Text in Afrikaans / In this study an instrument is suggested for implementation by the Educational Psychologist to design a support programme, aimed at handling family members' stress where a child has sustained a brain injury. Attention was paid to the phenomenon "brain injured child" to ascertain demands and needs (physical, cognitive, psychological and emotional). Specific note was taken of the toll on each family member in their observance, experience, assistance and giving· meaning to the child. Reference was made to existing support programmes for such family members from the acute care phase to the final acceptance and readjustment of the family. With this study the need for a continuous support programme and the contents of such a programme was addressed. Using these guidelines the Educational Psychologist will be able to prepare the family for the stress possibilities in dealing with the brain injured child. / Met hierdie studie is 'n instrument daargestel vir die ontwerp van 'n hulpverleningsprogram vir gebruik deur die Opvoedkundige Sielkundige. Hierdie hulpprogram het as doel, die hantering van stres, deur die gesin van 'n kind, wat 'n breinbesering opgedoen het. In die studie is aandag gegee aan die tipiese gedrag wat oor die algemeen van 'n breinbeseerde kind verwag kan word. Daar is ook gepoog om te bepaal hoe elke lid van die gesin die breinbeseerde kind beleef, aan hom betekenis gee, en hom probeer help ten opsigte van die eise (fisiek en emosioneel) wat hy stel. Verder is daar gekyk na bestaande hulpverlening (gerig op die hantering van stres) aan die gesinslede van 'n breinbeseerde kind vanaf die akute versorgingsfase tot en met die aanpassing en herorganisering van die gesin. Met hierdie studie is 'n behoefte aan 'n kontinue hulpverleningsprogram en die inhoud van so 'n program by gesinslede aangespreek. Aan die hand van die riglyne sal die Opvoedkundige Sielkundige 'n gesin kan voorberei op die stres wat hulle ten opsigte van die hantering van 'n breinbeseerde kind te wagte kan wees. / Psychology of Education / M. Ed. (Voorligting)

Indiana University-Purdue University Indianapolis (IUPUI) / Posttraumatic epilepsy, the development of temporal lobe epilepsy (TLE) following traumatic brain injury, accounts for 20% of symptomatic epilepsy. Reorganization of mossy fibers within the hippocampus is a common pathological finding of TLE. Normal mossy fibers project into the CA3 region of the hippocampus where they form synapses with pyramidal cells. During TLE, mossy fibers are observed to innervate the inner molecular layer where they synapse onto the dendrites of other dentate granule cells, leading to the formation of recurrent excitatory circuits. To date, the molecular mechanisms contributing to mossy fiber sprouting are relatively unknown. Recent focus has centered on the involvement of tropomycin-related kinase receptor B (TrkB), which culminates in glycogen synthase kinase 3β (GSK3β) inactivation. As the neurite outgrowth promoting collapsin response mediator protein 2 (CRMP2) is rendered inactive by GSK3β phosphorylation, events leading to inactivation of GSK3β should therefore increase CRMP2 activity. To determine the involvement of CRMP2 in mossy fiber sprouting, I developed a novel tool ((S)-LCM) for selectively targeting the ability of CRMP2 to enhance tubulin polymerization. Using (S)-LCM, it was demonstrated that increased neurite outgrowth following GSK3β inactivation is CRMP2 dependent. Importantly, TBI led to a decrease in GSK3β-phosphorylated CRMP2 within 24 hours which was secondary to the inactivation of GSK3β. The loss of GSK3β-phosphorylated CRMP2 was maintained even at 4 weeks post-injury, despite the transience of GSK3β-inactivation. Based on previous work, it was hypothesized that activity-dependent mechanisms may be responsible for the sustained loss of CRMP2 phosphorylation. Activity-dependent regulation of GSK3β-phosphorylated CRMP2 levels was observed that was attributed to a loss of priming by cyclin dependent kinase 5 (CDK5), which is required for subsequent phosphorylation by GSK3β. It was confirmed that the loss of GSK3β-phosphorylated CRMP2 at 4 weeks post-injury was likely due to decreased phosphorylation by CDK5. As TBI resulted in a sustained increase in CRMP2 activity, I attempted to prevent mossy fiber sprouting by targeting CRMP2 in vivo following TBI. While (S)-LCM treatment dramatically reduced mossy fiber sprouting following TBI, it did not differ significantly from vehicle-treated animals. Therefore, the necessity of CRMP2 in mossy fiber sprouting following TBI remains unknown.