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PubMedDate not supplied

Heterogeneity of antibody specificity in Taiwanese patients with polyneuropathy and IgM paraproteinemia.

About half of the Caucasian patients with chronic polyneuropathy and IgM paraproteinemia show serum anti-myelin-associated glycoprotein (MAG) and anti-sulfoglucuronosyl glycosphingolipid (SGGLs) activities. These antibody activities have been demonstrated to react with a carbohydrate epitope known as the HNK-1 or sulfoglucuronic acid (SGA) epitope. However, in Asian populations the occurrence of serum anti-SGA activities has been reported to be relatively rare. We investigated 5 cases of chronic polyneuropathy with IgM paraproteinemia from Taiwan and found that 3 of them had high-titer serum anti-SGA (SGGL/MAG) antibody activities. The clinical symptoms of these 3 patients were consistent with sensory dominant polyneuropathy with a severer involvement of the lower limbs than of the upper limbs. Electromyography and nerve conduction studies revealed severe sensory nerve involvement (no response in 3 cases) and moderate slowing of motor conduction velocity (MCV) without conduction block. The decrease in MCV correlated well with anti-SGA antibody titer (less than 30 m/s with the titration of 1:12, 800, normal 55-60 m/s). Pathological findings showed active demyelinating polyneuropathy with myelin ovoid and myelinated fiber loss. Our data suggest that anti-SGGL antibody activities may not be very rare among Asian populations. Additionally, there seems an intriguing possibility that the titer of this antibody correlates with the severity of peripheral nerve involvement in patients of demyelinating polyneuropathy with IgM paraproteinemia.

Aged↗
PubMed2005

No adrenergic sensitization of afferent neurons in painful sensory polyneuropathy.

INTRODUCTION: The aim of the present study was to determine (1) if an adrenergic sensitivity of afferent neurons is present in patients with painful polyneuropathy as compared with non-painful polyneuropathy and (2) if there is a correlation between adrenergic sensitisation and the severity of afferent and sympathetic small fiber damage. METHODS: 10 patients with painful and non painful polyneuropathy and 10 healthy controls were included. The function of small afferent and efferent sympathetic neurons was evaluated. Adrenergic sensitivity of afferent neurons was assessed by cutaneous iontophoresis of norepinephrine. Spontaneous pain, mechanical hyperalgesia as well as warm and heat pain thresholds were measured. RESULTS: Iontophoresis of norepinephrine did not induce or enhance spontaneous pain or mechanical allodynia, either in painless or painful polyneuropathies. There was no difference in norepinephrine-induced heat hyperalgesia between both neuropathy groups and healthy controls. The response of afferent neurons to norepinephrine was not correlated with the severity of damage to afferent small fibers or efferent sympathetic vasoconstrictor neurons. CONCLUSION: The results do not support the assumption that in painful polyneuropathies afferent neurons acquire an adrenergic sensitivity after nerve injury and that adrenergic stimulation leads to an exacerbation of spontaneous pain and thermal and mechanical hyperalgesia.

Aged↗
PubMed1994

Early detection of distal symmetrical polyneuropathy during HIV infection by paired stimulation of sural nerve.

In 203 HIV infected patients in various clinical stages neurological examination, paired stimulation (LPSS), nerve conduction velocity (NCVS) and amplitude (AMPS) of the sural nerve, distal latency (DLP), nerve conduction velocity (NCVP), amplitude (AMPP) and F waves of the peroneal nerve were recorded. Neurological examination revealed symptoms and clinical signs of polyneuropathy in 67 (33%) (WR 1-6) of the patients. LPSS after paired stimulation was abnormal in 25.5%, NCVS in 14.2%, AMPS in 9.8%, NCVP in 11.8%, DLP in 11.2%, AMPP in 5.9% and FWP in 14.6%. Our findings indicate a high incidence of peripheral nerve system involvement during HIV infection. In 11.5% of all patients only LPSS proved polyneuropathy. Neurophysiological results from HIV infected patients with symptoms and clinical signs of polyneuropathy were statistically significantly different from HIV infected patients without symptoms and clinical signs of polyneuropathy. The delay of LPSS represents the most sensitive neurophysiological indicator of polyneuropathy during HIV infection and announces the onset of peripheral nerve disease even in early stages of infection, according to Walter Reed staging classification 1 and 2 (approx. 20%).

Adult↗
PubMedDate not supplied

Polyneuropathy in Australian outpatients with type II diabetes mellitus.

In order to determine the local prevalence of polyneuropathy among adult outpatients with type II (non-insulin-dependent) diabetes mellitus, we applied a series of standardised measures to patients attending a multidisciplinary diabetes clinic. The study group comprised 94 men and 15 women; mean age, 70.6+/-7.8 years; mean duration of diabetes, 11.7+/-10.1 years; and mean HbA1c 8.3%+/-1.7%. Neuropathy Symptom Scores > or = 1 were present in 97% of patients (mean, 3+/-2; range, 0-12), and 95% had Neuropathy Disability Scores > or = 2 (mean, 27+/-19; range, 0-87). 52% of men reported impotence. Autonomic dysfunction on cardiovascular reflex testing was present in 46% of patients (39/84). Finger and toe vibration perception thresholds were greater than 3SD higher than mean thresholds measured in control subjects without diabetes in 43% and 58% of patients, respectively. Polyneuropathy, defined as lower limb sensory and motor nerve conduction velocity or latency outside mean +/-2 SD of that measured in age-matched controls, was present in 49% of patients (53/109). These results suggest that there is a high prevalence of polyneuropathy in Australian out-patients with type II diabetes mellitus. In this study, clinical assessment using Neuropathy Disability Scores was not diagnostically useful since only five patients had a normal score. Using nerve-conduction studies as the "gold standard" diagnostic criteria, the best alternative test for the presence of polyneuropathy was toe vibration perception threshold (sensitivity 74%, specificity 56%). In view of the emerging evidence that intensive glycaemic control reduces the rate of progression of polyneuropathy, we recommend that patients with type II diabetes mellitus have nerve-conduction studies performed for early detection of this important complication.

Adult↗
PubMed1987

Hereditary generalized amyloidosis with polyneuropathy. Clinicopathological study of 65 Japanese patients.

A clinicopathological study was made on 65 patients from a small area of Nagano Prefecture, Japan, with hereditary generalized amyloidosis with polyneuropathy to clarify the clinical variety of the disease. Forty-five patients from Ogawa village showed similar clinical features. The age of onset ranged widely from 16 to 62 years. The main neurological manifestations were polyneuropathy starting in the legs and autonomic dysfunction. Lower cranial nerves were also affected in the advanced stages. Severe cardiac and renal involvement was uncommon. All these clinical features are consistent with type I familial amyloid polyneuropathy (FAP). The remaining 20 patients from five unrelated kinships showed unique clinical pictures. Two families from Ogawa village had type I FAP, but 4 out of the 5 affected patients showed marked nephropathy with heavy proteinuria from an early stage. Of the three other families, one, with 10 patients, was notable for the involvement of the central nervous system. Most of the patients showed cerebellar ataxia and pyramidal tract signs in addition to a sensorimotor and autonomic peripheral neuropathy. Another family had 2 siblings who had severe amyloid heart disease from the onset and developed polyneuropathy with autonomic features at an advanced stage. In the third family, onset occurred in the sixth decade in all 3 patients and the course was mild in 2, although the clinical features were those of typical type I FAP. Immunohistochemical study revealed that the amyloid fibril proteins in the patients with all four unusual clinical phenotypes were related to plasma prealbumin. The most common form of hereditary generalized amyloidosis in Japan is type I FAP, but the disease shows considerable variety in the age of onset and involves more systemic organs than previously recognized. The newly recognized clinical forms of hereditary generalized amyloidosis with severe amyloid heart disease or central nervous dysfunction indicate clinical heterogeneity of hereditary amyloidosis with polyneuropathy.

Adolescent↗
PubMed1983

Chronic cryptogenic polyneuropathy. The search for a cause.

91 patients with chronic symptoms of polyneuropathy without any previously known underlying disorder underwent extensive clinical and laboratory investigations in an attempt to reveal the cause of the polyneuropathy. A definite or probable origin of polyneuropathy was detected in only 8 patients (9%) and a possible but questionable cause was found in 16 (17%), while the cause in 74% remained undetermined. In only 1 patient could effective treatment be instituted. No evidence was found for an association between polyneuropathy and reduced glucose tolerance without manifest diabetes mellitus. The findings suggest that only a limited investigation is justified in most cases of chronic polyneuropathy without obvious cause.

Adult↗
PubMed1997

Double filtration plasmapheresis in the treatment of inflammatory polyneuropathy.

Twelve cases of recognized inflammatory polyneuropathy were treated by plasmapheresis (PP) at Shin-Kong Wu Ho-Su Memorial Hospital from November 1993 to November 1995. These include 6 cases of acute inflammatory demyelinating polyneuropathy (AIDP), 4 cases of chronic inflammatory demyelinating polyneuropathy (CIDP), one case of Fisher syndrome, and one case of Sjögren's syndrome with polyneuropathy. The patients chosen for PP met the inclusion criteria of severely disabled, i.e., Grade 4 (bed or chair bound) or Grade 5 (required assisted ventilation), or an unremittingly progressive course. Plasmapheresis was carried out by the double filtration method. Each patient received a standard course of at least 4 sessions of pheresis. All the patients receiving PP showed a beneficial response. The treatment for 10 patients was judged to be effective. The other 2 patients (one AIDP and one CIDP), though improved, were unable to reach Grade 2. Among the complications of PP, only 4 episodes of symptomatic hypotension were noted in a total of 73 sessions of PP. In conclusion, PP is safe and effective in treating inflammatory polyneuropathy.

Adult↗
PubMed1984

Polyneuropathy in critically ill patients.

Five patients developed a severe motor and sensory polyneuropathy at the peak of critical illness (sepsis and multiorgan dysfunction complicating a variety of primary illnesses). Difficulties in weaning from the ventilator as the critical illness subsided and the development of flaccid and areflexic limbs were early clinical signs. However, electrophysiological studies, especially needle electrode examination of skeletal muscle, provided the definite evidence of polyneuropathy. The cause is uncertain, but the electrophysiological and morphological features indicate a primary axonal polyneuropathy with sparing of the central nervous system. Nutritional factors may have played a role, since the polyneuropathy improved in all five patients after total parenteral nutrition had been started, including the three patients who later died of unrelated causes. The features allow diagnosis during life, and encourage continued intensive management since recovery from the polyneuropathy may occur.

Adult↗
PubMed1986

Critically ill polyneuropathy: electrophysiological studies and differentiation from Guillain-Barré syndrome.

A polyneuropathy of varying severity has been observed in association with sepsis and critical illness in 15 patients. Since clinical evaluation is often difficult, electrophysiological studies provided definitive evidence for polyneuropathy. These revealed reductions in the amplitudes of compound muscle and sensory nerve action potentials, the most marked abnormality. Near-nerve recordings confirmed such reductions for sensory fibres. Needle electromyography revealed signs of denervation of limb muscles. Phrenic nerve conduction and needle electromyographic studies of chest wall muscles suggested that the polyneuropathy partially explained difficulties in weaning patients from the ventilator, an early clinical sign. No defect in neuromuscular transmission was demonstrated, despite the use of aminoglycoside antibiotics in some patients. In those who survived the critical illness, clinical and electrophysiological improvement occurred. The 15 critically ill polyneuropathy patients were compared with 16 Guillain-Barré syndrome patients observed during the same period. The analysis showed that the two polyneuropathies are likely to be separate entities that can be distinguished in most instances by the predisposing illness, electrophysiological features and cerebrospinal fluid results.

Aged↗
PubMed1989

Hypothyroidism and polyneuropathy.

The prevalence and characteristics of polyneuropathy were assessed using standard clinical and electrophysiological criteria in 39 consecutive outpatients with primary hypothyroidism, 15 of whom were previously untreated. Subjective complaints, mainly paraesthesiae, were recorded from 25 cases (64%) and objective findings supporting a clinical diagnosis of polyneuropathy were present in 13 (33%). Using standard electrophysiological criteria, a definite diagnosis of polyneuropathy was made in 28 cases (72%). The commonest sites of abnormal nerve conduction were the sensory nerves, especially the sural nerve. Polyneuropathy was generally mild. None of the clinical and biochemical indicators of hypothyroidism were significantly correlated with the electrophysiological signs of peripheral nerve impairment or the diagnosis of polyneuropathy.

Adolescent↗
PubMed1993

Chronic idiopathic polyneuropathy presenting in middle or old age: a clinical and electrophysiological study of 75 patients.

The clinical and electrophysiological features were prospectively studied of 75 patients (46 men and 29 women) with chronic polyneuropathy presenting in middle or old age in whom a diagnosis could not be made even after extensive evaluation and a follow up of six months. The mean age at the onset of symptoms was 56.5 years. The clinical features of chronic idiopathic polyneuropathy are heterogeneous. On clinical grounds 44 patients had a sensorimotor, 29 patients a sensory, and two patients a motor polyneuropathy. The overall clinical course in chronic idiopathic polyneuropathy was slowly progressive. None of the patients became severely disabled. Electrophysiological and nerve biopsy studies were compatible with an axonal polyneuropathy. Antibodies against myelin associated glycoprotein, gangliosides, and sulphatides were assessed in 70 patients and found to be negative.

Age of Onset↗
PubMed1995

Electrodiagnostic criteria for polyneuropathy and demyelination: application in 135 patients with Guillain-Barré syndrome. Dutch Guillain-Barré Study Group.

Since the development of effective but expensive therapeutic strategies for the treatment of Guillain-Barré syndrome, early confirmation of the diagnosis has become very important. Electrodiagnostic criteria were developed for the discrimination of polyneuropathy and in particular for demyelination. The sensitivity and specificity of these criteria were determined in 135 patients with Guillain-Barré syndrome in an early stage of the disease, along with 45 healthy volunteers. The algorithms used to develop our criteria consisted of sets of selected electrodiagnostic variables, each of them relevant to the detection of polyneuropathy. Each set was applied on all of three consecutive electrodiagnostic examinations within one month of disease onset. Application of the best set resulted in 85% of patients with Guillain-Barré syndrome fulfilling the criteria for polyneuropathy at the first examination (mean time interval six days of disease onset), whereas none of the healthy volunteers fulfilled the criteria (sensitivity 85%, specificity 100%). The set of criteria for the detection of demyelination was fulfilled by 60% during the first examination (by 66% and 72% during the second and third examination). Application of criteria for demyelinating polyneuropathy as defined by others resulted in substantially lowered incidence (3%-46%). It is concluded that these criteria for the electrodiagnostic delineation of polyneuropathy are the most sensitive to date, with respect to the early confirmation of the diagnosis of Guillain-Barré syndrome.

Adult↗
PubMed1976

Shoe-makers' polyneuropathy in Italy: the aetiological problem.

Since 1957, when the first cases of the so-called shoe-makers' toxic polyneuropathy were reported, nearly 400 cases have been described in the Italian literature. The substance that was considered to be responsible for the disease was triorthocresylphosphate (TOCP) contained in glues, artificial leathers, and some types of paints. However numerous chemical analyses of glues and leathers taken from factories where cases of the disease occurred have shown that in almost all instances little or no TOCP was present. In addition the disease manifests itself more frequently during winter and spring and this is not consistent with the absorption of the causative agent through the skin and/or gastrointestinal tract. In order to clarify the aetiology of the disease 122 workers in the shoe industry affected by toxic polymeuropathy during the period 1971-74 were studied. Workplaces where cases of polyneuropathy had occurred were visited and samples of glues and solvents were taken for chemical analysis. The polyneuropathy chiefly affects workers engaged in glueing and in the cleaning process, but it also affects those who do not have direct contact with glues or solvents. The disease is more common in women (68%) than in men (32%) and, in its more severe form begins with overwhelming prevalence during winter and early spring regardless of the job performed. No direct relationship has been found between the severity of the disease and the number of years of work in the shoe industry or of specific exposure (that is the number of years of work in the activity performed at the onset of the disease). The polyneuropathy is found almost exclusively among workers of the artisam type in small shoe factories, where standards of hygiene are low. Chemical analysis of glues and cleaning fluids collected from five different factories, where 20 cases of polyneuropathy occurred, showed the presence of paraffin hydrocarbons with a low boiling point (pentane, 2-methyl-pentane, 3-methyl-pentane, n-hexane, etc.) in concentrations of more than 80% by weight.

Adolescent↗
PubMed2007

Simplified electrodiagnostic criteria of diabetic polyneuropathy in field study (KCIS No. 14).

This study sought to determine the sensitivity of sural sensory action amplitude (SAP) and peroneal motor conduction velocity (MCV) for differentiating the status of other nerve conduction velocities and identifying important correlates of diabetic polyneuropathy. Subjects (n = 708) with type 2 diabetes from one community completed a preliminary questionnaire. Among the 298 subjects with positive questionnaire results, 272 completed nerve conduction tests. The means of 6 nerve conduction velocities of subjects with both SAP and MCV abnormalities were compared to those of normal controls. The mean conduction velocities of all motor and sensory nerves were slower (p < 0.05) in subjects with polyneuropathy than without polyneuropathy. Important known correlates of diabetic polyneuropathy can also be identified by this electrophysiological definition. The sural SAP and peroneal MCV together serve as a good diagnostic for diabetic polyneuropathy and can be used as a simplified criterion in field studies.

Action Potentials↗
PubMed1988

Clinical and neurophysiologic features in paraneoplastic polyneuropathy.

Three of 8,954 in- patients have been selected as affected by paraneoplastic polyneuropathy. In all of them the polyneuropathy had a steadily progressive course, with symptoms beginning in the lower limbs and spreading to the upper limbs in a few months. An increase in protein content of the cerebrospinal fluid was evident in each case. No other possible causes of polyneuropathy were found, and the association with malignancy was histologically proved in all 3 cases. A bronchogenic ("oat cell") carcinoma was present in the first patient, who had an almost exclusively motor neuropathy. An osteosarcoma was diagnosed in the second case, and its association with a polyneuropathy seems to be exceptional. A sigmoid adenocarcinoma was discovered in the third patient. Neurophysiologic investigations were indicative of a polyneuropathy with predominant axonic involvement in all 3 cases.

Action Potentials↗
PubMed2004

Thioctic acid for patients with symptomatic diabetic polyneuropathy: a critical review.

Diabetic neuropathy represents a major health problem, as it is responsible for substantial morbidity, increased mortality, and impaired quality of life. Near-normoglycemia is now generally accepted as the primary approach to prevention of diabetic neuropathy, but is not achievable in a considerable number of patients. A growing body of evidence suggests that oxidative stress resulting from enhanced free-radical formation and/or defects in antioxidant defense is implicated in the pathogenesis of diabetic neuropathy. Markers of oxidative stress such as superoxide anion and peroxynitrite production are increased in diabetic patients in relation to the severity of polyneuropathy. In experimental diabetic neuropathy, oxygen free-radical activity in the sciatic nerve is increased, and treatment with thioctic acid, a potent lipophilic antioxidant, results in prevention or improvement of the diabetes-induced neurovascular and metabolic abnormalities in various organ systems. Pharmacodynamic studies have shown that thioctic acid favorably influences the vascular abnormalities of diabetic polyneuropathy such as impaired microcirculation, increased indices of oxidative stress, and increased levels of markers for vascular dysfunction, such as thrombomodulin, albuminuria, and nuclear factor-kappaB. Thus far, seven controlled randomized clinical trials of thioctic acid in patients with diabetic neuropathy have been completed (Alpha-Lipoic Acid in Diabetic Neuropathy [ALADIN I-III], Deutsche Kardiale Autonome Neuropathie [DEKAN], Oral Pilot [ORPIL], Symptomatic Diabetic Neuropathy [SYDNEY], Neurological Assessment of Thioctic Acid in Neuropathy [NATHAN] II) using different study designs, durations of treatment, doses, sample sizes, and patient populations. Recently, a comprehensive analysis was undertaken of trials with comparable designs that met specific eligibility criteria for a meta-analysis to obtain a more precise estimate of the efficacy and safety of thioctic acid (600mg intravenously for 3 weeks) in diabetic patients with symptomatic polyneuropathy. This meta-analysis included the largest sample of diabetic patients (n = 1258) ever to have been treated with a single drug or class of drugs to reduce neuropathic symptoms, and confirmed the favorable effects of thioctic acid based on the highest level of evidence (Class Ia: evidence from meta-analyses of randomized, controlled trials). The following conclusions can be drawn from these trials: (i) short-term treatment for 3 weeks using intravenous thioctic acid 600 mg/day reduces the chief symptoms of diabetic polyneuropathy to a clinically meaningful degree; (ii) this effect on neuropathic symptoms is accompanied by an improvement of neuropathic deficits, suggesting potential for the drug to favorably influence underlying neuropathy; (iii) oral treatment for 4-7 months tends to reduce neuropathic deficits and improve cardiac autonomic neuropathy; and (iv) clinical and postmarketing surveillance studies have revealed a highly favorable safety profile of the drug. Based on these findings, a pivotal long-term multicenter trial of oral treatment with thioctic acid (NATHAN I) is being conducted in North America and Europe to investigate effects on progression of diabetic polyneuropathy, using a clinically meaningful and reliable primary outcome measure that combines clinical and neurophysiological assessment.

Animals↗
PubMed2004

Cooling detection thresholds in the assessment of diabetic sensory polyneuropathy: comparison of CASE IV and Medoc instruments.

OBJECTIVE: Cooling detection threshold testing may be an important quantitative method for assessing polyneuropathy, in that it has traditionally been viewed as a measure of small-fiber involvement. The present study sought to determine the agreement between two common testing devices and to determine whether these are concordant in their association with predictor variables for diabetic sensory polyneuropathy. RESEARCH DESIGN AND METHODS: A total of 83 patients with diabetes (10 patients with type 1 diabetes and 73 patients with type 2 diabetes) and a wide spectrum of diabetic sensory polyneuropathy severity underwent concurrent cooling detection threshold testing using the Medoc and CASE IV instruments. Common predictor variables for diabetic sensory polyneuropathy were measured on the same day. RESULTS: Measurements of cooling detection thresholds by both instruments were highly correlated (Spearman's correlation coefficient 0.81, P < 0.001) and demonstrated a high degree of agreement by the method of Bland and Altman (95% distribution critical values for the difference in cooling detection thresholds, +7.5 and -5.6 degrees C). Cooling detection thresholds by both instruments were strongly correlated with clinical indicators of large-fiber neuropathy but not with the symptoms of small-fiber neuropathy (pain). CONCLUSIONS: These two instruments available for assessment of cooling detection thresholds are interchangeable for research in diabetic sensory polyneuropathy. However, this modality is equivalent to other modalities of quantitative sensory threshold testing in its association with indicators of large-fiber neuropathy and does not seem to provide an advantage for the prediction of small-fiber involvement.

Diabetic Neuropathies↗
PubMed2000

[Familial amyloid polyneuropathy type I complicated by chronic glaucoma: 3 cases].

PURPOSE: We report 3 cases of familial amyloid polyneuropathy type I (FAP) with amyloid infiltration of the vitreum and glaucoma. PATIENTS AND METHODS: We reviewed the records of three patients, 2 females and one male, aged 41, 47 and 83 years respectively. The 3 patients had familial amyloid polyneuropathy type I with vitreous infiltration and open angle glaucoma. The two women underwent a liver graft four years earlier. Vitrectomy allowed confirmation of the diagnosis in the 83-year-old patient. Two patients underwent trabeculectomy, histological analysis of the iris and the trabeculum was obtained for one patient. RESULTS: The tree patients presented a polyneuropathy, vitreous infiltration and open angle glaucoma. Results of light microscopy of the iris and the trabeculum showed amyloid deposits in the iris and the trabecular meshworks. CONCLUSION: Familial amyloid polyneuropathy is a hereditary disease which may have a wide range of ocular manifestations. Glaucoma is among the most serious complications of familial amyloid polyneuropathy.

Adult↗