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Volume 3
Journal of Neurology and Clinical Neuroscience
Neurosurgery 2019 & Neuroimmunology 2019
May 22-23, 2019
Page 24
Neurosurgery and Neurological Surgeons
Neuroscience and Neuroimmunology
May 22-23, 2019 London, UK
6
th
Annual Meeting on
9
th
Global Summit on
&
J Neurol Clin Neurosci, Volume 3
Guillain-Barre Syndrome (GBS) andGBS-like Syndrome: Clinical, neuropathological and immunological
correlations
GBS is an auto-immune life-threatening inflammatory polineuropathy that
may produce severe functional disability. Vaccines, viral, fungine or bacterial
infections may trigger the disease. On the basis of neuropathological and
neurophysiological findings, GBS is classified in demyelinating and axonal
forms. In both features, functional disability is directly correlated to axonal
loss. Involvement of amyelinic axons is responsible for autonomic disturbances,
which, along with bulbar spread of the disease, represent a potential cause of
death in GBS. A consistent number of patients both in the early or recovery
phases may complain of neuropathic pain that requires an adequate treatment. Immunological aspect of the disease,
i.e auto-antibodies directed against GM1 (Gangliosidosis) and recently to contactin-associated protein 1 (Caspr) of the
paranodal region of myelinated nerves, have already been investigated. We have demonstrated that TNF-alpha (Tumor
Necrosis Factor) was immunolocalized in both myelinated and unmyelinated axons the sural nerve of GBS patients. We
concluded that this substance may be directly responsible for axonal loss( G.A. Putzu et al, J. Neurol Sci, 2000).
Interferon-gamma, which is a stimulator of IL28A was also easily detected in the sural nerve of GBS patients. The role
of adhesion molecules like ICAM in the immune process of GBS will be also discussed. The therapeutic approach of
GBS is aimed to avoid death in the acute phase (respiratory failure in Landry paralysis, cardiac rhythm anomalies in
disautonomia). The efficacy of plasmapheris and intravenous immunoglobulins in the treatment of GBS is nowadays
clearly demostrated. The next frontier is the theoretical possibility to use monoclonal antibodies (i.e, anti-INF Interferon-
gamma) as a therapeutic tool in GBS.
We also reviewed the literature on GBS-like conditions that may clinically mimick GB.
Biography
The Author is a Medical Doctor since 1992, with specialization in Paediatric Neurology. He achived his PhD in 1996. During PHD studies, He
was a Research Fellow in Hammersmith Hospital of London, UK in 1992, then He moved to Marseille (France) to work at INSERM (Genetics)
and in Neurophathology. The Author has published more than 15 papers in the field of Neuromuscular Disorders.
puzzugio@gmail.comGiovanni Antioco Putzu
Casa di Cura Sant’Elena, Quartu Sant’Elena, Italy
Immune localization of TNF-alpha on myelin and axons
in the sural nerve of acute GBS, double immunostaining
technique, longitudinal section,x 400