Antibodies to peripheral nerve myelin proteins in chronic inflammatory demyelinating polyradiculoneuropathy and Guillain–Barré syndrome

2007 ◽  
Vol 118 (5) ◽  
pp. e157-e158
Author(s):  
D. Allen ◽  
K. Giannopoulos ◽  
N. Gregson ◽  
A. Makowska ◽  
J. Pritchard ◽  
...  
Keyword(s):  
Peripheral Nerve ◽  
Chronic Inflammatory Demyelinating Polyradiculoneuropathy ◽  
Guillain Barre Syndrome ◽  
Myelin Proteins ◽  
Guillain Barré Syndrome ◽  
Guillain Barré

scholarly journals Treatment-related fluctuation in Guillain-Barre syndrome

2011 ◽  
Vol 02 (02) ◽  
pp. 168-170 ◽  
Author(s):  
Thirunavukkarasu Thivakaran ◽  
Ranjanie Gamage ◽  
Inuka Kishara Gooneratne
Keyword(s):  
Immune Activation ◽  
Early Treatment ◽  
Disease Onset ◽  
Immunoglobulin Therapy ◽  
Chronic Inflammatory Demyelinating Polyradiculoneuropathy ◽  
Guillain Barre Syndrome ◽  
Disability Scale ◽  
Guillain Barré Syndrome ◽  
Immunoglobulin Treatment ◽  
Guillain Barré

ABSTRACTGuillain-Barre syndrome (GBS) is usually a monophasic illness but relapses occur. A 55-year-old female with hypertension and vitiligo presented with acute inflammatory demyelinating polyradiculoneuropathy. She improved with immunoglobulin treatment started on day 6 of illness, but relapsed on day 14 warranting repeat immunoglobulin therapy. Thereafter recovery was complete. Her relapse was due to treatment-related fluctuation (TRF). TRF is improvement in the GBS disability scale of at least one grade after completion of immunotherapy followed by worsening of the disability scale of at least one grade within the first 2 months after disease onset. Recurrent GBS and chronic inflammatory demyelinating polyradiculoneuropathy were excluded. During the peak of the illness ANA titres were transiently high. The presence of other medical conditions, predominant proximal weakness and the absence of preceding diarrhea are predictors for TRF seen in this patient. Early treatment and evidence of ongoing immune activation have contributed toward TRF.

Guillain-Barré Syndrome and Chronic Inflammatory Demyelinating Polyradiculoneuropathy in Pregnancy

2018 ◽  
Author(s):  
Pariwat Thaisetthawatkul ◽  
Eric Logigian
Keyword(s):  
Fetal Outcome ◽  
Chronic Inflammatory Demyelinating Polyradiculoneuropathy ◽  
Guillain Barre Syndrome ◽  
Progressive Muscle Weakness ◽  
Immune Mediated ◽  
Guillain Barré Syndrome ◽  
Viral Illness ◽  
Life Threatening ◽  
Depolarizing Agents ◽  
Guillain Barré

Guillain-Barré syndrome (GBS) and chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) are both immune-mediated diseases of the peripheral nervous system that typically present with symmetric, progressive muscle weakness, areflexia, and sensory symptoms or signs. GBS evolves rapidly with a nadir at 2–4 weeks usually with an antecedent viral illness, while CIDP progresses more slowly over months to years. GBS is sometimes complicated by life-threatening respiratory failure or dysautonomia. Onset of GBS and relapse of CIDP can occur during pregnancy or postpartum. But with appropriate supportive care and immunotherapy, maternal and fetal outcome in both conditions is typically excellent. The exception is fetal outcome in GBS triggered by maternal CMV or Zika infection transmitted to the fetus. Full-term vaginal delivery and regional anesthesia are preferred in maternal GBS and CIDP, but if C-section and general anesthesia are indicated, non-depolarizing agents such as succinylcholine should be avoided.

T cell responses to myelin proteins in Guillain-Barré syndrome

1992 ◽  
Vol 111 (2) ◽  
pp. 200-203 ◽  
Author(s):  
A. Khalili-Shirazi ◽  
R.A.C. Hughes ◽  
S.W. Brostoff ◽  
C. Linington ◽  
N. Gregson
Keyword(s):  
T Cell ◽  
T Cell Responses ◽  
Guillain Barre Syndrome ◽  
Myelin Proteins ◽  
Cell Responses ◽  
Guillain Barré Syndrome ◽  
Guillain Barré

Serial peripheral nerve ultrasound in Guillain–Barré syndrome

2016 ◽  
Vol 127 (2) ◽  
pp. 1652-1656 ◽  
Author(s):  
Siti Nur Omaira Razali ◽  
Thaarani Arumugam ◽  
Nobuhiro Yuki ◽  
Faizatul Izza Rozalli ◽  
Khean-Jin Goh ◽  
...  
Keyword(s):  
Peripheral Nerve ◽  
Guillain Barre Syndrome ◽  
Nerve Ultrasound ◽  
Guillain Barré Syndrome ◽  
Guillain Barré

scholarly journals Guillain-Barré syndrome following Zika virus infection is associated with a diverse spectrum of peripheral nerve reactive antibodies

2021 ◽  
Author(s):  
Alexander J Davies ◽  
Cinta Lleixà ◽  
Ana M Siles ◽  
Dawn Gourlay ◽  
Georgina Berridge ◽  
...  
Keyword(s):  
Peripheral Nerve ◽  
Zika Virus ◽  
Target Identification ◽  
Guillain Barre Syndrome ◽  
Igg Antibody ◽  
Humoral Immune ◽  
Cellular Models ◽  
Inflammatory Neuropathy ◽  
Guillain Barré Syndrome ◽  
Guillain Barré

Introduction Recent outbreaks of Zika virus (ZIKV) in South and Central America have highlighted significant neurological side effects. Concurrence with the inflammatory neuropathy Guillain-Barré syndrome (GBS) is observed in 1:4000 ZIKV cases. Whether the neurological symptoms of ZIKV infection are a consequence of autoimmunity or direct neurotoxicity is unclear. Methods We employed rat dorsal root ganglion (DRG) neurons, Schwann cells (SCs), and human stem cell-derived sensory neurons myelinated with rat SCs as cellular models to screen for anti-peripheral nerve reactive IgG and IgM autoantibodies in sera of ZIKV patients with and without GBS. In this study, 52 ZIKV-GBS patients were compared with 134 ZIKV-infected patients, and 91 non-ZIKV controls. Positive sera were taken forward for target identification by immunoprecipitation and mass spectrometry, and candidate antigens validated by ELISA and cell-based assays. Autoantibody reactions against glycolipid antigens were also screened on an array. Results Overall, IgG antibody reactivity to rat SCs (6.5%) and myelinated co-cultures (9.6%) were significantly higher, albeit infrequently, in the ZIKV-GBS group compared to all controls. IgM antibody immunoreactivity to DRGs (32.3%) and SCs (19.4%) was more frequently observed in the ZIKV-GBS group compared to other controls, while IgM reactivity to co-cultures was as common in ZIKV and non-ZIKV sera. Strong axonal-binding ZIKV-GBS serum IgG antibodies from one patient were confirmed to react with neurofascin-155 and 186. Serum from a ZIKV non-GBS patient displayed strong myelin-binding and anti-lipid antigen reaction characteristics. There was however no significant association of ZIKV-GBS with any anti-glycolipid antibodies. Conclusion Autoantibodies in ZIKV associated GBS patient sera target heterogeneous peripheral nerve antigens suggesting heterogeneity of the humoral immune response despite a common prodromal infection.

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