Guillain-Barre Syndrome (GBS

Guillain-Barre’ Syndrome (GBS) is a common cause of acute onset weakness. It is an immune-mediated disease that is usually preceded by gastrointestinal or respiratory tract infection in most of the cases. Various pathogens like Mycoplasma pneumonia, Campylobacter jejuni, Epstein Bar virus and Cytomegalovirus are involved in its pathogenesis and immune response directed against these organisms may cross react with myelin sheath and other neural tissues causing weakness.1 it occurs in whole world with various proportions in all seasons. The incidence varies between 0.4-1.7 cases per 100,000 persons in one year.1
Core clinical feature of GBS is rapidly progressive ascending weakness starting from lower limbs in the most of cases. Maximum weakness is reached within 2-4 weeks from the onset of illness.2 After reaching maximum weakness, patients may have a plateau phase of disease lasting from several days to weeks or many months. This phase is followed by slower recovery phase of illness of varying duration of several months to years. Half of patients may have different cranial nerves involvement. In Europe, about a third of patients with GBS are mildly affected and they keep on walking with mild difficulty.3 Combination of rapidly progressive weakness in legs and arms, areflexia/hyporeflexia and protein cell
Other cranial nerves like bulbar abducent and oculomotor nerves are less often affected.5 Miller Fisher Syndrome is a clinical variant of GBS in which patients may have a triad of ataxia, areflexia and ophthalmoplegia.6,7 Brainstem (Bickerstaff) encephalitis is another overlapping syndrome that presents with sudden onset of weakness having multiple cranial or peripheral nerve involvement. Later on disturbances of consciousness and even coma may occur in the course of this disease. Recognition of this disease is important, because this illness may improve after the start of