Objective To evaluate the therapeutic effect of vitrectomy on bullous retinal detachment. Methods The clinical data of 7 patients (9 eyes) with bullous retinal detachment who had undergone vitrectomy due to useless photocoagulation were retrospectively analyzed. Bullous retinal detachment of the patients had been diagnosed by examination of slit-lamp microscope, three-mirror gonioscope, indirect ophthalmoscope, B-mode ultrasound, and fundus fluorescein angiography. All of the affected eyes underwent vitrectomy with closed triple incisions through the pars plana after release of subretinal liquid under the local anaesthesia. The cortex of vitreous body was taken out, and exsuction of subretinal liquid was carried out via retinal incision. Photocoagulation closed the incision and the effusion area of the retina, and intraocular filling matter was injected after exchange of air and liquid. The follow-up period lasted 3 months to 8 years with the average period of 47 months. Results Reattached retina was found in all of the affected eyes during the follow-up period. One eye underwent a second vitrectomy due to local retinal redetachment caused by a new retinal hole formed by the pull of pre-retinal proliferative membrane and a silicon vesicle entered the subretinal space, but the retina reattached after 1-year follow-up examination. The visual acuity impr oved in different degree after the operation in 8 eyes, but remained unchanged in 1 eye. Conclusion Vitrectomy for terminal bullous retinal detachment may promote the reattachment of retina safely and effectively, and save partial visual acuity of the affected eyes. (Chin J Ocul Fundus Dis, 2006, 22:299-301)
Epilepsy is a complex disease spectrum, because of long-term recurrent seizures and seriously affect the quality of life of patients, it is of great significance to explore the pathogenesis of epilepsy and actively seek new therapeutic targets. In this paper, the pathogenesis of epilepsy related to mitochondrial pathway was discussed from the aspects of energy depletion, oxidative stress damage, impaired calcium homeostasis, increased glutamic acid release, mitochondrial DNA mutation, Coenzyme Q10 deficiency, abnormal mitochondrial movement and change, and relevant therapeutic ideas were proposed. This paper shows that mitochondrial function affects the onset of epilepsy from various ways. Further understanding of the relationship between mitochondria and the onset of epilepsy is beneficial to find new therapeutic targets and develop new therapies beyond the control of epilepsy.