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Guillain-Barré Syndrome (guillain-barré + syndrome)
Selected AbstractsImproved outcome of EAN, an animal model of GBS, through amelioration of peripheral and central inflammation by minocyclineJOURNAL OF CELLULAR AND MOLECULAR MEDICINE, Issue 2 2009Zhi-Yuan Zhang Abstract Experimental autoimmune neuritis (EAN) is a widely used animal model of the human acute inflammatory demyelinating polyradiculoneuropathy, which is the most common subtype of Guillain-Barré Syndrome. EAN is pathologically characterized by breakdown of the blood-nerve barrier, infiltration of reactive immune cells, local inflammation, demyelination in the peripheral nervous system and mechanical allodynia. Minocycline is known to have neuroprotective and anti-inflammatory effects. Furthermore, relieve of neuropathic pain following minocycline administration was observed in a variety of animal models. Here, we investigated the effects of minocycline on rat EAN. Suppressive treatment with minocycline (50 mg/kg body weight daily immediately after immunization) significantly attenuated the severity and duration of EAN. Macrophage and T-cell infiltration and demyelination in sciatic nerves of EAN rats treated with minocycline were significantly reduced compared to phosphate-buffered saline (PBS)-treated EAN rats. mRNA expressions of matrix metallopeptidase-9, inducible nitric oxide synthase and pro-inflammatory cytokines interleukin-1 , and tumour necrosis factor-, in EAN sciatic nerves were greatly decreased by administration of minocycline as well. Furthermore, minocycline attenuated mechanical allodynia in EAN rats and greatly suppressed spinal microglial activation. All together, our data showed that minocycline could effectively suppress the peripheral and spinal inflammation (immune activation) to improve outcome in EAN rats, which suggests that minocycline may be considered as a potential candidate of pharmacological treatment for autoimmune-mediated neuropathies. [source] Guillain-Barré syndrome in a child with pain: lessons learned from a late diagnosisACTA PAEDIATRICA, Issue 10 2010Danielle B. Pier Abstract Children with Guillain-Barré Syndrome (GBS) often do not present like adults with an ascending paralysis and sensory abnormalities, but typically have pain and gait difficulties as predominant symptoms. We present a case of paediatric GBS that was not diagnosed until late in the course because of limited neurological examination, erroneous interpretation of newly acquired data and insufficient familiarity with the disorder in children. Through this case, essentials of paediatric GBS are reviewed. Conclusion:, pain and gait difficulties can be the main features of paediatric GBS at presentation. In addition, a comprehensive neurological exam in any case of weakness or diffuse pain combined with ongoing critical interpretation of a disease course allows for adjustment of a preliminary diagnosis towards a potentially life-threatening disease. [source] Diagnosis of motor neuropathyEUROPEAN JOURNAL OF NEUROLOGY, Issue 3 2001J. -M. Motor neuropathy is a clinical entity which leads to consideration of a wide spectrum of peripheral nerve disorders. Firstly, it may be distinguished from other causes of peripheral motor involvement such as muscle diseases and disorders of the neuromuscular junction. Secondly, it may be discussed in two different forms: acute and chronic. Acute chronic neuropathies are mainly observed in Guillain-Barré syndrome, in which electrophysiological studies allow us to recognize the classical demyelinating form and the axonal form. The other causes of acute motor neuropathy are mainly poliomyelitis and porphyrias. Chronic motor neuropathies are mainly observed in motor neuron diseases, mainly amyotrophic lateral sclerosis, but also Kennedy's disease and other lower motor neuron diseases which may be inherited or acquired. The other causes are multifocal motor neuropathy and the predominantly motor forms of chronic inflammatory demyelinating polyneuropathy. The characterization of these different types of chronic neuropathy is of major importance because of the therapeutic consequences which may lead to the proposal of specific treatments. [source] Matrix metalloproteinase-2 is involved in myelination of dorsal root ganglia neuronsGLIA, Issue 5 2009Helmar C. Lehmann Abstract Matrix metalloproteinases (MMPs) comprise a large family of endopeptidases that are capable of degrading all extracellular matrix components. There is increasing evidence that MMPs are not only involved in tissue destruction but may also exert beneficial effects during axonal regeneration and nerve remyelination. Here, we provide evidence that MMP-2 (gelatinase A) is associated with the physiological process of myelination in the peripheral nervous system (PNS). In a myelinating co-culture model of Schwann cells and dorsal root ganglia neurons, MMP-2 expression correlated with the degree of myelination as determined by immunocytochemistry, zymography, and immunosorbent assay. Modulation of MMP-2 activity by chemical inhibitors led to incomplete and aberrant myelin formation. In vivo MMP-2 expression was detected in the cerebrospinal fluid (CSF) of patients with Guillain-Barré syndrome as well as in CSF and sural nerve biopsies of patients with chronic inflammatory demyelinating polyneuropathy. Our findings suggest an important, previously unrecognized role for MMP-2 during myelination in the PNS. Endogenous or exogenous modulation of MMP-2 activity may be a relevant target to enhance regeneration in demyelinating diseases of the PNS. © 2008 Wiley-Liss, Inc. [source] Starch and albumin mixture as replacement fluid in therapeutic plasma exchange is safe and effectiveJOURNAL OF CLINICAL APHERESIS, Issue 5 2008Gladys P. Agreda-Vásquez Abstract Therapeutic plasma exchange (TPE) is an effective treatment in Myasthenia gravis (MG) and Guillain-Barré syndrome (GBS) and 5% human albumin is the replacement fluid of choice; however, it is expensive. More recently, it has been suggested that starch is a safe and cheaper choice to human albumin. Objective: To evaluate our 5-year experience using 3% hydroxyethyl starch (HES) and 5% human albumin mixture, as replacement fluid in TPE for these diseases. Materials and methods: Retrospective study carried out from January 2001 through September 2006. We included those patients with MG and GBS undergoing TPE. We analyzed clinical outcome (CO) and adverse events (AE) and our results were compared with a previous study which included similar patients undergoing TPE using just 5% human albumin. Results: Thirty-one procedures were carried out in 26 patients, a total of 147 TPE sessions. In the group of MG we had 57% complete responses (CR) and 86% overall response (OR) while in the group of GBS we had 40% CR and 60% OR. When we analyzed our CO with the previous study no statistical differences were found. Mean processed plasma volume (PPV) was 4.2 in MG and 5.5 in GBS. Twenty patients had AE, being hypotension and catheter dysfunction the most frequent ones, while tachycardia, hypertension and paresthesias were statistically more frequent in the HES/albumin group. Conclusions: TPE with a mixture of 3% HES and 5% human albumin is as effective and safe as 5% human albumin alone for patients with these diseases. J. Clin. Apheresis, 2008. © 2008 Wiley-Liss, Inc. [source] Topology and patch-clamp analysis of the sodium channel in relationship to the anti-lipid a antibody in campylobacteriosisJOURNAL OF NEUROSCIENCE RESEARCH, Issue 15 2008Seigo Usuki Abstract An infecting strain VLA2/18 of Campylobacter jejuni was obtained from an individual with campylobacteriosis and used to prepare chicken sera by experimental infection to investigate the role of serum anti-ganglioside antibodies in Guillain-Barré syndrome. Both sera of the patient and chicken contained anti-ganglioside antibodies and anti-Lipid A (anti-Kdo2-Lipid A) antibodies directed against the lipid A portion of the bacterial lipooligosaccharide. The anti-Kdo2-Lipid A activities inhibited voltage-gated Na (Nav) channel of NSC-34 cells in culture. We hypothesized that anti-Kdo2-Lipid A antibody acts on the functional inhibition of Nav1.4. To test this possibility, a rabbit peptide antibody (anti-Nav1.4 pAb) against a 19-mer peptide (KELKDNHILNHVGLTDGPR) on the , subunit of Nav1.4 was produced. Anti-Nav1.4 pAb was cross-reactive to Kdo2-Lipid A. Anti-Kdo2-lipid A antibody activity in the chicken serum was tested for the Na+ current inhibition in NSC-34 cells in combination with ,-Conotoxin and tetrodotoxin. Contrary to our expectations, the anti-Kdo2-Lipid A antibody activity was extended to Nav channels other than Nav1.4. By overlapping structural analysis, it was found that there might be multiple peptide epitopes containing certain dipeptides showing a structural similarity with v-Lipid A. Thus, our study suggests the possibility that there are multiple epitopic peptides on the extracellular domains of Nav1.1 to 1.9, and some of them may represent target sites for anti-Kdo2-Lipid A antibody, to induce neurophysiological changes in GBS by disrupting the normal function of the Nav channels. © 2008 Wiley-Liss, Inc. [source] Transient cardiomyopathy as the presenting feature of Guillain-Barré syndromeJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 2 2010Rossen T. Rousseff No abstract is available for this article. [source] Improving fatigue assessment in immune-mediated neuropathies: the modified Rasch-built fatigue severity scaleJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 4 2009Sonja I. Van Nes Abstract Fatigue is a major disabling complaint in patients with immune-mediated neuropathies (IN). The 9-item fatigue severity scale (FSS) has been used to assess fatigue in these conditions, despite having limitations due to its classic ordinal construct. The aim was to improve fatigue assessment in IN through evaluation of the FSS using a modern clinimetric approach [Rasch unidimensional measurement model (RUMM2020)]. Included were 192 stable patients with Guillain-Barré syndrome (GBS), chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) or polyneuropathy associated with monoclonal gammopathy of undetermined significance (MGUSP). The obtained FSS data were exposed to RUMM2020 model to investigate whether this scale would meet its expectations. Also, reliability and validity studies were performed. The original FSS did not meet the Rasch model expectations, primarily based on two misfitting items, one of these also showing bias towards the factor ,walking independent.' After removing these two items and collapsing the original 7-point Likert options to 4-point response categories for the remaining items, we succeeded in constructing a 7-item Rasch-built scale that fulfilled all requirements of unidimensionality, linearity, and rating scale model. Good reliability and validity were also obtained for the modified FSS scale. In conclusion, a 7-item linearly weighted Rasch-built modified FSS is presented for more proper assessment of fatigue in future studies in patients with immune-mediated neuropathies. [source] Treating nerves: a call to armsJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 2 2008Richard A. C. Hughes Abstract The process of proving that new treatments for peripheral nerve diseases work has often been slow and inefficient. The lack of adequate evidence for some existing treatments has been highlighted by Cochrane systematic reviews. This article uses four different conditions to illustrate the need for more research. Both corticosteroid injections and surgical decompression of the median nerve are efficacious in carpal tunnel syndrome, but whether corticosteroid injections avoid the need for operation needs to be discovered. Corticosteroids are efficacious for Bell's palsy, but the role of antiviral agents needs clarification, which should come from ongoing trials. Intravenous immunoglobulin (IVIg) and plasma exchange are both efficacious in Guillain-Barré syndrome, but corticosteroids are not. More trials are needed to discover the best dose of IVIg in severe cases and whether mild cases need treatment. In chronic inflammatory demyelinating polyradiculoneuropathy, corticosteroids, IVIg and plasma exchange are all efficacious, at least in the short term, but trials are needed to discover whether and which other immunosuppressive agents help. The Peripheral Nerve Society has formed a standing committee, the Inflammatory Neuropathy Consortium (http://pns.ucsd.edu/INC.htm), to facilitate the trials needed to answer the remaining questions in the inflammatory neuropathies. [source] Guillain-Barré syndrome after combined CHOP and rituximab therapy in non-Hodgkin lymphomaJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 2 2007Fabrizia Terenghi [source] 14-3-3 protein in the CSF of inflammatory peripheral neuropathiesJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 2 2004A Bersano 14-3-3 proteins are a highly conserved protein family of unknown function, although some authors suggested a role in cellular proliferation and differentiation, neurotransmitters biosynthesis and apoptosis. The expression of these proteins increases during development, in particular, in large projection neurons such as spinal motor neurons. Recently the protein was described in cerebrospinal fluid (CSF) of patients with spongiform encephalopathies, in particular Creutzfeld-Jacob disease, where the protein is considered a highly sensitive and specific marker. 14-3-3 protein has been also detected in CSF of other prion-unrelated dementias and other neurodegenerative (Parkinson disease, stroke and paraneoplastic syndromes) and inflammatory diseases like Multiple Sclerosis. The aim of our study was to evaluate whether the 14-3-3 protein is also present in the CSF of peripheral nervous system diseases. We studied by Western Blot the CSF of 120 patients including 38 with Guillain-Barré syndrome (GBS), 23 with chronic inflammatory demyelinating polyneuropathy (CIDP), 12 with multifocal motor neuropathies (MMN), 20 motor neuron disease (MND), 8 paraneoplastic syndrome, 14 other neuropathies or radiculopathies (OPN), and 5 normal subjects (NC). We found the 14-3-3 protein in the CSF of 21 (55%) patients with GBS, 13 (56%) with CIDP, 1 (5%) with MND, 3 (21%) with OPN and none with paraneoplastic syndrome, MMN or NC. Our results reveal that 14-3-3 protein can be detected not only in central but also in peripheral nervous system diseases where it is significantly associated (p < 0.0001) with GBS and CIDP. [source] Structure Of Campylobacter Jejuni Lipopolysaccharides Determines Antiganglioside Specificity And Clinical Features Of Guillain-Barre, And Miller Fisher PatientsJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 3 2002CW Ang Ganglioside mimicry in the lipopolysaccharide (LPS) fraction of Campylobacter jejuni isolated from Guillain-Barré syndrome (GBS) and Miller Fisher syndrome (MFS) patients was compared with isolates from patients with an uncomplicated enteritis. The antibody response to C. jejuni LPS and gangliosides in neuropathy patients and controls was compared as well. LPS from GBS and MFS-associated isolates more frequently contained ganglioside-like epitopes compared to control isolates. Almost all neuropathy patients showed a strong antibody response against LPS and multiple gangliosides in contrast to enteritis patients. Isolates from GBS patients more frequently had a GM1-like epitope than isolates from MFS patients. GQ1b-like epitopes were present in all MFS-associated isolates and was associated with anti-GQ1b antibody reactivity and the presence of oculomotor symptoms. These results demonstrate that the expression of ganglioside mimics is a risk factor for the development of post-Campylobacter neuropathy. This study provides additional evidence for the hypothesis that the LPS fraction determines the antiganglioside specificity and clinical features in post-Campylobacter neuropathy patients. [source] PERIPHERAL NERVOUS SYSTEM DEMYELINATION AND iNOS EXPRESSIONJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 1 2002Article first published online: 11 MAR 200 Conti G.1, Pasquale C.1, Rostami A.3, De Pol A.2, Galimberti D.1, Scarpini E.1, Baron P.L.1, Scarlato G.1 1 Milano Italy, 2 Modena, Italy, 3Philadelphia USA. Nitric oxide (NO), during CNS demyelination, is synthesised in inflammatory cells from L-arginine by the nitric oxide synthases (NOS). NO can subserve different functions, from cytotoxicity to neuroprotection and trigger either necrotic or apoptotic cell death. In this study we detected inducible form of NOS (iNOS) gene expression in experimental allergic neuritis (EAN), induced in Lewis rats by injection of "SP26," emulsified in complete Freund's adjuvant, which clinical, electrical, and pathological features resemble those of "Guillain-Barré" syndrome. Northern blot, single nerve fiber immmunostaining, and immuno-electron microscope showed that both iNOS mRNA and protein were induced in the PNS of EAN rats by day 14 after immunization, at the beginning of EAN clinical signs. However, with the same experimental procedures, we failed to find iNOS expression during Wallerian degeneration following nerve cut. These data support the hypothesis that iNOS regulation has an active role in cell-mediated demyelination. [source] Severe backache in Guillain-Barré syndromeMUSCLE AND NERVE, Issue 3 2002Marisa Sánchez-Guerra MD No abstract is available for this article. [source] Prediction of respiratory insufficiency in Guillain-Barré syndromeANNALS OF NEUROLOGY, Issue 6 2010Christa Walgaard MD Objective Respiratory insufficiency is a frequent and serious complication of the Guillain-Barré syndrome (GBS). We aimed to develop a simple but accurate model to predict the chance of respiratory insufficiency in the acute stage of the disease based on clinical characteristics available at hospital admission. Methods Mechanical ventilation (MV) in the first week of admission was used as an indicator of acute stage respiratory insufficiency. Prospectively collected data from a derivation cohort of 397 GBS patients were used to identify predictors of MV. A multivariate logistic regression model was validated in a separate cohort of 191 GBS patients. Model performance criteria comprised discrimination (area under receiver operating curve [AUC]) and calibration (graphically). A scoring system for clinical practice was constructed from the regression coefficients of the model in the combined cohorts. Results In the derivation cohort, 22% needed MV in the first week of admission. Days between onset of weakness and admission, Medical Research Council sum score, and presence of facial and/or bulbar weakness were the main predictors of MV. The prognostic model had a good discriminative ability (AUC, 0.84). In the validation cohort, 14% needed MV in the first week of admission, and both calibration and discriminative ability of the model were good (AUC, 0.82). The scoring system ranged from 0 to 7, with corresponding chances of respiratory insufficiency from 1 to 91%. Interpretation This model accurately predicts development of respiratory insufficiency within 1 week in patients with GBS, using clinical characteristics available at admission. After further validation, the model may assist in clinical decision making, for example, on patient transfer to an intensive care unit. ANN NEUROL 2010;67:781,787 [source] Pharmacokinetics of intravenous immunoglobulin and outcome in Guillain-Barré syndrome,ANNALS OF NEUROLOGY, Issue 5 2009Krista Kuitwaard MD Objective Intravenous immunoglobulin (IVIg) is the first choice treatment for Guillain-Barré syndrome (GBS). All patients initially receive the same arbitrary dose of 2g per kg body weight. Not all patients, however, show a good recovery after this standard dose. IVIg clearance may depend on disease severity and vary between individuals, implying that this dose is suboptimal for some patients. In this study, we determined whether the pharmacokinetics of IVIg is related to outcome in GBS. Methods We included 174 GBS patients who had previously participated in 2 randomized clinical trials. At entry, all patients were unable to walk unaided and received a standard dose of IVIg. Total IgG levels in serum samples obtained immediately before and 2 weeks after the start of IVIg administration were determined by turbidimetry and related to clinical outcome at 6 months. Results The increase in serum IgG (,IgG) 2 weeks after IVIg treatment varied considerably between patients (mean, 7.8g/L; standard deviation, 5.6g/L). Patients with a low ,IgG recovered significantly more slowly, and fewer reached the ability to walk unaided at 6 months (log-rank p < 0.001). In multivariate analysis adjusted for other known prognostic factors, a low ,IgG was independently associated with poor outcome (p = 0.022). Interpretation After a standard dose of IVIg treatment, GBS patients show a large variation in pharmacokinetics, which is related to clinical outcome. This may indicate that patients with a small increase in serum IgG level may benefit from a higher dosage or second course of IVIg. Ann Neurol 2009;66:597,603 [source] The Critical Role of IL-12p40 in Initiating, Enhancing, and Perpetuating Pathogenic Events in Murine Experimental Autoimmune NeuritisBRAIN PATHOLOGY, Issue 4 2002Lei Bao Interleukin 12 (IL-12) is a proinflammatory cytokine with important immunoregulatory activities and is critical in determining the differentiation and generation of Th1 cells. For the present study, we investigated the role of endogenous IL-12 in the pathogenesis of experimental autoimmune neuritis (EAN), which is a CD4+ T-cell mediated autoimmune inflammatory disease of the peripheral nervous system. EAN is used as an animal model for Guillain-Barré syndrome of humans. Here, EAN was established in IL-12 p40 deficient mutant (IL-12 -/- ) C57BL/6 mice by immunization with P0 peptide 180,199, a purified component of peripheral nerve myelin, and Freund's complete adjuvant. In these IL-12 -/- mice the onset of clinical disease was delayed, and the incidence and severity of EAN were significantly reduced compared to that in wild-type mice. The former group's clinical manifestations were associated with less P0-peptide 180,199 induced secretion of interferon-, (IFN-,) by splenocytes in vitro and low production of anti-P0-peptide 180,199 IgG2b antibodies in serum. Fewer IFN-, and TNF-, producing cells, but more cells secreting IL-4, were found in sciatic nerve sections from IL-12 -/- mice, consistent with impaired Th1 functions and response. However, the IL-12 deficiency appeared not to affect P0 peptide 180,199-specific T-cell proliferation. These results indicate that IL-12 has a major role in the initiation, enhancement and perpetuation of pathogenic events in EAN by promoting a Th1 cell-mediated immune response and suppressing the Th2 response. This information augments consideration of IL-12 as a therapeutic target in Guillain-Barré syndrome and other T-cell-mediated autoimmune diseases. [source] Can we face the challenge of expanding use of intravenous immunoglobulin in neurology?ACTA NEUROLOGICA SCANDINAVICA, Issue 5 2010I. Elovaara Elovaara I, Hietaharju A. Can we face the challenge of expanding use of intravenous immunoglobulin in neurology? Acta Neurol Scand: 2010: 122: 309,315. © 2010 The Authors Journal compilation © 2010 Blackwell Munksgaard. The use of high-dose polyclonal intravenous immunoglobulin (IVIG) in the treatment of autoimmune neurological diseases has expanded over the last decade. Based on controlled clinical trials IVIG can be considered currently as the first-line treatment in Guillain-Barré syndrome, chronic inflammatory demyelinating polyneuropathy and multifocal motor neuropathy, and it may be used as a rescue therapy in worsening myasthenia gravis. IVIG is a second-line therapy in dermatomyositis, stiff-person syndrome and pregnancy-associated or postpartum relapses of multiple sclerosis. Although the biological efficacy of IVIG is due to multiple effects on the immune system, many mechanisms are still unknown. The awareness of risks and complications of IVIG therapy has increased, but severe side effects are still considered rare. Due to increasing costs of this treatment, careful selection of patients who will benefit from IVIG is extremely important. [source] Tongue weakness is associated with respiratory failure in patients with severe Guillain-Barré syndromeACTA NEUROLOGICA SCANDINAVICA, Issue 6 2009D. Orlikowski Objective,,, Swallowing impairment may worsen respiratory weakness and conduct to respiratory complications such as aspiration pneumonia in Guillain-Barré syndrome (GBS). We prospectively evaluate how tongue weakness could be associated to bulbar dysfunction and respiratory weakness in severe GBS patients. Measurements and main results,,, Tongue strength, dysphagia and respiratory parameters were measured in 16 GBS patients at intensive care unit (ICU) admission and discharge and in seven controls. Tongue strength was decreased in the GBS patients compared with the controls. At admission, patients with dysphagia and those requiring mechanical ventilation (MV) had greater tongue weakness. All the patients with initial tongue strength <150 g required MV during ICU stay. Tongue strength correlated significantly with respiratory parameters. Conclusion,,, This study confirms the strong association between bulbar and respiratory dysfunction in GBS admitted to ICU. Tongue weakness may be present in GBS, especially during the phase of increasing paralysis, and resolves during the recovery phase. Tongue strength and indices of global and respiratory strength vary in parallel throughout the course of GBS. Further studies are needed to assess if, when used in combination with other respiratory tests, tongue strength measurement could contribute to identify patients at high risk for respiratory complications. [source] Guillain-Barré syndrome in a child with pain: lessons learned from a late diagnosisACTA PAEDIATRICA, Issue 10 2010Danielle B. Pier Abstract Children with Guillain-Barré Syndrome (GBS) often do not present like adults with an ascending paralysis and sensory abnormalities, but typically have pain and gait difficulties as predominant symptoms. We present a case of paediatric GBS that was not diagnosed until late in the course because of limited neurological examination, erroneous interpretation of newly acquired data and insufficient familiarity with the disorder in children. Through this case, essentials of paediatric GBS are reviewed. Conclusion:, pain and gait difficulties can be the main features of paediatric GBS at presentation. In addition, a comprehensive neurological exam in any case of weakness or diffuse pain combined with ongoing critical interpretation of a disease course allows for adjustment of a preliminary diagnosis towards a potentially life-threatening disease. [source] Assessment of coronary morphology and flow in a patient with guillain-barré syndrome and st-segment elevationCLINICAL CARDIOLOGY, Issue 3 2001Nikolaos Dagres M.D. Abstract Patients with Guillain-Barré syndrome often have cardiac disturbances as a manifestation of autonomic dysfunction. Such abnormalities consist of arrhythmias and disturbances of heart rate and blood pressure. We report a case of a patient with Guillain-Barré syndrome who developed ST-segment elevation in the inferolateral leads, suggestive of an acute coronary syndrome. Cardiac catheterization revealed angiographically normal coronary arteries. Intracoronary ultrasound was also normal. Intracoronary Doppler flow measurements revealed an elevated baseline coronary flow velocity of up to 41 cm/s and decreased coronary flow reserve, particularly in the left circumflex artery. Myopericarditis as cause of the electrocardiographic changes could be ruled out by echocardiography and endomyocardial biopsy. We postulate that the intracoronary Doppler findings are caused by autonomic dysfunction with decrease of coronary resistance and redistribution of the transmural myocardial blood flow. [source] Treatment for guillain-barré syndrome,ANNALS OF NEUROLOGY, Issue 5 2009David R. Cornblath MD No abstract is available for this article. [source] Assessment of coronary morphology and flow in a patient with guillain-barré syndrome and st-segment elevationCLINICAL CARDIOLOGY, Issue 3 2001Nikolaos Dagres M.D. Abstract Patients with Guillain-Barré syndrome often have cardiac disturbances as a manifestation of autonomic dysfunction. Such abnormalities consist of arrhythmias and disturbances of heart rate and blood pressure. We report a case of a patient with Guillain-Barré syndrome who developed ST-segment elevation in the inferolateral leads, suggestive of an acute coronary syndrome. Cardiac catheterization revealed angiographically normal coronary arteries. Intracoronary ultrasound was also normal. Intracoronary Doppler flow measurements revealed an elevated baseline coronary flow velocity of up to 41 cm/s and decreased coronary flow reserve, particularly in the left circumflex artery. Myopericarditis as cause of the electrocardiographic changes could be ruled out by echocardiography and endomyocardial biopsy. We postulate that the intracoronary Doppler findings are caused by autonomic dysfunction with decrease of coronary resistance and redistribution of the transmural myocardial blood flow. [source] | |||||||||||||