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At least 19 recordsLinked to original sources
PubMed1993

[Meningoencephalitis associated with polyradiculoneuropathy with increased HSV IgG antibody--report of three cases].

We report three patients presented with meningoencephalitis associated with polyradiculoneuropathy with increased HSV IgG antibody titer. The first patient was a 27-year-old woman with meningoencephalitis who developed status epilepticus. The CSF showed pleocytosis and increase in HSV IgG antibody titer. Herpes encephalitis was suspected, and she was treated with acyclovir. The symptoms of meningoencephalitis improved, but she developed flaccid tetraplegia. The NCV study was compatible with polyradiculoneuropathy. About two months later from the onset, muscle atrophy appeared in her all limbs. The second patient was a 23-year-old woman with meningoencephalitis, which was followed by ascending motor paralysis. The CSF showed pleocytosis and increase in HSV IgG antibody titer. The symptoms of meningoencephalitis improved by administration of acyclovir, but paralysis didn't improve. About two months later from the onset, muscle atrophy of all limbs appeared. The NCV study was compatible with polyradiculoneuropathy. The third patient was a 43-year-old man presenting somnolence, neck stiffness and ascending motor paralysis developing into flaccid tetraplegia. The CSF showed pleocytosis and increase in HSV IgG antibody titer. Somnolence and neck stiffness improved by administration of acyclovir but tetraplegia didn't improve. The NCV study was compatible with polyradiculoneuropathy. Immuno-absorption therapy and administration of prednisolone were performed. Meningoencephalitis associated with increased HSV IgG antibody titer is rare. Auto-allergic process which is initiated by HSV infection may be involved in the pathogenesis of polyradiculoneuropathy in these patients.

Adult↗
PubMed1999

Polyradiculoneuropathy revealing a solitary plasmacytoma of the ilium. A new case-report.

Neurological manifestations are uncommon in myeloma patients, and subacute polyradiculoneuropathy as the inaugural manifestations of solitary plasmacytoma of bone is exceedingly rare. We report the case of a 52-year-old man who was evaluated for a three-month history of flaccid tetraplegia with a gradually ascending onset and for a deterioration in general health. Electromyography findings were consistent with polyradiculoneuropathy. Laboratory tests showed a moderate amount of a monoclonal IgG-lambda antibody. Findings were normal from a radiographic bone survey and a radionuclide bone scan. Computed tomography of the pelvis disclosed a solitary osteolytic lesion in the right iliac crest, which was found upon biopsy to be a malignant plasmacytoma. Radiation therapy and chemotherapy were given. Subacute or chronic polyradiculoneuropathy as the inaugural manifestation of solitary plasmacytoma is exceedingly rare and should be distinguished from the sensorimotor polyneuropathy produced by plasma cell infiltration in some multiple myeloma patients. The polyradiculoneuropathy of solitary plasmacytoma can be likened to the neuropathies seen in some forms of multiple myeloma (sclerotic myeloma and POEMS syndrome). The pathophysiology of these neuropathies remains obscure. The case reported here suggests that patients with unexplained lasting polyradiculoneuropathy should be investigated for a plasma cell proliferation even if they have no serum monoclonal component. Because plasmacytomas are painless, imaging studies are needed for their diagnosis. The management of the neuropathy consists in treatment of the tumor.

Bone Neoplasms↗
PubMed1993

Glomerulonephritis associated with inflammatory demyelinating polyradiculoneuropathy: a case report and review of the literature.

A patient developed relapsing inflammatory demyelinating polyradiculoneuropathy associated with nephrotic syndrome. Renal biopsy showed focal-segmental glomerulosclerosis. The review of the literature disclosed that glomerulonephritis with and without nephrotic syndrome seems to be not uncommon in inflammatory demyelinating polyradiculoneuropathy, such as Guillain-Barré syndrome. membranous glomerulonephritis is the most frequent histologic diagnosis while minimal change nephropathy, 'acute glomerulonephritis' and postinfectious type glomerulonephritis are not often present. This is the first case of inflammatory demyelinating polyradiculoneuropathy associated with nephrotic syndrome due to focal-segmental glomerulosclerosis. Larger prospective studies are necessary and may contribute to the understanding of the pathogenesis of both, glomerulonephritis and inflammatory demyelinating polyradiculoneuropathy.

Adult↗
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↗
PubMed2000

Pathogenesis and treatment of inflammatory demyelinating polyradiculoneuropathy.

Inflammatory demyelinating polyradiculoneuropathy causes a spectrum of conditions ranging from acute (Guillain-Barré syndrome), through subacute to chronic forms. The pathogenesis of acute forms is related to antibody responses against glycolipid epitopes which mimic bacterial, especially Campylobacter jejuni, structures but T cells are also involved. The pathogenesis of chronic forms is poorly understood. Different forms differ in their responses to steroids. Chronic inflammatory demyelinating polyradiculoneuropathy responds to steroids but a variant multifocal motor neuropathy and the acute forms of inflammatory demyelinating polyradiculoneuropathy do not. Acute and chronic forms respond to plasma exchange and intravenous immunoglobulin.

Gangliosides↗
PubMed1989

[Chronic inflammatory demyelinating polyradiculoneuropathy of acute onset: relapse after temporary improvement by plasma exchange and longstanding remission by corticosteroid therapy].

A 59-year-old woman became tetraparetic and unable to stand or walk acutely in several days after she had first developed weakness of her legs and dysesthesia of both hands. Neurological examination revealed facial weakness, proximal dominant tetraparesis, areflexia and acrodysesthesia. The cerebrospinal fluid protein was elevated without pleocytosis, and the nerve conduction velocity was markedly slowed. The sural nerve biopsy indicated demyelination. The tentative diagnosis was Guillain-Barré syndrome (GBS). The initial and second courses of plasma exchanges temporarily improved the weakness, but relapses occurred within a few weeks. The third course of plasma exchange was, therefore, immediately followed by corticosteroid therapy, which successfully improved the tetraparesis. However, weakness again worsened during the rapid reduction of corticosteroid. A high dose of corticosteroid was again started and maintained for two months. The patient recovered gradually and relapses had not occurred so far after gradual reduction of the dose of corticosteroid. Her disease was finally diagnosed as corticosteroid-dependent chronic inflammatory demyelinating polyradiculoneuropathy, although the onset had been as acute as that of GBS. The present case suggests that corticosteroid-dependent chronic inflammatory demyelinating polyradiculoneuropathy may present as a case of acute onset polyradiculoneuropathy resembling GBS, and that corticosteroid therapy must be tried in such a case when plasma exchanges are not effective or relapses occur.

Acute Disease↗
PubMed1995

Chronic relapsing polyradiculoneuropathy in IgG lambda monoclonal gammopathy of undetermined significance (MGUS)--complete remission following carmustine treatment.

A previously healthy 43 year-old female developed IgG lambda monoclonal gammopathy of undetermined significance (MGUS) and ascending sensorimotor polyradiculoneuropathy which relapsed 11 times within 2 years. Marked improvement was noted repeatedly after plasmapheresis. However, on each occasion symptoms and signs of polyradiculoneuropathy recurred almost exactly 3 weeks after plasma-pheresis. Following 6 weeks of treatment with carmustine (70 mg/week), nearly complete recovery was established, which has persisted up to now (82 months after the end of therapy). The close temporal correlation between clinical relapse and recurrence of the IgG paraprotein and its permanent absence in stable clinical remission after carmustine treatment suggest a causal relationship between the paraprotein and the polyradiculoneuropathy. However, further studies are required to confirm this observation, as well as the efficacy of carmustine therapy.

Adult↗
PubMed1994

[The clinical picture and pathogenesis of polyradiculoneuropathy in tick-borne encephalitis].

Based on examination of tick-borne encephalitis patients with ascending polyradiculoneuropathy the authors describe the character of the disease, its clinical picture and the results of laboratory studies, etc. Differential diagnosis is made between the indicated syndrome associated with tick-borne encephalitis and sporadic polyradiculoneuropathies. A detailed description is given for the first time of the clinical and pathomorphological picture of that gravest form of tick-borne encephalitis. As regards the character of the clinical and pathomorphological alterations, the ascending polyradiculoneuropathy associated with tick-borne encephalitis is meningoencephalomyelitis with the radicular syndrome which often determines the disease gravity and prognosis.

Adolescent↗
PubMed1994

[A pathogenic study of chronic inflammatory demyelinating polyradiculoneuropathy in a patient with hepatitis B infection].

We immunologically examined the pathogenesis of chronic inflammatory demyelinating polyradiculoneuropathy in a patient with HB hepatitis. A 41-year-old male clerk has been suffered from muscle weakness, tingling and numbness in the distal portion of all limbs. All symptoms were compatible with the typical patterns of chronic inflammatory demyelinating polyradiculoneuropathy. We examined the patient's serum and biopsied sural nerve, using histochemical and immunological techniques. We detected the band that reacted with anti-HBs antibody in the sural nerve in western blotting. The result indicated that HBs antigen was expressed on the peripheral nerves in the patient. There were no anti-peripheral nerve antibodies neither in the sural nerve or serum. There was no increase of immune complex in the serum. No deposition of immunoglobulins and complements were detected in the sural nerve. Immunoadsorption therapy had no effect on this patient, but administration of prednisolone improved his symptoms drastically. These findings suggest that a cytotoxic T cell may had played a more important role than humoral factors in this patient's nerve injury. Though the pathogenesis of chronic inflammatory demyelinating polyradiculoneuropathy remains unclear, our findings seem to be very interesting in that they go some way toward clarifying the pathogenesis of this disease.

Adult↗
PubMed1994

The spectrum of acquired demyelinating polyradiculoneuropathy.

Guillain-Barré Syndrome (GBS) is best viewed as a clinical syndrome which can have at least two clinical substrates: the commonest is an acquired demyelinating polyradiculoneuropathy and the other is an acute motor axonal neuropathy. An acute acquired neuropathy can also sometimes cause the Miller Fisher syndrome of ophthalmoplegia, areflexia and ataxia, and even more rarely a pure sensory neuropathy. The demyelinating form of GBS also forms one end of a spectrum which has Chronic Idiopathic Demyelinating Polyradiculoneuropathy (CIDP) at its other pole. CIDP usually produces a mixed sensory and motor, albeit predominantly motor deficit, but some patients have pure multifocal motor neuropathy (MMN) and other even less common patients have pure sensory CIDP. According to the definitions of international committees, the symptoms of GBS reach their nadir within 4 weeks and those of CIDP in not less than 8 weeks. The spectrum is completed by patients with a monophasic illness reaching its nadir in 4 to 8 weeks (subacute idiopathic demyelinating polyradiculoneuropathy (SIDP). In addition there are patients with discrete attacks of acute demyelinating neuropathy which have been called recurrent GBS. The differential diagnosis of acquired demyelinating neuropathy differs according to the position of the individual case on this spectrum. The pathogenesis of each case may depend on the nature of the autoantigen, the balance between T cell and antibody-mediated autoimmune mechanisms, and the tempo of the inflammatory process. These differences may explain the empirical observations that steroids are helpful in CIDP but not GBS. Removal of antibodies by plasma exchange or flooding the immune system with normal immunoglobulin is beneficial in GBS and some cases of CIDP.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
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↗
PubMed1989

Chronic inflammatory demyelinating polyradiculoneuropathy. Clinical characteristics, course, and recommendations for diagnostic criteria.

Over a 10-year period, we followed up 60 patients (35 men and 25 women) with chronic inflammatory demyelinating polyradiculoneuropathy. Diagnosis was based on previously outlined criteria. Patients were treated in a uniform manner and the overwhelming majority, 56 (94.9%) of 59 treated patients, initially responded to immunosuppressive therapy. The time for initial improvement was 1.9 +/- 3.6 months while the time to reach a clinical plateau was 6.6 +/- 5.4 months. The course was monophasic in 32 patients (53.3%) and relapsing in 28 (46.6%). Despite the initial responsiveness, only 24 (40%) of 60 patients are in partial or complete remission, receiving no medication. Two patients died. We were unable to identify specific clinical or laboratory features at the time of diagnosis that predicted outcome. Our data analysis, along with previous reports, suggests that chronic inflammatory demyelinating polyradiculoneuropathy may be more heterogeneous than previously emphasized. In this light, we have proposed diagnostic criteria that allow for the heterogeneity but at the same time provide for a more consistent approach to better establish the natural history of this condition.

Biopsy↗
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↗
PubMed1994

Cervical magnetic stimulation in children and adolescents: normal values and evaluation of the proximal lesion of the peripheral motor nerve in cases with polyradiculoneuropathy.

Cervical magnetic stimulation was used to establish the normal values of the peripheral motor nerve conduction of the upper extremity muscle in normal children and adolescents. Seven patients with peripheral neuropathy were also examined to evaluate a lesion in the proximal site of the peripheral motor nerve. In normal subjects, onset latencies and negative wave durations tended to increase with age. The developmental profile of the latency, corrected for arm length, revealed a significant decline until the age of about 5 years. In 4 cases with polyradiculoneuropathy, motor evoked potentials following cervical magnetic stimulation showed increased latencies, prolonged durations and polyphasic shapes. The time differences between latencies by magnetic stimulation and peripheral motor conduction times by F technique were significantly prolonged. Motor evoked potentials obtained in 3 cases of axonal degeneration, on the other hand, showed slightly increased latencies and normal durations. The time differences between latencies and peripheral motor conduction times were within the normal range. Thus, we consider that cervical magnetic stimulation is a useful method for study of peripheral motor conduction in children and adolescents, and in particular to evaluate the proximal lesion of the nerve in patients with polyradiculoneuropathy.

Adolescent↗
PubMed1999

Multifocal polyradiculoneuropathy and carcinoma of the thymus.

We studied a patient with polyradiculoneuropathy with anaplastic carcinoma of the thymus. Motor manifestations dominated. Postmortem examinations indicated that the primary changes were in the spinal nerve roots, peripheral nerves and, possibly, the spinal anterior horn cells. The posterior funiculi and posterior root ganglia were also affected, implying multifocal and multiphasic degeneration. This unusual polyradiculoneuropathy is a form of carcinomatous neuropathy.

Aged↗
PubMed1984

Beneficial effects of plasma exchange in acute inflammatory polyradiculoneuropathy.

The results of a controlled trial in which 38 patients with severe acute inflammatory polyradiculoneuropathy took part indicate that plasma exchange favourably influenced the course of the disease. Significant benefits were seen in time until onset of improvement, course of muscular weakness, improvement in disability grades over the first 2 months, and working capacity after 1 month. Cost-benefit analysis showed that the exchange treatment resulted in net financial savings. The results suggest that plasma exchange may have a role in the treatment of severe acute inflammatory polyradiculoneuropathy.

Acute Disease↗
PubMed1986

Plasma exchange in chronic inflammatory demyelinating polyradiculoneuropathy.

Plasma exchange has been reported to be efficacious in chronic inflammatory demyelinating polyradiculoneuropathy. We performed a prospective double-blind trial in which patients with static or worsening disease were randomly assigned to plasma exchange (n = 15) or to sham exchange (n = 14) for three weeks. After three weeks, we observed statistically significant differences in combined measurements of nerve conduction (total, motor, proximal, velocity, and amplitude) favoring patients who had received plasma exchange. Improvement to a greater degree than for any patient receiving sham exchange was detected in the neurologic-disability score in five patients (P = 0.025) and in subset scores for weakness and reflex in four patients (P less than 0.057). We conclude that for some patients with chronic inflammatory demyelinating polyradiculoneuropathy, plasma exchange has an ameliorating effect on neurologic dysfunction and nerve conduction, but in others no improvement is observed. Because plasma was replaced with normal serum albumin, a humoral factor or factors may have a role in the neurologic deficit of this disorder.

Chronic Disease↗