Our study showed men are more likely to have GBS than women which was consistent with most of the GBS studies[14-16]. GBS can affect people of all ages, but majority of patients were below the age of 40 years. Our result was similar to an Indian study showing high prevalence below 40 years and only few patients were above 50 years[17]. Similarly, a Northern Chinese study has also reported younger age-group GBS patients have higher incidence than elderly population[18]. In contrast to this, few studies reported the increase in incidence of GBS with age and rate is high among those are 50 years and above[19]. British studies has reported a bimodal peak of incidence among 2 age-groups 15-24 years and 65-74 years [20].
Histologically, GBS can be classified into two types of neuropathy: axonal and demyelinating. Neurophysiological study further can distinguish different patterns of axonal or demyelinating neuropathy. AIDP is reported as most common variants in western countries (80-90%) while 20-40% in Asian countries like Japan, China and India[21]. Our study results are consistent with most other Asian studies as demyelinating and axonal variants was 30% and 70% respectively[2, 5, 22]. Incidence of MFS is often less frequently reported in previous studies [23, 24], as no MFS patients were reported during our study period.
Typical clinical manifestations of GBS are: monophasic, rapidly progressive limb weakness with symmetricity, and absence or reduced tendon reflexes. Deep tendon reflexes have been reported to be preserved in some cases of AMAN variant [2]. All of the GBS patients of our study satisfied those typical clinical presentations except 1 patient of AMAN variant had preserved tendon reflexes during the emergency presentation in 48 hours, it got gradually reduced in next 48 hours. Most of our GBS patients had ascending pattern of weakness, but 2 patients (4.3%) had descending pattern, and 3 patients (6.5%) had simultaneous pattern of onset. An Indian study reported GBS patients had similar pattern of weakness with simultaneous involvement of upper and lower limbs was reported in 27.1% and descending pattern of weakness in 6.8% [15]. Facial palsy was seen in more than half of the GBS patients and bilateral weakness pattern was seen in most of them which was consistent with previous studies[25, 26]. Bulbar and neck muscles weakness were other important presenting features in our GBS patients and were also reported in previous studies[22, 25]. Although sensory symptoms are not usually disabling in GBS, it is one of the presenting complain in most patients[1]. Three-fourth of our patients had some sensory symptoms during admission. Dysautonomia, an important cause of death in GBS and is commonly associated with patients of severe limb weakness or bulbar involvement [27, 28]. Axonal variants which are the severe form of GBS are likely to have more risk of having dysautonomia[29]. Similar to our finding, Dysautonomia is a common manifestation seen in GBS in other studies, but no specific correlation with axonal pattern has been studied [6, 30].
Increase in CSF protein is one of the important supportive factor for diagnosis of GBS. But only 50% patient might show some slight increase in 1st week, and subsequently protein elevation is seen after 1st week[6]. Since lumbar puncture was done in range of 5-15 days, 54% of CSF protein were in normal range. Some of the studies has reported up to 80-95% of CSF protein elevation in GBS patients[17, 31, 32]. A recent Iranian study has reported CSF protein elevation in 20% of their patient, but the duration of CSF analysis and disease onset has not been specified[33]. Link et al found that leukocyte counts may increase between 10 days to 4 months and gradually normalizes later[34]. But all of our patients had cell counts in normal range. CSF findings may change over time in GBS patients which might confuse the treating physician suggesting judicious management is warranted correlating with clinical findings[35].
Western studies have higher AIDP incidence, whereas axonal variants in most Asian studies[2, 4]. In this current study, we also found predominant axonal variants, AMAN being the commonest variant. Nerve conduction studies were done between 1 and 3 weeks of symptoms onset and all of the patients showed patterns correlating with one of the GBS variants. Kokubun et al found that conduction studies done in early period might show majority with equivocal reports, but few weeks later axonal variants will be predominant[13]. Axonal variants present as reversible conduction block during early period which shows the importance of follow-up neurophysiological evaluation. Hadden et al also studied about repeat conduction studies at 5 weeks and found Wallerian like degeneration might be the reason for transformation of demyelinating to axonal variant later[21]. However, there were also cases of axonal pattern which transformed in to demyelinating pattern and the above hypothesis couldn’t explain it clearly. An Iranian study reported that sensory amplitude is usually affected later than motor amplitude resulting in sensory involvement is lately found[32].
Feasby et al found that axonal variants were found to be clinically severe than demyelinating variants[36]. Our study also showed axonal variants were found to be clinically more severe than demyelinating group with high ODSS and GBS disability score both at nadir and discharge. Among GBS variants, AMAN was found to have higher GBS disability score than AIDP. During discharge, both ODSS and GBS disability score of AMAN were significantly higher than AIDP. Delayed recovery in AMAN could be due to severe axonal loss[29, 36]. An early recovery in AIDP patients was found which could be due to demyelination without severe secondary axonal injury[5]. However, Mitsui et al and Ho et al didn’t find any difference in clinical outcome between axonal and demyelinating variants[37, 38].
Previous studies had shown that poor prognosis was associated with older age, antecedent diarrhea, need for mechanical ventilation, rapid onset of weakness and severe muscle weakness during admission[39, 40]. In age group comparison (<40 and ³ 40 years), no significant difference in clinical outcome reported till discharge and hospital stay duration was found. No significant difference was found among antecedent infections (acute gastrointestinal infection, upper respiratory tract infection and non-infective events) which was measured by ODSS and GBS disability score at discharge. In this current study, axonal variants were more prone to need for mechanical ventilation than demyelinating variant, which was similar to an Indian study[6]. In contrast to our findings, a French study reported demyelinating variant as a predictor of need for mechanical ventilation [41].
It is a single center study and less number of patients were recruited, but none of them were lost to follow-up. Other GBS variants besides AMAN, AMSAN and AIDP couldn’t be recruited in our study. We didn’t repeat nerve conduction study in 4-6 weeks which could be an important predictor of long term outcome. Laboratories facilities to isolate organisms of antecedent infection and measurement of ganglioside antibodies are the other supportive means for the diagnosis of GBS which is not available at our center.