9%). Weakness

(leg disability grade 5 or more and arm disability grade 3 or more) was seen in 40 (85.1%) patients, sensory symptoms in 19 (40.0%) patients, cranial nerve palsy in 15 (31.9%) patients and autonomic dysfunction in 7 (14.9%) patients. Twenty-seven (57.4%) patients needed mechanical ventilation. All patients received IVIG and 31 patients (66%) underwent plasmapheresis. There was no recorded mortality among patients studied. Table I shows the relationship between antiganglioside antibodies and electrodiagnosis findings. Patients with unclassified electrodiagnosis findings were further excluded from the rest of the study analysis. Fig. 1 shows distribution of patients in the study according to electrodiagnosis findings, Galunisertib clinical trial and antiganglioside antibodies results. Table II shows total and specific learn more IgG antiganglioside antibodies results

in both subtypes of GBS. Table III shows the clinical features in the AMAN compared with AIDP groups. Table IV shows the clinical features in the antiganglioside positive compared with negative patients. Table V shows the clinical features of GBS according to both the electrodiagnosis findings and the antiganglioside antibody positivity. In the present study, AMAN subtype constituted a major form of GBS in Egyptian children. Similar reports are found all over the world. In Asia, it is reported that AMAN is a major form of GBS, in Central and South America the frequency is 35–65% [11], [12] and [13]. In the present study, most of AMAN patients were antiganglioside antibody positive. On the other hand, most AIDP patients were seronegative. The strong correlation between antiganglioside antibodies and the subtype of GBS has been confirmed in previous studies [11], [14] and [15]. Similar to our study, previous studies found a correlation between GD1b antibody and AMAN subtypes [16], [17], [18], [19] and [20]. In another studies, it was anti-GD1a or anti-GM1 [21], [22] and [23]. Clinical presentation in antiganglioside positive patients was more frequently associated with severe motor weakness, which

necessitated mechanical ventilation and was also associated with antecedent diarrhea than the seronegative patients. Our findings confirmed that antiganglioside antibodies determine the ALOX15 clinical severity and the pathophysiology of GBS patients which was in accord with previous studies [6], [10], [23], [24] and [25]. Antiganglioside positive AIDP patients shared also many features with those with AMAN subtypes indicating that these antibodies play a significant role in determining the clinical features of GBS subtypes, this fact was confirmed with previous studies [11] and [17]. Out of 21 antiganglioside positive patients, 95% failed to respond to IVIG and responded well to plasmapheresis compared to only 41% of antiganglioside negative patients (P < 0.001). The exact mechanism is still debated and an ongoing challenge.