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PubMed1997

Evaluation of neuropathy in patients on suramin treatment.

Suramin, a promising chemotherapeutic agent, causes a dose-limiting sensorimotor polyneuropathy. We undertook a phase 1 study of suramin that included serial neurologic and electrophysiologic examinations as part of the safety evaluation. We found that 6 of 41 (15%) patients developed suramin-induced demyelinating neuropathy which resembled Guillain-Barre syndrome clinically. There was 1 asymptomatic patient with electrophysiologic abnormalities suggestive of a demyelinating neuropathy. In addition, 1 patient with mild axonal neuropathy at baseline had deterioration of his symptoms during suramin treatment. Four asymptomatic patients developed electrophysiologic findings suggestive of a mild axonal neuropathy. We conclude that: (1) serial electrophysiologic monitoring is helpful for early detection of suramin-induced neuropathy; and (2) fixed dosing schedule of suramin without adaptive control does not lead to an increased incidence of demyelinating neuropathy when compared to adaptively controlled dosing schedules.

Adult↗
PubMed1999

Autoantibodies associated with peripheral neuropathy.

High titers of serum antibodies to neural antigens occur in several forms of neuropathy. These include neuropathies associated with monoclonal gammopathy, inflammatory polyneuropathies, and paraneoplastic neuropathies. The antibodies frequently react with glycosylated cell surface molecules, including glycolipids, glycoproteins, and glycosaminoglycans, but antibodies to intracellular proteins have also been described. There are several correlations between antibody specificity and clinical symptoms, such as anti-MAG antibodies with demyelinating sensory or sensorimotor neuropathy, anti-GM1 ganglioside antibodies with motor nerve disorders, antibodies to gangliosides containing disialosyl moieties with sensory ataxic neuropathy and Miller-Fisher syndrome, and antibodies to the neuronal nuclear Hu antigens with paraneoplastic sensory neuronopathy. These correlations suggest that the neuropathies may be caused by the antibodies, but evidence for a causal relationship is stronger in some examples than others. In this review, we discuss the origins of the antibodies, evidence for and against their involvement in pathogenic mechanisms, and the implications of these findings for therapy.

Antibody Specificity↗
PubMed1978

Carcinomatous versus radiation-induced brachial plexus neuropathy in breast cancer.

A retrospective study was performed of 18 women in whom ipsilateral brachial plexus neuropathy developed after treatment for carcinoma of the breast. In the absence of metastatic tumor elsewhere, the only distinguishing feature between carcinomatous neuropathy and radiation-induced neuropathy was the symptom-free interval after mastectomy and radiation therapy. Women with an interval of less than a year have radiation-induced neuropathy. Brachial plexus exploration in difficult diagnostic situations will permit early treatment and avoid debilitating loss of function. Brachial plexus exploration for biopsy is safe and free of complications if performed carefully. Treatment of carcinomatous neuropathy is most likely to succeed if the tumor is hormonally sensitive, but radiotherapy may also be effective. Treatment of radiation-induced neuropathy remains largely ineffective.

Adenocarcinoma↗
PubMed2006

Immunotherapy for IgM anti-myelin-associated glycoprotein paraprotein-associated peripheral neuropathies.

BACKGROUND: Serum monoclonal anti-myelin associated glycoprotein antibodies may be pathogenic in some people with IgM paraprotein and demyelinating neuropathy. Immunotherapies aimed at reducing the level of these antibodies might be expected to be beneficial. OBJECTIVES: To examine the efficacy of any form of immunotherapy in reducing disability and impairment resulting from IgM anti-myelin associated glycoprotein paraprotein-associated demyelinating peripheral neuropathy. SEARCH STRATEGY: We searched the Cochrane Neuromuscular Disease Group Register (March 2005), MEDLINE (January 1966 to March 2005) and EMBASE (January 1980 to March 2005) for controlled trials. We also checked bibliographies and contacted authors and experts in the field. SELECTION CRITERIA: We included randomised or quasi-randomised controlled trials of participants of any age treated with any type of immunotherapy for anti-myelin-associated glycoprotein antibody associated demyelinating peripheral neuropathy with monoclonal gammopathy of undetermined significance of any severity. Our primary outcome measure was change in the Neuropathy Impairment Scale or Modified Rankin Scale at six months after randomisationSecondary outcome measures were: Neuropathy Impairment Scale or the Modified Rankin Score at 12 months after randomisation; ten-metre walk time, subjective clinical scores and electrophysiological parameters at six and 12 months after randomisation; IgM paraprotein levels and anti-myelin associated glycoprotein antibody titres at six months after randomisation and adverse effects of treatments. DATA COLLECTION AND ANALYSIS: We identified eight possible trials. Of these, five randomised controlled trials were included after discussion between the authors. One author extracted and the other checked the data. No missing data could be obtained from trial authors. MAIN RESULTS: The five eligible trials (97 participants) tested intravenous immunoglobulin, interferon-alpha or plasma exchange. Only two, of intravenous immunoglobulin, had comparable interventions and outcomes but both were short-term. There were no significant benefits of the treatments used in the outcomes predefined for this review, but not all the predefined outcomes were used in every included trial. Intravenous immunoglobulin showed benefits in terms of improvement in Modified Rankin Scale at two weeks and 10-metre walk time at four weeks. Serious adverse effects of intravenous immunoglobulin are known to occur from observational studies but none were encountered in these trials. AUTHORS' CONCLUSIONS: There is inadequate reliable evidence from trials of immunotherapies in anti-myelin associated glycoprotein paraproteinaemic neuropathy to recommend any particular immunotherapy treatment. Intravenous immunoglobulin is relatively safe and may produce some short-term benefit. Large well-designed randomised trials of at least six to 12 months duration are required to assess existing or novel therapies.

Demyelinating Diseases↗
PubMed1993

Peripheral neuropathy after occupational exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

Reports of human exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) describe signs and symptoms consistent with exposure-related peripheral neuropathy. In a cross-sectional study, prevalence of peripheral neuropathy was measured in 265 workers exposed 15 years earlier to chemicals contaminated with TCDD and in 244 unexposed, age-, race-, gender- and community-matched comparisons. Cases of peripheral neuropathy were defined from examination, electrophysiologic and quantitative sensory tests, and symptoms. Exposure was assessed by measuring lipid-adjusted serum TCDD levels. The mean serum TCDD level for workers (220 parts per trillion (ppt)) was significantly higher than for referents (7 ppt) (p < .0001). Thirty-two percent of both worker and referent groups met the case definition for peripheral neuropathy. In the logistic regression analyses, serum TCDD level was not related to peripheral neuropathy. These data suggest that despite continued high serum TCDD levels, peripheral neuropathy is not a long-term sequela of high exposure to TCDD-contaminated chemicals. However, the study cannot preclude the occurrence and subsequent resolution of acute effects caused by high exposure, as experienced in Seveso and possibly by some workers, while exposed to high levels of TCDD-contaminated substances.

Adult↗
PubMed2003

FK506 is neuroprotective in a model of antiretroviral toxic neuropathy.

Antiretroviral toxic neuropathy is the most common neurological complication of human immunodeficiency virus infection. This painful neuropathy not only affects the quality of life of human immunodeficiency virus-infected patients but also severely limits viral suppression strategies. We have developed an in vitro model of this toxic neuropathy to better understand the mechanism of neurotoxicity and to test potential neuroprotective compounds. We show that among the dideoxynucleosides, ddC appears to be the most neurotoxic, followed by ddI and then d4T. This reflects their potency in causing neuropathy. AZT, which does not cause a peripheral neuropathy in patients, does not cause significant neurotoxicity in our model. Furthermore, in this model, we show that the immunophilin ligand FK506 but not cyclosporin A prevents the development of neurotoxicity by ddC, as judged by amelioration of ddC-induced "neuritic pruning," neuronal mitochondrial depolarization, and neuronal necrotic death. This finding suggests a calcineurin-independent mechanism of neuroprotection. As calcineurin inhibition underlies the immunosuppressive properties of these clinically used immunophilin ligands, this holds promise for the neuroprotective efficacy of nonimmunosuppressive analogs of FK506 in the prevention or treatment of antiretroviral toxic neuropathy.

Animals↗
PubMed1988

Peripheral neuropathies associated with human immunodeficiency virus infection.

Peripheral neuropathies may complicate all stages of infection with human immunodeficiency virus (HIV). Acute inflammatory demyelinating polyneuropathy, sensory ganglioneuritis, and acute cranial nerve palsy all may occur 2 to 3 weeks after acute HIV infection. Acute inflammatory demyelinating polyneuropathy, chronic inflammatory demyelinating polyneuropathy, and polyradiculopathy may occur with otherwise asymptomatic HIV virus infection. Neuropathy is one of the most common neurological manifestations of the acquired immunodeficiency syndrome (AIDS)-related complex, occurring in as many as 20% of these patients. Acute or chronic inflammatory demyelinating polyneuropathy (38%) and mononeuropathy multiplex (29%) are most frequently seen, and usually there is a good prognosis, with the neuropathy resolving spontaneously or with steroids or plasmapheresis. Neuropathy occurring with AIDS is reportedly uncommon but probably is underreported, especially in seriously ill patients. By contrast with AIDS-related complex, the neuropathy associated with AIDS is usually a distal symmetrical polyneuropathy (72%), with inflammatory neuropathy, mononeuropathy multiplex, and polyradiculopathy occurring rarely. The pathogenesis of acute or chronic inflammatory demyelinating polyneuropathy and possibly of mononeuropathy multiplex is probably autoimmune. The pathogenesis of distal symmetrical polyneuropathy is less clearly established and may be infectious, toxic, or nutritional. Polyradiculopathy most likely is infectious; cytomegalovirus is a leading contender for infectious agent, but herpes simplex virus and HIV are other possibilities.

AIDS-Related Complex↗
PubMed1994

Peripheral neuropathy from taxol and cisplatin combination chemotherapy: clinical and electrophysiological studies.

Taxol is a novel antineoplastic agent that has demonstrated impressive clinical activity in breast, ovarian, lung, and head and neck cancers. This broad antitumor activity of taxol in cisplatin-sensitive tumors suggests that the combination of taxol and cisplatin may become one of the most commonly used taxol-based chemotherapeutic regimen in the treatment of solid tumors. Both taxol and cisplatin, however, are neurotoxic. To study the neurotoxic effects of these two agents when used in combination, we prospectively evaluated neurological function at baseline, during, and following treatment, in 21 cancer patients treated with taxol (135-350 mg/m2), cisplatin (75-100 mg/m2), and granulocyte-colony stimulating factor (5 micrograms/kg). Twenty of the 21 patients (95%) developed a sensory-motor neuropathy 1 to 21 weeks after the initiation of therapy, that was progressive with each additional course of chemotherapy. The neuropathy was symmetrical, length dependent, axonal in nature by physiological studies, and more pronounced in those patients who received higher doses of taxol. The neuropathy appeared earlier and at lower taxol doses in those patients with preexisting neuropathies. We conclude that sensory-motor neuropathy is a frequent dose-dependent toxicity of combined cisplatin and taxol use. Peripheral neuropathy is likely to become the major dose-limiting toxicity of taxol-cisplatin combination chemotherapy when higher doses of these agents are administered with granulocyte-colony stimulating factor.

Adult↗
PubMed1994

Leber's hereditary optic neuropathy mitochondrial DNA mutations in multiple sclerosis.

The observation of a multiple sclerosis (MS)-like illness in patients, particularly women, who carry the most common Leber's hereditary optic neuropathy mitochondrial DNA (mtDNA) mutation may indicate a contributory role for mitochondrial genes in genetic susceptibility to MS. We screened 307 unrelated MS patients, ascertained from population surveys, for the pathogenic Leber's hereditary optic neuropathy mutations at positions 11778 and 3460 of mtDNA, and also studied 20 patients with prominent and early optic nerve involvement. In addition, these 307 patients and 129 control subjects were investigated for the base change at position 13708, which has been suggested to play a role in the pathogenesis of Leber's hereditary optic neuropathy. Neither of the pathogenic mtDNA mutations occurred in the unselected MS patients. The 13708 base change was present in MS patients at a frequency similar to that in healthy control subjects. Three of the patients selected on the basis of severe optic nerve involvement had either the 11778 (one) or 3460 (two) mutations associated with Leber's hereditary optic neuropathy. All were women and none had affected relatives. We conclude that these mutations do not contribute to genetically determined susceptibility in typical MS patients, although a mitochondrial genetic component in the etiology of MS remains possible. A subgroup of MS patients, particularly females with severe bilateral visual failure due to optic neuropathy, may harbor a Leber's hereditary optic neuropathy mutation and we suggest that mtDNA analysis is appropriate in these patients.

Adult↗
PubMed1996

Deletions of chromosome 17p11.2 in multifocal neuropathies.

We investigated 51 patients with multifocal neuropathies for the deletion of chromosome 17p11.2 described in families with hereditary neuropathy with liability to pressure palsies (HNPP). The deletion was detected in 24 patients, including 19 patients from 14 of 15 families in whom HNPP had been considered likely on clinical, neurophysiological, and/or pathological grounds. One patient with a deletion had rather unusual clinical features for HNPP, presenting with a progressive scapuloperoneal syndrome. Overall, 7 (37%) of the 19 index patients with the deletion had no affected relatives, and less than half had evidence of a generalized neuropathy on examination. Peripheral nerve lesions were related to pressure in only 15 (62%) of the patients with the deletion. Nerve conduction studies in 23 of 25 patients and relatives studied showed a fairly uniform pattern of moderate prolongation of distal sensory and motor latencies and slowing of conduction velocities, and variable reduction of sensory or evoked muscle action potential amplitudes. The patients investigated who did not have a deletion of 17p11.2 were heterogeneous and included those with recurrent and/or familial neuralgic amyotrophy, two or more peripheral nerve lesions at common sites of entrapment, or a patchy axonal neuropathy of unknown etiology. In 1 patient a diagnosis of HNPP remains most likely. DNA analysis for the deletion of 17p11.2 is clearly useful in establishing the diagnosis of HNPP, which should be considered regardless of family history or clinical evidence of a generalized neuropathy, and in patients with multifocal neuropathies that do not conform to the classic clinical practice of HNPP.

Adolescent↗
PubMedDate not supplied

Sonography of entrapment neuropathies in the upper limb (wrist excluded).

The progressive refinement of broadband transducers with frequencies higher than 10 MHz and improved near-field resolution has enhanced the potential of sonography to evaluate a variety of nerve entrapment syndromes occurring in the upper limb, such as suprascapular neuropathy in the area of the spinoglenoid-supraspinous notch, the quadrilateral space syndrome (axillary neuropathy), radial neuropathy in the area of the spiral groove, the supinator syndrome (posterior interosseous neuropathy), the cubital tunnel syndrome (ulnar neuropathy), and the Kiloh-Nevin syndrome (anterior interosseous neuropathy). In these settings, high-resolution sonography can depict changes in the nerve's shape and echotexture and can depict many extrinsic causes of nerve entrapment.

Humans↗
PubMed2003

Autonomic and peripheral neuropathy in endstage liver disease and following liver transplantation.

Severe chronic liver disease may be associated with a peripheral somatic and an autonomic neuropathy. There are only a limited number of reports on the incidence and features of these neuropathies. In addition the effects of liver transplantation on these neuropathies have not been well studied. We examined peripheral somatic and autonomic nerve function in 42 patients with endstage liver disease prior to transplantation and also examined the effect of liver transplantation on these neuropathies in 14 patients. Peripheral somatic neuropathy (93%) and autonomic neuropathy (50%) were common in patients with endstage liver disease and were more frequent than previously reported. Abnormalities improved in some patients after liver transplantation, particularly if there was return of normal hepatic function.

Adolescent↗
PubMed2004

Absence of sensory neuropathy among workers with occupational exposure to chlorpyrifos.

Several studies have reported the occurrence of sensory neuropathy with exposure to chlorpyrifos and other organophosphorus insecticides, at levels not associated with overt toxicity. We evaluated 113 chemical workers, including 53 of 66 (80%) eligible chlorpyrifos workers and 60 of 74 (81%) randomly selected referent workers, to identify evidence of sensory neuropathy or subclinical neuropathy. Compared to referents, chlorpyrifos subjects had significantly longer duration of work in chlorpyrifos-exposed areas (9.72 vs. 0.01 years; P < 0.0001), greater cumulative chlorpyrifos exposure (64.16 vs. 0.69 mg/m(3). day; P < 0.0001), higher urine 3,5,6-trichloro-2-pyridinol (TCP) excretion (108.6 vs. 4.3 microg/g creatinine; P < 0.0001), and lower plasma butyrylcholinesterase (BuChE) activity (7281 vs. 8176 mU/ml; P = 0.003). Despite exposures among chlorpyrifos subjects to levels at which well-described physiological effects on B-esterases exist, the frequency of symptoms or signs of neuropathy did not differ significantly between groups, and the only 2 subjects fulfilling criteria for confirmed neuropathy were both in the referent group. Mean nerve conduction study results were comparable to established control values and did not differ significantly between groups. We found no evidence of sensory neuropathy or isolated peripheral abnormalities among subjects with long-term chlorpyrifos exposure at levels known to be associated with the manufacturing process.

Adolescent↗
PubMed2004

Porphyric neuropathy.

The hepatic porphyrias are a group of rare metabolic disorders characterized by enzymatic defects in the biosynthesis of heme, a metalloporphyrin that is the principal product of porphyrin metabolism. The hepatic porphyrias are genetically transmitted as autosomal-dominant disorders with variable expression that produce a particularly severe form of neuropathy. Most medical students readily recognize acute attacks of porphyria when the classic triad of abdominal pain, psychosis, and neuropathy is present. Yet, porphyric neuropathy is a source of confusion in practice, and patients with porphyria rarely receive the correct diagnosis early in the course of the illness. Porphyric neuropathy is manifest by symptoms, signs, and cerebrospinal fluid abnormalities resembling acute Guillain-Barré syndrome. However, accompanying psychological features, a proximal predilection of asymmetric weakness, and electrodiagnostic findings indicative of an axonal polyradiculopathy or neuronopathy all suggest the diagnosis of porphyria. Confirmation of the diagnosis depends on use of appropriate laboratory studies. The underlying pathophysiology of porphyric neuropathy has not been established, but it may be related to direct neurotoxicity of elevated levels of delta-aminolevulinic acid. The severity of the neuropathy and the availability of potential treatments, including avoidance of provocative factors, make identification important.

Animals↗
PubMed1982

Peripheral neuropathy in patients with benign monoclonal gammopathy--a pilot study.

It is well known that peripheral neuropathy occurs in patients with myeloma or macroglobulinaemia, but its pathogenesis is still obscure. In recent years, neuropathy has also been reported in association with benign monoclonal or oligoclonal gammopathy. Modern histo-immunological methods have revealed evidence of antibody production to peripheral nerve tissue, probably the myelin sheath. The present study included 21 unselected, consecutive patients with benign monoclonal gammopathy observed in the Division of Haematology. Clinical and laboratory investigations included electrophysiological examination and analyses of the M components. Of the 21 patients 11 had noticed slight neuropathic symptoms in their extremities; in 5 both clinical and electrophysiological findings were compatible with neuropathy; 6 showed positive clinical signs of neuropathy; 4 had either positive electromyographic or electroneurographic findings. In summary, 15 of 21 patients had some signs of peripheral neuropathy. In spite of the screening design of the study, this strikingly high frequency is comparable with other recent reports. Haematological studies did not reveal any significant differences between the patient groups with positive or negative neurological findings. The findings indicate that even benign gammopathies may be associated with peripheral neuropathy.

Adult↗
PubMed1977

[Unmyelinated nerve fibers in senile nerves and in late thalidomide neuropathy: a quantitative electron microscopic study (author's transl)].

Sural nerve biopsies of four patients, aged 54--76 years, with a predominantly sensory type of neuropathy following high dosages of thalidomide were examined by light and electron microscopy. The present study includes a qualitative and quantitative evaluation of unmyelinated nerve fibers. Despite severe neuropathy, increased numbers of small unmyelinated axons per endoneurial area were noted in all patients. This numerical increase appeared to be independent of aging, since it was not seen in two senile controls, studied at the age of 83 and 88 years. The increase in the endoneurial density of unmyelinated axons, especially of small sized fibers, is likely to be related to regeneration following degeneration of unmyelinated axons although endoneurial shrinkage secondary to loss of large myelinated fibers could have caused an additional increase in the number of axons per endoneurial area. Axonal sprouting, despite degeneration of large numbers of myelinated and unmyelinated fibers, appears to be consistent with some of the characteristic clinical features of thalidomide neuropathy such as paresthesias, hyperesthesia for pain and temperature, and disturbances of autonomic functions. On the other hand, a variable number of empty Schwann cells (bands of Büngner) and pockets at the surface of many Schwann cells noted in the four patients with neuropathy were also seen in both senile controls with no signs of neuropathy. Thus, it is obvious that pockets and empty Schwann cells may be related to aging or other causes of slow axonal wasting with Schwann cell proliferation and are not necessarily associated with clinically manifest neuropathy.

Aged↗
PubMed1987

The leakage of serum proteins across the blood-nerve barrier in hereditary and inflammatory neuropathies. An immunohistochemical and morphometric study.

The leakage of eight different serum proteins and immunoglobulins across the blood-nerve barrier (BNB) was studied by means of the peroxidase-antiperoxidase method in hereditary and inflammatory neuropathies and graded semiquantitatively with respect to endoneurial staining intensity and distribution. These data were compared with the degree of alterations of the myelinated nerve fibre population evaluated by morphometric analysis. Our series of 18 human sural nerve biopsies included seven hereditary neuropathies (three HMSN I, two HMSN II, two tomaculous neuropathies), nine inflammatory neuropathies (seven polyneuritis, two hypertrophic neuritis) and two normal controls. In HMSN II and in tomaculous neuropathy there was no enhanced endoneurial staining for serum proteins despite of a severe nerve fibre loss, whereas in HMSN I a rise of serum proteins of small and moderate molecular size like albumin and IgG was demonstrated in the endoneurial space indicating an impaired BNB function. Qualitative changes of the BNB with leakage also of high molecular weight proteins were observed in polyneuritis and hypertrophic neuritis, irrespective of the degree of nerve fibre changes. Our results show that fibre loss and alteration of the BNB are not correlated. The unselective leakage of serum proteins through the BNB appears to be a characteristic change in inflammatory neuropathies leading to proteinous edema. With regard to the subperineurial accentuation of the endoneurial edema it will be discussed that the vascular diffusion barrier is more fragile than the perineurial diffusion barrier.

Adolescent↗
PubMed1994

Ischemic monomelic neuropathy: an under-recognized complication of hemodialysis access.

During the past 3 years six episodes of ischemic monomelic neuropathy (IMN) have been identified in five patients as a complication of upper extremity dialysis grafts. All patients had long-standing insulin-dependent diabetes, peripheral neuropathy, and brachial artery graft origins, whereas 60% had peripheral vascular disease. Five episodes occurred immediately after graft placement, whereas one was due to a graft-related thromboembolus. Diagnostic delay was common with initial findings attributed to anesthesia, positioning, or surgical trauma. Electrophysiologic studies showed underlying diabetic neuropathy with severe multifocal neuropathy distal to the grafts. Digital pressure indices were reduced but there was no critical ischemia. In three cases ischemia was completely corrected with improvement in one. One patient had proximal balloon angioplasty with no improvement and of the two untreated patients, one improved slightly. Ischemic monomelic neuropathy is a rare but disabling complication of dialysis access in diabetic uremic patients. Its occurrence is unpredictable and diagnostic delay is common. Correction of ischemia is indicated but usually does not improve the neuropathy. Prevention requires further research to more accurately characterize the patients at risk.

Arm↗