Figure 2

pS6 in FCD subtypes. FCD II: (A) Intense labelling was confirmed in dysmorphic neurones in FCDIIa and FCD IIb (B) as anticipated, highlighting the tigroid appearance of the cytoplasm (B). Dysmorphic neurones were also intensely positive with pS6 235/6 (C), although the cytoplasm of balloon cells appeared somewhat weaker. (D) Double labelling of pS6 with DCX confirmed the balloon cells as pS6 positive, with some balloon cells co-labelling with DCX (arrowhead, inset); small DCX bipolar cells were not always pS6 labelled (arrow) and wrapping of a DCX-positive cell processes around a pS6-positive balloon cell (inset) was also noted. FCD IIIa: (E) FCD type IIIa (adjacent to HS) with laminar neuronal loss demonstrated with NeuN labelling and clusters of neurones in layer II accompanied by mark superficial cortical gliosis (F); in these cases labelling of the residual neurones in layer II with pS6 ser 235/6 (G) and pS6 ser 240/244 (H) was noted. Double labelling studies confirmed co-localisation of pS6 240/244 with GFAPdelta isoform in the cortex (I) and white matter (J) and between nestin and pS6 235/6 in small glial cells particularly in perivascular regions (K), as well as focally between DCX-positive small cells and pS6 235/236 (L). FCD IIIb: pS6 highlighted intense labelling of scattered cortical neurones in adjacent dyslaminar cortex, as well as neurones trapped within the tumour (inset), but negative labelling of the small tumour cells (M). FCDIIId: Disrupted cortex adjacent to an old perinatal infarct in this case showed a prominent ‘tramline’ labelling pattern of pyramidal cells (N); inset shows prominent labelling of astroglial cells in the region of chronic cortical scarring in an FCD IIId case. Bar in A, B, C, D, I, J, K and L equivalent to approximately 35 microns, in e,f,g,h and m to 50 microns and in n to 100 microns.