ABSTRACT
BACKGROUND: The protective effect of excitatory amino acid antagonists for CA3 hippocampal neuronal loss has been well documentated. From a clinical point of view, however, alternative therapies should also be explored because excitatory amino acid antagonists have relatively deleterious side effects. Administration of lecithinized superoxide dismutase (PC-SOD) has recently been demonstrated to reduce brain edema after traumatic brain injury (TBI) in the cerebral cortex. In this study, we investigated the effectiveness of PC-SOD on CA3 hippocampal cell loss by examining hematoxylin and eosin-stained sections. METHODS: Rats were divided at random into three groups. The first group received 1 mL of saline (contusion + saline group, n = 5). Rats of the second group were treated with 3000 IU/kg of PC-SOD (contusion + SOD 1 group, n = 5), while the third group received 5000 IU/kg of PC-SOD (contusion + SOD 2 group, n = 5). All agents were administered intraperitoneally 1 minute after traumatic insult and every 24 hours until 2 or 3 days post-TBI. Animals were sacrificed 3 or 7 days after contusion injury. RESULTS: PC-SOD prevented CA3 neuronal loss 3 days after TBI, and increased the number of surviving CA3 neurons 7 days after TBI. CONCLUSION: Our findings suggest that PC-SOD may serve as a pharmacological agent in the treatment of neuronal loss after TBI.
Subject(s)
Brain Injuries/complications , Brain Injuries/drug therapy , Hippocampus/drug effects , Hippocampus/injuries , Nerve Degeneration/etiology , Nerve Degeneration/prevention & control , Phosphatidylcholines/therapeutic use , Superoxide Dismutase/therapeutic use , Animals , Brain Injuries/pathology , Cell Count , Disease Models, Animal , Dose-Response Relationship, Drug , Drug Administration Schedule , Hippocampus/pathology , Male , Nerve Degeneration/pathology , Phosphatidylcholines/administration & dosage , Rats , Rats, Sprague-Dawley , Superoxide Dismutase/administration & dosage , Time FactorsABSTRACT
The authors present three cases of refractory chronic subdural hematoma (CSDH) treated by embolization of the middle meningeal artery (MMA) after several unsuccessful drainage procedures. The patients were initially treated by the usual method of burr hole and irrigation of the hematoma. After recurrence, several percutaneous puncture and drainage procedures were unable to prevent re-collection of the hematoma. Then the authors embolized the MMA which was thought to be the feeding artery of the outer membrane of the hematoma cavity. No enlargement of the hematoma was seen after embolization and, gradually, complete resolution of the hematoma was obtained. The outcome of the patients was excellent in all three cases. This new therapeutic approach to recurrent CSDH is discussed.
