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Barré Syndrome (barré + syndrome)
Selected AbstractsCase report: Hepatitis A preceding Guillain,Barré Syndrome,JOURNAL OF MEDICAL VIROLOGY, Issue 8 2006Shobha D. Chitambar Abstract A case of acute hepatitis A with Guillain,Barré Syndrome subtype AMAN (acute motor axonal neuropathy) in a 17-year-old male is reported. Serum and cerebrospinal fluid were positive for anti-hepatitis A virus (HAV) IgM, IgG, and IgA. The onset of the syndrome was evident in week 3 of illness. The remarkably high titers of serum anti-HAV IgG appeared unique to a hepatitis A patient with the syndrome. Phylogenetic analysis of the HAV genome detected in the serum and feces revealed genotype IIIA, circulating commonly in Pune, western India. J. Med. Virol. 78:1011,1014, 2006. © 2006 Wiley-Liss, Inc. [source] Prevalence and mechanism of bladder dysfunction in Guillain,Barré Syndrome,NEUROUROLOGY AND URODYNAMICS, Issue 5 2009Ryuji Sakakibara Abstract Aim To examine the prevalence and mechanism of urinary dysfunction in GBS. Methods Urinary symptoms were observed and neurological examinations made repeatedly during hospitalization of 65 consecutive patients with clinico-neurophysiologically definite GBS. The patients included 41 men, 24 women; mean age, 41 years old; mean Hughes motor grade, 3; AIDP, 28, AMAN, 37. Urodynamic studies consisted of uroflowmetry, measurement of post-micturition residuals, medium-fill water cystometry, and external anal sphincter electromyography. Results Urinary dysfunction was observed in 27.7% of GBS cases (urinary retention, 9.2%). Urinary dysfunction was related to the Hughes motor grade (P,<,0.05), defecatory dysfunction (P,<,0.05), age (P,<,0.05), and negatively related to serum IgG class anti-ganglioside antibody GalNAc-GD1a (P,<,0.05). Urinary dysfunction was more common in AIDP (39%) than in AMAN (19%). No association was found between antibody titer against neuronal nicotinic acetylcholine receptors and urinary dysfunction. Urodynamic studies in nine patients, mostly performed within 8 weeks after disease onset, revealed post-void residual in 3 (mean 195 ml), among those who were able to urinate; decreased bladder sensation in 1; detrusor overactivity in 8; low compliance in 1; underactive detrusor in 7 (both overactive and underactive detrusor in 5); and nonrelaxing sphincter in 2. Conclusion In our series of GBS cases, 27.7% of the patients had urinary dysfunction, including urinary retention in 9.2%. Underactive detrusor, overactive detrusor, and to a lesser extent, hyperactive sphincter are the major urodynamic abnormalities. The underlying mechanisms of urinary dysfunction appear to involve both hypo- and hyperactive lumbosacral nerves. Neurourol. Urodynam. 28:432,437, 2009. © 2009 Wiley-Liss, Inc. [source] Methods: Retrospective hospital-based searches for cases of acute flaccid paralysisAUSTRALIAN AND NEW ZEALAND JOURNAL OF PUBLIC HEALTH, Issue 1 2002R.M. D'Souza Objective: Australia had to demonstrate adequate acute flaccid paralysis (AFP) surveillance by achieving a rate of one per 100,000 in children under the age of 15 to fulfil one of the requirements of the Regional Commission for the Certification of Poliomyelitis Eradication to be declared polio free. To increase the ascertainment rate of AFP cases, a hospital search was conducted to identify cases not reported to the active AFP surveillance. Methods: A computerised search of hospital admissions in New South Wales (NSW) and Western Australia (WA) on ICD-9 codes of Guillain Barré Syndrome (GBS), unspecified encephalitis, poliomyelitis, vaccine-associated paralytic polio (VAPP) and flaccid paralysis was conducted for the period 1995,98. Medical records of cases that were not reported to the active surveillance were reviewed in three hospitals of NSW and two hospitals in WA. Results: Twenty additional cases recorded as GBS and five as transverse myelitis (TM) were identified through the searches, which increased the average four-year AFP rate from 1.0 to 1.4 per 100,000 in children under the age of 15 years in these two states and the overall AFP rate in Australia increased from 0.78 to 1.14. There were no cases of polio or VAPP found. Nine cases of GBS and five of TM reported to the active AFP surveillance were not found in the hospital searches. Conclusion: A combination of active surveillance and hospital-based searches increased the investigated AFP rate, which fulfilled one of the certification requirements for Australia to be certified polio free. Implications: Until global certification is achieved, AFP surveillance needs to be improved to identify cases of importation of wild poliovirus. [source] Neurological manifestations of antiphospholipid syndromeEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 4 2010Carlos E. M. Rodrigues Eur J Clin Invest 2010; 40 (4): 350,359 Abstract Background, Neurologic disorders are among the most common and important clinical manifestations associated with the antiphospholipid syndrome (APS). It is characterized by diverse neurological manifestations. These include stroke, transient ischaemic attack, Sneddon's syndrome, convulsions/epilepsy, dementia, cognitive deficits, headaches/migraine, chorea, multiple sclerosis-like, transverse myelitis, ocular symptoms and Guillain,Barré syndrome. Material and methods, We review the latest data about neurologic disorders and APS. Results, In patients under 45 years of age, 20% of strokes are potentially associated with APS. Our study group recently reported a correlation between primary APS and peripheral neuropathy. Only one study investigated the occurrence of peripheral neuropathy in patients diagnosed with PAPS through electrophysiological study and showed alterations in 35% of patients. The mechanism of nervous system involvement in APS is considered to be primarily thrombotic. However, other mechanisms have been described, such as antiphospholipid antibodies that bind to the neural tissue, deregulating their functions and having an immediate pathogenic effect. Conclusions, This review summarizes the latest data regarding the clinical aspects, radiological and therapeutic of major neurologic manifestations associated with antiphospholipid antibodies. [source] Sensory Guillain,Barré syndrome after Campylobacter jejuni infectionEUROPEAN JOURNAL OF NEUROLOGY, Issue 3 2007Y. A. Rajabally No abstract is available for this article. [source] Guillain,Barré syndrome in southern Taiwan: clinical features, prognostic factors and therapeutic outcomesEUROPEAN JOURNAL OF NEUROLOGY, Issue 6 2003B.-C. Cheng To determine the clinical features, prognostic factors, and therapeutic results of Guillain,Barré syndrome (GBS) in order to improve the therapeutic strategy for this disease. We retrospectively reviewed the electrodiagnostic study and medical records of patients with GBS admitted to Chang Gung Memorial Hospital, Kaohsiung, between January 1986 and December 2000. Outcomes and prognosis were followed-up after 1 year. Ninety-six patients were enrolled in this study. According to the clinical and electrophysiological findings, 77 patients were acute inflammatory demyelinating polyradiculoneuropathy, seven were Miller Fisher syndrome, and six were axonal forms, and six were unclassified. At a follow-up of 1 year, 61 patients (64%) recovered, 30 (31%) had residua and five (5%) died. Amongst these 30 had residua, including unassisted gait in 19, assisted gait in four, and wheel/bed bound in seven. According to the statistical analysis, disabilities at the nadir (P < 0.0001) and at admission (P = 0.014) were significant prognostic factors. Variables used for the stepwise logistic regression, and the results revealed that after analysis for all the above variables, only disability at the nadir (P < 0.0001) was independently associated with the treatment failure rate. Our study revealed 27% of cases in need of respiratory support during hospitalization, and 5% of hospital-treated patients die from the complications. Furthermore, 31% had residua at a follow-up of 1 year or more. If prognostic factors are considered, disability at the nadir during hospitalization demonstrates consistently poor therapeutic outcomes. Therefore, early diagnosis, choice of appropriate treatment, and preventing complications during acute stages are essential to maximize the potential for survival. [source] Erratum: Longer duration of viremia and unique amino acid substitutions in a hepatitis A virus stain associated with Guillain,Barré syndrome (GBS)JOURNAL OF MEDICAL VIROLOGY, Issue 11 2010Madhuri S. Joshi No abstract is available for this article. [source] Clinical presentation and prognosis of childhood Guillain,Barré syndromeJOURNAL OF PAEDIATRICS AND CHILD HEALTH, Issue 7-8 2008Jung Hwan Lee Aim: Guillain,Barré syndrome (GBS) is an acute inflammatory polyneuropathy commonly characterised by rapidly progressive, symmetric weakness and areflexia. This study is to assess the clinical characteristics of paediatric GBS, as well as its long-term functional prognosis. Methods: We retrospectively assessed the clinical manifestations, results of electrodiagnostic tests, functional status and prognosis of 56 children diagnosed with GBS. Based on clinical and electrophysiological findings, the patients were classified as having acute inflammatory demyelinating polyradiculoneuropathy ([AIDP]n = 34), acute motor axonal neuropathy ([AMAN]n = 14), acute motor and sensory axonal neuropathy (n = 1) and Miller Fisher syndrome ([MFS]n = 7). Results: Upper respiratory infection was the most frequent preceding event, and limb weakness was the most frequent symptom at GBS onset. There was no significant difference in the mean time from the onset of illness to nadir between any of these groups. Both the AIDP and AMAN groups showed significantly poorer functional status, measured by the Hughes scale, than the MFS group. Two years after nadir, however, the three groups did not differ significantly. Functional status at nadir, as estimated by the Hughes scale, is a more important factor than electrophysiological types in predicting long-term outcome. Conclusion: The most common symptom at onset in paediatric GBS was limb weakness. Functional status at nadir in AMAN was not significantly different from that of AIDP, and both types achieved good functional outcome for ambulation after 2 years. Functional status at nadir was more important than the electrophysiological type in predicting long-term outcomes. [source] Guillain,Barré syndrome in childhoodJOURNAL OF PAEDIATRICS AND CHILD HEALTH, Issue 5-6 2005Monique M Ryan Abstract:, The Guillain,Barré syndrome (GBS) is characterized by the acute onset of rapidly progressive, symmetric muscle weakness with absent or decreased muscle stretch reflexes. GBS is the most common cause of acute flaccid paralysis in childhood, with an incidence in Australia of 0.8 per 100 000 children per year. Recent advances in this field have included identification of a number of clinical and neurophysiologic subtypes of GBS, enabling improved characterization of etiology and improved prognostication in this disorder. [source] Polyneuritis cranialis with contrast enhancement of cranial nerves on magnetic resonance imagingJOURNAL OF PAEDIATRICS AND CHILD HEALTH, Issue 1 2003A Morosini Abstract: The disorder of multiple cranial nerve palsies without spinal cord involvement is referred to as polyneuritis cranialis (PC) and is rare. It is thought to be an acute post-infective polyneuropathy or a variant of Guillain,Barré syndrome. Electrophysiological evidence of demyelination has been reported, but no radiological abnormalities of the affected cranial nerves have been noted. We report a case of PC where contrast enhanced magnetic resonance imaging (MRI) showed enhancement of the peripheral segments of the oculomotor and abducens nerves. This case illustrates the utility of MRI in the assessment of cranial nerve palsies. [source] Infantile botulism: Clinical and laboratory observations of a rare neuroparalytic diseaseJOURNAL OF PAEDIATRICS AND CHILD HEALTH, Issue 2 2000E Urdaneta-Carruyo Abstract: A 3-month-old male infant was admitted to the University Hospital of Los Andes with a history of constipation, weak crying, poor feeding, flaccidity and later bilateral ptosis and hyporeflexia. The admission diagnosis was septicaemia until an electrophysiological study reported postetanic facilitation with 50 Hz/seg stimulations four days later. The Clostridium botulinum toxin type B was isolated from the infant's stool samples and the organism grew in anaerobic cultures. The patient recovered completely and was discharged 2 months later. Although infant botulism is an uncommon disease in our environment, this diagnosis must be suspected in all afebrile infants with constipation, affected cranial nerves and generalized hypotonia. The principal differential diagnoses are Landry-Guillain,Barré syndrome, poliomyelitis, myasthenia gravis and infant muscular atrophy. [source] Selective contrast enhancement of anterior spinal nerve roots on magnetic resonance imaging: a suggestive sign of Guillain,Barré syndrome and neurobrucellosisJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 3 2003Article first published online: 12 AUG 200 No abstract is available for this article. [source] Genes Differentially Expressed By Schwann Cells Of Motor Versus Sensory NervesJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 1 2001D Imperiale Charcot-Marie-Tooth (CMT) disease includes a heterogeneous group of inherited demyelinating peripheral neuropathies related to genetic defects of myelin-forming Schwann cells (SC). In CMT, as in other common acquired demyelinating neuropathies (Guillain Barré syndrome, chronic inflammatory demyelinating polyneuropathy), motor nerves are invariably more involved than sensory nerves. Also in transgenic mouse models of peripheral neuropathy, there is a preferential demyelination of motor districts independent of the type of genetic alteration. The basis for differential susceptibility to demyelination is unknown. The aim of this study was to identify differences in gene and protein expression that may underlie the differential susceptibility to demyelination of motor and sensory myelin-forming SC. Since spinal roots are the only portion of mammalian PNS in which motor and sensory axons are segregated, we extracted RNA from adult rat dorsal (sensory) and ventral (motor) spinal roots and compared corresponding cDNAs by an RNA fingerprint approach. Four differentially displayed bands were isolated. We first characterized the most differentially expressed band, which was highly enriched in sensory roots. Sequence analysis showed that the band encoded a portion of rat sarco/endoplasmic reticulum calcium transporting ATPase type 1 coding sequence (SERCA1). RT-PCR experiments confirmed SERCA1 enrichment in dorsal sensory roots. SERCA enzymes are ubiquitous calcium regulatory systems in muscle and non-muscle cells and SERCA1 is selectively enriched in skeletal muscle. To our knowledge, no studies have investigated SERCA isoform expression in peripheral nerve. Identification of a calcium regulatory molecule in SC is interesting, as calcium is essential for the proper structure and function of the nodal and paranodal portions of SC, as well as the myelin sheath. However, calcium homeostasis in SC is relatively unexplored. Experiments to localize SERCA1 transcript and protein in different PNS districts and to clarify its functional role in peripheral nerve are underway. [source] Disseminated intravascular large-cell lymphoma with initial presentation mimicking Guillain,Barré syndromeMUSCLE AND NERVE, Issue 1 2010Qin Li Jiang MD Abstract We report a patient with intravascular large B-cell lymphoma who initially presented with acute ascending weakness and sensory changes. Electrodiagnostic testing and cerebral spinal fluid (CSF) studies were initially suggestive of a demyelinating polyneuropathy. Further clinical evaluation and testing were consistent with mononeuropathy multiplex. Autopsy revealed disseminated intravascular large-cell lymphoma. Intravascular large-cell lymphoma should be considered in the differential diagnosis of a rapidly evolving neuropathy associated with other organ involvement. Muscle Nerve, 2010 [source] Contribution of central and peripheral factors to residual fatigue in Guillain,Barré syndromeMUSCLE AND NERVE, Issue 1 2007Marcel P.J. Garssen MD Abstract Many patients with Guillain,Barré syndrome (GBS) suffer from severe residual fatigue that has an uncertain basis. We determined the relative contribution of peripheral and central factors during a 2-min fatiguing sustained maximal voluntary contraction (MVC) in 10 neurologically well-recovered GBS patients and 12 age- and sex-matched healthy controls. Physiological fatigue was defined as the decline of voluntary force during an MVC of the biceps brachii. Relative amounts of peripheral fatigue and central activation failure were determined combining voluntary force and force responses to electrical stimulation. Surface electromyography was used to determine muscle-fiber conduction velocity. During the first minute of sustained MVC, peripheral fatigue developed more slowly in patients than in controls. Central fatigue only occurred in patients. The muscle-fiber conduction velocity was higher in patients. The initial MVC, decrease of MVC, initial force response, and initial central activation failure did not significantly differ between the groups. Although peripheral mechanisms cannot be excluded in the pathogenesis of residual fatigue after GBS, these results suggest that central changes are involved. This study thus provides further insight into the factors contributing to residual fatigue in GBS patients. Muscle Nerve, 2007 [source] Lymphoma and peripheral neuropathy: A clinical reviewMUSCLE AND NERVE, Issue 3 2005John J. Kelly MD Abstract Lymphoma occasionally affects the peripheral nervous system. When it does, the diagnosis can be elusive since many patients present without known lymphoma. Most peripheral nerve complications are due to non-Hodgkin's lymphoma (NHL), which infiltrates nerves causing axonal damage. This disorder can affect nerve roots and cranial nerves, often associated with lymphomatous meningitis. NHL may also infiltrate peripheral nerves and cause plexopathy, mononeuropathy, or generalized neuropathy. These neuropathies may resemble an asymmetric mononeuropathy multiplex or a generalized disorder such as chronic inflammatory demyelinating polyradiculoneuropathy. When NHL infiltrates diffusely, the term neurolymphomatosis is used. Hodgkin's lymphoma (HL), by contrast, rarely infiltrates nerves. More often, HL causes immunological disorders of the peripheral nervous system such as inflammatory plexopathy or Guillain,Barré syndrome. Other rare lymphomas such as intravascular lymphoma and Waldenström's macroglobulinemia can also affect peripheral nerves in specific ways. In addition, other malignant and nonmalignant lymphoproliferative disorders enter into the differential diagnosis of lymphomatous neuropathy. This review discusses the multiple peripheral nerve presentations of lymphoma from the clinician's point of view and provides a guide to the evaluation and diagnosis of these uncommon, challenging disorders. Muscle Nerve, 2005 [source] Advances in understanding and treatment of immune-mediated disorders of the peripheral nervous systemMUSCLE AND NERVE, Issue 2 2004Bernd C. Kieseier MD Abstract During recent years, novel insights in basic immunology and advances in biotechnology have contributed to an increased understanding of the pathogenetic mechanisms of immune-mediated disorders of the peripheral nervous system. This increased knowledge has an impact on the management of patients with this class of disorders. Current advances are outlined and their implication for therapeutic approaches addressed. As a prototypic immune-mediated neuropathy, special emphasis is placed on the pathogenesis and treatment of the Guillain,Barré syndrome and its variants. Moreover, neuropathies of the chronic inflammatory demyelinating, multifocal motor, and nonsystemic vasculitic types are discussed. This review summarizes recent progress with currently available therapies and,on the basis of present immunopathogenetic concepts,outlines future treatment strategies. Muscle Nerve 30: 131,136, 2004 [source] Immunotherapy of idiopathic inflammatory neuropathiesMUSCLE AND NERVE, Issue 3 2003Peter D. Donofrio MD Abstract Evaluation of peripheral neuropathy is a common reason for referral to a neurologist. Recent advances in immunology have identified an inflammatory component in many neuropathies and have led to treatment trials using agents that attenuate this response. This article reviews the clinical presentation and treatment of the most common subacute inflammatory neuropathies, Guillain,Barré syndrome (GBS) and Fisher syndrome, and describes the lack of response to corticosteroids and the efficacy of treatment with plasma exchange and intravenous immunoglobulin (IVIG). Chronic inflammatory demyelinating polyneuropathy, although sharing some clinical, electrodiagnostic, and pathologic similarities to GBS, improves after treatment with plasma exchange and IVIG and numerous immunomodulatory agents. Controlled trials in multifocal motor neuropathy have shown benefit after treatment with IVIG and cyclophosphamide. Also discussed is the treatment of less common inflammatory neuropathies whose pathophysiology involves monoclonal proteins or antibodies directed against myelin-associated glycoprotein or sulfatide. Little treatment data exist to direct the clinician to proper management of rare inflammatory neuropathies resulting from osteosclerotic myeloma; POEMS syndrome; vasculitis; Sjögren's syndrome; and neoplasia (paraneoplastic neuropathy). Muscle Nerve 28: 273,292, 2003 [source] Comparison between impairment and disability scales in immune-mediated polyneuropathiesMUSCLE AND NERVE, Issue 1 2003Ingemar S.J. Merkies MD Abstract The ability of a scale to detect clinical relevant changes over time, i.e., its "responsiveness," may help clinicians to choose among valid and reliable measures. Therefore, we investigated the responsiveness' rank ordering (best to worse) of six selected valid and reliable scales, namely the Medical Research Council (MRC)-sumscore, sensory-sumscore, grip-strength (Vigorimeter), nine-hole peg, ten-meters walking, and a disability-sumscore, in immune-mediated polyneuropathies. Patients with newly diagnosed Guillain,Barré syndrome (n = 7) or chronic inflammatory demyelinating polyneuropathy (n = 13) were examined over 52 weeks. Responsiveness of each scale was measured using different methods (effect-size, standardized response mean score, Wilcoxon matched-pairs signed-rank, and a newly devised Schmitz's distribution-free responsiveness score), and the obtained scores in each method were plotted against the follow-up period, thus allowing area-under-the-curve calculations (higher area-under-the-curve indicating better responsiveness). Also, longitudinal correlations were performed between the scales' values and patients' own clinical judgments (deteriorated, unchanged, improved) (higher correlation = better responsiveness). A consistent rank ordering was observed in each technique with the disability-sumscore, MRC-sumscore, and Vigorimeter being among the best responsive scales. Hence, the primary use of these measures is suggested in studies of immune-mediated polyneuropathies. Muscle Nerve 28: 93,100, 2003 [source] Immunoglobulin IgG Fc-receptor polymorphisms and HLA class II molecules in Guillain,Barré syndromeACTA NEUROLOGICA SCANDINAVICA, Issue 1 2010S. Sinha Sinha S, Prasad KN, Jain D, Nyati KK, Pradhan S, Agrawal S. Immunoglobulin IgG Fc-receptor polymorphisms and HLA class II molecules in Guillain,Barré syndrome. Acta Neurol Scand: 2010: 122: 21,26. © 2010 The Authors Journal compilation © 2010 Blackwell Munksgaard. Objective,,, To analyze host genetic factors immunoglobulin G Fc receptors (Fc,Rs) and human leukocyte antigen (HLA) class II in GBS patients. Methods,,, Fc,RIIA, IIIA and IIIB polymorphisms were studied in 80 each GBS patients and healthy controls by allele specific PCR. HLA class II DR,1 and DQ,1 typing was performed at the two-digit level by PCR in randomly selected 54 GBS patients and 202 controls. Results,,, Fc,RIIA-H/H (56% vs 9%; P < 0.0001) and Fc,RIIIA-V/V (40% vs 13%; P < 0.0001) genotypes, H131 allele frequencies (0.73 vs 0.26, P < 0.0001) and HLA DQ,1*060x (OR, 1.96; 95% CI, 1.26,3.04; P < 0.01) were significantly increased in GBS than controls. DR,1*0701 alone (OR, 10; 95% CI, 45.90,2.25; P < 0.001) and together with Fc,RIIA-H/H (OR, 11.03; 95% CI, 2.63,46.20; P < 0.001) was significantly associated with GBS patients having microbiological evidence of recent infection. Conclusions,,, The study indicates that homozygous Fc,RIIA and Fc,RIIIA genotypes and Fc,RIIA H131 allele are associated with GBS. HLA class II molecule DR,1*0701 is identified as novel genetic risk factor for development of GBS in patients with preceding infection. [source] Is there a need for long-term follow-up in chronic idiopathic polyneuropathy?ACTA NEUROLOGICA SCANDINAVICA, Issue 5 2009T. Rudolph Objective ,, To evaluate the long-term functional status and well-being in patients with chronic idiopathic polyneuropathy (CIP) in comparison to Guillain,Barré syndrome (GBS) and healthy controls. Materials and methods ,, Forty-two CIP and 42 GBS-patients were examined at median 5 and 6 years after disease onset and were compared with 50 healthy controls. The Fatigue Severity Scale (FSS), Visual Analogue Scale for pain (VAS), Disability Rating Index (DRI) and Medical Outcome Study 36-item short-form health status scale (SF-36) were used. Variables at onset and symptoms at follow-up were correlated with outcome measurements in GBS. Results ,, Patients with CIP and GBS had more pain and disability than healthy controls. Additionally, CIP-patients were more fatigued than healthy controls. Patients with CIP were more fatigued [FSS 4.9 (SD 1.6) vs 3.8 (SD 1.8); P < 0.01] and disabled [DRI 4.1 (SD 2.3) vs 2.5 (SD 2.1); P = 0.05] than those with GBS. Physical functioning on the SF-36 was more impaired in CIP than GBS, compared with healthy controls. Conclusions , Patients with CIP and GBS seem to develop persistent impairment on long-term functional status and well-being, more clearly in CIP, reflecting the importance of long-term follow-up in further disease management. [source] Asymmetric pharyngeal,cervical,brachial weakness associated with anti-GT1a IgG antibodyACTA NEUROLOGICA SCANDINAVICA, Issue 4 2002Y. Osaki Osaki Y, Koga M, Matsubayashi K, Yuki N. Asymmetric pharyngeal,cervical,brachial weakness associated with anti-GT1a IgG antibody. Acta Neurol Scand 2002: 106: 234,235. © Blackwell Munksgaard 2002. We report a case of markedly asymmetric pharyngeal,cervical,brachial weakness. Acute progression of symptoms, albuminocytologic dissociation in cerebrospinal fluid, electrophysiologic evidence of demyelination and elevation of IgG anti-GT1a antibody titer paralleled the clinical course, support the diagnosis of Guillain,Barré syndrome. Guillain,Barré syndrome should be considered in the differential diagnosis of cranial neuropathy, even in cases where there is marked asymmetry. [source] Overlapping Guillain,Barré syndrome and Bickerstaff's brainstem encephalitis associated with anti-GQ1b IgG antibody after herpes simplex virus infectionACTA NEUROLOGICA SCANDINAVICA, Issue 1 2001N. Yuki Herpes simplex virus (HSV) is a rare, antecedent infectious agent in Guillain,Barré syndrome (GBS). We report a patient with overlapping GBS and Bickerstaff's brainstem encephalitis (BBE). The patient had a vesicular lesion on her nose. Antecedent HSV type 1 (HSV-1) infection was confirmed by isolation of the virus and detection of the presence of serum anti-HSV-1 IgM antibody during the acute phase. Her serum IgG had high anti-GQ1b antibody titer. External ophthalmoplegia has been noted in 2 of 4 reported cases of HSV-associated GBS. Herpetic brainstem encephalitis cases of poor prognosis are known, but only 2 cases of benign brainstem encephalitis secondary to HSV infection, in which there was acute ophthalmoplegia and clinical features consistent with those of BBE have been reported. [source] Antecedent symptoms in Guillain,Barré syndrome: an important indicator for clinical and serological subgroupsACTA NEUROLOGICA SCANDINAVICA, Issue 5 2001M. Koga Objectives, To examine whether Guillain,Barré syndrome (GBS) can be classified in clinical and immunological subgroups based on the type of prior illness. Background, The existence of antecedent symptoms supports the diagnosis of GBS in patients who experience acute muscle weakness progression. However, little is known about additional meanings of determining antecedent symptoms. Materials and methods, Prospective investigation of prior infectious illness in GBS and related disorders (n=176). Results, The frequent antecedent symptoms in GBS and related disorders were fever (52%), cough (48%), sore throat (39%), nasal discharge (30%), and diarrhea (27%). Patients who had sore throats or coughs frequently had ophthalmoparesis (respectively P=0.0004, P=0.001) and IgG anti-GQ1b antibody (P=0.01, P=0.007). Fever was associated with bulbar palsy (P=0.047) and headache with facial palsy (P=0.04). Patients with diarrhea often had anti-ganglioside IgG (anti-GM1 [P=0.0006] and anti-GM1b [P=0.008]), IgM (anti-GM1 [P=0.03], anti-GM1b [P=0.02], and anti-GalNAc-GD1a [P=0.047]) antibodies and rarely showed ophthalmoparesis or bulbar palsy (respectively P=0.02, P=0.04). Diarrhea and abdominal pain were closely associated with Campylobacter jejuni serology (respectively P<0.0001, P=0.01), whereas other symptoms were not related to pathogens such as cytomegalovirus, Epstein,Barr virus, or Mycoplasma pneumoniae. Conclusions, Our comprehensive study showed that GBS preceded by sore throat, cough, fever, headache, or diarrhea respectively forms clinical or serological subgroups, or both. This association is not necessarily dependent on infection by the known trigger pathogens. [source] Is Campylobacter lipopolysaccharide bearing a GD3 epitope essential for the pathogenesis of Guillain,Barré syndrome?ACTA NEUROLOGICA SCANDINAVICA, Issue 2 2000N. Yuki The hypothesis has been proposed that the GD3 ganglioside-like lipopolysaccharide (LPS) is essential for and functions in the development of Guillain,Barré syndrome (GBS) and Miller Fisher syndrome (MFS) subsequent to Campylobacter jejuni enteritis. Our study showed that patients with GBS or MFS who had previously suffered diarrhea had anti-GD3 antibodies less often than those who had not had diarrhea. Sera from patients who showed GBS or MFS with the serologic evidence of prior C. jejuni infection had anti-GD3 antibodies less frequently than sera from those without evidence of infection. Statistical analysis showed that anti-GD3 antibodies were less frequent in patients with GBS or MFS from whom C. jejuni had been isolated than were other anti-ganglioside antibodies, such as anti-GM1 antibodies. These results could not support the above hypothesis. [source] | ||||||||||