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PubMed2005

EFNS guidelines on the use of skin biopsy in the diagnosis of peripheral neuropathy.

Skin biopsy has become a widely used tool to investigate small calibre sensory nerves including somatic unmyelinated intraepidermal nerve fibres (IENF), dermal myelinated nerve fibres, and autonomic nerve fibres in peripheral neuropathies and other conditions. Different techniques for tissue processing and nerve fibre evaluation have been used. In March 2004, a Task Force was set up under the auspices of the European Federation of Neurological Societies (EFNS) with the aim of developing guidelines on the use of skin biopsy in the diagnosis of peripheral neuropathies. We searched the Medline database from 1989, the year of the first publication describing the innervation of human skin using immunostaining with anti-protein-gene-product 9.5 (PGP 9.5) antibodies, to 31 March 2005. All pertinent papers were rated according to the EFNS guidance. The final version of the guidelines was elaborated after consensus amongst members of the Task Force was reached. For diagnostic purposes in peripheral neuropathies, we recommend performing a 3-mm punch skin biopsy at the distal leg and quantifying the linear density of IENF in at least three 50-mum thick sections per biopsy, fixed in 2% PLP or Zamboni's solution, by bright-field immunohistochemistry or immunofluorescence with anti-PGP 9.5 antibodies (level A recommendation). Quantification of IENF density closely correlated with warm and heat-pain threshold, and appeared more sensitive than sensory nerve conduction study and sural nerve biopsy in diagnosing small-fibre sensory neuropathy. Diagnostic efficiency and predictive values of this technique were very high (level A recommendation). Confocal microscopy may be particularly useful to investigate myelinated nerve fibres, dermal receptors and dermal annex innervation. In future, the diagnostic yield of dermal myelinated nerve fibre quantification and of sweat gland innervation should be addressed. Longitudinal studies of IENF density and regeneration rate are warranted to correlate neuropathological changes with progression of neuropathy and to assess the potential usefulness of skin biopsy as an outcome measure in peripheral neuropathy trials (level B recommendation). In conclusion, punch skin biopsy is a safe and reliable technique (level A recommendation). Training in an established cutaneous nerve laboratory is recommended before using skin biopsy as a diagnostic tool in peripheral neuropathies. Quality control at all levels is mandatory.

Biopsy↗
PubMed1993

Immunohistochemical findings in vasculitic neuropathies.

Fifteen sural nerve biopsies of vasculitic neuropathies have been compared with 11 cases of different non-vasculitic neuropathies and normal nerves from brain-dead organ donors. The APAAP (alkaline phosphatase monoclonal anti-alkaline phosphatase) immunostaining method was applied to cryostat sections from unfixed snap-frozen tissue samples. Immunoglobulins IgG, IgM, IgA, complement factors and light chains were reactive in biopsies of normal nerves as well as of vasculitic and nonvasculitic neuropathies. A strong reaction against IgE in the epineurial vessel walls was only seen in cases of Churg-Strauss-vasculitis. Antibodies against MHC class II (HLA DR) were positive in most of vasculitic infiltrates. Vascular endothelial cells were positive with anti MHC class I in all biopsies. A typical finding in all vasculitic neuropathies was the infiltration of epineurial vessels with CD4 positive and, to a lesser extent, CD8 positive lymphocytes. CD22 positive lymphocytes (B cells) have only been seen in about one third of vasculitic neuropathies. CD16 positive cells (NK-cells or neutrophils) could be demonstrated only in two biopsies. CD68 positive cells (macrophages) are frequently seen in most cases of neuropathy regardless of their etiology. The results support the concept of a primary T-cell mediated process against epineurial vessels as the most important mechanism in the pathogenesis of vasculitic neuropathies. In some cases with small epineurial infiltrates the vasculitic process can only be recognized with antibodies against CD4 or CD8. Therefore, the immunohistochemical evaluation of sural nerve biopsies may be helpful for identifying cases with microvasculitis.

Adolescent↗
PubMed1997

Peripheral neuropathy in acrodermatitis chronica atrophicans - a late Borrelia manifestation.

Clinical and/or neurophysiological signs of peripheral neuropathy were found in 64% of 63 consecutive untreated patients with the late borrelial manifestation acrodermatitis chronica atrophicans (ACA). The neuropathy frequency was significantly higher in the patients than in 30 age- and sex-matched control persons of whom 27% had neuropathy findings. The most common neuropathy in ACA was a symmetric distal sensory polyneuropathy. In a subgroup of patients with localized or asymmetric neuropathy, the changes were found more often in extremities with than without visible ACA lesions. Neuropathy symptoms, most often pain and/or paresthesia, were present in 64% of the patients, compared to in 13% of the control persons. Thus, both symptoms and signs of neuropathy were significantly more frequent in patients with untreated ACA than in control subjects.

Acrodermatitis↗
PubMed1997

Peripheral neuropathy in individuals with HIV infection in Zimbabwe.

Peripheral neuropathy is associated with HIV infection. The prevalence and types of peripheral neuropathy encountered in a randomly-selected HIV infected African population at different stages of disease were investigated. HIV positive individuals were categorized into 1 of 3 groups: asymptomatic, symptomatic and AIDS. HIV negative individuals formed the control group. Nerve conduction data were obtained using standard electrophysiological procedures and CD4+ levels were measured. The type of neuropathy was determined from the history, clinical presentation and electrophysiological abnormalities. The prevalence of peripheral neuropathy was 44%: subclinical neuropathy (SCN) accounted for 56%, acute inflammatory demyelinating polyneuropathy (AIDP) for 15% and distal symmetrical polyneuropathy (DSPN) for 22% of cases of neuropathy. SCN was found in all categories whereas AIDP predominated in the symptomatic category and DSPN in individuals with AIDS. The pattern and frequency of neuropathies seen in our African population is similar to that reported from other continents.

Adult↗
PubMed2005

Antinuclear antibodies define a subgroup of paraneoplastic neuropathies: clinical and immunological data.

OBJECTIVE: Paraneoplastic neuropathy is a clinical and immunological heterogeneous disorder and attempts have been made to classify subgroups of this disease. Only 30-50% of the clinical defined cases have antineuronal antibodies. METHODS: The clinical and immunological features of 36 patients with paraneoplastic neuropathy from the authors' database were analysed including the type and course of the neuropathy, associated tumours, and the presence of antineuronal and other autoantibodies. RESULTS: Antineuronal antibodies were detected in 17/36 patients (47%) and anti-Hu was the most frequent antineuronal antibody. Nine patients had high titre antinuclear antibodies (ANA, median titre 1/1000) without antineuronal antibodies. ANA reactivities were different in most patients. Comparison of the ANA positive and ANA negative patients revealed that ANA positive paraneoplastic neuropathy is more frequently associated with breast cancer but is not associated with lung cancer (p<0.05). The main clinical type in these patients was sensorimotor neuropathy. No ANA positive patient had central nervous system involvement. Although the Rankin score at the time of diagnosis was not different, the functional outcome in ANA positive patients was better than in ANA negative patients (p<0.05). CONCLUSIONS: Paraneoplastic neuropathy is a heterogeneous disorder. ANA may define a subgroup of paraneoplastic neuropathy with different clinical and immunological features and may be related to better prognosis of the neuropathic symptoms.

Aged↗
PubMed2005

Clinical spectrum of cryoglobulinaemic neuropathy.

BACKGROUND AND OBJECTIVE: Cryoglobulinaemic neuropathy (CN) is probably common, as it is usually related to HCV infection. The aim of this study was to delineate the clinical spectrum of CN in a large series and to investigate the factors influencing its expression. METHODS: Seventy one consecutive patients (12 men, 59 women), diagnosed as having CN on the basis of clinical features of neuropathy, clinical and serological findings of mixed cryoglobulinaemia, and exclusion criteria, were identified during a six year period. All patients underwent clinical examination, and electrophysiological and laboratory investigations. RESULTS: Results of the patients with "pure" CN (n = 54) and those with comorbidities (n = 17) were evaluated separately. Of the former 76% had sensory neuropathy (including selective small fibre sensory neuropathy (SFSN) in 14 patients), 15% had sensorimotor polyneuropathy, and 9% had mononeuritis multiplex. The pattern of distribution was similar in the patients with comorbidities. In 30/54 patients, CN was the first manifestation of cryoglobulinaemia. Patients with mild cryoglobulinaemic syndrome had sensory neuropathy more frequently than patients with active syndrome (p < 0.001), in particular SFSN (p < 0.001). The latter group had more severe features, with significantly more cases of reduced or absent motor (p = 0.028) and sensory action potentials (p < 0.001), and a tendency towards higher Rankin scores (p = 0.06). CONCLUSIONS: Sensory neuropathy, often in the form of SFSN, is by far the commonest form of CN. Cryoglobulinaemia should be vigorously investigated in the diagnosis of sensory neuropathy, especially in older women. Activity of the cryoglobulinaemic syndrome is a major factor influencing the clinical expression and severity of CN.

Aged↗
PubMed1997

Axonal neuropathy associated with monoclonal gammopathy of undetermined significance.

OBJECTIVE: The neuropathy associated with monoclonal gammopathy of undetermined significance (MGUS) is typically a predominantly demyelinating process that may have additional features of axonal degeneration. Sixteen patients with MGUS and a pure or predominantly axonal neuropathy are reported and compared with 20 consecutive patients with demyelinating neuropathy and MGUS who were seen during the same period. METHODS: Retrospective review of a consecutive series of patients with neuropathy and MGUS evaluated during a five year period. RESULTS: The axonal group had mild, symmetric, slowly progressive, predominantly sensory neuropathy, usually limited to the legs. There were no differences in the age of onset or duration of symptoms at the time of presentation, initial symptoms, or the severity of weakness between the axonal and demyelinating cases. However, the axonal process was associated with less vibration and proprioceptive loss, did not include leg ataxia (present in 55% of patients with demyelinating type), less often had generalised areflexia (19% v 70%), IgM gammopathy (19% v 80%), and anti-MAG antibodies (0% v 40%), and had lower CSF protein concentrations (mean, 49 v 100 mg/dl). The illness was also generally milder with less disability (mean Rankin score 2.1 v 2.8). Fewer patients with axonal neuropathy improved with immunomodulating therapy (27% v 75%). CONCLUSION: There is an axonal neuropathy associated with MGUS that is clinically and electrophysiologically distinct from the more typical demyelinating pattern.

Adrenal Cortex Hormones↗
PubMed2002

Clinical validation of methods of diagnosis of neuropathy in a field study of United Kingdom sheep dippers.

OBJECTIVES: To investigate the reproducibility of measured indices of chronic peripheral neuropathy from a field study of sheep dippers when compared with similar measurements carried out in a clinical setting. METHODS: A stratified random sample of field study subjects was invited to attend a clinic. Neuropathy was measured both in the field and at the clinic with a modified version of a standard symptoms questionnaire and quantitative sensory thresholds for hot, cold, and vibration. These were combined into a classification of the likelihood of neuropathy with a neuropathy scoring system. Indicators of sensory abnormality were based on comparison of sensory thresholds to age dependent reference values derived from an external reference group. RESULTS: Only 51% of subjects were assigned similar classifications in the field and clinic based on the neuropathy scoring system. Of the component indices, grouped symptom scores, with 65% of subjects showing exact agreement, proved to be more reproducible than quantitative sensory test indicators. There were biases in the comparison of field and clinic measurements of hot and vibration sensations, but no evidence of greater variation between individual people in sensory thresholds in the field relative to at the clinic. CONCLUSIONS: The neuropathy scoring system proved to be of limited reproducibility, due in a large part to the lack of reproducibility of the indicators of sensory test abnormality caused by inadequate temperature control. However, the symptoms score and measured sensory thresholds could be used separately as indices of neuropathy in exposure-response analyses.

Adult↗
PubMed2003

Autonomic neuropathy in patients with hepatic cirrhosis.

BACKGROUND: Autonomic neuropathy has been reported in patients with alcoholic liver disease but information on its occurrence in patients with non-alcoholic liver disease is contradictory. AIM: To assess autonomic functions in patients with alcoholic and non-alcoholic liver disease. STUDY DESIGN: Autonomic function using five standard tests was examined in 20 cirrhotics (10 alcoholics and 10 non-alcoholics) and 20 age and sex matched controls. The extent of autonomic dysfunction was determined in the patients and a comparison between the characteristics of patients with and without autonomic neuropathy was made. RESULTS: Sixteen (80%) of the cirrhotic subjects were found to have evidence of autonomic neuropathy. Of these, three (15%) patients had early parasympathetic damage, five (25%) had definite parasympathetic damage, and eight (40%) had combined (that is, both parasympathetic and sympathetic) damage. Nine (90%) of the alcoholics and seven (70%) of the non-alcoholics had autonomic dysfunction. Only one patient belonging to the alcoholic group had clinical evidence of peripheral neuropathy. Moreover, there was no significant association between subjective symptoms of autonomic neuropathy and objective evidence of autonomic damage as assessed by autonomic function tests. Autonomic dysfunction was significantly more frequent in advanced liver disease compared with early liver damage. Nine (75%) out of 12 cirrhotic subjects belonging to Child class B and six (85.7%) of the seven patients belonging to Child class C had autonomic neuropathy. CONCLUSION: This study shows that autonomic neuropathy is common in cirrhotic subjects, that it is found with comparable frequency in alcoholics and non-alcoholics, and that it increases in severity with increase in extent of liver damage, suggesting that liver damage contributes to the neurological deficit.

Autonomic Nervous System Diseases↗
PubMed2006

Contribution of nerve biopsy to unclassified neuropathy.

OBJECTIVES: To evaluate the diagnostic yield of nerve biopsy in patients with peripheral neuropathy of undetermined cause despite extensive diagnostic workup. METHODS: From November 2001 through January 2004, 38 patients underwent nerve biopsy because of unclassified neuropathy. RESULTS: The etiology of the neuropathies could be defined in 14 patients (37%), i.e. in 15% of chronic symmetric, 30% of chronic asymmetric, 50% of subacute symmetric and 62.5% of subacute asymmetric neuropathies. The biopsy was diagnostic in 6 patients (16%), where it showed a vasculitis, and supportive in 8 patients (21%). CONCLUSIONS: The contribution of nerve biopsy to the diagnosis of peripheral neuropathy was highest in acute and subacute asymmetric forms of neuropathy and lowest in chronic symmetric forms. The main indication for nerve biopsy remains the diagnosis of vasculitic neuropathy, a potentially treatable disorder.

Aged↗
PubMed2006

Mitochondrial abnormalities in patients with LHON-like optic neuropathies.

PURPOSE: To investigate certain biochemical and molecular characteristics of mitochondria in patients with Leber hereditary optic neuropathy (LHON)-like optic neuropathies. METHODS: Patients who had LHON-like optic neuropathies in both eyes were selected from neuro-ophthalmology clinics. Evaluation included clinical examination, neuroimaging, and assessment of several mitochondrial parameters in the blood, including sequencing the entire mitochondrial (mt)DNA coding region, measuring relative mtDNA content, studying mitochondrial respiratory function in some patients, and sequencing the OPA1 and OPA3 genes. RESULTS: Thirty-five patients (21 men and 14 women; average age at onset 19.0 +/- 8.7 years) met inclusion and exclusion criteria for LHON-like optic neuropathies with median visual acuity approximately 20/200. Other hereditary retinopathies and optic neuropathies were unlikely because of inclusion and exclusion criteria, because ERGs were normal, and because no patient had pathogenic sequence changes in the OPA1 or OPA3 genes. Compared with control subjects, these patients had more potentially pathogenic nonsynonymous mtDNA changes, greater relative mtDNA content (P < 0.001), and less mitochondrial respiratory activity (P < 0.001). Only six patients (17%) had primary LHON mutations; however, even the 29 patients without primary LHON mutations had significant evidence of mitochondrial abnormalities. Mitochondrial haplogroup distribution was similar in patients and control subjects. CONCLUSIONS: Primary LHON mutations are less common in patients with LHON-like optic neuropathy selected from a clinical setting than in patients with LHON from multigenerational families. The results suggest that mitochondrial dysfunction plays a role in this type of optic neuropathy whether or not primary LHON mutations are present. This information has implications for diagnostic testing and for future investigations into mechanisms of disease.

Adolescent↗
PubMed2006

Metronidazole: newly recognized cause of autonomic neuropathy.

Metronidazole is a commonly used antibiotic prescribed for the treatment of anaerobic and protozoal infections of the gastrointestinal and genitourinary tracts. It is associated with numerous neurologic complications, including peripheral neuropathy. Neuropathy is typically detected in patients on chronic therapy, although it has been documented in those taking large doses for acute infections. Numerous case reports have been published describing motor and sensory neuropathy, yet autonomic neuropathy has not been described with metronidazole use. A previously healthy 15-year-old girl presented with complaints of burning pain in her feet following a short course of metronidazole for vaginitis. She could obtain pain relief only by submerging her feet in ice water. Examination revealed cold and swollen lower extremities that became erythematous and very warm when removed from the ice water. Temperature perception was reduced to the upper third of the shin bilaterally. Deep tendon reflexes and strength were preserved. Nerve conduction studies demonstrated a peripheral neuropathy manifested by reduced sensory nerve and compound muscle action potentials. Reproducible sympathetic skin potential responses could not be obtained in the hand and foot, providing evidence of a concurrent autonomic neuropathy. A thorough evaluation revealed no other cause for her condition. Repeated nerve conduction studies and sympathetic skin potentials returned to normal over the course of 6 months, paralleling the patient's clinical improvement. Metronidazole is a potential cause of reversible autonomic neuropathy.

Action Potentials↗
PubMed2004

Sensory neuropathy in vasculitis: a clinical, pathologic, and electrophysiologic study.

BACKGROUND: Vasculitis is not usually considered as a cause of symmetric sensory neuropathy. OBJECTIVE AND METHODS: To present the clinical, pathologic, and electrophysiologic features of 17 (16%) cases of sensory neuropathy in vasculitis (SNV) among 106 cases with histologically proven vasculitic neuropathy that were collected over the last 30 years. RESULTS: In 41% of cases, SNV was found as systemic vasculitic neuropathy in association with primary vasculitic disease. The most common clinical presentation was symmetric polyneuropathy, seen in 53% of cases. The most common nerve conduction pattern was diffuse neuropathy pattern of axonal degeneration. Sural nerve biopsy was diagnostic in 88% of cases. In two cases, muscle biopsy was necessary for the definite diagnosis of vasculitis. Non-systemic SNV is usually benign. Of 11 patients followed for longer than 2 years, none developed motor weakness due to neuropathy. CONCLUSION: Sensory neuropathy, regardless of symmetry, can be due to vasculitis.

Adult↗
PubMed2005

Residual neuropathy in long-term population-based follow-up of Guillain-Barré syndrome.

OBJECTIVE: To estimate the occurrence of residual neuropathy and its self-reported health consequences in a population-based group of patients with Guillain-Barré syndrome (GBS) and to characterize quantitatively the concomitant motor, sensory, and autonomic impairments. METHODS: Forty patients (mean age 46 years) with a confirmed diagnosis of GBS were studied a mean of 7 years (range 1 to 13 years) after the acute attack together with 40 healthy control subjects. The Dyck minimal criteria of neuropathy, the Neuropathy Symptom Score, the Neuropathy Disability Score, the Short Form-36 (SF-36) generic health questionnaire, isokinetic dynamometry at ankle and wrist, quantitative sensory testing of thresholds for vibration, cold, and pain, autonomic function tests, nerve conduction studies, and a summed Neuropathy Rank Sum Score (NRSS) were applied. RESULTS: Nineteen patients (48%) had residual neuropathy, which was independent of follow-up time. The patients with GBS reported lower health status than control subjects on the SF-36 Physical Component Summary Scale (PCS; p = 0.01), and the PCS scores correlated with the NRSS (r = -0.41, p = 0.009). In patients with GBS, muscle strength at ankle dorsal flexion was reduced by 13.9% (p = 0.001), sensory thresholds for vibration were increased in the foot (p < 0.05), and sensory thresholds for cold were increased in the hand and foot (p < 0.05), whereas autonomic functions and pain thresholds were unaffected. CONCLUSIONS: Residual neuropathy affecting large- and medium-sized myelinated fibers endures long after the acute attack of Guillain-Barré syndrome in approximately half of all patients, leads to motor and sensory dysfunction, and shows a trend toward impairing self-reported physical health status.

Adult↗
PubMed1989

Peripheral neuropathy in primary Sjögren's syndrome.

Sjögren's syndrome (dryness of eyes, mouth, and other mucous membranes) may be associated with disease of joints, blood, internal organs, skin, and central and peripheral nervous systems. We reviewed 33 cases of primary Sjögren's syndrome and peripheral neuropathy evaluated by neurologic examinations and EMG at the Mayo Clinic from 1976 to 1988, and studied sural nerve biopsy specimens in 11 of them. Symmetric sensorimotor polyneuropathy occurred most frequently, followed by symmetric sensory neuropathy. Autonomic neuropathy, mononeuropathy, or cranial neuropathy (especially trigeminal neuropathy) was superimposed on generalized neuropathy in approximately one-fourth of patients. The course generally was slowly progressive, except for a few patients who may have improved with prednisone therapy. Although spinal ganglion involvement might have accounted for some of the clinical and neurophysiologic findings, we found evidence that necrotizing vasculitis was involved in fiber degeneration. All nerve biopsies revealed perivascular inflammatory infiltrates and other vessel abnormalities, which were diagnostic in two cases and strongly suggestive of necrotizing vasculitis in six cases. Axonal degeneration predominated over demyelination and sometimes was focal or multifocal. In neuropathy of unknown cause, particularly if it is sensory, autonomic, or involves trigeminal nerve, consider Sjögren's syndrome.

Adult↗
PubMed1994

Cytomegalovirus multifocal neuropathy in AIDS: analysis of 15 consecutive cases.

A severe multifocal neuropathy caused by cytomegalovirus (CMV-MN) can occur in the late stage of human immunodeficiency virus (HIV) infection. In a retrospective study, we identified 15 consecutive HIV-positive patients with a diagnosis of CMV-MN based on (1) markedly asymmetric neuropathy, (2) fewer than 100 CD4+ cells per mm3, (3) exclusion of other causes of neuropathy, and (4) characteristic CMV cytopathic changes on neuromuscular biopsy (2 patients), positive CSF culture for CMV (2 patients), or clinical improvement on anti-CMV therapy given for concurrent extraneurologic CMV disease (8 patients) or neuropathy (3 patients). All patients were men and had severe immunosuppression (mean CD4+ cell count, 18 per mm3). The initial symptoms were numbness and painful paresthesias showing a patchy, multifocal distribution. After a mean of 11 weeks (range, 1 to 10 months), the patients developed moderate or severe sensorimotor asymmetric neuropathy. Extraneurologic CMV infection occurred in 10 patients before diagnosis. Electrophysiologic studies showed axonal neuropathy and CMV DNA was present in CSF by the polymerase chain reaction (PCR) technique in 90% of patients tested. Fourteen patients showed a marked improvement 1 to 4 weeks after starting ganciclovir or foscarnet therapy. During follow-up on maintenance therapy (13 patients), the neuropathy relapsed in three patients and probable or confirmed CMV encephalitis occurred in five. Twelve patients died during follow-up, at a mean interval of 9.5 months after their first symptoms. These results extend the clinical spectrum of CMV-MN and show that PCR detection of CMV DNA in CSF may be a useful diagnostic marker.

Acquired Immunodeficiency Syndrome↗
PubMed2004

The frequency of peripheral neuropathy in a group of HIV positive patients in Brazil.

UNLABELLED: Peripheral neuropathy is a common neurological complication occurring in asymptomatic and symptomatic stages of HIV infection. The most common syndromes are distal symmetric polyneuropathy, inflammatory demyelinating polyneuropathy, poliradiculopathy, mononeuropathy, mononeuropathy multiplex and autonomic neuropathy. PURPOSE: To evaluate the frequency of peripheral neuropathy in a group of HIV seropositive outpatients in São Paulo, Brazil. METHOD: Over a period of 17 months, 49 HIV+ patients where evaluated clinically. Laboratory analysis and electroneuromyography were requested to all patients. RESULTS: >Thirty four (69.4%) of the 49 patients had the diagnosis of peripheral neuropathy established on clinical grounds. The most common sign was impairment (97.1%) of sensibility. Thirteen (33.3%) of the 39 that were subjected to electroneuromyography had features of peripheral neuropathy, being a sensitive-motor axonal neuropathy the most common. No abnormalities were found in the laboratory analysis performed in 42 patients, except in four who had VDRL positive. CONCLUSION: A peripheral neuropathy was frequently found upon clinical examination in our group of HIV positive individuals.

Adult↗
PubMed2003

Pain-related differential expression of NGF, GDNF, IL-6, and their receptors in human vasculitic neuropathies.

OBJECTIVE: Pain-related differential expressions of nerve growth factor (NGF), glial cell line-derived neurotrophic factor (GDNF) and interleukin-6 (IL-6), and their receptors were investigated in human vasculitic neuropathies. MATERIALS AND METHODS: The mRNA levels of pain-related neurotrophic factors, NGF, GDNF and IL-6, were examined in the sural nerves of 22 painful and non-painful patients with acute necrotizing vasculitic neuropathies, together with their concomitant soluble receptors (p75, GFR(alpha)-1 and IL-6R(alpha)). RESULTS: The mRNAs for these factors and receptors in the lesioned nerves were up-regulated to a variable extent in both groups. NGF mRNA expression was more closely correlated with that of p75 in painful neuropathy with relatively preserved large fiber density, compared with non-painful neuropathy, though the NGF mRNA level in painful neuropathy was lower than that in non-painful neuropathy. GDNF was closely associated with GFR(alpha)-1 in mRNA levels regardless of the pain state, but IL-6 was not associated with IL-6R(alpha). CONCLUSION: The differential expression of neurotrophic factors and their cognate soluble receptors in human vasculitic neuropathy suggests that NGF, which was effectively transferred to sensory axons with p75, may induce pain.

Adult↗