A web-based videoconferencing approach to training caregivers in rural areas to compensate for problems related to traumatic brain injury.

OBJECTIVE: To describe the development and the implementation of a Web-based, videoconferencing training program for caregivers of adults with traumatic brain injury in rural areas to manage cognitive and behavioral changes in the person with the injury. DESIGN: Feasibility study, with satisfaction and perceived utility assessed. INTERVENTION: Six Web-based videoconference sessions, combining didactic education and interactive problem-solving. PARTICIPANTS: Fifteen caregivers of persons with complicated mild, moderate, or severe traumatic brain injury, who were admitted to a level III trauma center in a rural area of Texas. MEASURES: Satisfaction survey and perceived utility questions conducted immediately following training and at an average of 18 months after training. RESULTS: Participants' overall satisfaction and comfort with the training was high. They perceived that they gained knowledge that was applicable to the everyday problems being experienced. At follow-up, all participants reported having used the knowledge gained to help cope with problems and all had referred to the written materials at least once since the training. CONCLUSIONS: Web-based videoconferencing can be used to provide training to caregivers to manage cognitive and behavioral problems resulting from traumatic brain injury. However, there are obstacles related to willingness to seek help among persons in rural areas that must be overcome.

Role of GABAergic antagonism in the neuroprotective effects of bilobalide.

Bilobalide, a constituent of Ginkgo biloba, has neuroprotective properties. Its mechanism of action is unknown but it was recently found to block GABA(A) receptors. The goal of this study was to test the potential role of a GABAergic mechanism for the neuroprotective activity of bilobalide. In rat hippocampal slices exposed to NMDA, release of choline indicates breakdown of membrane phospholipids. NMDA-induced choline release was almost completely blocked in the presence of bilobalide (10 microM) and under low-chloride conditions. Bicuculline (100 microM), a competitive antagonist at GABA(A) receptors, reduced NMDA-induced choline release to a small extent (-23%). GABA (100 microM) partially antagonized the inhibitory action of bilobalide. Exposure of hippocampal slices to NMDA also caused edema formation as measured by increases of tissue water content. NMDA-induced edema formation was suppressed by bilobalide and by low-chloride conditions. Bicuculline exerted partial protection (by 30%) while GABA reduced bilobalide's effect by about one third. To investigate bilobalide's interaction with GABA(A) receptors directly, we measured binding of [(35)S]-TBPS to rat cortical membranes. TBPS binding was competitively inhibited by bilobalide in the low micromolar range (IC(50)=3.7 microM). As a functional test, we determined (36)chloride flux in rat corticohippocampal synaptoneurosomes. GABA (100 microM) significantly increased (36)chloride flux (+65%), and this increase was blocked by bilobalide, but with low potency (IC(50): 39 microM). We conclude that, while antagonism of GABA(A) receptors may contribute to bilobalide's neuroprotective effects, additional mechanisms must be postulated to fully explain bilobalide's actions.