polyneuropathies/lodhja

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Clinical correlates of fatigue in chronic inflammatory demyelinating polyneuropathy.

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Fatigue is a recognised manifestation of immune-mediated neuropathies, but its causes and implications are unclear. This study aimed to explore the correlates of fatigue amongst a number of clinical parameters in patients with chronic inflammatory demyelinating polyneuropathy (CIDP),

Fatigue in immune-mediated neuropathies.

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Fatigue, a highly debilitating symptom, is reported in most patients with immune-mediated neuropathies, particularly in Guillain-Barré syndrome, chronic immune-mediated demyelinating polyradiculoneuropathy, monoclonal gammopathy of undetermined significance related polyneuropathy, and multifocal

Amantadine for treatment of fatigue in Guillain-Barre syndrome: a randomised, double blind, placebo controlled, crossover trial.

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OBJECTIVE Fatigue is a major complaint in patients with immune mediated polyneuropathies. Despite apparently good physical recovery after Guillain-Barré syndrome (GBS), many patients remain restricted in daily and social activities, and have a decreased quality of life. In this trial, the effect of

Fatigue as the main presenting symptom of chronic inflammatory demyelinating polyradiculoneuropathy: a study of 11 cases.

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Fatigue has been shown to be more frequent than previously thought in immune-mediated polyneuropathies. However, fatigue has not been reported as the main cause of referral in chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) patients. Between January 2001 and December 2003, we

[Acute progressive polyneuropathy in a patient with Waldenström macroglobulinemia].

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A case of Waldenström's macroglobulinemia (WM) (IgM-kappa type) associated with acute-onset demyelinating peripheral neuropathy is reported. A 49-year-old woman was admitted to our hospital because of general fatigue and recurrent syncope attacks. She was treated with vincristine, cyclophosphamide,

Tafamidis, a Noninvasive Therapy for Delaying Transthyretin Familial Amyloid Polyneuropathy: Systematic Review and Meta-Analysis.

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Tafamidis functions to delay the loss of function in transthyretin familial amyloid polyneuropathy (TTR-FAP), which is a rare inherited amyloidosis with progressive sensorimotor and autonomic polyneuropathy. This systematic literature review and meta-analysis evaluated the efficacy and

[Myocardiopathy caused by Portuguese-type familial amyloidotic polyneuropathy. Sequential morphologic and functional study of 60 patients].

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OBJECTIVE To assess the cardiac involvement of familial amyloidotic polyneuropathy--Portuguese type (FAP) in a prospective study. BACKGROUND FAP is a sensitive, motor and autonomic familial polyneuropathy, due to amyloid deposits on nerve and vascular structures, related to abnormal transthyretin

Association of small-fiber polyneuropathy with three previously unassociated rare missense SCN9A variants

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Background: Small fiber polyneuropathy (SFN) involves ectopic firing and degeneration of small-diameter, somatic/autonomic peripheral axons. Causes include diabetes, inflammation and rare pathogenic mutations, including in SCN9-11

[Plasmapheresis, immunotherapy and chemotherapy in polyneuropathies].

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BACKGROUND Although the precise cause of many of the polyneuropathies evaluated clinically is unknown, there is substantial evidence that many are caused by autoimmune disorders. Currently treatment is directed towards production of immunomodulation or immunosuppression. CONCLUSIONS The degree of

Randomized controlled trial of the combined monoaminergic and opioid investigational compound GRT9906 in painful polyneuropathy.

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GRT9906 is an investigational novel compound with μ-opioid receptor agonism and inhibition of noradrenalin/serotonin re-uptake. In this randomized, double-blind, placebo-controlled, three-way cross-over trial in painful polyneuropathy, the efficacy and safety of GRT9906 was assessed and compared

PDXK mutations cause polyneuropathy responsive to pyridoxal 5'-phosphate supplementation.

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To identify disease-causing variants in autosomal recessive axonal polyneuropathy with optic atrophy and provide targeted replacement therapy.We performed genome-wide sequencing, homozygosity mapping, and segregation analysis for novel disease-causing gene

Evidence of small-fiber polyneuropathy in unexplained, juvenile-onset, widespread pain syndromes.

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OBJECTIVE We tested the hypothesis that acquired small-fiber polyneuropathy (SFPN), previously uncharacterized in children, contributes to unexplained pediatric widespread pain syndromes. METHODS Forty-one consecutive patients evaluated for unexplained widespread pain beginning before age 21 had

Self-reported fatigue following intensive care of chronically critically ill patients: a prospective cohort study.

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UNASSIGNED Protracted treatment on intensive care unit (ICU) sets the patients at increased risk for the development of chronic critical illness (CCI). Muscular and cardio-respiratory deconditioning are common long-term sequelae, going along with a state of chronic fatigue. At present, findings

Scientific Advances in and Clinical Approaches to Small-Fiber Polyneuropathy: A Review.

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Small-fiber polyneuropathy involves preferential damage to the thinly myelinated A-delta fibers, unmyelinated C sensory fibers, or autonomic or trophic fibers. Although this condition is common, most patients still remain undiagnosed and untreated because of lagging medical and public

[A Case of Severe Peripheral Polyneuropathy Occurring after Entecavir Treatment in a Hepatitis B Patient].

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Entecavir (Baraclude®) is an oral antiviral drug used for the treatment of HBV. Entecavir is a reverse transcriptase inhibitor which prevents the HBV from multiplying. Most common adverse reactions caused by entecavir are headache, fatigue, dizziness, and nausea. Until now, there has been no report

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