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At least 19 recordsLinked to original sources
PubMed1991

Serum interleukin-2 concentrations in Guillain-Barré syndrome and chronic idiopathic demyelinating polyradiculoneuropathy: comparison with other neurological diseases of presumed immunopathogenesis.

Serum concentrations of the cytokine interleukin-2 (IL-2) were quantitated by enzyme-linked immunosorbent assay in 42 patients with Guillain-Barré syndrome, 15 patients with chronic idiopathic demyelinating polyradiculoneuropathy, 37 patients with other neuropathies, 54 patients with other noninflammatory, nondemyelinating neurological disorders, and 26 healthy control subjects. We found markedly increased serum levels of IL-2 in patients with Guillain-Barré syndrome and to a much lesser extent, in patients with chronic idiopathic demyelinating polyradiculoneuropathy. Increased serum concentrations of IL-2 in patients with Guillain-Barré syndrome returned to normal in parallel with recovery from the disease. These findings suggest ongoing T-cell proliferation in patients with Guillain-Barré syndrome and some patients with chronic idiopathic demyelinating polyradiculoneuropathy. IL-2 levels were also raised in patients with active multiple sclerosis, myasthenia gravis, and herpes simplex encephalitis, and some patients with polymyositis, invoking T cells in the pathogenesis of these diseases.

Autoimmune Diseases↗
PubMed1991

The epidemiology of inflammatory polyradiculoneuropathy. A critical review of the distribution, characteristics and outcome of the disease. Plasmapheresis Study Group.

An outline of the principal reports dealing with the definition, distribution, course and treatment of the inflammatory polyradiculoneuropathies, including the Guillain-Barré syndrome (GBS) and chronic inflammatory demyelinating polyneuropathy (CIDP), is given. Current diagnostic criteria for GBS are reaffirmed while the diagnosis of CIDP lacks proper standardization. Then, the boundaries between the two disorders are ill-defined. While GBS is rare and homogeneously distributed across developed and developing countries, the prevalence rate of CIDP is unknown. Several antecedent events have been implicated in the pathogenesis of GBS; yet, except for the swine-flu vaccine, the relation between infectious or toxic agents and the occurrence of the disease is purely anecdotal. The only factors known to influence the outcome of GBS are age, severity of opening symptoms, abnormal electrophysiologic characteristics of peripheral nerve function, and plasmapheresis. However, responders and non-responders to current treatment are far from defined. Although similarities have been found between experimental allergic neuritis and experimental allergic encephalomyelitis, the degree of CNS impairment in patients with inflammatory polyradiculoneuropathies needs further refinement. To provide a tentative answer to some of the unsolved questions on inflammatory polyradiculoneuropathies, a multicenter cohort study on newly diagnosed patients submitted to standard clinical and laboratory evaluation, and given common therapeutic regimes, is awaited.

Central Nervous System↗
PubMedDate not supplied

[Immunochemical findings in the cerebrospinal fluid in patients with inflammatory demyelinating polyradiculoneuropathy].

The aim of the study was to check the hypothesis of involvement of the structure of the central nervous system on the basis of the analysis of the integrity of blood-brain barrier and the degree of IgG synthesis in the intrathecal space of patients with inflammatory demyelinization polyradiculoneuropathy. The study involved 27 patients with acute and 14 patients with chronic inflammatory demyelinization polyradiculoneuropathy. The analysis of liquor was performed in different stages of the disease. The results have shown that in the acute phase, in the phase of the maximal functional deficit there are signs of damaged integrity of the blood-brain barrier but without signs of increased intrathecal IgG synthesis. It has been concluded that there are no reliable signs of increased immunologic activity in the intrathecal space of patients with inflammatory demyelinization polyradiculoneuropathy.

Adult↗
PubMed1977

Polyradiculoneuropathy accompanying procainamide-induced lupus erythematosus: evidence for drug-induced enhanced sensitization to peripheral nerve myelin.

Factors involved in the development of an insidious polyradiculoneuropathy in association with a procainamide-induced, lupuslike syndrome were explored. A 73-year-old man with this clinical syndrome had sural nerve changes consisting of loss of large myelinated fibers with evidence of remyelination and Schwann cell proliferation. The patient's lymphocytes showed marked incorporation of tritiated thymidine when cultured with either procainamide or extracts of human peripheral nerve myelin, and there was an enhanced response with the combination. We also found that procainamide-treated rats showed acceleration of lymphocyte sensitization to peripheral nerve myelin as judged by the early development of inhibition of macrophage migration and positive skin tests to extracts of peripheral nerve myelin. These studies suggest that procainamide can enhance lymphocyte sensitization to peripheral nerve myelin and may have predisposed this individual to development of a polyradiculoneuropathy.

Aged↗
PubMed1979

Progressive polyradiculoneuropathy: treatment with Azathioprine.

A case is presented of a 64-year-old male with chronic inflammatory polyradiculoneuropathy (CIP) relentlessly progressing (despite steroids) to virtually complete quadriplegia over seven months. Once commenced on Azathioprine he dramatically improved over a six week period. The truly progressive form of CIP is rare. It is, however, immunologically similar to relapsing CIP and to the more common acute inflammatory polyradiculoneuropathy (AIP). Although the place of steroid therapy is still in doubt it would seem that cytotoxic immunosuppressives have something definite to offer in these conditions where there is progression beyond 4-5 weeks. In the largest series of CIP available (where the patients were untreated, or treated with steroids alone) the mortality rate was 11%, and the "complete recovery" rate only 5%. Although only isolated case reports are available, it would seem that if more aggressive immunosuppressive therapy was used more frequently, the prognosis might be considerably improved.

Azathioprine↗
PubMed1990

Focal neuropathy preceding chronic inflammatory demyelinating polyradiculoneuropathy by several years.

We report three patients who exhibited an unusual clinical course of chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) in which mononeuropathic limb weakness developed 2, 11 and 23 years, respectively, before the development of generalized polyradiculoneuropathy. The eventual diagnosis remained uncertain until other causes of neuropathy were excluded, and the clinical disorder progressed to involve the other limbs. Focal or regional variants of CIDP suggest that the pathologic, and perhaps the immunologic, abnormalities can be localized and selective for prolonged periods of time. Although this clinical variant seems to account for a small number of CIDP cases, its recognition may aid in making an early diagnosis.

Adult↗
PubMed1979

Facial myokymia with polyradiculoneuropathy.

Two patients had bilateral facial myokymia in association with polyradiculoneuropathy. Characteristic electromyographic findings allow polyradiculoneuropathy to be differentiated from other causes of facial movements, and support the possibility that extraaxial facial nerve involvement is another cause of facial myokymia.

Adult↗
PubMed1992

Subacute idiopathic demyelinating polyradiculoneuropathy.

Seven cases of subacute idiopathic demyelinating polyradiculoneuropathy had a monophasic illness characterized by progressive weakness of all four limbs that evolved during 4 to 8 weeks. Neurophysiological investigations implied demyelination in all seven cases. In two patients, sural nerve biopsy specimens that were taken showed macrophage-associated demyelination. All patients made substantial or complete recoveries with oral prednisolone (four cases) or without treatment (three cases). None of the patients required ventilation or had autonomic complications. These cases provide a link between the acute idiopathic demyelinating form of Guillain-Barré syndrome and chronic idiopathic demyelinating polyradiculoneuropathy.

Adult↗
PubMed1986

Acute and chronic demyelinating inflammatory polyradiculoneuropathy. Association with autoimmune diseases and lymphocyte response to human neuritogenic protein.

Of 66 patients (31 female and 35 male) with demyelinating inflammatory polyradiculoneuropathy (DIP), 12% (8/66) had a chronic relapsing and/or progressive course (CR-DIP) and 88% (58/66) had an acute monophasic illness (acute Guillain-Barré syndrome or GBS). Ten (15%) of the 66 had one or more associated putative autoimmune diseases; of these ten, five had CR-DIP and five had GBS. Cell-mediated immune responsiveness (CMI) of 30 cases with DIP was tested in vitro by lymphocyte transformation. Peripheral nervous system neuritogenic protein (NP) and central nervous system encephalitogenic myelin basic protein were the challenge antigens. Eighteen (60%) of the 30 patients had CMI to NP of human peripheral nervous system origin when a stimulation index (SI) of 2 or more was evaluated as positive; eight 27% (1) had CMI to NP when a positive SI was 3 or more. Of the 44 control patients with other neuropathies, only two (4.6%) demonstrated CMI to NP (SI, greater than or equal to 2). The in vitro response of patients with DIP to myelin basic protein (7/30) was not significantly different from that of the control population (16/44). The high incidence of DIP associated with autoimmune diseases and the CMI to NP in this group suggest that DIP may be an autoimmune disease with NP as one possible major antigen.

Acute Disease↗
PubMed1979

Treatment of chronic relapsing inflammatory polyradiculoneuropathy by plasma exchange.

A 58-year-old man developed recurrent episodes of symmetrical motor weakness associated with acroparesthesias and areflexia. The cerebrospinal fluid protein was elevated and nerve conduction velocities were slowed. There was no evidence of systemic disease or toxic exposure, and a diagnosis of chronic relapsing inflammatory polyradiculoneuropathy was made. The patient improved during treatment with corticosteroids, but steroid-induced complications necessitated discontinuance. A recrudescence of symptoms prompted a search for alternative therapy, and plasma exchange was tried. A marked improvement in strength was noted following each course of plasma exchange, suggesting that further similar trials are justified.

Chronic Disease↗
PubMed1991

Antibodies in sera from patients with inflammatory demyelinating polyradiculoneuropathy react with ganglioside LM1 and sulphatide of peripheral nerve myelin.

Sera from 23 patients with acute Guillain Barré syndrome (GBS), 15 patients with chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) and from 40 age-matched blood donors were analysed for antibodies to acidic glycosphingolipids from human brain and peripheral nerve. Antibodies to ganglioside LM1, the major ganglioside of peripheral nerve myelin. were found in 43% of GBS and in 67% of CIDP patients' sera, and in 20% of the blood donors. However, antisulphatide antibodies were detected in 65% and 87% of the sera from GBS and CIDP patients, respectively, but only in 15% of the control sera. Sulphatide is the major acidic glycosphingolipid in myelin and its concentration in peripheral nerve myelin is 100 times higher than that of LM1. The high frequency of LM1 and, in particular of sulphatide antibodies, might thus be relevant to the pathogenesis of the GBS and CIDP.

Adolescent↗
PubMed1992

Are CSF or serum ganglioside antibodies related to peripheral nerve demyelination in neuroborreliosis, Guillain-Barré syndrome, or chronic inflammatory demyelinating polyradiculoneuropathy?

Cerebrospinal fluid (CSF) and serum IgG and IgM antibodies to seven gangliosides were determined in patients with neuroborreliosis (NB) (n = 20), Guillain-Barré syndrome (GBS) (n = 13), and chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) (n = 10). The incidence of elevated antibodies was highest in NB and lowest in CIDP. Correlation between CSF and serum antibodies was only observed for IgG antibodies to GM1, GD1b and GT1b in GBS. The strong IgM antibody reactivity to gangliosides in the CSF of NB patients may be involved in the variety of neurological disorders attributed to Borrelia burgdorferi infection. Since one CIDP and three GBS patients had serologic evidence of prior or concurrent borrelia infection, this infection may belong to the infections that can trigger GBS or CIDP. The lack of specific ganglioside antibody patterns in these four patients suggests that ganglioside antibodies are not the link between Borrelia burgdorferi infection and the demyelination of peripheral nerves in GBS and CIDP.

Adult↗
PubMed1987

Fulminant demyelinating polyradiculoneuropathy resembling brain death.

A fulminant polyradiculoneuropathy resulted in a clinical state like brain death. Sequential EEG studies showed normally reactive alpha activity and spontaneous variability between wakefulness, drowsiness and sleep. EEG studies are valuable in such states in suggesting at least partial integrity of cortical neuronal activities, where no clinical measure is available.

Brain Death↗
PubMed1991

P2 specific lymphocyte transformation in Guillain-Barré syndrome and chronic idiopathic demyelinating polyradiculoneuropathy.

Thymidine incorporation proliferation assays to whole bovine P2 protein and its 58-81 and 14-25 synthetic peptides were performed on blood mononuclear cells from ten patients with Guillain-Barré syndrome (GBS), six patients with chronic idiopathic demyelinating polyradiculoneuropathy (CIDP), and age and sex matched normal subjects. The only patients whose cells showed any response were two out of four with very early GBS. One responded to P2 and both synthetic peptides. One responded to P2 but to neither peptide. The results support a role for cell mediated immunity to P2 protein in some patients with Guillain-Barré syndrome.

Adult↗
PubMed1988

Class and IgG subclass distribution of antibodies against peripheral nerve myelin in sera from patients with inflammatory demyelinating polyradiculoneuropathy.

An enzyme-linked immunosorbent assay (ELISA) was used to quantify antibodies against peripheral nerve myelin (PNM) in sera from 90 patients with Guillain-Barré syndrome (GBS) and from 70 patients with chronic inflammatory demyelinating polyradiculoneuropathy (CIDP). Fifty-nine percent of the patients with GBS and 51% of the patients with CIDP had increased levels of anti-PNM antibodies. Antibodies were also found in 0%-14% of sera from patients with other neurological diseases and in 8% of normal blood donors. Mean levels of IgG, IgM and IgA anti-PNM antibodies were increased in sera from patients with GBS, and mean IgG and IgA anti-PNM antibody levels were increased in sera from patients with CIDP when compared with sera from normal blood donors. The mean IgG anti-PNM antibody response observed in patients with GBS or CIDP was dominated by the IgG1 and IgG3 subclasses.

Adolescent↗
PubMed1990

CNS involvement in Japanese patients with chronic inflammatory demyelinating polyradiculoneuropathy.

Thirteen consecutive Japanese patients with chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) were studied by MRI, evoked potentials, and EEG. We found 3 of these patients exhibited symptoms of CNS disorders. Of these 3, 2 with abnormal MRI and visual evoked potentials, and one with abnormal brainstem auditory evoked potentials were detected. Another case without clinical CNS signs showed abnormal EEG findings. The subclinical CNS abnormalities found in the Japanese patients were considered to be less frequent than in cases from Western countries reported previously.

Adolescent↗
PubMed1978

Polyradiculoneuropathy associated with heroin abuse.

Neurological complications of heroin addiction have occurred only sporadically in the United Kingdom. We report the case of a young female patient who developed an acute polyradiculoneuropathy when she recommended intravenous heroin after four years abstinence. Another possible aetiological factor was a preceding flu-like illness but, after full investigations, we concluded that heroin abuse was the most likely cause of the neurological symptoms.

Adult↗