People interested in the research are advised to contact the author for the final version of the publication, or visit the DOI to the publisher's website.• The final author version and the galley proof are versions of the publication after peer review.• The final published version features the final layout of the paper including the volume, issue and page numbers. Link to publication General rightsCopyright and moral rights for the publications made accessible in the public portal are retained by the authors and/or other copyright owners and it is a condition of accessing publications that users recognise and abide by the legal requirements associated with these rights.• Users may download and print one copy of any publication from the public portal for the purpose of private study or research. • You may not further distribute the material or use it for any profit-making activity or commercial gain • You may freely distribute the URL identifying the publication in the public portal.(dorsal hemisection T13-L1) of adult rats has only marginal effects on severed axons (i.e. corticospinal axons were found more closely to the lesion site, but not not cross the lesion). This lack of axon regeneration could, however, be related to the characteristics of the scaffold material; the break-down products of poly(D,L)-lactide are acidic which may be detrimental for good integration of the scaffold within the spinal cord lesion; also the matrices used only supported seeding OEC on the matrix surface leaving the grafted cells directly exposed to the toxic environment of the injured spinal cord (Deumens 2006a). (Human) neural stem cellsAnother promising cell-based therapy for repair of the injured spinal cord involves (human) neural stem cells. These cells have the potential to provide cell-replacement for both neurons and glia.However, it has been -and still can be-a main problem that neural stem cells tend to mostly differentiate into astrocytes, which, in some cases, can support neuronal hyperexcitability (Hofstetter 2005, Martino 2006, Setoguchi 2004). Neuronal and oligodendroglia differentiation would certainly lead to better therapeutic effects of neural stem cell treatment (Abematsu 2010, Cummings 2005, Keirstead 2005). Neurons derived from neural stem cells are able to fully integrate into the host circuitry and their oligodendrocytes effectively remyelinate axons (Englund 2002, Keirstead 2005). Human fetal spinal cord derived neural stem cells (HSSC) grown in a monolayer, have shown to give rise to neurons, astrocytes, and oligodendrocytes in a rodent SCI model (Yan 2007). Furthermore, these HSSC were shown to be able to reduce spasticity (and improve locomotor function) after intraspinal grafting in a rodent SCI model of spasticity, which was attributed to their differentiation in inhibitory (γ-aminobutyric acid-ergic (GABA) and glycinergic neurons (Cizkova 2007). Lack of inhibition might be an important mechanism for neuronal hyperexcitability underlying pain and spasticity after SCI (Gwak 2011b). Furthermore, by impr...