Abstract
Introduction. Guillain Barre Syndrome (GBS) is a post infectious polyneuropathy involving mainly motor but sometimes sensory and autonomic nerves. It is an acquired disease of the peripheral nerves that is characterized by rapidly progressing paralysis, areflexia and albumino-cytological dissociation in CSF. Methodology: Prospective, descriptive, observational, hospital based study was carried out to find out the clinico-epidemiological features of GBS including existing treatment modalities and its outcome. All cases fulfilled the criteria for AFP (Acute flaccid Paralysis) surveillance was included. Cases were reviewed for full medical history and examinations. To confirm the diagnosis, necessary investigations were carried out and combined with clinical symptoms. Results: Thirty patients were included in the study during study period. Among them 90% were diagnosed as GBS, 7.4% patients of GBS were associated with hypokalemic paralysis, 7.4% diagnosed as transverse myelitis and 3.7% diagnosed as idiopathic neuropathy. Different types of GBS were classified as AIDP (Acute inflammatory demyelinating polyneuropathy) 62.96%, AMAN (Acute motor axonal neuropathy) - 25.52%, AMASAN (Acute motor and sensory axonal neuropathy) - 3.3% and MFS (Miller fisher's syndrome) - 6.6% according to NCV result. Male female ratio is 1.7:1.0. There was 14.8% patients had relapse within 5 year. Associated diseases were URTI, pneumonia, sore throat and diarrhea. Facial Nerve palsy was commonest cranial nerve involvement.Sixty percentage of patients presented with sensory symptoms. There was transient bowel and bladder involvement in 20% of the cases. 69.2% patients became bed ridden at the nadir. There was albumin-cytological dissociation in 80% case. Majority of patients improved with supportive treatment alone, 19.5% patient required ventilator support among them 40% died. 7.4% of cases expired during treatment. Half of the patients fully recovered within 3 months. Conclusion: GBS is the commonest cause of AFP, AIDP being commonest subtype in our setting. We have to improve our existing treatment facilities and extend to different centers to detect and treat GBS. Most of the patients improve with supportive treatment alone. Ventilator support indicates grave prognosis. Key words: GBS (Gullein Barre Syndrome); AFP (Acute flaccid Paralysis); AIDP (Acute inflammatory demyelinating polyneuropathy; AMAN (Acute motor axonal neuropathy); AMASAN (Acute motor and sensory axonal neuropathy); MFS (Miller fisher's syndrome). DOI: 10.3126/jnps.v31i2.4065 J Nep Paedtr Soc 2010;31(2):93-97
Highlights
Guillain Barre Syndrome (GBS) is a post infectious polyneuropathy involving mainly motor but sometimes sensory and autonomic nerves
A comprehensive pathological account of GBS was that of Haymaker & Kernohan (1949) who stressed that edema of the peripheral nerves was the important changes in the early stage of disease[3]
Among them 27 (90%) were diagnosed as GBS, 2 (7.4%) patients of GBS were associated with hypokalemic paralysis, 2 patients (7.4%) diagnosed as transverse myelitis and 1 patient (3.7%) diagnosed as idiopathic neuropathy
Summary
Guillain Barre Syndrome (GBS) is a post infectious polyneuropathy involving mainly motor but sometimes sensory and autonomic nerves. Guillain Barre Syndrome (GBS) is a post infectious polyneuropathy involving mainly motor but sometimes sensory and autonomic nerves[1].GBS is an acquired disease of the peripheral nerves that is characterized clinically by rapidly progressing paralysis, areflexia and albumino-cytological dissociation[2]. Earliest description of this disease is probably that of Word Rob and Oliver in 1834, but the syndrome as first described in 1859 by Jean Baptiste Octave Landry, who identified. The watershed development in the last decade, has been the characterization of variants of GBS and recognition of pathological association of campylobacter jejuni infection with the motor axonal form of GBS3
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