No abstract

Acute radiation injury leads to thymic involution, adrenal enlargement, leukopenia, thrombocytopenia, gastrointestinal ulceration, and impaired wound healing. The authors hypothesized that supplemental vitamin A would mitigate these adverse effects in rats exposed to acute whole-body radiation. This hypothesis was based on previous experiments in their laboratory that showed that supplemental vitamin A is thymotropic for normal rodents and lessens the thymic involution, lymphopenia, and adrenal enlargement that follows stress, trauma, and neoplasia, largely obviates the impaired wound healing induced by the radiomimetic drugs streptozotocin and cyclophosphamide, lessens the systemic response (thymic involution, adrenal enlargement, leukopenia, lymphocytopenia) to local radiation, and shifts the median lethal dose (LD50/30) following whole-body radiation to the right. To test their hypothesis, dorsal skin incisions and subcutaneous implantation of polyvinyl alcohol sponges were performed in anesthetized Sprague-Dawley rats at varying times following sham radiation or varying doses of whole-body radiation (175-850 rad). In each experiment, the control diet [which contains about 18,000 IU vit. A/kg chow (3 X the NRC RDA for normal rats)] was supplemented with 150,000 IU vit. A/kg diet beginning at, before, or after sham radiation and wounding or radiation and wounding. The supplemental vitamin A prevented the impaired wound healing and lessened the weight loss, leukopenia, thrombocytopenia, thymic involution, adrenal enlargement, decrease in splenic weight, and gastric ulceration of the radiated (750-850 rad) wounded rats. This was true whether the supplemental vitamin A was begun before (2 or 4 days) or after (1-2 hours to 4 days) radiation and wounding; the supplemental vitamin A was more effective when started before or up to 2 days after radiation and wounding. The authors believe that prevention of the impaired wound healing following radiation by supplemental vitamin A is due to its enhancing the early inflammatory reaction to wounding, including increasing the number of monocytes and macrophages at the wound site; possible effect on modulating collagenase activity; effect on epithelial cell (and possible mesenchymal cell) differentiation; stimulation of immune responsiveness; and lessening of the adverse effects of radiation.

We describe a 65-year-old man who had medically refractory craniofacial dystonia with blepharospasm (Meige syndrome) and spasmodic torticollis (video, part 1). Initial botulinum toxin injections had been discontinued because of adverse side effects and a loss of efficacy. After informed consent, the patient received bilateral pallidal electrodes for deep brain stimulation (DBS). With neurostimulation, symptoms nearly resolved (video, part 2), with sustained efficacy at 4-month follow-up. Our case is in line with the few anecdotal descriptions of treatment for Meige syndrome with pallidal DBS.1,2 Our case demonstrates the efficacy of bilateral pallidal DBS for Meige syndrome and spasmodic torticollis.1. Capelle HH, Weigel R, Krauss JK. Bilateral pallidal stimulation for blepharospasm-oromandibular dystonia (Meige syndrome). Neurology

Groups of healthy wounded rats with and without comminuted femoral fractures, and maintained on nutritionally complete commercial rat chow with and without supplemental vitamin A, were studied. The test wounds were standard dorsal skin incisions and s.c. polyvinyl alcohol sponge implants. In some experiments the rats were pair-fed; the rats with femoral fracture not receiving supplemental vitamin A were the lead group for determining food allowanced. In other experiments, the rats were allowed food ad libitum. We found that wound healing of rats with femoral fracture was increased when supplemental vitamin A was given, but the supplemental vitamin A did not completely obviate the adverse effects of fracture. The ratio of the breaking strengths of the skin incisions after formalin fixation to the breaking strengths of the incisions in the fresh state was higher in the unsupplemented rats, supporting the results of our earlier experiments that vitamin A increases the rate of collagen cross-linking.