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PubMed1986

An outbreak of N-hexane induced polyneuropathy among press proofing workers in Taipei.

The objective of this study was to determine the prevalence and the etiology of polyneuropathy observed among press proofing workers in Taipei. Neurological examinations of 59 workers, from 16 press proofing factories, were conducted. Fifty-four of those workers subsequently underwent studies of nerve conduction velocities. Samples of bulk solvent from the involved factories were analyzed for their contents using gas chromatography. Fifteen (25%) of the study group were found to have polyneuropathy. All 15 patients with polyneuropathy were from factories in which solvents containing n-hexane were regularly used, and there was a significant association between n-hexane concentration in the bulk samples and prevalence of polyneuropathy. The air concentration of n-hexane in one factory in which all six employees developed polyneuropathy was 190 ppm. Workers who were exposed to n-hexane at air levels of less than 100 ppm but who frequently worked overtime showed a significant slowing of motor nerve conduction velocities on median, ulnar, and peroneal nerves. Of 13 workers who regularly slept in the factory, 12 (92%) had polyneuropathy compared to three (7%) of 46 workers who did not sleep in the factory. The outbreak of polyneuropathy was attributed to a combination of the use of solvents with high contents of n-hexane, poor ventilation, and the practice of sleeping in the factories between shifts.

Adolescent↗

PubMed1984

[Polyneuropathies in old age].

70 patients were examined in a prospective study to clarify causes of polyneuropathies becoming manifest beyond the age of 60. 29 patients (41.4%) had mixed symmetrical sensorimotor polyneuropathy and 21 (30%) symmetrical sensory polyneuropathy. Peripheral neurological deficits were asymmetrically distributed in 20 patients (28.6%). Polyneuropathy was monocausal in 31 patients (44.3%), whereas a variety of pathogenetic factors was found in 29 patients (41.4%). Aetiology remained undetermined in 10 patients (14.3%). The causes of polyneuropathies differ markedly in elderly patients from those found in studies not restricted to specific age groups. Insufficient gastrointestinal absorption, in particular, appears to be a prominent pathogenetic factor, more often than even diabetes mellitus (n = 39, corresponding to 55.7%). However, diabetes was the underlying pathogenetic factor in 90% of patients with asymmetrically distributed polyneuropathies. In spite of this, multifactorial pathogenesis in the elderly would require a search for causes other than diabetes even in asymmetrically distributed polyneuropathies.

Aged↗

PubMed1999

Absence of polyneuropathy among workers previously diagnosed with solvent-induced toxic encephalopathy.

An association between polyneuropathy and occupational exposure to trichloroethylene, trichloroethane, perchloroethylene, or similar solvents alone or in combination is controversial. We sought to determine whether workers previously diagnosed with solvent-induced toxic encephalopathy had objective evidence of polyneuropathy. Thirty railroad workers previously diagnosed with toxic encephalopathy were examined in the context of litigation against their employers. All described long-term occupational solvent exposure averaging 20 years in duration (range, 10 to 29 years) and producing acute intoxication on a regular basis. The diagnosis of subclinical or clinical polyneuropathy was established using a combination of symptoms, signs, and nerve conduction study (NCS) measures, consistent with standard clinical practice. Potential confounders were identified. NCS results were compared with historical controls, including unexposed workers matched by gender, age, and body mass index. Dose-response relationships were evaluated using simple linear and stepwise regression models. Three workers fulfilled clinical polyneuropathy criteria. The only worker fulfilling NCS criteria for confirmed clinical polyneuropathy had diabetes mellitus. Mean NCS values for most measures were similar to control values, and existing differences in sensory amplitudes disappeared when compared with the matched control group. NCS measures were not significantly influenced by exposure duration or job title. Separation into groups on the basis of the presence or absence of polyneuropathy symptoms, previous diagnosis of polyneuropathy, disability status, and severity or type of encephalopathy did not demonstrate significant NCS differences. The complaints of these workers claiming neurotoxic injury from occupational solvent exposure are not explained by peripheral nervous system dysfunction.

Adult↗

PubMed1995

Chronic symmetric symptomatic polyneuropathy in the elderly: a field screening investigation in two Italian regions. I. Prevalence and general characteristics of the sample. Italian General Practitioner Study Group (IGPSG).

The prevalence and general characteristics of chronic symmetric symptomatic polyneuropathy were assessed in two elderly populations living in Varese, northern Italy, and San Giovanni Rotondo, southern Italy. We interviewed 4,191 subjects (3,027 in Varese and 1,164 in San Giovanni Rotondo), 55 years and older, seen in office consultations by 27 general practitioners. A neurologist examined 734 patients who had two or more symptoms of polyneuropathy. A diagnosis of possible polyneuropathy (screening neuropathic symptoms and one of the following findings: bilateral impairment of strength; bilateral impairment of sensation; bilateral impairment of deep tendon reflexes) was made in 213 patients (7.0%) in Varese and 94 (8.1%) in San Giovanni Rotondo. Probable polyneuropathy (screening symptoms and at least two of the physical findings) was present in 111 Varese patients (3.7%) and 40 San Giovanni Rotondo patients (3.4%). The age- and sex-adjusted prevalence rate of probable polyneuropathy was 3.6 per 100 in Varese and 3.3 per 100 in San Giovanni Rotondo. The disease was more prevalent in women in Varese and in men in San Giovanni Rotondo and was significantly correlated with age in Varese. Diabetes was found in association with probable polyneuropathy in 43.7% of patients. Muscle cramps and distal paresthesia were the main symptoms. In general, polyneuropathy was mild to moderate, impairment of deep tendon reflexes and sensation being the most common findings.

Aged↗

PubMed2002

Statins and risk of polyneuropathy: a case-control study.

BACKGROUND: Several case reports and a single epidemiologic study indicate that use of statins occasionally may have a deleterious effect on the peripheral nervous system. The authors therefore performed a population-based study to estimate the relative risk of idiopathic polyneuropathy in users of statins. METHOD: The authors used a population-based patient registry to identify first-time-ever cases of idiopathic polyneuropathy registered in the 5-year period 1994 to 1998. For each case, validated according to predefined criteria, 25 control subjects were randomly selected among subjects from the background population matched for age, sex, and calendar time. The authors used a prescription register to assess exposure to drugs and estimated the odds ratio of use of statins (ever and current use) in cases of idiopathic polyneuropathy compared with control subjects. RESULTS: The authors verified a diagnosis of idiopathic polyneuropathy in 166 cases. The cases were classified as definite (35), probable (54), or possible (77). The odds ratio linking idiopathic polyneuropathy with statin use was 3.7 (95% CI 1.8 to 7.6) for all cases and 14.2 (5.3 to 38.0) for definite cases. The corresponding odds ratios in current users were 4.6 (2.1 to 10.0) for all cases and 16.1 (5.7 to 45.4) for definite cases. For patients treated with statins for 2 or more years the odds ratio of definite idiopathic polyneuropathy was 26.4 (7.8 to 45.4). CONCLUSIONS: Long-term exposure to statins may substantially increase the risk of polyneuropathy.

Aged↗

PubMed2003

Intravenous immunoglobulin G is remarkably beneficial in chronic immune dysschwannian/dysneuronal polyneuropathy, diabetes-2 neuropathy, and potentially in severe acute respiratory syndrome.

Chronic Immune Dysschwannian/Dysneuronal Polyneuropathy is an autoimmune peripheral-nerve and/or nerve-root disorder known to usually respond to intravenous immunoglobulin-G treatment. Benefit can involve any combination of motor-nerve fibers and large and small sensory-nerve fibers responsible for a progressively crippling, unbalancing, discomforting or painful disorder. "Diabetic neuropathy" is commonly considered untreatable. However, 81% of my 48 recently-summarized type-2 diabetes patients with polyneuropathy, adequately-treated with intravenous immunoglobulin-G, off-label, were relieved, sometimes completely, of various motor and sensory symptoms, including pain, thereby resembling Chronic Immune Dysschwannian/Dysneuronal Polyneuropathy. Spinal fluid protein in them is often elevated, higher values seeming to auger a better intravenous immunoglobulin-G response. Continuing the improvement requires continuing the intravenous immunoglobulin-G treatment, indicating both intravenous immunoglobulin-G responsiveness and dependency. The intravenous immunoglobulin-G responsive type-2 diabetes polyneuropathy usually is dysschwannian, sometimes mainly dysneuronal intravenous immunoglobulin-G, the most beneficial and safest treatment, is costly, but if intravenous immunoglobulin-G-treatability of a dysimmune component of type-2 diabetes neuropathy is overlooked, dismissed or rejected, as commonly happens, other costs are high regarding the patient's worsening morbidity and disability, and resultant need for increased medical care. A novel intravenous immunoglobulin-G regimen effective for fragile patients is Two Non-Consecutive-Days Every Week, using 0.4 gm/kg body wt/day. Possible molecular mechanisms of intravenous immunoglobulin-G benefit are discussed. I propose that a) there is a higher incidence of Chronic Immune Dysschwannian/Dysneuronal Polyneuropathy-like neuropathy in type-2 diabetes patients and in patients with a strong family history of type-2 diabetes, and b) the intravenous immunoglobulin-G-treatable neuropathy in type-2 diabetes can be brought on by the genetico-diabetoid-2 state. The genetic-metabolic milieu (but not necessarily glucose dysmetabolism per se.) of type-2 diabetes putatively predisposes to the presumably-dysimmune intravenous immunoglobulin-G-responsive polyneuropathy. In some of our patients, especially ones having a strong type-2 diabetes genetic background, the intravenous immunoglobulin-G-responsive neuropathy preceded the diagnosis of type-2 diabetes by 5-10 years. Accordingly, Chronic Immune Dysschwannian/Dysneuronal Polyneuropathy patients having a strong type-2 diabetes genetic background are designated "genetico-diabetoid-2 neuropathy" prior to their manifesting type-2 diabetes. Intravenous immunoglobulin-G is herein suggested as a treatment for Severe Acute Respiratory Syndrome, a recent, and feared-repetitive, pandemic with many fatalities caused by a highly-contagious mutant coronavirus, for which there is no definitive treatment. Intravenous immunoglobulin-G might: a) combat a dysimmune component of Severe Acute Respiratory Syndrome, including the reactive cytokine-chemokine storm against respiratory tissues; b) contain some antibodies effective against the coronavirus non-specific components of Severe Acute Respiratory Syndrome; c) block host-cell receptors for the virus; and d) counteract secondary infections.

Chronic Disease↗

PubMed2001

MRI of the brachial plexus in polyneuropathy associated with monoclonal gammopathy.

On magnetic resonance (MR) imaging of the brachial plexus increased signal intensity and swelling of the brachial plexus has been found in chronic inflammatory demyelinating polyneuropathy (CIDP). Whether these proximal abnormalities are also present in the distal polyneuropathy associated with monoclonal gammopathy is unknown. Therefore, we performed MR imaging of the brachial plexus in 21 patients with polyneuropathy associated with IgM monoclonal gammopathy (11 IgM with anti-MAG antibodies, 10 IgM without anti-MAG antibodies). For comparison we studied 9 patients with polyneuropathy associated with IgG monoclonal gammopathy and 8 patients with CIDP. Among the 30 patients with monoclonal gammopathy, 24 patients had demyelinating polyneuropathy. Among these 24 patients, there was increased signal intensity of the brachial plexus on the T2-weighted images regardless of whether clinical deficits were generalized or purely distal in location. No association was found with the isotype of the monoclonal gammopathy. Of the 8 patients with CIDP, 5 had brachial plexus abnormalities. None of the 6 patients with axonal polyneuropathy associated with monoclonal gammopathy had such abnormalities. Thus, MR imaging of the brachial plexus shows that the distal demyelinating polyneuropathy associated with monoclonal gammopathy is more generalized than presumed.

Adult↗

PubMed1994

Abnormalities in T-lymphocyte populations in blood from patients with demyelinating polyneuropathy associated with monoclonal gammopathy.

Patients with monoclonal gammopathy secrete monoclonal antibodies (M-component), that in some patients are associated with polyneuropathy. The M-component has been shown to react with peripheral nerve myelin in some of these patients. However, it is not known whether the M-component secreting B-cells are autonomous or subject to regulation by T-cells or if other cellular abnormalities may occur. In order to define circulating lymphocyte subpopulations, flow cytometry was done on blood samples from patients with monoclonal gammopathy and demyelinating polyneuropathy (n = 13) and patients with monoclonal gammopathy without polyneuropathy (n = 11), and were compared to healthy controls. Significantly increased proportions of primed T-helper (CD4+) cells, i.e. those expressing helper/inducer function (CD29+ CD4+), providing help for antibody secretion, as well as decreased proportions of naive, unprimed suppressor/inducer (CD45RA+ CD4+) T-helper cells were found in patients with M-component associated polyneuropathy. Within the T-cytotoxic/suppressor population (CD8+) we found an increased proportion of killer/effector (S6F1+ CD8+) cells and a decreased proportion of suppressor/effector (S6F1- CD8+) cells in patients with monoclonal gammopathy and polyneuropathy. Similar findings were found in monoclonal gammopathy patients without polyneuropathy, although the deviations in general were less pronounced and did not reach statistical significance compared to the controls. The proportion of natural killer (NK) cells (CD56+) was markedly decreased in all patients with monoclonal gammopathy. In the whole group of patients with monoclonal gammopathy, we found clear proportions of interleukin-2 receptor (CD25+) expressing lymphocytes, indicating the presence of activated T-cells. No clear correlation between abberations in T-cell subtypes and clinical severity of the demyelinating polyneuropathy or titres of anti-PNM antibodies was found.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMedDate not supplied

Painful polyneuropathy in patients with and without diabetes: clinical, neurophysiologic, and quantitative sensory characteristics.

OBJECTIVES: To study pain characteristics and peripheral nerve involvement in patients with painful diabetic and nondiabetic polyneuropathy in comparison with patients with non-painful polyneuropathy. PATIENTS AND METHODS: Fifty-five patients with polyneuropathy (37 with painful polyneuropathy, of whom 19 had diabetes and 18 had no diabetes; and 18 with painless polyneuropathy of different etiologies) were examined clinically using quantitative sensory tests and neurophysiology. Pain intensity and characteristics were analyzed by daily ratings on a 10-step verbal scale and by a questionnaire. RESULTS: Most patients experienced pain of more than one character. There was no clear difference in character or duration of pain between patients with and without diabetes. The mean value of the daily rating of pain intensity showed that pain was more severe in the evenings than in the mornings and that diabetic patients reported worse pain than nondiabetic patients. Thirty-two of the 37 patients with pain had paresthesias and/or dysesthesias, whereas only 7 of 18 patients without pain had paresthesias. Pain was always located in the feet, and, in most patients, also in the lower part of the legs. Some patients also experienced pain in the hands. Tactile sensibility, measured by quantitative tests, was more affected in both diabetic and nondiabetic patients with painful polyneuropathy compared with patients without pain (p = 0.02). Temperature, pain, and vibratory sensibility were equally affected in all patient groups. Nerve conduction velocity, amplitudes, and distal latency were equally affected in the pain group as compared with the control group, indicating that both thin and thick nerve afferents are affected in patients with painful as well as non-painful polyneuropathy and that etiology has no clear impact on nerve involvement. CONCLUSIONS: Neuropathy pain was always located in the feet and more severe in diabetic patients compared with patients with neuropathy pain of other etiologies. The authors also found evidence for a greater tactile sensibility involvement in patients with neuropathy pain, irrespective of etiology, whereas other quantitative sensibility and neurography parameters were equally affected in all patient groups.

Adult↗

PubMedDate not supplied

[Polyneuropathy deficiency among Xavante indians].

UNLABELLED: The authors present two cases of polyneuropathy deficiency among Xavante indians where the sole food was rice in case 1 and almost so in case 2. The rice consumed by these indians was processed or hulled. Intoxication by cyanide from maniot or other vegetable was excluded. CASE REPORT: Two indians aged 18 and 25 years with a progressive history of weaness, decrease in muscular force and thinning were observed in their villages. On removal to the Hospital São Paulo, atrophy of the distal musculature of the upper and lower limbs, motor deficit distally with zero degree in the flexor musculature, abolished deep reflexes, plantar cutaneous reflex without response bilaterally, decreased tactile, painful and pallesthetic sensitivity distally in the lower limbs were noted on neurological examination of case 1. On neurological examination of case 2 proximal hyporeflexia in the upper limbs, areflexia in the distal portions of the upper and lower limbs, tactile and painful hypoesthesia in the feet, right hypoacousis were noted. Electromyography showed abnormalities compatible with symmetric sensorimotor polyneuropathy with an axonal demyelination pattern in case 1 and predominantly demyelinizing in case 2. Cerebrospinal fluid tests were normal. DISCUSSION: Polyneuropathy was characterized by the clinical history and by neurological, electromyographic and cerebrospinal fluid tests. The diagnosis of polyneuropathy deficiency was established by the clinical history and by electromyography suggesting peripheral polyneuropathy of nutritional origin. This neuropathy deficiency does not fit myeloneuropathies such as ataxic tropical neuropathy, spastic paraparesis and Cuba neuropathy. CONCLUSION: The Xavante polyneuropathy deficiency is caused by thiamine (vitamin B1) deficiency, that is dry beriberi, owing to consumption of industrially processed rice as sole or almost sole food. The Xavante polyneuropathy is different from the neuropathy observed among Kreen-Akrore indians and from that of adolescent indians in the Xingu Park.

Adolescent↗

PubMed1990

[Factors affecting the incidence and severity of polyneuropathy in type I diabetes mellitus].

194 type I diabetics were subjected to neurological and electromyographic examinations. In 161 patients, i.e. in 83%, signs of polyneuropathy were detected, the severity of which was evaluated according to a 5-grade scale where grade 1 was the mildest and the 5th grade the most severe one. The authors proved a statistically significant correlation of the incidence and severity of polyneuropathy and the duration of diabetes. It was found that the decisive period of persistence of diabetes was 6-10 years. During this period the incidence of polyneuropathies increased from 30 to 87%. After 20 years duration of diabetes there was not only a 100% incidence of polyneuropathy, but severe affections--grade 3-5--predominated in 78%. In patients with severe grades of polyneuropathy diabetes was manifested at a significantly lower age than in patients without polyneuropathy and with a milder affection. The authors did not detect a significant relationship between the height of the patients and the incidence of polyneuropathy nor significant differences between men and women.

Adult↗

PubMed1990

[Relation of diabetic polyneuropathy to vascular and organ complications in type I diabetes mellitus].

The authors investigated in 194 type I diabetics the incidence and severity of diabetic polyneuropathy in relation to other organ and vascular complications, incl. autonomous neuropathy. It was revealed that the increasing severity of polyneuropathy was significantly v séru (Cr equal to or less than 130-200 mumol/l); 4--Cr greater than 200 mumol/l; associated with severe stages of nephropathy and proliferative retinopathy with amaurosis. The concurrent presence of hypertension and polyneuropathy was surprising and striking--even in patients with the mildest grade 1 polyneuropathy hypertension was present in 10% and the incidence increased significantly with the increasing severity of polyneuropathy. Ischaemic heart disease and ischaemia of the lower extremities was significantly more frequent only in patients with grade 5 polyneuropathy. In patients with grade 4 and 5 neuropathy there was a 100% incidence of autonomous neuropathy in the cardiovascular sphere. The authors did not reveal significant differences between men and women as regards the relationship between the incidence of polyneuropathy and organ and vascular complications.

Autonomic Nervous System Diseases↗

PubMed1986

[Sensorimotor and autonomous polyneuropathies in diabetic children and adolescents].

In 28 juvenile and adolescent diabetics (14 males, 14 females) ranging in age between 9 and 20 years (mean: 14.9) we investigated several electrophysiological parameters, the vibration threshold and the cardiovascular reflexes in order to determine the incidence of sensomotor and autonomic polyneuropathy. 6 patients showed evidence of sensomotor polyneuropathy, 2 more had signs of autonomic polyneuropathy. Both groups with polyneuropathy did not differ significantly from the whole group of diabetics concerning the mean onset of illness and several metabolic parameters. The mean duration of illness and the average age was clearly higher in the patients with sensomotor polyneuropathy than in the whole group. Out of 5 patients with diabetic retinopathy 3 had signs of sensomotor polyneuropathy. No patient was clinically affected by polyneuropathy. In 1 patient the distal latency and the amplitude of the compound muscle action potential of the peroneal nerve showed pathologic values, in a second patient the maximal conduction velocity of the median nerve was slowed. 4 patients had abnormally high vibration threshold. The heart rate variation during rest was reduced in 2 patients. Significant differences between the diabetics and the controls could only be found concerning the maximum conduction velocities of the peroneal and the median nerve. Our results will be compared and discussed.

Adolescent↗

PubMed1997

Diabetic polyneuropathy in the elderly. Prevalence and risk factors in two geographic areas of Italy. Italian General Practitioner Study Group (IGPSG).

OBJECTIVE: To assess the prevalence and the risk factors of diabetic polyneuropathy in representative samples of elderly individuals. PATIENTS: 4191 subjects 55 years and older from two areas of Italy were screened by their general practitioners (GPs) and those positive for neuropathic symptoms were subjected to a standard clinical examinations. METHODS: The screening questionnaire included a list of clinical conditions possibly causing polyneuropathy, including diabetes. In patients with diabetes, the date of diagnosis, the most recent fasting and post-prandial blood glucose value and glycosylated hemoglobin were sought. Probable polyneuropathy was diagnosed through impairment of 2 or 3 nerve functions (strength, sensation, tendon reflexes) in the extremities with symmetrical and distal distribution. RESULTS: The sample included 347 patients with diabetes (8.3%). Sixty-six of them (19%) had symptoms and signs consistent with probable polyneuropathy (overall prevalence 1.6%). The disease prevailed in women and in subjects aged 75 years and older. Diabetic patients with polyneuropathy had a longer disease course (P < 0.02) and high mean fasting (P < 0.001) and post-prandial (P < 0.02) blood glucose. CONCLUSION: Diabetic polyneuropathy in the elderly is a fairly common clinical condition prevailing in women and in subjects 75 years and older. Risk factors for polyneuropathy include prolonged disease duration and high mean fasting and post-prandial blood glucose.

Aged↗

PubMed2003

[Diagnosis and treatment of polyneuropathy: what can the family doctor do?].

Polyneuropathies are common disorders of the peripheral nervous system. Early diagnosis and therapy enables to stop the progression of the polyneuropathy and to ameliorate polyneuropathic symptoms in most cases. Clinical examination is sufficient to diagnose polyneuropathy. However, to reveal the etiology of a polyneuropathy additional diagnostic procedures are necessary. The general practitioner should recognize the signs and symptoms of a polyneuropathy and start necessary investigations. If the etiology of the polyneuropathy is revealed specific therapy can be started. Furthermore, polyneuropathic symptoms can be ameliorated independently of the underlying cause.

Alcoholic Neuropathy↗

PubMed2003

Chronic acquired demyelinating symmetric polyneuropathy classified by pattern of weakness.

OBJECTIVES: To study a representative group of patients with chronic acquired symmetric demyelinating polyneuropathies, and to evaluate classification by pattern of weakness and by presence of immunoglobulin monoclonal protein (M protein). METHODS: In Vest-Agder County, Norway, an unselected population of patients with chronic symmetric polyneuropathies who fulfill electrodiagnostic criteria for demyelination are registered in a database and followed up prospectively. Data were taken from the database on April 2, 2001. Patients with proximal as well as distal weakness were classified as having chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), and patients with only distal symptoms as having distal acquired demyelinating symmetric polyneuropathy (DADS). RESULTS: A total of 29 patients had chronic acquired symmetric demyelinating polyneuropathy; 15 had CIDP and 14 had DADS. The 2 categories differed regarding spinal protein level (mean +/- SD, 0.102 +/- 0.060 g/dL in CIDP vs 0.065 +/- 0.029 g/dL in DADS; P =.05); clinical course (remitting in 6 of 13 patients with CIDP vs 0 of 14 with DADS; P =.02); disability score at diagnosis (mean +/- SD, 3.3 +/- 1.0 in CIDP vs 1.9 +/- 0.6 in DADS; P<.001) and at peak of symptoms (mean +/- SD, 3.6 +/- 1.1 in CIDP vs 2.3 +/- 0.6 in DADS; P<.001); and response to immunosuppressive treatment (11 of 12 patients with CIDP vs 2 of 7 with DADS; P =.01). An M protein was detected in 8 patients (3 with CIDP and 5 with DADS). Patients with polyneuropathy with and without M protein were similar in clinical features, course, disability, and treatment response. CONCLUSION: Classification by presence or absence of proximal weakness separates patients with chronic acquired symmetric demyelinating polyneuropathy into groups that are different in clinical course, disability, and treatment response.

Adult↗

PubMed1999

Amplitude-dependent slowing of conduction in amyotrophic lateral sclerosis and polyneuropathy.

The mechanism of motor nerve conduction slowing in amyotrophic lateral sclerosis (ALS) is thought primarily to be loss of large, fast-conducting motor fibers; this is less certain in axonal polyneuropathy. We compared motor conduction studies in 64 patients with axonal polyneuropathy with 72 patients with ALS. Compound motor action potential amplitude, distal motor latency, and conduction velocity were converted to a percentage of the upper or lower limit of normal and then represented as a square root (SQRT) transformation, plotted with SQRT amplitude as the independent variable and SQRT latency or SQRT conduction velocity as the dependent variables. Regression analysis of the lower extremity nerve data showed that prolongation of latency and slowing of velocity were amplitude-dependent and were virtually identical in ALS and polyneuropathy. In the upper extremity, amplitude-dependent prolongation of latency was similar in both groups, but amplitude-dependent slowing of velocity was seen in ALS and not in axonal polyneuropathy. Our data support the hypothesis that the major mechanism of slowing is similar in both polyneuropathy and ALS and is the loss of large, fast-conducting fibers. However, the presence of distal but not proximal slowing in the upper extremity of axonal polyneuropathy suggests that additional mechanisms may be contributory.

Action Potentials↗

PubMed2006

Do carbamates cause polyneuropathy?

Carbamates are reversible inhibitors of acetylcholinesterase, and some also inhibit neuropathy target esterase (NTE), the target in organophosphate-induced delayed polyneuropathy. However, based on mechanistic considerations, these carbamates were thought to be unable to initiate polyneuropathy. Consequently, clinical reports of polyneuropathy associated with carbamate exposures have been disregarded. We discuss three cases of polyneuropathy that occurred after severe poisoning by methylcarbamates. In addition, high repeated doses of phenyl N-methyl N-benzylcarbamate caused nearly 100% NTE inhibition and polyneuropathy in the hen model. These data suggest the need to reconsider the long-standing tenet that carbamates cannot cause polyneuropathy. Alternatively, a preexisting subclinical neuropathy in these individuals may have been amplified by carbamates, as observed in animal models. We suggest that individuals with underlying neuropathy (e.g., diabetics) who are poisoned by carbamates should be followed closely. In addition, procedures for the current risk assessment of carbamate pesticides may need to be reconsidered.

Adult↗