ORIGINAL ARTICLE How Different is AMAN from AIDP in Childhood GBS? A Prospective Study from North India Pradeep Kumar Gupta 1 & Pratibha Singhi 2 & Sunit Singhi 3 & Ananthanarayanan Kasinathan 4 & Naveen Sankhyan 5 Received: 14 February 2018 /Accepted: 6 December 2018 # Dr. K C Chaudhuri Foundation 2019 Abstract Objectives To compare the clinical profile and short-term outcome of children with axonal and demyelinating subtypes of childhood Guillain Barré syndrome (GBS). Methods This is a prospective observational study conducted in a tertiary care teaching hospital in North India. Consecutive children with Guillain Barré syndrome were recruited to compare the clinical profile and short term outcome among the subtypes. Results Among 9847 children admitted to the emergency, 95 had acute flaccid paralysis; 57 of whom had GBS. Electrophysiological studies were completed in 57; of whom 20 had acute inflammatory demyelinating polyneuropathy (AIDP); 19 had acute motor axonal neuropathy (AMAN); 12 had non-reactive nerves; five were unclassifiable; 1 had acute motor sensory axonal neuropathy (AMSAN). More children in AMAN group had preceding gastroenteritis (4 vs. 2), while AIDP group had upper respiratory infections (12 vs. 7). Ataxia was only seen in AIDP subtype while wrist drop, foot drop and hyperreflexia were seen only with AMAN subtype. Respiratory muscle involvement (6 vs. 3) and artificial ventilation (5 vs. 2) was more in AMAN. At discharge, children with AIDP were less likely to be non-ambulant (12 vs. 6, p = 0.036). Mean disability scores at hospital discharge (4.9 ± 1.2 vs. 4 ± 0.9, p = 0.015) and at last follow-up (0.7 ± 1.01 vs. 0.05 ± 0.2, p = 0.016) were higher in AMAN. Children with AIDP were more likely to achieve normalcy on follow-up (19 vs. 12, p = 0.023). Conclusions Children with AMAN appear to have a more severe clinical course; higher short-term morbidity; and slower recovery than those with AIDP. Keywords Acute inflammatory demyelinating polyneuropathy . Acute motor axonal neuropathy . Clinical features . Guillain-Barré syndrome . Neurophysiology Introduction Guillain Barré syndrome (GBS) is the leading cause of acute flaccid paralysis characterized by the archetypal description of Bsymmetrical, ascending paralysis with areflexia^. It has an estimated annual incidence of 1.34 cases per 100,000 in chil- dren less than 15 y of age [1]. Since the earliest depiction in France in 1916, GBS is regarded as a constellation of diverse clinical findings of peripheral nerve dysfunction secondary to post infectious inflammatory mechanism. Two-thirds of GBS have potent antecedent triggers such as Campylobacter jejuni, Cytomegalovirus, Mycoplasma, Varicella zoster and Hepatitis E. The best-known subtypes of GBS encompass acute inflam- matory demyelinating polyneuropathy (AIDP); acute motor axonal neuropathy (AMAN); acute motor sensory axonal neu- ropathy (AMSAN); Miller Fisher syndrome (MFS) and * Naveen Sankhyan drnsankhyan@yahoo.co.in 1 Department of Pediatrics, Siddhi Memorial Hospital, Kathmandu, Nepal 2 Pediatric Neurology and Neurodevelopment, Medanta, The Medicity, Gurugram, Haryana, India 3 Division of Pediatrics, Medanta, The Medicity, Gurugram, Haryana, India 4 Department of Pediatrics, Mahatma Gandhi Medical College and Research Institute, Sri Balaji Vidyapeeth University, Puducherry, India 5 Pediatric Neurology Unit, Department of Pediatrics, Advanced Pediatrics Centre, Postgraduate Institute of Medical Education and Research, Chandigarh 160012, India The Indian Journal of Pediatrics https://doi.org/10.1007/s12098-018-2835-5