%) to CDC 3 (55%). At least one neurophysiological result was impaired in CDC 1 in 25% and in CDC 3 in 45%. Significant correlation between neurophysiological changes and CDC4(+)-cells and beta-microglobuline were detected for stage CDC 3 C. CONCLUSION: Results show stage related prevalence of distal symmetric polyneuropathy already in early stages. In late stages of HIV-infection prevalence of distal symmetric polyneuropathy seems to be directly correlated to immunodeficiency syndrome. The pathogenesis of distal symmetric polyneuropathy during HIV-infection is up to now incompletely understood, but results indicate a clear dependency between progressive immunological dysfunction and neuropathy. High active antiretroviral therapy in patients suffering from distal symmetric polyneuropathy is a main topic of future studies.

Adult↗

PubMedDate not supplied

An open-label study of the lidocaine patch 5% in painful idiopathic sensory polyneuropathy.

OBJECTIVE: Painful idiopathic distal sensory polyneuropathy is common, but has been largely ignored as a model for the evaluation of neuropathic pain therapies. We have therefore conducted a safety, tolerability, and effectiveness study of the lidocaine patch 5% in painful idiopathic distal sensory polyneuropathy. DESIGN: A prospective open-label, flexible dosing, 3-week study period with a 5-week extension. SETTING: Peripheral Neuropathy clinics and Anesthesiology Clinical Research Center at a tertiary care facility. PATIENTS: Twenty subjects with a diagnosis of idiopathic distal sensory polyneuropathy (with or without associated impaired glucose tolerance), with a baseline mean pain daily rating of > or =4 on a visual analog scale. Intervention. Lidocaine patch 5%, maximum of four patches daily for 18 hours. MAIN OUTCOME MEASURE: Change from baseline week to week 3 mean daily diary pain ratings. Secondary endpoints included assessments of safety and tolerability as well as quality of life measures. RESULTS: Subjects with idiopathic distal sensory polyneuropathy, both with and without impaired glucose tolerance, showed significant improvements in pain and quality of life outcome measures over a 3-week treatment period. These improvements were maintained in a subgroup of patients treated for an additional 5 weeks and permitted a taper of concomitant analgesics in 25% of subjects. The lidocaine patch 5% was well tolerated. CONCLUSIONS: The lidocaine patch 5% appeared well tolerated and potentially effective in the management of painful idiopathic distal sensory polyneuropathy. Idiopathic distal sensory polyneuropathy is an appropriate patient population for the conduct of clinical trials of neuropathic pain therapies.

Administration, Topical↗

PubMed2000

Polyneuropathies of cats.

Polyneuropathies of cats have a variety of clinical presentations. Areflexic flaccid quadriparesis, or quadriplegia, progressing over a 24- to 48-hour period, may be associated with polyneuropathies, as can chronic insidiously progressive tremors and muscle weakness that wax and wane or progress slowly over weeks or months, and which can go undiagnosed for years. In addition, these neurological signs may be due to spinal cord, neuromuscular junction or muscle disorders, so the diagnosis of polyneuropathy can be a challenge even for the most astute of clinicians. Polyneuropathies may have congenital, inherited, inflammatory, metabolic and toxic causes. Sometimes the underlying aetiology is not found and a diagnosis of idiopathic polyneuropathy is made. Since the treatment and prognosis of polyneuropathies in cats vary, the purpose of this review is to assist the veterinary practitioner to recognise, appropriately manage and provide an accurate prognosis for these challenging cases.

Animals↗

PubMed2005

Diphtheria with polyneuropathy in a closed community despite receiving recent booster vaccination.

INTRODUCTION AND METHODS: We report 20 patients aged 18-24 years from Latvia with diphtheritic polyneuropathy. All lived in a closed community and 80% were known to have been fully vaccinated against diphtheria until at least 14 years old. Diphtheria antitoxin had been administered within 3 days of the onset of upper respiratory tract infection in 16 patients and 15 received antibiotics. RESULTS: Neurological symptoms developed after a median of 43 days (range 35-58) compared to only 10 days in previous studies of unvaccinated patients. All showed evidence of mild limb polyneuropathy with electrophysiological evidence of polyneuropathy. Only 30% showed early bulbar abnormalities compared to the usual rate of over 95% in diphtheritic polyneuropathy. However, 45% had later bulbar deterioration coinciding with the limb polyneuropathy. CONCLUSIONS: These patients show that an attenuated form of polyneuropathy of later onset, with less prominent early bulbar features, can occur in patients vaccinated against diphtheria according to schedule but living in a closed community in a country where diphtheria remains endemic.

Adolescent↗

PubMed2000

Current perception threshold: an adjunctive test for detection of acquired demyelinating polyneuropathies.

Current Perception Threshold (CPT) evaluation quantifies the sensory threshold to transcutaneous electrical stimulation of three sensory fiber subtypes: A-beta (2,000 Hz), A-delta (250 Hz) and C fibers (5 Hz). Demyelinating polyneuropathies tend to affect larger myelinated fibers before smaller unmyelinated fibers, and they usually begin at the proximal nerve roots or terminal axons, due to relative weakness of the blood-nerve barrier in these locations. Axonal polyneuropathies tend to affect smaller fibers before larger fibers, in a distal to proximal gradient. Ten patients with demyelinating polyneuropathy and ten patients with axonal polyneuropathy underwent CPT testing. CPT comparisons were made with regard to side-to-side asymmetries, fiber type involvement, and the ratio of fiber types involved. The C2, lateral antebrachial cutaneous, and sural distributions were examined bilaterally. Demyelinating polyneuropathies were detected with 50% sensitivity and 100% specificity. This diagnostic sensitivity is similar to that of published criteria based upon motor nerve conduction. CPT testing can distinguish demyelinating from axonal polyneuropathies. It may be particularly helpful in patients with predominantly sensory symptoms in whom EMG/NCS data may be equivocal, or in patients who decline EMG/NCS studies.

Action Potentials↗

PubMed2001

[The value of electroneurography in recognition of peripheral ischaemic polyneuropathy in patients suffering from critical leg ischaemia].

Peripheral arteries disorders cause not only leg ischaemia, but also peripheral polyneuropathy. Polyneuropathy increases ischaemic pain. The aim of this study was to estimate how many patients suffering from critical leg ischaemia have symptoms of peripheral polyneuropathy. 40 patients were investigated: 37 men and 3 women; mean age was 57 years. All patients underwent electroneurographic examination. It consisted of measurements of motor conduction in tibial and peroneal nerves, wave F, sensory conduction in sural nerve. Polyneuropathy was observed in 95% of patients. The frequency of polyneuropathy was also significantly enlarged in leg with non critical ischaemia. We did not observe the greater risk of polyneuropathy in diabetic patients. The work is an introduction to the following clinical studies.

Adult↗

PubMed1997

Sural/radial amplitude ratio in the diagnosis of mild axonal polyneuropathy.

As proximal nerves are relatively spared in length-dependent, axonal polyneuropathy, we theorized that a sural/radial amplitude ratio (SRAR) might be a sensitive indicator of mild polyneuropathy. In this study, sural amplitudes and SRARs in patients with signs of mild axonal polyneuropathy were compared to those of normal, age-matched control subjects. Sural and radial sensory responses were measured in a standard fashion in all subjects. Thirty polyneuropathy patients had an average SRAR of 0.29 as compared to 0.71 for the 30 normal subjects. An SRAR of less than 0.40 was a strong predictor of axonal polyneuropathy, with 90% sensitivity and 90% specificity, as compared to an absolute sural amplitude of less than 6.0 microV, which had sensitivity of only 66%. Additionally, unlike the sural amplitude, the ratio did not vary significantly with age. We conclude that the SRAR is a sensitive, specific, age-independent electrodiagnostic test for mild axonal polyneuropathy.

Adult↗

PubMed1992

The relative diagnostic sensitivity of different F-wave parameters in various polyneuropathies.

We studied F-wave minimum latency, persistence, and chronodispersion in the median and ulnar nerves of 70 controls and 75 patients with various polyneuropathies. Prolonged minimum latency was the most frequent F-wave abnormality in all groups of patients with polyneuropathy. The finding of decreased persistence or absence of F-responses was comparable in sensitivity to prolonged minimum latency in Guillain-Barré syndrome (GBS) and chronic inflammatory demyelinating polyneuropathy (CIDP), whereas chronodispersion had a comparable sensitivity only in CIDP. Decreased persistence of obtained F-responses, and the absence of F-responses in nerves with low compound muscle action potential amplitudes, were nonspecific findings. F-wave studies often provide useful additional information in the evaluation of patients suspected of having a polyneuropathy. In patients with axonal polyneuropathies, we found that F-wave studies are significantly more sensitive than standard motor conduction studies in identifying physiological abnormalities of motor axons. Furthermore, in a patient with an acquired polyneuropathy, the finding of markedly prolonged minimum latency, or the absence of F-responses in nerves with normal CMAP amplitude, is highly specific for the presence of demyelination.

Adult↗

PubMed1982

Microneurographic findings in diabetic polyneuropathy with special reference to sympathetic nerve activity.

Microneurographic recordings of naturally occurring nerve activity in the median or peroneal nerve were made in 25 patients with diabetes mellitus, 17 of whom had signs of polyneuropathy. In patients without polyneuropathy, the electrical findings did not differ from those in healthy subjects. In patients with polyneuropathy, sensory afferent impulses were always normal qualitatively, whereas muscular afferent activity was weak or entirely absent in some patients. Sympathetic activity, if found, showed normal characteristics in muscle and skin fascicles, except that it was difficult to obtain a good signal-to-noise ratio. In 16 of 25 recordings with the electrode positioned intraneurally, sympathetic activity could not be detected in patients with polyneuropathy. The failures correlated with impaired skin sympathetic effector organ responses and reduction of motor nerve conduction velocity. The results suggest that impairment of sympathetic outflow occurs frequently in diabetic polyneuropathy and that sympathetic involvement occurs earlier than in many other types of polyneuropathy.

Diabetic Neuropathies↗

PubMed1996

Critical illness polyneuropathy in multiple organ dysfunction syndrome and weaning from the ventilator.

BACKGROUND: Acute axonal polyneuropathy has been found in patients with multiple organ dysfunction syndrome. This 'critical illness polyneuropathy' (CIP) has been associated with difficult weaning from the ventilator in retrospective studies. OBJECTIVE: To test the hypothesis that CIP is related to the degree and number of organ dysfunctions, and to weaning problems. DESIGN: Prospective study of 18 months. SETTING: A multidisciplinary intensive care unit in a general hospital SUBJECTS: Thirty-eight patients under 75 years of age who had been mechanically ventilated for more than 7 days, without previous signs of or risk factors for polyneuropathy. MEASURES: Organ dysfunctions were quantified using a dynamic scoring system (0-12 points). Electromyography studies were performed during mechanical ventilation to identify patients with and without CIP. RESULTS: CIP was present in 18 out of 38 patients and associated with an increased organ dysfunction score (5.3 +/- 1.8 vs. 3.6 +/- 1.5; p = 0.003) and number of organs involved [median (range): 4 (3-5) vs. 2 (1-4); p = 0.009], in particular cardiovascular (p = 0.003), renal (p = 0.04), and hematopoietic failure (p = 0.04). Patients with polyneuropathy were ventilated longer, but this was not clearly due to more difficult weaning [median: 16.5 (1-48) vs. 9.5 (1-38) days; p = 0.26]. Polyneuropathy was present in 2 of 4 patients with normal weaning. CONCLUSIONS: Axonal polyneuropathy is related to the severity of multiple-organ-dysfunction syndrome. Its presence does not necessarily implicate difficult weaning from artificial ventilation.

APACHE↗

PubMed1993

Immunofixation superior to plasma agarose electrophoresis in detecting small M-components in patients with polyneuropathy.

Monoclonal immunoglobulins (M-components) in blood are found in some patients with polyneuropathy and are thought to be of pathogenetic importance, especially if the M-component is of IgM isotype. As the finding of an M-component may indicate a treatable polyneuropathy, the potential of the method to uncover an M-component is of importance. Cellulose acetate or agarose electrophoresis used in routine practice may miss small M-components covered by other proteins. We therefore applied the uncovering and specific method of immunofixation in comparison with agarose electrophoresis on patients investigated for polyneuropathy. Of 83 consecutive patients, 5 had M-components. Two of these 5 patients, one with an axonal polyneuropathy and the other with a lower motor neuron syndrome, had extra bands on agarose electrophoresis, verified as IgG M-components by immunofixation. In the 3 additional patients an M-component was uncovered only by immunofixation, not seen in the agarose electrophoresis of plasma; 2 of them were of IgM isotype and one was of IgG isotype. These 3 patients were diagnosed as having a demyelinating (i.e., possibly immune-mediated) polyneuropathy by means of neurophysiology and in one by means of nerve biopsy. A 6th patient had 2 small bands in the gamma region on the agarose electrophoresis, verified as oligoclonal bands of IgG isotype by immunofixation but was not judged as an M-component. Three out of the 83 patients, were judged as having motor neuron diseases. All remaining 80 were found to have polyneuropathy.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed2003

Interdigital nerve conduction study of the foot for an early detection of diabetic sensory polyneuropathy.

OBJECTIVE: To report on the value of interdigital nerve (IDN) conduction study (NCS) of the foot for the recognition of diabetic sensory polyneuropathy with normal routine NCS and the nature of electrophysiological abnormality in early diabetic sensory polyneuropathy. METHODS: The sensory nerve conductions in the two digital and 4 IDNs of the foot were obtained orthodromically using the near-nerve needle and signal averaging technique. RESULTS: In 21 patients with diabetic sensory polyneuropathy with normal routine NCS, a definite neuropathy pattern (abnormalities in more than 3 of 6 tested nerves) was observed in 12 patients (57.1%). The most common abnormalities that were found were a low amplitude in the sensory compound nerve action potential and an absent potential, indicating that early diabetic sensory polyneuropathy is due to axonal degeneration. CONCLUSIONS: Interdigital NCS of the foot using near-nerve needle technique can identify neuropathy in diabetic sensory polyneuropathy with normal routine NCS. This technique offers a useful means of detecting nerve conduction abnormalities in the early stage of diabetic polyneuropathy.

Adult↗

PubMed1992

Plasma-cell dyscrasia with polyneuropathy. The spectrum of POEMS syndrome.

BACKGROUND: The POEMS (polyneuropathy, organomegaly, endocrinopathy, monoclonal gammopathy, and skin changes) syndrome and osteosclerotic myeloma (polyneuropathy and sclerotic bone lesions) may both be manifestations of plasma-cell dyscrasia, but the interrelation of these diseases is not clear. We therefore set out to define the clinical spectrum of disease in patients with plasma-cell dyscrasia and polyneuropathy who have the complete or incomplete form of the POEMS syndrome or osteosclerotic myeloma. METHODS: Among 2714 patients with plasma-cell dyscrasia who were identified between 1973 and 1989, we reviewed the cases of those with polyneuropathy and plasma-cell dyscrasia who fulfilled the criteria for the POEMS syndrome or osteosclerotic myeloma. RESULTS: Thirty-eight patients (1.4 percent) with a median age of 51 years were identified, 22 of whom were male. By definition, all had polyneuropathy (37 combined sensorimotor, and 1 primarily motor). Other findings included osteosclerotic bone lesions (82 percent), skin abnormalities (58 percent), lymphadenopathy (42 percent), papilledema (37 percent), peripheral edema (29 percent), hepatomegaly (24 percent), splenomegaly (21 percent), and ascites (11 percent). Thirty-three patients (87 percent) had an abnormal M protein in serum or urine (17 had IgA lambda, and 12 IgG lambda). Five patients fulfilled all the criteria for the POEMS syndrome. The estimated five-year survival in the 38 patients was 60 percent, which was significantly better than the 20 percent survival in 869 patients with multiple myeloma (P < 0.05). The clinical course was similar among the patients with the complete form of the POEMS syndrome and those with the incomplete form. CONCLUSIONS: Plasma-cell dyscrasia with polyneuropathy is a rare multisystem disease that often presents with osteosclerotic bone lesions. The differentiation of the POEMS syndrome from so-called osteosclerotic myeloma with peripheral neuropathy appears to have no clinical value.

Adult↗

PubMed1992

Clinical examination versus neurophysiological examination in the diagnosis of diabetic polyneuropathy.

Several methods have been used to diagnose diabetic polyneuropathy and to quantitate the degree of affection of peripheral nerves. Using a newly developed scoring system we compared bedside clinical examination with neurophysiological examination in a group of 78 diabetic patients. Individual scores for clinical examination were significantly correlated with scores for neurophysiological examination (r = 0.7, p < 0.0005). All 78 patients had at least one clinical symptom or sign of polyneuropathy. Clinical examination indicated polyneuropathy in three patients with neuropathic complaints, while neurophysiological examination in these patients showed no abnormalities. In 12 out of 14 patients with normal neurophysiological sensory nerve function, clinical examination showed at least one abnormal sensory modality. Comparing the four different sensory modalities, light touch sense and pinprick sense indicated polyneuropathy better than vibration or position senses. An abnormal Hoffmann reflex of the soleus muscle was always associated with a decreased or absent ankle jerk. The scoring system for the clinical examination proved useful for diagnosing and quantitating the severity of diabetic polyneuropathy. Clinical sensory deficits could not be inferred from the results of neurophysiological testing of sensory nerve function. Pinprick sense, light touch sense, and ankle jerks were the most important parameters in the clinical diagnosis of diabetic polyneuropathy.

Diabetic Neuropathies↗

PubMed2005

Foot temperature in diabetic polyneuropathy: innocent bystander or unrecognized accomplice?

AIM: To explore mechanisms by which temperature could influence the pathogenesis and symptoms of diabetic polyneuropathy. METHODS: We conducted a literature review attempting to identify mechanisms by which diabetic polyneuropathy could be affected by temperature. RESULTS: Cooling can theoretically hasten the progression of diabetic polyneuropathy through several different mechanisms. Specifically, cooling can enhance neuronal ischaemia, increase formation of reactive oxygen species, slow axonal transport, increase protein kinase C activity, and interfere with immune function. Short-term temperature fluctuations (both warming and cooling) can initiate and exacerbate neuropathic pain by causing neuronal hyperexcitability and functional deafferentation. Although normal fluctuations of distal extremity temperature may be sufficient for these effects, impaired thermoregulation may make the distal extremities more susceptible to temperature extremes. Eventually, a 'vicious cycle' may ensue, resulting in neuronal deterioration with further disruption of temperature regulation. Limited epidemiological data suggest a higher prevalence of diabetic polyneuropathy in populations living in colder locations, supporting our hypothesis. CONCLUSIONS: Variations in foot temperature may play an important but as yet unrecognized role in the development and symptoms of diabetic polyneuropathy. Further basic and clinical research exploring this concept could help elucidate the natural history of diabetic polyneuropathy and lead to novel therapeutic strategies.

Body Temperature↗

PubMed1996

Anti-GM1 antibodies in polyneuropathies of unknown origin.

This study was undertaken to determine whether anti-GM1 titres are raised in polyneuropathies of unknown origin and whether determination of these titres is useful for diagnosing these conditions. The study population comprised 20 controls (aged 36-88 years), 12 patients with polyneuropathies of known origin (aged 31-81 years) and 15 patients with polyneuropathies of unknown origin (aged 40-77 years). Antibody levels were measured using a commercial GM1 enzyme linked immunosorbent assay kit (Buehlmann Laboratories). Mean anti-GM1 IgG and IgM antibody titres were not raised in patients with polyneuropathies of unknown origin. Anti-GM1 IgG antibody titres were raised in one and GM1 IgM antibody titres in none of the patients with polyneuropathies of unknown origin. In conclusion, GM1 antibody levels are rarely raised in polyneuropathies of unknown origin and probably play a minor role in the pathogenesis of these conditions.

Adult↗

PubMed1987

Neurotoxic effects of n-hexane on the human central nervous system: evoked potential abnormalities in n-hexane polyneuropathy.

An outbreak of n-hexane polyneuropathy as a result of industrial exposure occurred in printing factories in Taipei area from December 1983 to February 1985. Multimodality evoked potentials study was performed on 22 of the polyneuropathy cases, five of the subclinical cases, and seven of the unaffected workers. The absolute and interpeak latencies of patterned visual evoked potential (pVEP) in both the polyneuropathy and subclinical groups were longer than in the normal controls. The pVEP interpeak amplitude was also decreased in the polyneuropathy cases. Brainstem auditory evoked potentials (BAEP), showed no difference of wave I latency between factory workers and normal controls, but prolongation of the wave I-V interpeak latencies was noted, corresponding with the severity of the polyneuropathy. In somatosensory evoked potentials (SEPs), both the absolute latencies and central conduction time (CCT) were longer in subclinical and polyneuropathy cases than in the unaffected workers and normal controls. From this evoked potentials study, chronic toxic effects of n-hexane on the central nervous system were shown.

Adolescent↗