A case of recurrent Guillain-Barré syndrome with myocarditis]

We report a 35-year-old man who recovered from an initial episode of Guillain-Barré syndrome (GBS) and had acute relapse after two years of asymptomatic interval. He had an acute muscle weakness with areflexia in his extremities following an upper respiratory tract infection in 1993. He was treated with plasma exchange and recovered completely within two months. Two years later he had a relapse of muscle weakness in the same distribution as the initial episode following the symptoms and signs of congestive heart failure. Biopsy of the heart muscle disclosed mild infiltration of lymphocytes with edema and fibrosis: the diagnosis of healing myocarditis was made. He underwent plasma exchange after the heart failure resolved and fully recovered neurologically within three months. The association of GBS and myocarditis is extremely rare. Moreover, there have been no reports describing recurrent GBS with myocarditis. Since GBS with myocarditis sometimes takes a fatal outcome, careful observation and treatment are mandatory.     

A case of Guillain-Barré syndrome following a family outbreak of Campylobacter jejuni enteritis

We describe an outbreak of Campylobacter jejuni enteritis involving three family members of whom one developed Guillain-Barré syndrome (GBS). The patients' serum reacted strongly with several gangliosides and with the lipopolysaccharide (LPS) fractions from the C. jejuni strains isolated from his family members. Only low titer anti-ganglioside antibodies were found in his siblings. HLA-typing did not indicate a locus associated with auto-antibody production. Comparing the immune response in GBS patients and C. jejuni enteritis patients can be of great value in determining the additional factors that lead to post-Campylobacter GBS. Ganglioside mimicry alone is necessary but not sufficient for the induction of anti-ganglioside antibodies. Other susceptibility factors are required to induce an anti-neural immune response.     

Risk of cancer in patients with Guillain-Barré syndrome (GBS)

Abstract. The possible relationship between Guillain-Barré syndrome (GBS) and cancer is still controversial and the existence of a paraneoplastic GBS remains unconfirmed. To better define whether there is a relationship between GBS and malignancy, we compared the observed and the expected number of patients with tumours in a population-based cohort of subjects with GBS. Clinical differences between GBS patients with or without malignancies were analysed. Data were obtained from the Piemonte and Valle dAosta Register for GBS (PARGBS) (years 1990–1998). GBS was diagnosed according to NINCDS criteria. The number of expected cases of malignancy in the PARGBS population was calculated using the incidence rate of all types of cancer (ICD codes 140–208) in Piemonte [1985–1987], and in the most important town of this region, that is Turin (years 1993–1997). In the nine-year period, 435 incident patients with GBS were found. Nine of them developed cancer in the six months preceding or following GBS; in seven of them, the diagnosis of cancer and GBS was concomitant. The expected number of malignant tumours was 3.7 (using the incidence in Piemonte) and 3.8 (using the incidence in Turin); therefore, the odds ratios were 2.43 (95 % CI, 1.11–4.62) and 2.37 (95% CI, 1.09–4.50), respectively (p < 0.01). Although the cases with malignancies were clinically similar to the other cases of GBS observed through the Register, the mortality in GBS patients with cancer was higher and was the final cause of death in two patients affected by severe cancer. These results suggest a possible correlation between some cases of GBS and cancer. However, GBS in cancer patients does not meet all the criteria for paraneoplastic diseases.* Piemonte and Valle dAosta Register for GBS (PARGBS): Coordinating center: 2^nd Division of Neurology, Department of Neuroscience, University of Torino, Italy. Project coordinator: A. Chiò, MD. Study monitors: A. Calvo, MD, N. Di Vito, MD, M. Vercellino, MD. Scientific Committee: A. Bertolotto, MD, E. Bottacchi, MD, A. Chiò, MD, D. Cocito, MD, M. T. Giordana, MD, M. Leone, MD, L. Mazzini, MD, G. Mora, MD. Collaborating centers: A. Chiò, MD, A. A. Terreni, MD, D. Schiffer, MD, R. Mutani, MD, D. Cocito, MD, B. Bergamasco, MD, I. Rainero, MD (Department of Neuroscience, Section of Neurology, University of Torino, and Azienda Ospedaliera San Giovanni Battista, Torino), A. Bertolotto, MD, A. Tribolo, MD, R. Sciolla, MD, F. Mondino, MD, M. T. Giordana, MD (Department of Neuroscience, Section of Neurology, University of Torino, and Azienda Ospedaliera San Luigi Gonzaga, Orbassano), M. Leone, MD, P. Gaviani, MD, F. Monaco, MD (Department of Neurology, Amedeo Avogadro University, Novara), M. De Mattei, MD, E. Morgando, MD (Department of Neurology, Azienda Ospedaliera San Giovanni, Torino), L. Sosso, MD, M. Gionco, MD (Department of Neurology, Ospedale Mauriziano, Torino), U. Morino, MD, M. Nobili, MD (Department of Neurology, Ospedale Martini, Torino), L. Appendino, MD (Department of Neurology, Ospedale Maria Vittoria, Torino), D. Piazza, MD (Department of Neurology, Ospedale S. Giovanni Bosco, Torino), E. Oddenino, MD, W. Liboni, MD (Department of Neurology, Ospedale Gradenigo, Torino), G. Vaula, MD, G. Ferrari, MD (Department of Neurology, Ivrea), M. Favero, MD, C. Doriguzzi Bozzo, MD (Department of Neurology, Pinerolo), P. Santamaria, MD (Department of Neurology, Vercelli), U. Massazza, MD, E. Bollani, MD (Department of Neurology, Biella), A. Villani, MD, R. Conti, MD (Department of Neurology, Domodossola), G. Mora, MD, C. Balzarini, MD (Department of Neurological Rehabilitation, Fondazione S. Maugeri, Clinica del Lavoro e della Riabilitazione, IRCCS, Scientific Institute of Veruno), M. Palermo, MD (Department of Neurology, Alessandria), F. Vergnano, MD (Department of Neurology, Casale Monferrato), S. Cordera, MD, C. Buffa, MD (Department of Neurology, Novi Ligure), M. T. Penza, MD (Department of Neurology, Tortona), F. Fassio, MD (Department of Neurology, Asti), P. Meineri, MD (Department of Neurology, Azienda Ospedaliera Santa Croce e Carle, Cuneo), A. Cognazzo, MD, C. Mocellini, MD, A. Dutto, MD, A. Cucatto, MD (Department of Neurology, Savigliano), C. Cavestro, MD, W. Troni, MD (Department of Neurology, Alba), G. Corso, MD, E. Bottacchi, MD (Department of Neurology, Aosta).     

Guillain-Barré syndrome following COVID-19: new infection,old complication?

Journal of Neurology -     

Proteome analysis of cerebrospinal fluid in Guillain-Barré syndrome (GBS)

We used two-dimensional difference in-gel electrophoresis (2-D-DIGE) for proteome analysis of cerebrospinal fluid (CSF) in Guillain-Barré syndrome (GBS). Spots showing >2-fold difference between GBS and controls were analysed using MALDI-TOF mass spectrometry. Proteins that were up-regulated in GBS included haptoglobin, serine/threonine kinase 10, alpha-1-antitrypsin, SNC73, alpha II spectrin, IgG kappa chain and cathepsin D preprotein, while transferrin, caldesmon, GALT, human heat shock protein 70, amyloidosis patient HL-heart-peptide 127aa and transthyretin were down-regulated. Some of these proteins are reported in CSF of GBS for the first time. Accordingly, the 2-D-DIGE technology may be useful to identify disease-specific proteins in patients with GBS.     

Guillain-Barré syndrome following chickenpox: a case series

Guillain–Barré syndrome (GBS) is an acute, immune-mediated polyradiculoneuropathy, usually triggered by an infectious episode, mostly of viral origin. Varicella zoster virus (VZV) is a rare cause of GBS, mainly in the case of latent infection reactivation. We report on three adult patients who developed GBS following chickenpox, after a short period of latency. They were promptly treated with intravenous immunoglobulin, and the first one with plasma exchange additionally. All the patients experienced almost complete clinical recovery. Our experience suggests that primary VZV infection constitutes a GBS triggering event.     

Guillain-Barré syndrome after septicemia following clozapine-induced agranulocytosis. A case report

We report the case of a patient with schizophrenia, who experienced agranulocytosis during clozapine treatment, followed by bronchopulmonal infection and Guillain-Barré syndrome. The case was recorded within the German surveillance project "drug safety in psychiatry" (AMSP).     

A case of pharyngeal-cervical-brachial variant of Guillain-Barré syndrome with positive anti-galactocerebroside (Gal-C) IgM antibody]

A 49-year-old man presented with hoarseness, dysphagia, muscle atrophy and weakness of deltoid, trapezius, sternocleidomastoid, rhomboid, anterior serratus, infraspinatus and supraspinatus. Anti-Gal-C IgM antibody was positive in the serum. The other antiganglioside antibodies (GM1, GM2, GM3, GD1a, GD1b, GD3, GT1a, GT1b, GQ1b, GA1, GalNAc-GD1a, GM1b) were negative. Patient contracted pneumonia but whether it was due to mycoplasma was not evident. Plasmapheresis improved his clinical state including a decrease of the antibody. This case was diagnosed pharyngeal-cervical-brachial variant of Guillain-Barré syndrome, and anti-Gal-C antibody seemed to be correlated with the pathogenesis of this syndrome. Gal-C is a major glycolipid of myelin and the cell membrane of the myelin-forming cell (oligodendrocytes and Schwann cells) and is free of specific localization and distribution. The mechanism how the anti-Gal-C IgM antibody induced bulbar paralysis and the symptoms localizing neck and upper limbs remains to be known.     

A case of Guillain-Barré syndrome after Campylobacter jejuni enterocolitis: anti-ganglioside antibody levels with or without Guillain-Barré syndrome]

A 38-year old man developed enterocolitis one day after he had ingested raw chicken. Nine days later, his grip strength weakened. Eleven days later, he was admitted to our hospital with weakness of four limbs, dysphagia and dysarthria. Serum anti-Campylobacter jejuni antibody and anti-ganglioside antibodies (GM1, GD1a, GD1b, GalNAc-GD1a) were positive, and motor action potentials were not evoked at all extremities. He was diagnosed as having Guillain-Barré syndrome. After receiving immune absorption therapy and plasma exchange therapy, the patient improved. Another person who had also consumed the same raw chicken developed colitis only. Five weeks later, the anti-GalNAc-GD1a-IgG antibody titers (O.D. 490 nm) of the patient and the other man who developed colitis were 0.324 and 0.118, respectively. It was suggested that the pathogenesis of Guillain-Barré syndrome after Campylobacter jejuni enterocolitis may be related to the type and titer of anti-ganglioside antibodies and also to the sensitivity of the individual.     

Response to “a fatal case of Guillain-Barré syndrome after infection with COVID-19”

Journal of NeuroVirology -     

A case of slowly progressive pharyngeal-cervical-brachial variant of Guillain-Barré syndrome (PCB)]

A 69-year-old woman was admitted to our hospital because of slowly progressive weakness in the neck, shoulders, proximal arms, oropharyngeal muscles. From a viewpoint of clinical course and signs, it was suspected that the patient was suffered from motor neuron disease. However, serial electrophysiological studies showed the existence of local demyelination of the motor nerves. The immunoadsorption was then performed and marked recovery of symptoms was obtained. In this case, we could not detect any established anti-ganglioside antibodies which was related to pharyngeal-cervical-brachial variant of Guillain-Barré syndrome(PCB) or Guillain-Barré syndrome (GBS). It is suggested that unknown anti-ganglioside antibody may play an important role in cases of PCB. Despite of atypical slowliness of clinical progression and negative results of immunological studies, this patient is considered to be suffered from PCB, because of the results of electrophysiological studies and effectiveness of immunoadsorption therapy. Accordingly it may be important to take the possibility of PCB into diagnostic consideration, whenever the patient shows slowly progressive weakness in proximal arms, oropharyngeal muscles.     

A case of neuropathy mimicking Guillain-Barré syndrome after arsenic intoxication

INTRODUCTION: Chronic arsenic toxicity is a global health problem affecting millions of people. Acute arsenic poisoning is less frequent and it is most often lethal. Therefore, its consequences are not well known, more precisely its neurological consequences. OBSERVATION: We report a case of Guillain-Barré-like syndrome and encephalopathy after acute arsenical poisoning in a 50 year-old man. After 4 month follow-up, the improvement was slow and limited with persistent motor and proprioceptive deficits. DISCUSSION: The most frequent neurological complication induced by acute arsenical poisoning is a distal, symmetrical, sensory, axonal polyneuropathy. Yet the clinical course and the electrophysiological findings may also suggest a Guillain-Barré like syndrome. Moreover, the chelating is not very effective on the neurological complications. CONCLUSION: Any discrepancies in the clinical course of a Guillain-Barré syndrome shall lead to reconsider the diagnosis. The association of gastro-intestinal disorders, skin lesions, and encephalopathy and mood disorders leads to discuss intoxication with heavy metal and more precisely with arsenic. Moreover, the chelating is not very effective on the neurological complications.     

Bilateral facial palsy with paresthesias,variant of Guillain-Barré syndrome following COVID-19 vaccine: A case series of 9 patients

Several cases of Guillain-Barré Syndrome (GBS) associated with COVID-19 vaccination have been reported, including the rare subtype known as Bilateral Facial Palsy with paresthesias (BFP). To date, it is not known whether a causal relationship may exist between the two. We report 9 cases of BFP in patients vaccinated against COVID-19 in the previous month. Nerve conduction studies revealed demyelinating polyneuropathy in 4 patients, and 5 presented bilateral, focal facial nerve involvement, exclusively. Ganglioside antibody panel was positive in 4 patients (anti-GM1=2, anti-GD1a=1 and anti-sulfatide=1). Seven patients received intravenous immunoglobulin treatment, one plasma exchange, and one patient died from sudden cardiac arrest following arrhythmia before treatment could be administered. Rates of BFP following COVID-19 vaccination, did not differ from those reported in previous series. Epidemiological studies are essential to determine whether a causal relationship may exist between this rare form of GBS and COVID-19 vaccination.     

A case of relapsing Guillain-Barré syndrome associated with exacerbation of chronic hepatitis B virus hepatitis

A patient with two episodes of acute polyradiculoneuropathy (Guillain-Barré syndrome) that both occurred during exacerbation of chronic hepatitis B and separated by a 2-year asymptomatic interval is described. The possible causative relation between the neuropathy and the chronic hepatitis B is discussed.     

Severe Guillain-Barré syndrome following head trauma

Fulminant forms of Guillain-Barré syndrome (GBS) present as acute onset tetraparesis and areflexia with absent brainstem reflexes, simulating brain death. Head trauma as an antecedent to fulminant GBS has been infrequently reported, and recognizing an association between GBS and head trauma may be crucial for patient management. Consequently, we report a patient with fulminant GBS with mixed demyelinating and axonal features preceded by a closed head injury, and discuss the possible pathophysiological mechanisms.     

Guillain-Barré syndrome following acute falciparum malaria

Plasmodium falciparum malaria is often complicated by involvement of the gastrointestinal, cardiovascular, and nervous systems. The development of Guillain-Barré syndrome in 10 patients who had had acute P. falciparum malaria during its seasonal exacerbation is reported.