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Guillain Baré

Hassan El Khatib, Amal Naous, Soha Ghanem, Ghassan Dbaibo, Mariam Rajab
Guillain-Barre Syndrome, an acute flaccid paralysis known to be caused by recent Gastro-intestinal infections mainly campylobacter, and Respiratory infections mainly mycoplasma pneumoniae and influenza. One reported case of severe invasive pneumococcal disease in a 68 year old female, that presented with Austrian's triad of meningitis, pneumonia and endocarditis, and progressed to develop Guillain Barre syndrome, an association never been documented before. We present a case of 13 year old male, presented with hypoactivity and inability to bare his own weight, developed septic shock due to pneumococcus with Acute Respiratory Distress Syndrome, and was found to have neurological findings of Guillain-Barre Syndrome...
2018: IDCases
Jens Kuhle, Axel Petzold
INTRODUCTION: Biomarker discovery studies are sometimes referred to as fishing exercises as the excitement of discovering a potentially important new biomarker is offset by the likelihood of finding something that is barely useful. For biomarkers to increase their prognostic value, biomarkers need to improve the current prognostic accuracy. In this regard, one potential advantage in biomarker discovery for acute neurological disease is that damage-related release of biomarkers can be timed, allowing for targeted sample collection...
July 2011: Expert Opinion on Medical Diagnostics
José Berciano, Antonio García, Nuria T Villagrá, Félix González, César Ramón, Isabel Illa, María T Berciano, Miguel Lafarga
We describe a clinicopathological study of a patient presenting with severe and electrophysiological axonal Guillain-Barré syndrome (GBS). An 83-year-old man had a 2-day history of distal acroparesthesias and ascending weakness culminating in quadriplegia, the patient dying 1 month after onset. On day 3, motor conduction velocity (MCV) and distal motor latency values were normal or minimally delayed; most F waves were present with latencies normal or barely delayed. Compound muscle action potential (CMAP) amplitudes were variably reduced...
March 2009: Journal of the Peripheral Nervous System: JPNS
Jan Tomcík, Michal Dufek, Jan Hromada, Ivan Rektor, Martin Bares
Miller Fisher syndrome (MFS) is a localized variant of Guillain-Barré syndrome (GBS), characterized by ophthalmoplegia, areflexia, and ataxia. Recent neurophysiological studies have suggested that abnormal terminal axon dysfunction occurs in some cases of Miller Fisher syndrome and Guillain-Barrd syndrome. We present a rare case report of recurrent MFS with abnormal terminal axon dysfunction. To the best of our knowledge, this is the first case report of recurrent MFS with terminal axon dysfunction that persisted up to nine months after the initial presentation of the second attack with positive antiganglioside antibodies and full clinical recovery...
December 2007: Acta Neurologica Belgica
Elzbieta Szupień, Bozena Ositek, Jarosław Pniewski
The following paper presents a case of presently rare serious and non-typical subacutely progressing neurological complications in Addison-Biermer disease in a period before the diagnosis, and effective treatment with vitamin B12 in the advanced process of the nervous system impairment. The patient was a 52-year-old woman with the following (increasingly severe) symptoms occurring over a period of 5 weeks, after an earlier non-related operation: paresis of lower limbs (up to paraplegia), slight paresis of upper limbs, sphincters disorder, numbness and the loss of sensation in the upper and lower limbs, and finally mental deterioration...
September 2004: Neurologia i Neurochirurgia Polska
E Uetz-von Allmen, M Sturzenegger, R Rieben, F Rihs, A Frauenfelder, U E Nydegger
So far, the pathogenic significance and use for diagnosis of antiganglioside GM1 antibodies (anti-GM1) are unclear. We therefore compared serum IgM and IgG antimonosialo ganglioside GM1 levels of 33 patients with presumed immune-mediated neuropathies, 100 patients with various other central or peripheral neurological disorders, and 110 controls by ELISA. We also measured the complement-activating capacity of anti-GM1 by C5b-9-GM1-ELISA to evaluate its value to distinguish between pathogenic and nonpathogenic autoantibodies...
1998: European Neurology
C L Koski, R Humphrey, M L Shin
The role of anti-peripheral nerve myelin antibody (anti-PNM Ab) in the pathogenesis of acquired demyelination of peripheral nerve is unclear, in part, due to the poor correlation between antibody and disease activity. Previous studies show that only 27-50% of patients with acute demyelinating neuropathy or Guillain-Barré syndrome (GBS) had serum Abs to peripheral nerve or PNM as demonstrated by consumption of hemolytic activity of serum complement 1 (C1) fixation and transfer assay, quantitative determinations of anti-PNM Ab showed significantly high titers in the serum of patients with GBS, chronic and recurrent polyneuritis, and paraproteinemia associated with peripheral neuropathy...
February 1985: Proceedings of the National Academy of Sciences of the United States of America
A Appiotti, F Trebini, G Scarzella
A clinical of 37 patients suffering form Guillain-Baré syndrome has been carried out. Because of their unusual onset and clinical course, two of the cases are reported in full. The first case presented atypical onset modalities characterised by dysarthria, dysphonia and dysphagia with subsequent diplegia of the facial nerve and motor involvement of all four extremities; the second was difficult to diagnose and over time it turned out to be disimmune chronic-recurrent polyneuropathy. The clinic instrumental diagnostic and therapeutic course of this case, which was characterised by the poor response to corticosteroid therapy as a result of which use of immunosuppressor (azatioprine) and plasma-feresis were employed with a reaosable improvement, is described in detail...
October 1990: Minerva Medica
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