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At least 127 records · Page 7Linked to original sources

PubMed1994

Upper limb pain in chronic demyelinating polyneuropathy: electrophysiological correlates.

Pain is not usually considered a symptom of chronic relapsing demyelinating polyneuropathy. We report two patients with chronic demyelinating polyneuropathies in whom clinical and electrophysiological worsening was associated with the development of deep and distressing upper limb aching discomfort. One patient had a MGUS-associated hypertrophic demyelinating and prednisone-dependent polyneuropathy, followed over a course of two and a half years. His discomfort regularly predicted electrophysiological relapse of neuropathy, before more obvious clinical signs had emerged. Resolution of the discomfort also predicted subsequent clinical and electrophysiological improvement. Upper limb pain may be an important feature of early relapse in some patients with demyelinating polyneuropathies. Standardized serial electrophysiological testing in patients with chronic demyelinating polyneuropathy can be an important management tool in conjunction with clinical signs and symptoms.

Arm↗

PubMed2005

Follow up of patients with signs and symptoms of polyneuropathy not confirmed by electrophysiological studies.

The outcome and final diagnoses of patients with symptoms and/or signs suggestive of polyneuropathy, but with normal electrophysiological studies, were investigated. All patients who presented at the outpatient clinic between 1993 and 1998 with signs and symptoms suggestive of polyneuropathy, but in whom electrophysiological studies were normal, were included. We retrospectively collected data from the medical records and then interviewed the patients and used the Sickness Impact Profile scale to investigate functional status at least 2 years after presentation. We included 74 patients, of whom 39 had neurological signs at neurological examination at the first visit. A final diagnosis was made in 24 of the 39 patients with neurological signs, and in three of the 35 patients without neurological signs but with symptoms. One (3%) of the 35 patients without neurological signs at the first visit had a poor outcome versus 15 (39%) of the 39 patients with neurological signs. In 11 (41%) of the 27 patients in the group with a final diagnosis the outcome was poor versus 5 (11%) of 47 patients without a final diagnosis. In 11 patients we concluded that they probably had small fibre neuropathy. Patients presenting with symptoms of polyneuropathy but who have neither neurological signs of polyneuropathy nor electrophysiological studies confirming a polyneuropathy have a good outcome at least 2 years after presentation. Further investigations are not indicated, except for patients fulfilling the criteria of small fibre neuropathy. In patients with neurological signs, as the outcome depends on the diagnosis and an explanation for these signs is often found, repeated investigations in this group are mandatory.

Adult↗

PubMed2001

Diagnostic investigation of patients with chronic polyneuropathy: evaluation of a clinical guideline.

OBJECTIVE: (1) To evaluate a clinical guideline for the diagnostic investigation of patients presenting with signs and symptoms (present for longer than 6 weeks) suggesting a chronic polyneuropathy. (2) To investigate the contribution of electrophysiological studies to a focused search for aetiology in these patients. METHODS: A chart review was carried out of a consecutive group of outpatients in 1993-7 at a university department of neurology, with signs and symptoms suggesting a polyneuropathy in whom the diagnostic investigation had been carried out according to a recently introduced guideline. Diagnostic tests were performed and final diagnoses were made. RESULTS: Unnecessary investigations were carried out in 108 (51%) of 213 patients and too few tests in 23 (11%) of these patients. In 82 (48%) of the 172 patients who fulfilled the inclusion criteria neurophysiological tests did not contribute to the final diagnosis. Neurophysiological criteria for demyelination were fulfilled in only 13 (8%) of the 172 patients. CONCLUSION: In patients presenting with signs and symptoms of chronic polyneuropathy the number of tests in the diagnostic investigation can be considerably reduced. In patients with signs and symptoms of polyneuropathy, providing the clinical phenotype is typical, in the presence of diabetes mellitus, renal failure, HIV infection, alcoholism, or use of potentially neurotoxic drugs further investigations are non-contributory. The significance of electrophysiological studies in the investigation of patients with polyneuropathy is rather to separate sensorimotor neuropathies from pure sensory neuropathies than to distinguish between demyelinating and axonal neuropathies.

Chronic Disease↗

PubMed2001

Postgastrectomy polyneuropathy with thiamine deficiency.

OBJECTIVE: Polyneuropathy has been reported after gastrectomy performed to treat various lesions. Although thiamine deficiency is a possible cause of this neuropathy, the pathogenesis still remains to be clarified. Seventeen patients with peripheral neuropathy with thiamine deficiency after gastrectomy are described. METHODS: Seventeen patients with polyneuropathy after gastrectomy accompanied by thiamine deficiency were selected. Patients were restricted to those with total or subtotal gastric resection to treat ulcer or neoplasm. Patients who had undergone operations to treat morbid obesity were excluded. RESULTS: Intervals between the operation and onset of neuropathy varied from 2 months to 39 years. Most patients did not seem malnourished. Serum concentrations of B vitamins other than thiamine were nearly normal. Symmetric motor-sensory polyneuropathy, predominantly involving the lower limbs, had progressed over intervals varying from 3 days to 8 years. Relative degrees of motor and sensory impairment also varied extensively. Some cases that progressed rapidly mimicked Guillain-Barré syndrome. Electrophysiological and pathological findings were those of axonal neuropathy. Substantial functional recovery from polyneuropathy was seen in most patients by 3 to 6 months after initiating thiamine supplementation. Motor recovery was better than sensory recovery. CONCLUSIONS: Various symptoms were seen in patients with postgastrectomy neuropathy. Thiamine deficiency should be considered in the differential diagnosis of motor-sensory polyneuropathy after gastrectomy.

Activities of Daily Living↗

PubMed2002

Clinimetric evaluation of a new overall disability scale in immune mediated polyneuropathies.

OBJECTIVES: To determine the validity, reliability, and responsiveness of a new overall disability sum score in immune mediated polyneuropathies. METHODS: Three impairment measures (MRC sum score, sensory sum score, grip strength (Vigorimeter)) and three disability scales (an overall disability sum score (ODSS), Hughes' functional scale (f score), Rankin scale) were assessed in a cross sectional group of 113 clinically stable patients (83 with Guillain-Barré syndrome, 22 with chronic inflammatory demyelinating polyneuropathy (CIDP), eight with a gammopathy related polyneuropathy). The ODSS was also used serially in 20 patients with recently diagnosed Guillain-Barré syndrome (n = 7) or CIDP (n = 13) and changing clinical conditions. Multiple regression studies were performed to compare the impact of impairment disturbances (independent variables) on the various disability scales (dependent variable). RESULTS: Moderate to good construct validity (stable group: Spearman's rank test (absolute values), r = 0.41-0.79; longitudinal group: multiple correlation coefficient, R = 0.69-0.89; p < 0.006 for all associations) and reliability (intraclass correlation coefficient, R = 0.90-0.95; p < 0.0001) were demonstrated for the ODSS. Its SRM values were high (> 0.8), indicating good responsiveness. Impairment measures accounted for a higher variance proportion of the ODSS compared with the f score and Rankin (R = 0.64 v 0.56 and 0.45, respectively). CONCLUSIONS: All clinimetric requirements were met by the overall (arm and leg) disability sum score in immune mediated polyneuropathies. Its use is therefore suggested in evaluating immune mediated polyneuropathies.

Adolescent↗

PubMed1976

[Motor nerve conduction velocity in uraemic polyneuropathy: correlation with metabolic factors (author's transl)].

The following parameters have been examined in twenty-one patients suffering from chronic renal failure (creatinine level between 4.5 and 18.8 mg/100 ml serum): maximum motor nerve conduction of the peroneal nerve, amplitude of the compound muscle action potential of the extensor digitorum brevis muscle, serum creatiine, total protein, serum globulins, serum albumins, alkali reserve, time of increase of serum creatinine above 4 mg/100 ml up to time of determination of the maximum motor nerve conduction, daily urinary excretion, mean blood pressure, (p less than 0.01) was found between maximum motor nerve conduction, as well as amplitude of the compound muscle action potential, and the serum albumin level only. Decreased levels of serum albumin, is correlated with diminished nerve conduction and a lower amplitude. The relationship between the electrophysiological data and serum albumin levels maybe explained on the basis of progression of a pre-existing polyneuropathy due to additional dietary malnutrition. A different interpretation is the assumption of an inactivation of neurotoxin on binding by albumins. A decrease in the albumin level would, therefore, result in an increased amount of unbound toxic agent. The values of the maximum motor nerve conduction were between 16 m/sec and 51 m/sec (mean value 42.2 m/sec), pointing to a polyneuropathy of primary axonal type rather that to primary demyelinization. The amplitudes of the compound muscle action potentials were not greatly reduced and thus the uraemic polyneuropathy seems to be of mixed type. In uraemic polyneuropathy different aetiological factors have to assumed. According to the prevalent factor a polyneuropathy of predominantly axonal or predominantly demyelinizing type may result.

Action Potentials↗

PubMed2000

[Polyneuropathy is an early finding in primary systemic amyloidosis].

BACKGROUND: Polyneuropathy is associated with several pathological conditions. Amyloidosis is a less common cause of polyneuropathy. Amyloidosis is caused by the accumulation of insoluble protein fibrils (amyloid) in the extracellular matrix. Primary systemic amyloidosis is caused by B-lymphocyte dyscrasia. Polyneuropathy is the first sign of primary systemic amyloidosis in about 20% of the cases, and is characterised by relentless progression, painfulness, and prominent symptoms of autonomic neuropathy. MATERIAL AND METHODS: We describe three cases of primary systemic amyloidosis that started with polyneuropathy. RESULTS: The diagnosis of primary systemic amyloidosis is often delayed more than two years after the onset of polyneuropathy. Biopsy of rectum, fat tissue, bone marrow, or peripheral nerve are diagnostic tools. INTERPRETATION: The survival of non-treated patients is about 18 months after the diagnosis. With chemotherapy the survival is prolonged to approximately 38 months.

Aged↗

PubMed2002

Chronic demyelinating polyneuropathy in graft-versus-host disease following allogeneic bone marrow transplantation.

In recent years a novel problem has arisen in organ transplantation medicine, namely GVHD. The nervous system has been involved mainly at the level of the CNS and this can lead to a serious outcome for the patient. In rare cases, peripheral nerves may be affected and show acute or chronic polyneuropathy. Here a case is reported of polyneuropathy associated with chronic GVHD. A 32-year-old man, suffering from chronic GVHD following an allogeneic bone marrow transplantation (BMT) for malignant lymphoma at the age of 25, developed a motor dominant polyneuropathy 5 years later. Electrophysiologic studies demonstrated the demyelinating type of polyneuropathy. Biopsy specimens from skin and skeletal muscle disclosed perivascular lymphocytic infiltrates expressing T-cell markers. The sural nerve showed a loss of myelinated nerve fibers with epineurial fibrosis and rare occurrence of T cells, but without obvious vasculitic changes. The present case suggested that polyneuropathy could develop in association with chronic GVHD in some patients with a long-standing disease course.

Adult↗

PubMed1992

[Polyneuropathies associated with lymphoplasmacytic dyscrasias: the clinical and instrumental characteristics of a 38-patient case load].

A varying percentage from 40 to 60% of patients having lymphoplasmacytic dyscrasias with a monoclonal component shows a clinical or subclinical polyneuropathy. From a different viewpoint, a monoclonal gammopathy has been detected in 10% of patients effected by chronic idiopathic polyneuropathy. A case study of 38 patients with lymphoplasmacytic dyscrasia subjected to clinical, immunohematological and electrophysiological examination revealed a high prevalence of polyneuropathy (84%), mainly axonal (72%) and often subclinical. The neuropathy was evenly distributed between patients having malignant and benign lymphoplasmacytic dyscrasias. No statistically significant correlation was found between the presence of neuropathy and the main clinical and immunohematological data. This supports the concept that the pathogenesis of polyneuropathy associated with lymphoplasmacytic dyscrasias may be multifactorial. Nor can it be ruled out that the paraprotein may in fact be secondary to the polyneuropathy or sometimes a simple coincidence.

Adult↗

PubMed1980

[Electrophysiological studies in vincristin-polyneuropathy (author's transl)].

21 Patients with malignant brain tumors were treated with vincristine (1,4 mg/m2) in the course of combination chemotherapie, given in 14 days series over 3 months up to 26 month. 18 patients developed clinical signs of a sensory and 4 patients of a sensomotoric polyneuropathy. Changes in nerve conduction velocity of the N. peronaeus and N. suralis and amplitude of the evoked muscle response (M. extensor digitorum brevis) and nerve action potential were studied in dependency of the total vincristine dosage. The following conclusions were drawn. 1. Clinical occurrence of vincristine polyneuropathy and decrease of nerve conduction velocity of peroneal and sural nerve and the amplitude of the muscle response and nerve action potential are dosage dependent. 2. Sensory fibres appear to be damaged earlier and more severe than motor fibers, but this difference was statistically not significant. 3. Nerve conduction velocity of peroneal and sural nerve is normal or slightly decreased in vincristine polyneuropathy, but the amplitude of the evoked response in extensor digitorum brevis muscle and of the nerve action potential of the suralis nerve are markedly diminished. This result indicates that vincristine polyneuropathy is of primary axonal orgin. 4. If vincristine dosage is reduced to half or vincristine is discontinued after a reduction of the potential amplitude in the extensor digitorum brevis muscle below 1 mV, severe, not reversible polyneuropathies may be avoided.

Action Potentials↗

PubMed1998

[A case of polyneuropathy associated with osteosclerotic myeloma].

A 50-year-old woman presented with sensorimotor polyneuropathy in the lower limbs. Biopsy of the muscle revealed neurogenic changes, and electrophysiological study and pathology of the biopsied nerve indicated myelinoaxonal degeneration. Her symptoms responded to neither plasmapheresis nor prednisolone. Pelvic radiography disclosed an osteosclerotic lesion that was subsequently diagnosed as IgA-lambda plasmacytoma by biopsy. Radiation therapy for this solitary osteosclerotic myeloma improved the patient's polyneuropathy. In Japan, reports of cases of polyneuropathy associated with osteosclerotic myeloma without multiorgan disorders as in our case have not previously been described; thus, such cases may be misdiagnosed. Therefore, in patients with polyneuropathy of unknown etiology, a systemic bone survey and repeated searches for M-protein are important. Treatment of bone lesions in patients with solitary osteosclerotic myeloma may improve the associated polyneuropathy.

Female↗

PubMed1998

Alcohol-related acute axonal polyneuropathy: a differential diagnosis of Guillain-Barré syndrome.

BACKGROUND: Chronic axonal polyneuropathy is a well-known clinical sequela of excessive alcohol consumption; however, acute axonal polyneuropathy related to alcohol abuse is less well recognized. OBJECTIVE: To describe alcohol-related acute axonal polyneuropathy in 5 chronic alcoholics who developed ascending flaccid tetraparesis and areflexia within 14 days. METHODS: Case series with clinical, laboratory, electrophysiological, and, in 1 patient, biopsy data. RESULTS: All 5 patients consumed a daily average of 250 g of alcohol, and 4 had lost a substantial amount of weight recently. Additional clinical features included painful paresthesia, myalgia, and glove and stocking-type sensory loss. Repeated cerebrospinal fluid examinations failed to show the marked increase of protein concentration with normal cell count typical of Guillain-Barré syndrome, although the protein level was mildly elevated in 1 patient. Blood laboratory findings were consistent with longstanding alcohol abuse. Compound muscle and sensory nerve action potentials were absent or reduced, while conduction velocities were normal or mildly reduced. Three to 4 weeks after onset, needle electromyography displayed moderate to severe fibrillations and positive sharp waves in addition to normal motor unit potentials, indicating an acute axonal polyneuropathy; this was confirmed by sural nerve biopsy in 1 patient. CONCLUSIONS: Excluding other factors, we assume that in these patients the combination of alcohol abuse and malnutrition caused severe acute axonal polyneuropathy. Its distinction from Guillain-Barré syndrome is important because treatment requires balanced diet, vitamin supplementation, and abstinence from alcohol, while immunotherapy may not be indicated.

Acute Disease↗

PubMed2004

Effectiveness, tolerability, and impact on quality of life of the 5% lidocaine patch in diabetic polyneuropathy.

BACKGROUND: The treatment of painful diabetic polyneuropathy (DPN) is often inadequate and frequently limited by the systemic adverse effects of medications, necessitating the evaluation of novel treatments. OBJECTIVE: To evaluate the effectiveness, tolerability, and impact on quality of life of the 5% lidocaine patch in painful diabetic polyneuropathy. DESIGN: Open-label, flexible-dosing, 3-week study with a 5-week extension. SETTING: Outpatient clinics and clinical research centers.Patients Volunteer sample of 56 patients with clinically defined painful diabetic polyneuropathy of longer than 3 months' duration. Intervention The 5% lidocaine patch, with a maximum of 4 patches daily for 18 hours. MAIN OUTCOME MEASURES: Change in mean daily pain diary ratings from baseline to week 3. Secondary end points included assessments of safety, tolerability, and quality of life. RESULTS: Patients with painful diabetic polyneuropathy showed significant improvements in pain and quality-of-life outcome measures during a 3-week treatment period. These benefits were maintained in a subgroup of patients treated for an additional 5 weeks, during which taper of concomitant analgesic therapy was permitted. Adverse events were minimal, and systemic accumulation of lidocaine did not occur. CONCLUSIONS: Up to four 5% lidocaine patches for up to 18 h/d are well tolerated in patients with painful diabetic polyneuropathy, significantly improve pain and quality-of-life ratings, and may allow tapering of concomitant analgesic therapy. Given the open-label design of this trial, a randomized controlled trial is necessary to confirm these results.

Administration, Topical↗

PubMed1981

Chronic relapsing (dysimmune) polyneuropathy: pathogenesis and treatment.

Chronic relapsing polyneuropathy is a distinct dysschwannian/demyelinating polyneuropathy characterized by usually slow onset, progressive or relapsing-remitting course, elevated cerebrospinal fluid (CSF) protein, marked slowing of nerve conduction velocity, segmental demyelination demonstrable in sural nerve biopsies, and absence of systemic illness or abnormal serum immunoglobulins. The cause of the disorder and the mechanisms underlying its chronicity and relapsing-remitting course are not clear. Immunoglobulin deposition observed in sural nerve biopsies and abnormal immunoglobulin patterns in the "CSF in some cases suggest a dysimmune pathogenesis; thus the term chronic relapsing (dysimmune) polyneuropathy (CRDP) is preferred. The disease is a treatable form of idiopathic polyneuropathy. In our series of 25 patients with CRDP, treatment with high-single-dose daily prednisone, slowly tapered to an alternate-day program, has been very successful in the majority. A low (10 to 20 mg) alternate-day-single-dose program, maintained indefinitely, seems to be required to prevent future recurrences. Evidence is provided that other immunosuppressants (azathioprine, cyclophosphamide, poly-ICLC) and possibly plasmapheresis, alone or in conjunction with corticosteroids, may have a beneficial role in controlling difficult cases of chronic relapsing polyneuropathy.

Adolescent↗

PubMed2001

Painful sensory polyneuropathy associated with impaired glucose tolerance.

We examined records of 121 patients coded as idiopathic polyneuropathy, extracting neuropathy symptoms, electromyographic data, and diagnostic blood work. Of 89 patients screened for glucose handling, 28 demonstrated frank diabetes mellitus. Of the remaining 61 patients, 15 (25%) had impaired glucose tolerance (IGT) by American Diabetes Association criteria (serum glucose 140--200 mg/dl 2 h after a 75-g glucose load). Excluding those with diabetes mellitus, 35% of patients with neuropathic pain had IGT, more than twice the prevalence found in large, unselected population studies. No other common etiology of polyneuropathy was identified. Two-hour oral glucose tolerance test results were often abnormal, whereas fasting glucose or hemoglobin A1c was normal. Bias due to referral pattern, body weight, or genetics might affect the comparison of our polyneuropathy cohort with a broader, population-based control. However, our results corroborate an association between IGT and painful sensory polyneuropathy and link these patients syndromically to the typical painful polyneuropathy of diabetes mellitus.

Adult↗

PubMed1995

Segmental median nerve conduction measurements discriminate carpal tunnel syndrome from diabetic polyneuropathy.

Median nerve conduction has been compared in CTS, with or without diabetes, and diabetic polyneuropathy. Approximately 90% of hands were correctly predicted as CTS or diabetic polyneuropathy by a comparison including the median antidromic sensory nerve conduction velocities in the elbow-to-wrist segment, wrist-to-palm segment, palm-to-finger segment, and the amplitude of the sensory nerve action potential. CTS with diabetes could not be distinguished from CTS without diabetes. The association between proximal and distal nerve conduction velocities was similar in CTS and diabetic polyneuropathy. A study in motor fibers showed that the hands could be classified through a combination of M-wave latency and the more proximal motor nerve conduction velocity measurements. Independent of severity, motor and sensory nerve conduction was influenced to an equal degree in CTS and diabetic polyneuropathy. The hypothesis that both CTS and diabetic polyneuropathy can be associated with neural ischemia is discussed.

Adult↗

PubMed1991

Chlorpyrifos-induced delayed polyneuropathy.

Chlorpyrifos [0,0-diethyl 0-(3,5,6-trichloro-pyridyl) phosphorothioate] caused delayed polyneuropathy in man. Contrary to previous studies, we report here that it also causes delayed polyneuropathy in the hen, the animal model for this toxicity. The minimal neuropathic dose was 60-90 mg/kg p.o., corresponding to 4-6 times the estimated LD50. Consequently, pralidoxime (2-PAM) in conjunction with atropine was necessary to reverse acetylcholinesterase (AChE) inhibition and cholinergic toxicity in hens given high enough doses of chlorpyrifos to cause neuropathy. Chlorpyrifos was slowly absorbed after single oral doses and the threshold of inhibition (greater than 70%) of neuropathy target esterase (NTE), the putative target for delayed neuropathy, was reached within 5-6 days. High AChE inhibition (greater than 90%), however, was measured within hours after dosing because of the higher potency of chlorpyrifos to inhibit this enzyme. In vitro studies showed that chlorpyrifos-oxon, the active metabolite of chlorpyrifos, was 10-20 times more active against AChE than against NTE, confirming the clinical observation. No differences were seen between human and hen enzymes in this respect. Hen and human brain homogenates contain A-esterases which hydrolysed chlorpyrifos to about the same extent in both species. In conclusion, chlorpyrifos causes delayed polyneuropathy in the hen, as was reported in man. The reasons for previous negative data in the hen are probably due to the relatively lower doses which were used. Judging from in vitro studies with hen and human enzymes, there are no differences in the two species as far as their relative sensitivity to delayed polyneuropathy. It is likely that delayed polyneuropathy would develop in both species only after severe cholinergic toxicity requiring aggressive antidotal treatment.

Animals↗

PubMed1996

Polyneuropathies in critically ill patients: a prospective evaluation.

OBJECTIVE: To determine the incidence, severity and course of polyneuropathies in patients with sepsis or systemic inflammatory response syndrome combined with multiple organ failure. DESIGN: Prospective study. SETTING: Division of Intensive Care Medicine of the Department of Anesthesiology and Intensive Care and Intensive Care Unit of the Department of Neurology, University Hospital Innsbruck, Austria. PATIENTS: Twenty-two patients between 23 and 77 years old with sepsis or systemic inflammatory response syndrome combined with multiple organ failure fulfilling strict inclusion and exclusion criteria. INTERVENTIONS: Clinical neurologic examination and electro myography/nerve conduction velocity measurements during the stay on the Intensive Care Unit and 2-3 months later. MEASUREMENTS AND RESULTS: In 9 of the 22 patients signs of polyneuropathy were found at the initial clinical investigation and in 7 patients at the follow-up investigation. Electrophysiologic investigation revealed signs of polyneuropathy in 18 patients initially and in 11 patients 2-3 months later. CONCLUSION: In our patient population the frequency of the development of polyneuropathy was high (81.8%). Electrophysiologic investigation is superior to clinical neurologic examination in the detection of polyneuropathies.

Activities of Daily Living↗