BACKGROUND: Recurrent Guillain Barre' syndrome (RGBS) is a rare condition and there is a paucity of clinical and neurophysiological studies. AIM: This study was undertaken to evaluate the clinical and neurophysiological changes in patients with recurrent GB syndrome and their outcome. METHODS: We report 11 patients with RGBS out of 200 patients with GB syndrome seen over last 10 years. These patients had 2 or more attacks of acute inflammatory demyelinating neuropathy with an onset to peak time of 4 weeks or less having complete or near complete recovery. All the patients underwent complete neurological evaluation. The disability was graded on a 0-10 clinical grading scale. Antinuclear antibody, rheumatoid factor C3, C4, urine test for porphyria, serum test for HIV and CSF examination were carried out in all the patients. Motor nerve conduction of median, ulnar, peroneal, F response and concentric needle electromyography were carried out in all. Sensory conduction of ulnar, median and sural, central motor conduction to abductor digiti minimi and tibialis anterior were also carried out. RESULTS: Patients' age ranged between 5 and 40 years and 6 were children. Eight patients had 2 attacks, 2 had 3 attacks and 1 had 4 attacks. The interval between attacks ranged between 4 months to 10 year (mean 39.5 month). The triggering events were noted in 7 patients and were identical to the previous event in 4 patients. Six patients had pure motor weakness, 4 had associated sensory symptoms and 1 had both sensory symptoms and signs. The severity of different attacks was not related to number of recurrences. Nerve conduction studies were consistent with demyelinating neuropathy. Central motor conduction was abnormal in 5 out of 7 episodes studied Eight patients recovered completely after initial attack and 3 had persistent foot drop at 6 month follow up. Following the second attack 4 patients recoveredfully and the remaining 7 had foot drop and in 2 there was mild proximal weakness as well. After the third attack 1 patient recoveredfully and the other 2 had residual deficit in the form of handgrip weakness and foot drop. There seems to be a tendency to accumulate neurological deficits with increasing frequency of attacks of GB syndrome.
BACKGROUND: Recurrent Guillain Barre' syndrome (RGBS) is a rare condition and there is a paucity of clinical and neurophysiological studies. AIM: This study was undertaken to evaluate the clinical and neurophysiological changes in patients with recurrent GB syndrome and their outcome. METHODS: We report 11 patients with RGBS out of 200 patients with GB syndrome seen over last 10 years. These patients had 2 or more attacks of acute inflammatory demyelinating neuropathy with an onset to peak time of 4 weeks or less having complete or near complete recovery. All the patients underwent complete neurological evaluation. The disability was graded on a 0-10 clinical grading scale. Antinuclear antibody, rheumatoid factor C3, C4, urine test for porphyria, serum test for HIV and CSF examination were carried out in all the patients. Motor nerve conduction of median, ulnar, peroneal, F response and concentric needle electromyography were carried out in all. Sensory conduction of ulnar, median and sural, central motor conduction to abductor digiti minimi and tibialis anterior were also carried out. RESULTS:Patients' age ranged between 5 and 40 years and 6 were children. Eight patients had 2 attacks, 2 had 3 attacks and 1 had 4 attacks. The interval between attacks ranged between 4 months to 10 year (mean 39.5 month). The triggering events were noted in 7 patients and were identical to the previous event in 4 patients. Six patients had pure motor weakness, 4 had associated sensory symptoms and 1 had both sensory symptoms and signs. The severity of different attacks was not related to number of recurrences. Nerve conduction studies were consistent with demyelinating neuropathy. Central motor conduction was abnormal in 5 out of 7 episodes studied Eight patients recovered completely after initial attack and 3 had persistent foot drop at 6 month follow up. Following the second attack 4 patients recoveredfully and the remaining 7 had foot drop and in 2 there was mild proximal weakness as well. After the third attack 1 patient recoveredfully and the other 2 had residual deficit in the form of handgrip weakness and foot drop. There seems to be a tendency to accumulate neurological deficits with increasing frequency of attacks of GB syndrome.